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  • December 20, 2016
  • 04:33 AM
  • 277 views

Generation R does gestational vitamin D levels and autistic traits

by Paul Whiteley in Questioning Answers

"Gestational vitamin D deficiency was associated with autism-related traits in a large population-based sample. Because gestational vitamin D deficiency is readily preventable with safe, cheap and accessible supplements, this candidate risk factor warrants closer scrutiny."So said the findings reported by Vinkhuyzen and colleagues [1] (open-access) reporting on data derived from "the Generation R Study, a population-based prospective cohort from fetal life onward, based in Rotterdam, The Netherlands." I've talked about this study initiative before on this blog (see here) but this time around its scientific eyes turned towards the possibility that vitamin D - the sunshine vitamin/hormone - might have some important connections to the presentation of some of the facets of autism or at least autistic traits. Yes, yet again, vitamin D and autism comes into view (see here)...The Vinkhuyzen paper is open-access for all to see (and has already received some media exposure) but here are a few choice details:Hypothesis: explore "the association between gestational 25OHD concentrations and a widely used parent-report continuous measure of autism-related traits—the Social Responsive Scale (SRS)." Said levels of 25-hydroxyvitamin D (25OHD) (the functional unit of vitamin D assessment) were obtained from "maternal mid-gestation sera and from neonatal sera (collected from cord blood)." SRS scores relevant to offspring were provided by parents "when the children were ~6 years of age."Results: well, this certainly wasn't an under-powered study as data for "4229 children and their mothers were available with measures of vitamin D concentrations drawn from maternal blood at mid-gestation and/or drawn from cord blood at time of birth as well as data on the SRS, 2489 children and their mothers were available with measures of vitamin D concentrations at both time points." Approximately 16% of mothers were classed as deficient based on that mid-gestation serum sample rising to 36% when looking at cord blood samples. As I've mentioned before, issues with vitamin D generally fall into a few bandings associated with insufficiency and deficiency at the lower end of typical."In all analyses, 25OHD deficiency or lower 25OHD concentrations were associated with higher (more impaired) SRS scores." This was based on the use of an "18-item abridged version of the questionnaire" that specifically looked at "behavioural features related to social cognition, social communication and autistic mannerisms." Remember, this was a study looking at autistic traits not autism diagnoses. Interestingly too, authors were also able to restrict their analysis to "offspring with European ethnicity" and reported similar results associating lower vitamin D levels and higher SRS scores. This subgroup analysis perhaps ties into other research where ethnicity has been suggested to be a factor in relation to vitamin D levels and diagnosed autism (see here).So, there you have it. Yet more evidence linking vitamin D and autism and/or autistic traits; this on the back of my previous entry not-so-long-ago (see here) talking about supplementation as a potential means to affect presentation of at least some autism, with appropriate caveats (see here). It's getting increasingly difficult to say that there is 'no connection' between the two factors.Strengths of the Vinkhuyzen study? Well, as I said, it was big in terms of participant numbers. I note also the authors proudly announce: "We used a gold standard assessment of 25OHD concentrations" in light of the application of "isotope dilution liquid chromatography-tandem mass spectrometry." A gold star for the authors indeed in light of some 'chaos' when it comes to the hows and whys of measuring vitamin D status. Limitations: well, as per every study that looks at the association between a small number of variables, there are potentially a million and one other factors that might also account for the results. Another gold star is due for the authors' mention of the fact that vitamin D seems to be 'associated' with various diagnostic labels outside of rickets these days (see here for example) and hence one cannot rule out that traits or diagnoses not specifically covered by the study could have exerted some effect. More so when one considers how much autistic traits might not be just autism-specific traits (see here). I might also add that subsequent work could/should also be looking at the genetics of vitamin D metabolism not just functional levels of the stuff (see here).A final quote from the authors to close: "Just as prenatal folate supplementation has reduced the incidence of spina bifida, we speculate that prenatal vitamin D supplementation may reduce the incidence of ASD." I know such sentiments might not be welcomed by everyone, and the assumption that autistic traits are 'always a negative thing' needs some continued careful consideration. The ideas however that: (a) nutrition might impact on both psychology and physiology and (b) that where appropriate and/or where wanted, use of vitamin D supplement might impact on risk of autism or the presentation of autism, are ideas that are deserving of a lot more investigation.And again, minus any charges of clinical or medical advice being given on this blog (they're not), here is what the UK Government (or parts of the UK) are currently saying about vitamin D and the population as a whole...----------[1] Vinkhuyzen AA. et al. Gestational vitamin D deficiency and autism-related traits: the Generation R Study. Mol Psychiatry. 2016 Nov 29.----------Vinkhuyzen AA, Eyles DW, Burne TH, Blanken LM, Kruithof CJ, Verhulst F, Jaddoe VW, Tiemeier H, & McGrath JJ (2016). Gestational vitamin D deficiency and autism-related traits: the Generation R Study. Molecular psychiatry PMID: 27895322... Read more »

Vinkhuyzen AA, Eyles DW, Burne TH, Blanken LM, Kruithof CJ, Verhulst F, Jaddoe VW, Tiemeier H, & McGrath JJ. (2016) Gestational vitamin D deficiency and autism-related traits: the Generation R Study. Molecular psychiatry. PMID: 27895322  

  • December 19, 2016
  • 03:19 AM
  • 264 views

Gut barrier integrity meets blood-brain barrier integrity with autism in mind

by Paul Whiteley in Questioning Answers

"In the ASD [autism spectrum disorder] brain, there is an altered expression of genes associated with BBB [blood-brain barrier] integrity coupled with increased neuroinflammation and possibly impaired gut barrier integrity."Although pretty enthused to see research linking names like Anna Sapone, Tim Buie and Alessio Fasano in the recent paper published by Maria Fiorentino and colleagues [1] (open-access), I was slightly less impressed with the use of the term 'the ASD brain' in their paper potentially joining two concepts that I've been quite interested in down my research years: gut barrier and blood-brain barrier function in the context of autism. Yes, I accept that those most precious of resources, donated brains from the deceased, represented some of the 'material' under scientific scrutiny, but if science has learned anything about autism down the years, it is that sweeping generalisations such as terms like 'the autism brain' don't reflect what the existing research tells us about the heterogeneity under the label. I might just as well use the term 'blogger brain' to denote some of my activities, but such a label tells you nothing about me aside from my pastime.After that little rant, the paper from Fiorentino is an interesting one in that the goal was to "investigate whether an altered BBB and gut permeability is part of the pathophysiology of ASD." To do this, tissue from both brain and gastrointestinal (GI) tract donated by a small number of deceased and non-deceased participants who were diagnosed with autism, schizophrenia or nothing related (not-autism controls) were analysed "for gene and protein expression profiles." This work was undertaken on the basis of "the interconnectivity of the gut–brain axis, [that] suggests that inappropriate antigen trafficking through an impaired intestinal barrier, followed by passage of antigens or activated immune complexes through a permissive blood–brain barrier (BBB), can be part of the chain of events leading to neuroinflammation and thereby subsequent disease." I might add that the use of the word 'disease' in that sentence is, I think, aiming to describe the physiological effects of 'leaky barriers' not the diagnosis of autism. It is unfortunate however that 'disease' still continues to be banded around in the context of autism [2].I think it's important to stress that the Fiorentino study was in effect two studies: one that looked at brain samples from one participant group who had died, and one that looked at GI samples from those who were still living (at the time of sample collection) and who presented with "GI symptoms undergoing esophagogastroduodenoscopy (EGD) for clinically indicated reasons." This was not a study where biological samples - brain and gut - came from the same person but rather a mash-up. Keep that in mind for now. The sorts of genes that were focused in on were those "associated with the formation, integrity, and function of the BBB and neuroinflammation" and included the claudins and something called MMP-9 and MMP-2 that have been discussed previously on this blog (see here) with leaky barriers in mind. The key words are 'barrier integrity' when it comes to the list of compounds that were under inspection.Results: well it was good to see the authors list details of each of the participants from which tissue were used in their study. Brain tissue from the deceased with autism for example, is subject to quite a few factors that can influence the outcome of any results obtained; not least whether specific comorbidity accompanied their autism diagnosis and the nature of their death. Indeed, looking through the various case report numbers, I'm struck by how young many participants, particularly those diagnosed with autism, were at the time of their death. This ties into other discussions and debates (see here)."Our molecular analysis of the BBB integrity and function shows an altered BBB in the ASD subjects evaluated." This was evidenced by elevations in the gene expression of MMP-9 and its proposed connection to disturbances of BBB integrity. Further: "Of the four claudins (i.e., CLDN-1, -3, -5 and -12) that to date are thought to be incorporated in the BBB... we found that two were significantly more expressed in the ASD brain as compared in HC [healthy controls]." Once again I might suggest the term 'healthy controls' is not an inappropriate one when it comes to determining not-autism or not-schizophrenia.Then to analysis of those [independent] gut biopsy samples: "results, showing increased expression levels of pore-forming (66% of the ASD samples) and decreased levels of barrier-forming (75% of the ASD samples) TJ [tight junction] components in the duodenal samples, suggest an impaired gut barrier and serve as a proof of concept to support the hypothesis of a gut–brain axis dysfunction in a subgroup of ASD patients." So, those compounds linked to making the gut barrier more 'leaky' were seemingly increased in expression, and those linked to making the gut barrier less 'leaky' were reduced in quite a few of the samples from those diagnosed with autism. Mmm...There is quite a bit more science included in the Fiorentino study but I think I've gone on long enough in this post. Suffice to say that the whole gut-brain axis thing with autism in mind gets a boost but more work is indicated, not least with larger sample groups and perhaps combining tissues from gut and brain from the same person. I would also like to see a little more done on this topic with some 'interventions' in mind, based on the other autism research that potentially links the authors (see here). Drawing for example, on a paper written by Prof Fasano titled: 'Zonulin, regulation of tight junctions, and autoimmune diseases' [3] suggesting that "gliadin, a storage protein present in wheat and that triggers celiac disease in genetically susceptible individuals, also affect the intestinal barrier function by releasing zonulin" one might see how far from being a set-in-stone state of affairs, dietary changes for some on the autism spectrum, might actually set in motion a host of biological changes pertinent to this area of work. And such changes might not be just confined to accepted gluten-related conditions either...----------[1] Fiorentino M. et al. Blood–brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders. Molecular Autism. 2016; 7:49.[2] Simms MD. When Autistic Behavior Suggests a Disease Other than Classic Autism. Pediatr Clin North Am. 2017 Feb;64(1):127-138.[3] Fasano A. Zonulin, regulation of tight junctions, and autoimmune diseases. Annals of the New York Academy of Sciences. 2012;1258(1):25-33.----------... Read more »

Fiorentino, M., Sapone, A., Senger, S., Camhi, S., Kadzielski, S., Buie, T., Kelly, D., Cascella, N., & Fasano, A. (2016) Blood–brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders. Molecular Autism, 7(1). DOI: 10.1186/s13229-016-0110-z  

  • December 18, 2016
  • 05:45 AM
  • 260 views

Fusion and sex in protocells & the start of evolution

by Artem Kaznatcheev in Evolutionary Games Group

In 1864, five years after reading Darwin’s On the Origin of Species, Pyotr Kropotkin — the anarchist prince of mutual aid — was leading a geographic survey expedition aboard a dog-sleigh — a distinctly Siberian variant of the HMS Beagle. In the harsh Manchurian climate, Kropotkin did not see competition ‘red in tooth and claw’, […]... Read more »

Sinai, S, Olejarz, J, Neagu, IA, & Nowak, MA. (2016) Primordial Sex Facilitates the Emergence of Evolution. arXiv. arXiv: 1612.00825v1

  • December 17, 2016
  • 05:51 AM
  • 247 views

Pregnancy influenza infection not linked to offspring autism

by Paul Whiteley in Questioning Answers

"There was no association between maternal influenza [flu] infection anytime during pregnancy and increased ASD [autism spectrum disorder] risk."So said the findings reported by Ousseny Zerbo and colleagues [1] continuing a research theme from this author (see here for example) looking at how various infections 'encountered' during critical periods of pregnancy may / may not impact on offspring autism risk. This time around the focus was on viral infections and in particular "maternal influenza infection and vaccination from conception date to delivery date" as derived from either diagnosis using ICD-9 criteria or "a positive laboratory result for influenza based on the Prodesse ProFlu+ Assay (Hologic), a multiplex real-time polymerase chain reaction in vitro diagnostic test." Said participants numbering nearly 200,000 children were all born "at Kaiser Permanente Northern California from January 1, 2000 to December 31, 2010, at a gestational age of at least 24 weeks." The press release accompanying the publication can be seen here."Maternal influenza infection during pregnancy was not associated with increased ASD risk in this study, and the association did not vary by the timing of influenza infection." Importantly, authors also looked at whether maternal influenza vaccination during pregnancy was also related to offspring ASD risk based on the data contained in their patient databases. The results pertinent to pregnancy flu vaccination and offspring risk were not exactly cut-and-dried as "in an initial analysis unadjusted for multiple comparisons" the authors reported seeing a 'slightly increased' risk for offspring autism associated with maternal vaccination during the first few months of pregnancy. This was set against data indicating no significant association between maternal influenza vaccination covering 'anytime' during pregnancy. Indeed, after "adjusting for the multiplicity of hypotheses tested" they concluded that the first trimester vaccination - offspring autism risk was potentially a 'chance finding'. Minus any scaremongering and to be on the safe side the authors suggested that "additional studies are warranted to further evaluate any potential associations between first-trimester maternal influenza vaccination and autism."Aside from a few potential 'weakness' attached to the Zerbo results including the fact that "subclinical infections or illnesses for which women did not seek medical attention" were not counted in the data, these are interesting results. Quite a few times on this blog I've covered the so-called maternal immune activation (MIA) hypothesis - where mum's reprogrammed pregnancy immune system is 'challenged' and potentially has implications for offspring development - and this work kinda falls into that category of autism science. Indeed, I've talked about the possibility quite recently (see here). Drawing also on data looking at season of conception/birth as potentially being important to pregnancy viral/bacterial exposure and onward offspring outcomes (see here) there has been a steady stream of peer-reviewed publications hinting at a potentially important 'association' between infection exposure in-utero and developmental outcomes for the child. The current Zerbo data however put a bit of a research spanner in the works when it comes specifically to any pregnancy flu and offspring autism risk suggestion albeit with the continued requirement for further investigations in this area covering other infections.----------[1] Zerbo O. et al. Association Between Influenza Infection and Vaccination During Pregnancy and Risk of Autism Spectrum Disorder. JAMA Pediatr. 2016 Nov 28.----------Zerbo O, Qian Y, Yoshida C, Fireman BH, Klein NP, & Croen LA (2016). Association Between Influenza Infection and Vaccination During Pregnancy and Risk of Autism Spectrum Disorder. JAMA pediatrics PMID: 27893896... Read more »

  • December 16, 2016
  • 05:25 AM
  • 232 views

Patient participation in clinical trials

by Joana Guedes in BHD Research Blog

Clinical trials are crucial to help doctors and scientists understand how to safely treat a particular condition, to evaluate new treatments and to test drug safety and efficacy. They have an important role in every step of managing a condition with different clinical trials helping with prevention, diagnosis, treatments and follow-up support.... Read more »

  • December 16, 2016
  • 05:00 AM
  • 204 views

Friday Fellow: Common Stonewort

by Piter Boll in Earthling Nature

by Piter Kehoma Boll It’s always hard to introduce a less charismatic species here. Not because they are less interesting to me, but because I cannot find good information available. But I try to do my best to show all … Continue reading →... Read more »

Ariosa, Y., Quesada, A., Aburto, J., Carrasco, D., Carreres, R., Leganes, F., & Fernandez Valiente, E. (2004) Epiphytic Cyanobacteria on Chara vulgaris Are the Main Contributors to N2 Fixation in Rice Fields. Applied and Environmental Microbiology, 70(9), 5391-5397. DOI: 10.1128/AEM.70.9.5391-5397.2004  

  • December 16, 2016
  • 03:16 AM
  • 239 views

Non-febrile seizures in children with autism vs unaffected siblings

by Paul Whiteley in Questioning Answers

"Children with idiopathic ASD [autism spectrum disorder] are significantly more likely to have non-febrile seizures than their unaffected siblings, suggesting that non-febrile seizures may be ASD-specific."So said the findings from Lena McCue and colleagues [1] (open-access) continuing a research theme looking at one of the important 'comorbidities' that seems to be over-represented when it comes to a diagnosis of autism (see here). Idiopathic autism or ASD refers to autism as the primary diagnosis and not something tied to an existing condition where autism can also present. Non-febrile seizures are seizures without fever (where fever can very much result in seizures).McCue et al "conducted a secondary analysis of data from a registry-based retrospective cohort study of 731 children with ASD and their 192 children unaffected siblings from the AGRE project for whom phenotypic data were collected." Data from around 320 families with at least one child diagnosed with an ASD (n=610) were compared with sibling data (n=160) in relation to the presence of non-febrile seizures. Siblings (not autism) were chosen as the control group because "siblings share, on average, fifty percent of genes as well as the same environment" so perhaps providing an alternative to just general population control groups.Results: "The prevalence of non-febrile seizures in the ASD group was 8.2% (50/610) and 2.5% in the unaffected siblings (4/160)." What this tells us, aside from the increased frequency of non-febrile seizures in those children diagnosed with autism, is that so-called 'unaffected' siblings are not completely immune to seizures or seizure-linked conditions minus fever. Further: "the odds of having non-febrile seizures increased with age..., presence of GI [gastrointestinal] dysfunction..., and those with a history of febrile seizures had five times the odds of reporting non-febrile seizures."I was particularly interested in the observations that: (a) gastrointestinal (GI) dysfunction, denoting functional bowel issues such as constipation or diarrhoea, were pretty well over-represented among the children with autism in this cohort, similar to other research (see here) and (b) said GI issues might itself/themselves 'up' the risk of non-febrile seizures in relation to autism. In these days of the 'gut-brain axis' where the grey/pinkish matter floating in the skull might not be totally separate and independent from the more mucus-y matter situated in the torso (see here for example), it strikes me as important that further investigations be carried out on how epilepsy might not just be a 'brain-thing'. We have for example, evidence pertinent to an autoimmune connection to some epilepsy (see here) that has implications for other autoimmune conditions affecting the gut too as per the notion that 'birds of an autoimmune feather may flock together'. That also one of the primary 'treatments' for epilepsy not responsive to the usual anti-epileptic medicines is the ketogenic diet (see here) is something else to consider when talking about gut and brain potentially being quite close neighbours."Our study found a five-fold higher lifetime prevalence of non-febrile seizures in children with idiopathic ASD from largely multiplex families compared to their unaffected siblings. These findings suggest that the reported non-febrile seizures may be ASD-specific and cannot be explained by genetic predisposition alone." With that conclusion from the study authors, one might similarly also suggest that the presence of autism in affected children vs. siblings also cannot be explained by genetic predisposition alone...----------[1] McCue LM. et al. Prevalence of non-febrile seizures in children with idiopathic autism spectrum disorder and their unaffected siblings: a retrospective cohort study. BMC Neurology. 2016; 16:245.----------McCue, L., Flick, L., Twyman, K., Xian, H., & Conturo, T. (2016). Prevalence of non-febrile seizures in children with idiopathic autism spectrum disorder and their unaffected siblings: a retrospective cohort study BMC Neurology, 16 (1) DOI: 10.1186/s12883-016-0764-3... Read more »

  • December 15, 2016
  • 02:59 AM
  • 271 views

ADHD, not autism, might count when it comes to 'comorbid psychiatric symptomatology'

by Paul Whiteley in Questioning Answers

A quote to begin this fairly brief post: "Our study concluded that higher levels of ADHD [attention-deficit hyperactivity disorder] severity-not ASD [autism spectrum disorder] severity-were associated with a higher prevalence of comorbid psychiatric symptomatology in school-age children with ASD. These findings may encourage clinicians to thoroughly assess ADHD symptomatology in ASD children to better inform treatment planning."That was the research bottom line reported by Rosleen Mansour and colleagues [1] following their examination of how a pretty common comorbidity accompanying a diagnosis of autism (see here) might well play an important role in terms of other 'comorbid psychiatric symptomatology' among those with autism.I'm interested in these findings for several reasons. A diagnosis of autism does seem to elevate the risk of receipt of various other psychiatric diagnoses (see here for example). As I've just said, ADHD is a pretty common comorbidity when it comes to autism (see here). A diagnosis of ADHD (and not the medication commonly used to manage such symptoms) seems to elevate the risk of receipt of various other psychiatric diagnoses too (see here). It's not too difficult to suggest that autism per se might not be 'the most important variable' when it comes to at least some people's risk of other psychiatric diagnoses being received. Indeed, there is another potentially important strand of evidence to include in this proposal, in terms of the continued experiences of some of those who 'move off the autism spectrum ' (see here).More research is implied with one important question to answer about the nature of the synergy between autism and ADHD when it comes to any enhanced risk of psychiatric comorbidity...So, Rogue One finally sees the cinematic light of day...----------[1] Mansour R. et al. ADHD severity as it relates to comorbid psychiatric symptomatology in children with Autism Spectrum Disorders (ASD). Res Dev Disabil. 2016 Nov 24;60:52-64.----------Mansour R, Dovi AT, Lane DM, Loveland KA, & Pearson DA (2016). ADHD severity as it relates to comorbid psychiatric symptomatology in children with Autism Spectrum Disorders (ASD). Research in developmental disabilities, 60, 52-64 PMID: 27889487... Read more »

  • December 14, 2016
  • 08:40 PM
  • 196 views

ZIKV replication and the induction of p53: a tale of three places ?

by thelonevirologist in Virology Tidbits

Zika Virus (ZIKV) is a mosquitoe-borne Flavivirus (MBFV), related to other Flavivirus’ that are transmitted by mosquitoes such as Dengue Virus (DENV), Yellow Fever Virus (YFV) or Tick Borne Encephalitis Virus (TBEV) and as such the viral genome is released into the cytoplasm following viral entry and translated into a single polyprotein that is cleaved by both viral and cellular proteases into the 3 structural and 7 non-structural proteins.
Here the induction of p53 dependent apoptosis and cell cycle delay by ZIKV is discussed with an emphasis on the viral Capsid protein. ... Read more »

Li H, Saucedo-Cuevas L, Shresta S, & Gleeson JG. (2016) The Neurobiology of Zika Virus. Neuron, 92(5), 949-958. PMID: 27930910  

Vasilakis N, & Weaver SC. (2016) Flavivirus transmission focusing on Zika. Current opinion in virology, 30-35. PMID: 27936448  

Barreto-Vieira DF, Barth OM, Silva MA, Santos CC, Santos Ada S, F JB Filho, & Filippis AM. (2016) Ultrastructure of Zika virus particles in cell cultures. Memorias do Instituto Oswaldo Cruz, 111(8), 532-4. PMID: 27581122  

Li H, Saucedo-Cuevas L, Regla-Nava JA, Chai G, Sheets N, Tang W, Terskikh AV, Shresta S, & Gleeson JG. (2016) Zika Virus Infects Neural Progenitors in the Adult Mouse Brain and Alters Proliferation. Cell stem cell, 19(5), 593-598. PMID: 27545505  

Pingen M, Bryden SR, Pondeville E, Schnettler E, Kohl A, Merits A, Fazakerley JK, Graham GJ, & McKimmie CS. (2016) Host Inflammatory Response to Mosquito Bites Enhances the Severity of Arbovirus Infection. Immunity, 44(6), 1455-69. PMID: 27332734  

Agarwal A, Joshi G, Nagar DP, Sharma AK, Sukumaran D, Pant SC, Parida MM, & Dash PK. (2016) Mosquito saliva induced cutaneous events augment Chikungunya virus replication and disease progression. Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 126-35. PMID: 26925703  

Hewitt G, Carroll B, Sarallah R, Correia-Melo C, Ogrodnik M, Nelson G, Otten EG, Manni D, Antrobus R, Morgan BA.... (2016) SQSTM1/p62 mediates crosstalk between autophagy and the UPS in DNA repair. Autophagy, 12(10), 1917-1930. PMID: 27391408  

Danthi P. (2016) Viruses and the Diversity of Cell Death. Annual review of virology, 3(1), 533-553. PMID: 27501259  

Parquet MC, Kumatori A, Hasebe F, Morita K, & Igarashi A. (2001) West Nile virus-induced bax-dependent apoptosis. FEBS letters, 500(1-2), 17-24. PMID: 11434919  

Zhao P, Han T, Guo JJ, Zhu SL, Wang J, Ao F, Jing MZ, She YL, Wu ZH, & Ye LB. (2012) HCV NS4B induces apoptosis through the mitochondrial death pathway. Virus research, 169(1), 1-7. PMID: 22542667  

Netsawang J, Noisakran S, Puttikhunt C, Kasinrerk W, Wongwiwat W, Malasit P, Yenchitsomanus PT, & Limjindaporn T. (2010) Nuclear localization of dengue virus capsid protein is required for DAXX interaction and apoptosis. Virus research, 147(2), 275-83. PMID: 19944121  

Licon Luna RM, Lee E, Müllbacher A, Blanden RV, Langman R, & Lobigs M. (2002) Lack of both Fas ligand and perforin protects from flavivirus-mediated encephalitis in mice. Journal of virology, 76(7), 3202-11. PMID: 11884544  

Tudzarova S, Mulholland P, Dey A, Stoeber K, Okorokov AL, & Williams GH. (2016) p53 controls CDC7 levels to reinforce G1 cell cycle arrest upon genotoxic stress. Cell cycle (Georgetown, Tex.), 15(21), 2958-2972. PMID: 27611229  

Abraham AG, & O'Neill E. (2014) PI3K/Akt-mediated regulation of p53 in cancer. Biochemical Society transactions, 42(4), 798-803. PMID: 25109960  

  • December 14, 2016
  • 07:43 AM
  • 191 views

The spotted gar genome illuminates vertebrate evolution and facilitates human-teleost comparisons

by Christian de Guttry in genome ecology evolution etc

The spotted gar genome illuminates vertebrate evolution and facilitates human-teleost comparisons About 450 mya bony vertebrates radiated into Lobe-finned fish, from which tetrapods appeared later, and Ray-finned fish, which include Teleost (Fig.1). Nowadays they make up to 96 percent of … Continue reading →... Read more »

Braasch I, Gehrke AR, Smith JJ, Kawasaki K, Manousaki T, Pasquier J, Amores A, Desvignes T, Batzel P, Catchen J.... (2016) The spotted gar genome illuminates vertebrate evolution and facilitates human-teleost comparisons. Nature genetics, 48(4), 427-37. PMID: 26950095  

  • December 14, 2016
  • 03:07 AM
  • 240 views

Urinary metabolomics in autism turns up tryptophan (again)

by Paul Whiteley in Questioning Answers

"The tryptophan metabolic pathway collectively displays the largest perturbations in ASD [autism spectrum disorder]."So said the findings reported by Federica Gevi and colleagues [1] (open-access) who provide yet more 'metabolomic' data when it comes to autism to add to the already quite voluminous peer-reviewed matter on this topic (see here for example).Just in case you aren't analytical chemistry-saavy, metabolomics is basically the study of the various chemical fingerprints that the multitude of cellular processes going on in the body leave behind. It's the technology available these days that makes metabolomics the discipline that it is, as words such as mass spectrometry and nuclear magnetic resonance (spectroscopy) fill the metabolomic airwaves coupled with some rather smart statistics and software to translate all that captured data into something meaningful.Gevi et al report results based on the analysis of urine samples from a small-ish group of children diagnosed with an ASD ("idiopathic ASD") compared with samples from a similar number of not autism controls. The aim was to focus on "autistic and unrelated typically developing children 2–8 years old, tightly matched by age, sex, Italian ancestry, and city of origin within the country" and look-see whether a particular HPLC-mass spec technique "hydrophilic interaction chromatography (HILIC)-LC-electrospray ionization (ESI)-MS" might provide some important data on autism vs. not autism.Results: well, it's always nice to get a research mention in such studies as per the line: "Data were normalized by urinary specific gravity, because creatinine excretion may be abnormally reduced in ASD children" with reference to some work published a few years back [2]. Indeed, this is not the first time creatinine has cropped up in autism metabolomic studies (see here) and is perhaps worthy of quite a bit more study itself (see here).The authors report that urine samples from those with autism vs. those with not-autism are "largely distinguishable" based on some nifty analysis of the compounds examined from those groups. They even provide a 'top 25 discriminating metabolites' summary to illustrate this fact. Before venturing further into this list, I would perhaps advise some caution however. Caution based on the fact that urine contains many hundreds/thousands of small molecules or chemical entities as a function of being a waste product and carrying waste products from a multitude of different biological processes. It's not outside the realms of possibility that with such a huge number of metabolites, any two groups could be separated out, not just those based on the appearance of autism or not...Anyhow: "The “metabolome overview” obtained through metabolic pathway analysis (MetPA) shows tryptophan metabolism, purine metabolism, vitamin B6 metabolism, and phenylalanine-tyrosine-tryptophan biosynthesis as the four most perturbed metabolic pathways in ASD." The reference to the aromatic amino acid called tryptophan (the stuff that eventually ends up as serotonin and melatonin) used in the title of this post kinda points to where the money might be when it came to these particular results. I've been interested in tryptophan metabolism and autism for quite a while now (see here for example) and how, outside of the whole serotonin/melatonin bit, there is quite a lot more to see besides. Mention of something called the kynurenine pathway by Gevi is interesting; not least because this pathway overlaps with other conditions/labels too (see here). This pathway might also have some important implications when it comes to epilepsy (see here) as a comorbidity to autism too.It's also interesting (to me at least!) to note that the authors found something related to the indoles in their analyses too. So: "we also detect a significant increase in indole derivatives of bacterial tryptophan including indolyl 3-acetic acid, indoxyl sulfate, and most prominently, indolyl lactate." Indoxyl sulfate, a uremic toxin - something that is not great for the kidneys - crops up yet again [3] and importantly, highlights how bacteria can also 'go to work' on tryptophan in the gut. Indole -3-acetic acid also brings back research memories in relation to an indole compound close to my research heart, indolyl-3-acrylolyglycine (IAG) [4] that has received a bit of a research bruising quite recently [5] (the authors of that study and another one [6] however, really need to rethink their paper titles insofar as them not actually testing whether dietary intervention actually 'affects' levels of IAG or related metabolites but nonetheless implying so).There are a range of other findings reported by Gevi and colleagues but I don't want to bore you with all the details. Suffice to say that metabolomics continues its research rise with autism in mind, and provides some rather interesting results. Of course there is more to do in this area; not least the focus on subgroups in these days of 'the autisms' and perhaps a little more metabolomic inquiry when it comes to the myriad of intervention options put forward 'for autism'. Who for example, wouldn't like to see metabolomic profiles pre- and post-folinic acid for example alongside the myriad of other interventions detailed in the peer-reviewed literature? Indeed, I might also advocate a little more investigation on whether specific patterns of urinary compounds might also be related to specific behavioural facets of autism. Given the move towards gut bacteria as potentially showing involvement in some of the results obtained by Gevi et al, it would also be interesting to see if 'altering' certain types of gut bacteria (see here for example) might also have some interesting knock-on effects when it comes to the metabolites detected too? There is quite a bit more to do.Music and more bad lip reading.... sick of blue milk?----------[1] Gevi F. et al. Urinary metabolomics of young Italian autistic children supports abnormal tryptophan and purine metabolism. Molecular Autism. 2016l 7: 47.[2] Whiteley P. et al. Spot urinary creatinine excretion in pervasive developmental disorders. Pediatr Int. 2006 Jun;48(3):292-7.[3] Diémé B. et al. Metabolomics Study of Urine in Autism Spectrum Disorders Using a Multiplatform Analytical Methodology. J Proteome Res. 2015 Dec 4;14(12):5273-82.[4] Bull G. et al. Indolyl-3-acryloylglycine (IAG) is a putative diagnostic urinary marker for autism sp... Read more »

  • December 13, 2016
  • 04:25 AM
  • 262 views

'My child is not talking'. Online concerns and internet-based screening for autism?

by Paul Whiteley in Questioning Answers

"Online communities are used as platforms by parents to verify developmental and health concerns related to their child."That was the starting point for the study results reported by Ben-Sasson & Yom-Tov [1] (open-access available here) who approached an increasingly important issue related to how the Internet and social media in particular, is fast becoming one of the 'go-to' options when it comes to parental concerns about their child's development and the question: could it be autism?So: "we analyzed online queries posed by parents who were concerned that their child might have ASD and categorized the warning signs they mentioned according to ASD [autism spectrum disorder]-specific and non-ASD-specific domains." The online queries included for study came from "the Yahoo Answers platform" between June 2006 and December 2013. There's a lesson there to reiterate that the Internet is an open platform and what you post is typically in the public domain and hence fodder for many different purposes...Authors turned up quite a few thousand queries, determining that over 1000 were "posted by parents who suspected their child might have autism". They randomly selected 195 to be used as the basis for this study. I personally don't know why 195 were selected and not rounded up to say 200, but ho-hum. Content analysis - analysing the content of the post! - was undertaken first "to rate a child's risk of ASD as either low, medium, or high". High risk was defined "as concerns related to at least two types of ASD-specific sign, 1 from the RRBI domain and another from the Social and Communication domains" among other things. Then content analysis was used to "identify the types of warning signs noted by parents." From these analyses: "each query received an ASD global risk score and was coded for either presence or absence of each sign domain and its subdomains."Results: from the 195 queries selected, the vast majority were posted in relation to a boy and most concerned a boy who was aged under 3 years. Contrary to the title of this blog post - 'My child is not talking' - the majority of queries were actually in relation to repetitive and restricted behaviors and interests (RRBI) although concerns related to language were not too far behind in frequency. In relation to those categorisations of low, medium and high risk groups, over half of the queries were labelled as high risk. Interestingly, there were fewer language concerns noted in those allocated to the low risk group than the medium or high risk groups, so perhaps I wasn't so far off with using those 'my child is not talking' words in the title.But things didn't just stop there for the authors, as the words "test the efficacy of machine learning tools in classifying the child's risk of ASD based on the parent's narrative" are also noted in their paper. Machine learning as in, 'giving computers the ability to learn without being explicitly programmed' according to one definition, is something that has cropped up on the blog before with autism in mind (see here for example). This led to the production of a decision tree - yes or no - "for distinguishing low-risk queries from medium- and high-risk queries." This is interesting but I'd perhaps like to see it tested independently before I say too much more.In these days of continued austerity and seemingly evermore limited resources when it comes to things like autism assessment and screening for various reasons, this kind of work has an important place. Certainly I don't think posting symptoms on-line with ever replace autism screening, and one has to bear in mind that at least here in the UK, we might have (knowingly or unknowingly) already initiated population autism screening in children (see here) as a consequence of changes to the Healthy Child Program. But with the technological advances being made where machine learning and the connected artificial intelligence are starting to make strides in relation to science and medicine, I don't doubt that one day parents will be typing in their child's symptoms on-line and somehow and somewhere Dr Google or some related system(s) might be talking back...Music and more bad lip reading applied to Star Wars: No, it's not the future (and watch Chewie holler).----------[1] Ben-Sasson A. & Yom-Tov E. Online Concerns of Parents Suspecting Autism Spectrum Disorder in Their Child: Content Analysis of Signs and Automated Prediction of Risk. J Med Internet Res. 2016 Nov 22;18(11):e300.----------Ben-Sasson A, & Yom-Tov E (2016). Online Concerns of Parents Suspecting Autism Spectrum Disorder in Their Child: Content Analysis of Signs and Automated Prediction of Risk. Journal of medical Internet research, 18 (11) PMID: 27876688... Read more »

  • December 12, 2016
  • 03:16 PM
  • 250 views

Bacteria Help Pitcher Plants Trap Prey

by Elizabeth Preston in Inkfish



Pity the insect that tumbles into a pitcher plant's trap. The slippery walls and waiting pool of water ensure it won't clamber back out. There's nothing left to do but wait to be digested.

The California pitcher plant (Darlingtonia californica) is also called the cobra lily for its curled-over shape that hides its exit from its victims. Unlike other pitcher plants, it doesn't fill its trap from above with rainwater but from below, drawing water up with its roots. But like others, it seems... Read more »

  • December 12, 2016
  • 04:37 AM
  • 249 views

Maternal immune activation (MIA) and Old World monkeys

by Paul Whiteley in Questioning Answers

Old World monkeys detailed in the title of this post, specifically refers to a type of animal called a rhesus macaque who were the 'participants' of choice as detailed in a recent study by Destanie Rose and colleagues [1] looking at a concept called maternal immune activation (MIA).Those who followed this blog down the years will no doubt have seen me discuss MIA before in the context of autism and/or schizophrenia (see here for example). The basic theory is that whilst in-utero and enjoying approximately nine months in a warm and comfortable environment with a reprogrammed maternal immune system to stop a mother's body from 'rejecting' a developing foetus, infections encountered by the mother at critical periods of pregnancy might themselves or through their effects on the maternal immune system, have the ability to 'affect' offspring outcomes in a variety of ways. The majority of work on the concept of MIA has been in smaller animals such as rodents, so the inclusion of rhesus macaques is an important step as it was in other work with the immune system and autism in mind (see here).So, take 21 pregnancy rhesus macaques and give them either "three injections over 72 hours of poly I:C-LC [an immune stimulant], a double stranded RNA analog (viral mimic), or saline as a control." Said injections were given either "near the end of the first trimester or near the end of the second trimester" to see whether timing of immune stimulation might be important. Macaque offspring were subsequently born and followed for about 4 years. Blood samples were collected from offspring "at the end of their first (year 1) and fourth (year 4) years to assess dynamic cellular immune function." At the same time, the behaviours of monkey offspring were also analysed to see if there were any effects from MIA exposure.Results: behaviour did seem to be affected by MIA exposure, particularly stereotyped behaviours, noted to be a core feature of autism. Similarly, researchers reported some important immune system 'changes' associated with MIA exposure: "elevated production of innate inflammatory cytokines including: interleukin (IL)-1β, IL-6, IL-12p40, and tumor necrosis factor (TNF)α" at 1 year of age. Immune system changes were also noted longer-term at 4-years: "the MIA exposed offspring continued to display elevated IL-1β, and there was also a pattern of an increased production of T-cell helper type (TH)-2 cytokines, IL-4 and IL-13." Although being careful not to generalise too much when it comes to immune system markers and what they mean for pro- or anti-inflammatory signals, the leaning towards the production of Th-2 cytokines is typically linked to atopy and 'the promotion of IgE and eosinophilic responses in atopy.' The authors - including some notable names from the MIND Institute - conclude by suggesting that: "Data from this study suggests long-term behavioral and immune activation was present in offspring following MIA."Accepting that animal models of something like MIA are not necessarily the same as human MIA and its responses, this is interesting work. If one however accepts the data on something like vaccine function being modelled in animals (see here for example) is akin to what happens in people, real people, there is some added strength to the information published by Rose and other groups on how MIA may indeed be a relevant factor when it comes to immune function potentially affecting offspring behaviour and development.This research also intersects with quite a lot of other peer-reviewed science talking about how (human) pregnancy infection does seem to be related to offspring risk for conditions such as autism (see here). That various immune-related conditions such as asthma in mothers might also 'prime' for offspring neurodevelopmental issues is another important strand of research potentially pertinent to this area (see here). And then also there is the idea of an 'inflammatory autism subtype' (see here) also previously suggested continuing the important theme of immune function and behaviour/development being linked. There are, as you can see, quite a few potentially important connections that can be made between the Rose results and other data on MIA and offspring development.Oh, and I'll be coming to the recent paper by Zerbo and colleagues all in good time...----------[1] Rose DR. et al. Long-term altered immune responses following fetal priming in a non-human primate model of maternal immune activation. Brain Behav Immun. 2016 Nov 19. pii: S0889-1591(16)30522-0.----------Rose, D., Careaga, M., Van de Water, J., McAllister, K., Bauman, M., & Ashwood, P. (2016). Long-term altered immune responses following fetal priming in a non-human primate model of maternal immune activation Brain, Behavior, and Immunity DOI: 10.1016/j.bbi.2016.11.020... Read more »

  • December 11, 2016
  • 02:07 PM
  • 230 views

MS2 mRNA imaging in yeast: more evidence for artefacts

by Gal Haimovich in Green Fluorescent Blog

Previously, on the story of MS2 in yeast: Last year, Roy Parker published a short article, in which he claimed that using the MS2 system in yeast causes the accumulation of 3′ RNA fragments, probably due to inhibition of mRNA … Continue reading →... Read more »

  • December 10, 2016
  • 04:28 AM
  • 301 views

"Are we expecting too much from the extreme male brain theory of autism?"

by Paul Whiteley in Questioning Answers

The title of this post reflects the commentary published by Andrew Whitehouse [1] (open-access) discussing the meaning of the findings reported by Kung and colleagues [2] who quite categorically stated that there was: "No relationship between prenatal androgen exposure and autistic traits" in their study.OK, androgen exposure and psychology basically refers to the extreme male brain theory and autism which suggests that the so-called over-representation of autism in males is potentially down to hormone exposure (testosterone). The theory implies that androgen exposure at critical points in early development are skewing brain development towards a more 'male brain'. The definition of a male brain: well, apparently men are better systemisers than empathisers (better engineers that priests, I assume). The extreme male brain (EMB) hypothesis is an extension of the 'Theory of Mind' (ToM) stuff, which quite a few years back suggested that those diagnosed as being on the autism spectrum have greater difficulties in decoding mental states such as intents and desires. Grand psychological theories at their very finest you might say.The problem is that whilst ToM and the EMB theory made great psychological textbook reading (certainly in their heyday between the mid-1980s up to the late 1990s) and have spawned a whole industry around testing and teaching ToM for example, the scientific evidence for these concepts being exclusively and universally attributable to the great heterogeneity that is autism is not actually all that great. A shocker I know; and don't even ask about how comorbidity around autism might also be pretty important to such psychological concepts (see here and see here for example).Whitehouse - who himself has done some research in this area - talks quite a bit about the hows and whys of quite a few negative findings when it comes to the EMB theory (yes, there are quite a few) and what perhaps needs to be done to "advance beyond this stalemate" in relation to the EMB theory and autism.  His suggestion: "future research must first understand how the prenatal hormone environment relates to individual behavioural dimensions, and then incorporate this knowledge into the investigation of links with the more aetiologically and phenotypically complex profile of ASD [autism spectrum disorder]."These are wise words indeed but I'd suggest this perhaps applies to any 'theory' in relation to autism, psychological, biological or genetic. Indeed, I believe that other authors (see here) have already staked their claim on how using the word 'autism' as a starting point for anything other than a descriptive label probably isn't going to move autism research along any time soon; autisms people, autisms. The challenge is also one of moving away from generalisations; so talking about male and female brains is probably about as useful as talking about left and right-sided brains. Indeed, I'll refer you to some discussions about 'gender brains' between the main proponent of the EMB theory and a psychologist a few years back (see here and see here) that kicked up some scientific dust.I personally do think there is something in the findings looking at androgen levels and cognitive styles in the same way that there is something in most (replicated) peer-reviewed research when it comes to autism. But as Prof. Whitehouse indicates, it's probably going to be more relevant to some on the autism spectrum than others, and even then, disentangling the 'cognitive' structure of autism is going to be important [3]. The days of grand over-arching psychological theories about autism do seem to be riding off into the scientific sunset as the huge diversity and 'burden' of over-represented comorbidity start to come into plain sight. And certainly I don't think it's too rude to end with the words 'about time too'.To close, I hark back to simpler days or should that be to a simpler future when Buck Rogers showed the 25th Century how to boogie. Tell him what you think Twiki.----------[1] Whitehouse AJO. Commentary: Are we expecting too much from the extreme male brain theory of autism? A reflection on Kung et al. (2016). J Child Psychol Psychiatry. 2016 Dec;57(12):1463-1464.[2] Kung KT. et al. No relationship between prenatal androgen exposure and autistic traits: convergent evidence from studies of children with congenital adrenal hyperplasia and of amniotic testosterone concentrations in typically developing children. J Child Psychol Psychiatry. 2016 Dec;57(12):1455-1462.[3] Happé F. et al. Time to give up on a single explanation for autism. Nat Neurosci. 2006 Oct;9(10):1218-20.----------Whitehouse AJ (2016). Commentary: Are we expecting too much from the extreme male brain theory of autism? A reflection on Kung et al. (2016). Journal of child psychology and psychiatry, and allied disciplines, 57 (12), 1463-1464 PMID: 27859346... Read more »

  • December 9, 2016
  • 04:53 AM
  • 265 views

'Big data' Taiwan and schizophrenia risk

by Paul Whiteley in Questioning Answers

Today I bring the findings reported by Chou and colleagues [1] (open-access available here) to the blogging table and how the research might of the Taiwan National Health Insurance Database (NHIRD) brought it's 'big data' ("n = 23 422 955") to bear on the question: what is the risk of developing schizophrenia where one or more first-degree or other relatives are affected?The answer: "Having an affected co-twin, first-degree relative, second-degree relative, or spouse was associated with an adjusted RR [relative risk] (95% CI) of 37.86 (30.55-46.92), 6.30 (6.09-6.53), 2.44 (1.91-3.12), and 1.88 (1.64-2.15), respectively. Compared with the general population, individuals with one affected first-degree relative had a RR (95% CI) of 6.00 (5.79-6.22) and those with 2 or more had a RR (95% CI) of 14.66 (13.00-16.53) for schizophrenia."To translate the science-talk: if one twin is diagnosed with schizophrenia, there is a hugely increased risk of the other twin also being affected. If a mother or father, sister or brother, or your child(ren) are diagnosed with schizophrenia, there is an enhanced risk but nothing like the risk to twins. As you move outwards to other outlying family members (uncles, aunts, grandparents, etc) affected, your risk continues to diminish albeit still noticeable. Interestingly, when it comes to spouses (husband or wife), there is a small but increased risk that if they are diagnosed with schizophrenia so the other partner is at some small, enhanced risk. This tallies with the concept of assortative mating [2] but does not necessarily rule out other shared non-genetic factors either.The final sentence in that quote provides some evidence for a cumulative effect too. So if one of your close family members is diagnosed with schizophrenia, so the risk to yourself might be heightened. If two or more close family members are diagnosed, the relative risk to yourself jumps quite a bit more."A family history of schizophrenia is therefore associated with a higher risk of developing schizophrenia, mood disorders, and delusional disorders. Heritability and environmental factors each account for half of the phenotypic variance of schizophrenia."To close, Yoda don't like seagulls...----------[1] Chou IJ. et al. Familial Aggregation and Heritability of Schizophrenia and Co-aggregation of Psychiatric Illnesses in Affected Families. Schizophr Bull. 2016 Nov 21. pii: sbw159.[2] Parnas J. Assortative mating in schizophrenia: results from the Copenhagen High-Risk Study. Psychiatry. 1988 Feb;51(1):58-64.----------Chou IJ, Kuo CF, Huang YS, Grainge MJ, Valdes AM, See LC, Yu KH, Luo SF, Huang LS, Tseng WY, Zhang W, & Doherty M (2016). Familial Aggregation and Heritability of Schizophrenia and Co-aggregation of Psychiatric Illnesses in Affected Families. Schizophrenia bulletin PMID: 27872260... Read more »

  • December 8, 2016
  • 05:12 PM
  • 300 views

Do We All Have Split Brains?

by Neuroskeptic in Neuroskeptic_Discover

When you're doing two things at once - like listening to the radio while driving - your brain organizes itself into two, functionally independent networks, almost as if you temporarily have two brains. That's according to a fascinating new study from University of Wisconsin-Madison neuroscientists Shuntaro Sasai and colleagues. It's called Functional split brain in a driving/listening paradigm



In referring to 'split brains' in their title, Sasai et al. are linking their work to the litera... Read more »

Sasai, S., Boly, M., Mensen, A., & Tononi, G. (2016) Functional split brain in a driving/listening paradigm. Proceedings of the National Academy of Sciences, 201613200. DOI: 10.1073/pnas.1613200113  

  • December 8, 2016
  • 03:14 PM
  • 109 views

ExAC presents a catalogue of human protein-coding genetic variation

by Kamil S. Jaron in genome ecology evolution etc

Exploration of variability of human genomes represents a key step in the holy grail of human genetics – to link genotypes with phenotypes, it also provides insights to human evolution and history. For this purpose Exome Aggregation Consortium (ExAC) have … Continue reading →... Read more »

Lek M, Karczewski KJ, Minikel EV, Samocha KE, Banks E, Fennell T, O'Donnell-Luria AH, Ware JS, Hill AJ, Cummings BB.... (2016) Analysis of protein-coding genetic variation in 60,706 humans. Nature, 536(7616), 285-91. PMID: 27535533  

  • December 8, 2016
  • 09:14 AM
  • 233 views

What are Hierarchical Orthologous Groups (HOGs)?

by Christophe Dessimoz in Open Reading Frame


One central concept in the OMA project and other
work we do to infer relationships between genes is that of Hierarchical
Orthologous Groups, or “HOGs” for the initiated.

We’ve written several papers on aspects pertaining to HOGs—how to infer
them,
how to evaluate them, they being
increasingly adopted by orthology
resources, etc.—but there is
still a great deal of confusion as to what HOGs are and why they matter.

Natasha Glover, talented postdoc in the lab, has prepared a brief video to
introduce HOGs and convey why in the Dessimoz lab we are all mad about them!

 



 

References

Altenhoff, A., Gil, M., Gonnet, G., & Dessimoz, C. (2013). Inferring Hierarchical Orthologous Groups from Orthologous Gene Pairs PLoS ONE, 8 (1) DOI: 10.1371/journal.pone.0053786

Boeckmann, B., Robinson-Rechavi, M., Xenarios, I., & Dessimoz, C. (2011). Conceptual framework and pilot study to benchmark phylogenomic databases based on reference gene trees Briefings in Bioinformatics, 12 (5), 423-435 DOI: 10.1093/bib/bbr034

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
... Read more »

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  

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