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  • February 3, 2017
  • 08:00 AM

American Alligator

by Jason Organ in Eatlemania!

The Eatles are munching on several juvenile American alligator skulls... Read more »

  • February 3, 2017
  • 05:00 AM

Friday Fellow: Northern Plaited Radiolarian

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Some weeks ago I introduced a diatom here and mentioned that, despite the fact that they are a very abundant group, little information on species is available. Today our species is a radiolarian and, just as … Continue reading →... Read more »

  • February 3, 2017
  • 03:03 AM

"Schizophrenia confers a high endogenous risk for diabetes"

by Paul Whiteley in Questioning Answers

"Schizophrenia confers a high endogenous risk for diabetes, and the risk is further increased by both first-generation and second-generation antipsychotics."So concluded Anto Rajkumar and colleagues [1] who relied on participant data in the thousands derived from several of those very helpful Scandinavian population registries (this time in Denmark) to add some further science to the idea that psychiatric diagnoses like schizophrenia seem to carry an elevated risk for all-manner of somatic conditions.From a total population of 2.7 millions people born in Denmark between 1977 and 2013, researchers reported that: "14,118 (0.52%) developed diabetes, and 8,945 (0.33%) developed schizophrenia during follow-up (49,582,279 person-years)." When looking at the risk of developing diabetes (bearing in mind there is more than one type of diabetes) in those with schizophrenia not following any antipsychotic medication regime, researchers reported that: "The adjusted hazard ratio for diabetes was 3.07 (95% confidence interval [CI], 1.71–5.41) in antipsychotic-naive schizophrenia compared with the general population." In other words, compared with those without a diagnosis of schizophrenia, there was something of an increased risk of developing diabetes in those diagnosed with schizophrenia.Then to the potential effect of antipsychotic medication, and as the authors note: "The risk for diabetes after starting antipsychotic treatment was significantly higher (adjusted hazard ratio, 3.64; 95% CI, 1.95–6.82) than the risk in antipsychotic-naive schizophrenia." The use of an adjusted hazard ratio means that researchers took into account potentially confounding variables such as a family history of diabetes known to potentially elevate the risk of the condition. The focus on medication is also perhaps the side of the whole schizophrenia-diabetes story that people might more readily recognise.If all that wasn't enough to convince you that schizophrenia - medicated and unmedicated - might show a rather important relationship with diabetes, perhaps the results reported by Pillinger and colleagues [2] might ease your scepticism and the suggestion (from the authors) that "higher levels of insulin, and increased levels of insulin resistance" are a facet of quite a few cases of schizophrenia alongside demonstrating that "people with schizophrenia had higher levels of glucose in the blood." On the basis of these and various other studies, the onus is on regular screening for diabetes and its symptoms alongside other related measures (see here for example) when it comes to schizophrenia under multiple 'medicated or not' conditions.Music to close, and having bumped into the excellent film 'Stand By Me' again recently, the song of the same name...----------[1] Rajkumar AP. et al. Endogenous and Antipsychotic-Related Risks for Diabetes Mellitus in Young People With Schizophrenia: A Danish Population-Based Cohort Study. Am J Psychiatry. 2017 Jan 20:appiajp201616040442.[2] Pillinger T. et al. Impaired Glucose Homeostasis in First-Episode Schizophrenia: A Systematic Review and Meta-analysis. JAMA Psychiatry. 2017 Jan 11.----------Rajkumar AP, Horsdal HT, Wimberley T, Cohen D, Mors O, Børglum AD, & Gasse C (2017). Endogenous and Antipsychotic-Related Risks for Diabetes Mellitus in Young People With Schizophrenia: A Danish Population-Based Cohort Study. The American journal of psychiatry PMID: 28103712... Read more »

  • February 2, 2017
  • 03:25 AM

Hyperuricemia present in both medicated and unmedicated kids with autism

by Paul Whiteley in Questioning Answers

I was intrigued to read the findings reported by Natchaya Vanwong and colleagues [1] talking about the presence of hyperuricemia - an excess of uric acid in the blood - in their cohort of children and young adults diagnosed with an autism spectrum disorder (ASD). Intrigued not only because the authors discuss how the use of the atypical antipsychotic risperidone might *correlate* with elevations of uric acid but also how: "Hyperuricemia was present in 44.70% of risperidone-naïve patients with ASD."Uric acid, more readily associated with the condition gout, has been mentioned before on this blog in the context of autism (see here) and other conditions/states (see here) not totally unfamiliar to autism. It's therefore not necessarily new news that elevations of the stuff might have been found again. The Vanwong study looked at uric acid levels in "127 children and adolescents with ASD treated with risperidone and 76 age-matched risperidone-naïve patients with ASD" alongside a few other biological parameters. They concluded that yes, quite a few participants in their cohort presented with hyperuricemia "defined as the level of uric acid concentration in the blood >5.5 mg/dL" bearing in mind no 'not-autism' control group was included for direct study (including those not diagnosed with autism but in receipt of risperidone).Implications following the Vanwong study? Well, bearing in mind that gout is traditionally seen as a disease of middle-to-older age, the first thing would be to screen for gout in those with high uric acid levels and keep monitoring just in case gout develops. Next up would be to perhaps also look at some of the "rare inherited genetic disorders that cause hyperuricemia" and whether they might 'overlap' with the presentation of autism; y'know in the context that 'autism genes are probably not just genes for autism' and all that. At this point, I'm also minded to remind readers of the important (but often forgotten work) by Mary Coleman and Ted Page [2] on the topic of autism and uric acid, bringing in purine metabolism 'issues' as something potentially important to some autism (uric acid comes about as a consequence of the metabolism of purines). This, in the context of the autisms (plural)...Insofar as the potential correlation posed between uric acid and risperidone usage, a word of caution is perhaps warranted but big words about 'risperidone causing hyperuricemia' are not required at this point in time without further study. Remember: "Hyperuricemia was present in 44.70% of risperidone-naïve patients with ASD and 57.50% of ASD patients treated with risperidone." I say this mindful that there are biological parameters that do need careful inspection when such antipsychotic therapy is put in place (see here) but the data is not yet so convincing when it comes to uric acid elevations and risperidone use.----------[1] Vanwong N. et al. Hyperuricemia in Children and Adolescents with Autism Spectrum Disorder Treated with Risperidone: The Risk Factors for Metabolic Adverse Effects. Front. Pharmacol. 2017. 5 Jan.[2] Page T. & Coleman M. Purine metabolism abnormalities in a hyperuricosuric subclass of autism. Biochim Biophys Acta. 2000 Mar 17;1500(3):291-6.----------Vanwong N, Srisawasdi P, Ngamsamut N, Nuntamool N, Puangpetch A, Chamkrachangpada B, Hongkaew Y, Limsila P, Kittitharaphan W, & Sukasem C (2017). Hyperuricemia in Children and Adolescents with Autism Spectrum Disorder Treated with Risperidone: The Risk Factors for Metabolic Adverse Effects. Frontiers in pharmacology, 7 PMID: 28105014... Read more »

  • February 1, 2017
  • 03:21 AM

Autism and a 'clear' reduction of behavioural severity in cases diagnosed

by Paul Whiteley in Questioning Answers

"This study provides the first clear evidence of a reduction over time in the behavioral severity of individuals diagnosed with Autistic Disorder during a period of stability in diagnostic criteria."So said the study findings reported by Andrew Whitehouse and colleagues [1] (a man not afraid to make waves when it comes to thinking about autism or about approaches to intervention) looking at "whether there were changes over time in the qualitative and quantitative phenotype of individuals who received the diagnosis of Autistic Disorder."Based on prospective registry data of new autism / autism spectrum disorder (ASD) cases (N=1252) in Western Australia (a research favourite) between 2000 and 2006, researchers reported that the severity of the presentation of autism seemed to 'change' between the years. They concluded: "A shift toward diagnosing individuals with less severe behavioral symptoms may have contributed to the increasing prevalence of Autistic Disorder diagnoses." At least in Australia that is...This is an interesting study. It kinda reiterates that when one talks about the quite phenomenal increase in diagnoses of autism being received, at least one factor contributory to that increase is the inclusion of a wider presentation of the condition. It also feeds into the discussions that have already happened, and will continue to happen, following the introduction of DSM-5 to autism diagnosis and in particular, the future role of the catch-all category that is social (pragmatic) communication disorder (SCD) (see here) when it comes to stiffer ASD diagnostic criteria not being met.But just before anyone breaks out with the sweeping generalisation that the increasing prevalence of autism over the past two decades is somehow all 'manufactured' (exhibit one) according to the diagnostic procedures used, the available data points to something far more multi-faceted and complex (see here for example)...----------[1] Whitehouse AJ. et al. Evidence of a reduction over time in the behavioral severity of autistic disorder diagnoses. Autism Res. 2017 Jan 19.----------Whitehouse AJ, Cooper MN, Bebbington K, Alvares G, Lin A, Wray J, & Glasson EJ (2017). Evidence of a reduction over time in the behavioral severity of autistic disorder diagnoses. Autism research : official journal of the International Society for Autism Research PMID: 28102641... Read more »

Whitehouse AJ, Cooper MN, Bebbington K, Alvares G, Lin A, Wray J, & Glasson EJ. (2017) Evidence of a reduction over time in the behavioral severity of autistic disorder diagnoses. Autism research : official journal of the International Society for Autism Research. PMID: 28102641  

  • January 31, 2017
  • 03:18 AM

S100B protein and autism continued

by Paul Whiteley in Questioning Answers

"Our findings showing an increase in peripheral concentrations of S100B and TNF-α provide limited support to the hypothesis about the roles of altered immune function and S100B in autism spectrum disorder (ASD)."So said the findings reported by Selin Aktan Guloksuz and colleagues [1] (open-access available here) continuing some discussions a few years back on a possible role for S100B in relation to at least some autism (see here).S100B - S100 calcium-binding protein B - is a compound involved in quite a few biological reactions not least "as a biomarker of global glial activity." Elevations of the S100B have been reported in relation to several states including that of [traumatic] brain injury. Outside of some research suggesting that elevations of S100B might also be a feature of diagnoses such as schizophrenia (see here), it has also been the topic of investigations with [some] autism in mind [2] too. The name of the game is elevations in S100B in relation to autism and more.Based on analyses of fasting blood samples from "40 unmedicated children with autism" (where autism diagnoses were confirmed by study researchers) and 35 asymptomatic control children, researchers measured levels of plasma S100B alongside various markers of immune function (cytokines). Among the suite of cytokines examined, levels of "tumor necrosis factor alpha (TNF-α), interferon gamma, interleukin (IL)-1β, IL-4, IL-6, IL-10, and IL-17A" were included. The idea of using unmedicated children with autism stems from the suggestion that at least one medication used for some autism might have the ability to elevate S100B [3].Results: as per the opening sentence to this post, levels of S100B and TNF-α were 'different' between the groups (both elevated) and this finding remained "after controlling for age, sex, and BMI [body mass index]." Researchers also reported some results looking at whether ASD symptom presentation might show any 'association' with S100B levels. On this topic they reported that: "Plasma S100B concentrations in children with severe ASD symptoms were higher than in children with mild-moderate ASD symptoms" but when again controlling for age, sex and BMI this association did not hold (significantly). As for the other cytokines outside of TNF-α... nothing came up as significant between the groups. This is interesting in light of recent work (see here) and even Guloksuz et al talk about future "prospective longitudinal studies investigating a broad set of immune markers, both in serum and CSF [cerebrospinal fluid], in large samples" and the pros- and cons of looking in CFS.Where next for this area of investigation? Well, taking into account the link between S100B and brain injury and what that could mean for cognitive processes for example, I'd be minded to suggest that more study is needed looking at the effect of S100B levels in relation to cognition and autism. Take for example the study results from Chen and colleagues [4] who reported that "serum S100B level was an independent contributor to the global cognitive dysfunctions, particularly for the speed of processing, attention/vigilance, visual learning and reasoning/problem solving subscores" in their cohort of participants with schizophrenia. Might similar correlations be present alongside S100B elevations in relation to autism? I'd also be minded to suggest looking at a possible role for comorbidities potentially accompanying a diagnosis of autism as being important for S100B elevations in light of other research on depression for example [5]. Depression (various types) and autism is very much an important area of overlap (see here for example) and might actually offer at least one way to target elevations in S100B.There is more to do on this topic.----------[1] Guloksuz SA. et al. Elevated plasma concentrations of S100 calcium-binding protein B and tumor necrosis factor alpha in children with autism spectrum disorders. Rev Bras Psiquiatr. 2017 Jan 12:0.[2] Al-Ayadhi LY. & Mostafa GA. A lack of association between elevated serum levels of S100B protein and autoimmunity in autistic children. J Neuroinflammation. 2012 Mar 16;9:54.[3] Quincozes-Santos A. et al. Effect of the atypical neuroleptic risperidone on morphology and S100B secretion in C6 astroglial lineage cells. Mol Cell Biochem. 2008 Jul;314(1-2):59-63.[4] Chen S. et al. Cognitive dysfunction correlates with elevated serum S100B concentration in drug-free acutely relapsed patients with schizophrenia. Psychiatry Res. 2017 Jan;247:6-11.[5] Rajewska-Rager A. & Pawlaczyk M. The role of S100B protein as a potential marker in affective disorders. Psychiatr Pol. 2016;50(4):849-857.----------Guloksuz SA, Abali O, Aktas Cetin E, Bilgic Gazioglu S, Deniz G, Yildirim A, Kawikova I, Guloksuz S, & Leckman JF (2017). Elevated plasma concentrations of S100 calcium-binding protein B and tumor necrosis factor alpha in children with autism spectrum disorders. Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) PMID: 28099628... Read more »

Guloksuz SA, Abali O, Aktas Cetin E, Bilgic Gazioglu S, Deniz G, Yildirim A, Kawikova I, Guloksuz S, & Leckman JF. (2017) Elevated plasma concentrations of S100 calcium-binding protein B and tumor necrosis factor alpha in children with autism spectrum disorders. Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999). PMID: 28099628  

  • January 30, 2017
  • 03:08 AM

High frequency of (self-reported) ADHD symptoms in eating disorders

by Paul Whiteley in Questioning Answers

"There is a high frequency of ADHD [attention-deficit hyperactivity disorder] symptoms in patients with binge eating/purging eating disorders that motivates further studies."That was the conclusion reached in the study by Nils Erik Svedlund and colleagues [1] (open-access) who, among other things, set out to "explore the prevalence and types of self-reported ADHD symptoms in a large, unselected group of ED [eating disorder] patients assessed in a specialized ED clinic." Participants (over 1100 of them) were "seeking help at the Stockholm Centre for Eating Disorders (SCED) from 4 February 2013 through 18 September 2015" and as well as being confirmed to have an eating disorder were also screened for ADHD-type behaviours using the WHO ADHD Self-Rating Scale for Adults (ASRS-screener). Notice the 'self-rated' part of that last sentence...Based on a ASRS screener score of 14 or above, researchers reported that some 30% of females (N=1094) self-reported 'issues' associated with a diagnosis of ADHD. Some 34% of men included for study (N=47) reported similar ADHD traits (31.3% of the total group including those diagnosed with 'Eating Disorder Not Otherwise Specified (EDNOS) type 5' were on or above the ASRS screener score of 14).Bearing in mind the presence of various types of different eating disorders in their cohort, researchers also looked at how those self-reported ADHD traits might correlate with sub-groupings. They report that: "The highest frequency of possible ADHD was found in BN [Bulimia Nervosa] and in AN-BP [Anorexia Nervosa bingeing/purging subtype], respectively." They also noted that specific symptoms of ED correlated with the ASRS-screener scores: binge eating, purging, loss of control over the eating and BMI [body mass index] > 17.5. I might add that based on responses to another schedule - the Comprehensive Psychiatric [Psychopathological] Rating Scale (CPRS) - included as part of the study, authors noted something of a link between the ASRS trait scores and "the CPRS scales for depression..., anxiety... and obsession-compulsion." But: "Psychiatric comorbidity correlated to ADHD symptoms without explaining the differences between eating disorder diagnoses."Keeping in mind that answering 6 questions on a screener questionnaire does not an ADHD diagnosis make, I am rather interested in these and other findings. I am by no means an expert on eating disorder but I have previously been interested in the suggestion that autistic traits may be 'over-represented' when it comes to ED (see here). Combined with the idea that autism and [diagnosed] ADHD might not also be unstrange diagnostic bedfellows (see here) and you can perhaps see that there is potentially more research to do in this area in these times of overlap and ESSENCE. And speaking of ESSENCE [2]...With a word or two of caution, I note the authors also talked about potential 'treatment' options given the overlap between ADHD traits (self-reported) and ED. So: "This motivates further randomized trials with stimulant treatment for bingeing/purging ED-patients with and without a concomitant ADHD diagnosis." Certain stimulants have quite a good track record when it comes to ADHD (see here) but the authors rightly note that 'appetite suppression' is a potential side-effect of such pharmacotherapy and something perhaps not ideal if someone is already underweight. More studies are indicated to disentangle what is linked to what.And while I'm on the topic, the link between autism traits and anorexia nervosa might actually be a little more tenuous that you perhaps think [3]...----------[1] Svedlund NE. et al. Symptoms of Attention Deficit Hyperactivity Disorder (ADHD) among adult eating disorder patients. BMC Psychiatry. 2017; 17: 19.[2] Karjalainen L. et al. Eating disorders and eating pathology in young adult and adult patients with ESSENCE. Compr Psychiatry. 2016 Apr;66:79-86.[3] Postorino V. et al. Investigation of Autism Spectrum Disorder and Autistic Traits in an Adolescent Sample with Anorexia Nervosa. J Autism Dev Disord. 2017. Jan 24.----------Svedlund, N., Norring, C., Ginsberg, Y., & von Hausswolff-Juhlin, Y. (2017). Symptoms of Attention Deficit Hyperactivity Disorder (ADHD) among adult eating disorder patients BMC Psychiatry, 17 (1) DOI: 10.1186/s12888-016-1093-1... Read more »

  • January 28, 2017
  • 07:52 PM

A Model for Phage Communication and the Implications for the Human Microbiome

by Geoffrey Hannigan in Prophage

Well we took a bit of a break these past couple of weeks, but we are back for the new year! Welcome to the Prophage blog 2017! The year has actually been off to a good start, with a lot of interesting papers being published this January. This week I want to kick things off by covering a very cool 2017 study by Erez et al that described an new and interesting mechanism by which bacteriophages communicate using...... Read more »

Erez, Z., Steinberger-Levy, I., Shamir, M., Doron, S., Stokar-Avihail, A., Peleg, Y., Melamed, S., Leavitt, A., Savidor, A., Albeck, S.... (2017) Communication between viruses guides lysis–lysogeny decisions. Nature, 541(7638), 488-493. DOI: 10.1038/nature21049  

  • January 28, 2017
  • 08:42 AM

Distortions of Reality

by The Neurocritic in The Neurocritic

President Trump this week repeated an assertion he made shortly after his election: that millions of ballots cast illegally by undocumented immigrants cost him the popular vote. If true, this would suggest the wholesale corruption of American democracy.

Not to worry: As far as anyone knows, the president’s assertion is akin to saying that millions of unicorns also voted illegally.

- In a

... Read more »

Preller, K., Herdener, M., Pokorny, T., Planzer, A., Kraehenmann, R., Stämpfli, P., Liechti, M., Seifritz, E., & Vollenweider, F. (2017) The Fabric of Meaning and Subjective Effects in LSD-Induced States Depend on Serotonin 2A Receptor Activation. Current Biology. DOI: 10.1016/j.cub.2016.12.030  

Wacker, D., Wang, S., McCorvy, J., Betz, R., Venkatakrishnan, A., Levit, A., Lansu, K., Schools, Z., Che, T., Nichols, D.... (2017) Crystal Structure of an LSD-Bound Human Serotonin Receptor. Cell, 168(3), 377-2147483647. DOI: 10.1016/j.cell.2016.12.033  

  • January 28, 2017
  • 04:15 AM

"Should gluten-free foods be available on prescription?"

by Paul Whiteley in Questioning Answers

Continuing the theme of blogging outside of the core material typically included on this site, I couldn't resist a mention of the 'head-to-head' debate talked about in the article by Matthew Kurien and colleagues [1] published in the British Medical Journal (BMJ).As per the title of this post, the name of the game was gluten-free products being available on prescription here in Blighty, and in particular, the prescribing of gluten-free products to patients diagnosed with coeliac disease. The head-to-headers were Matthew Kurien, Sarah Sleet & David Sanders* (*a name not unfamiliar to this blog) all in favour of keeping the status quo and James Cave presenting the opposing view and why prescriptions of gluten-free products to those with coeliac disease might not be the only way.OK, first things first. A gluten-free diet is not some dietary 'fad' for people living with coeliac disease (CD); it is a clinically-indicated treatment tool for this autoimmune condition. As I've said a few times on this blog, not only are there are physiological effects linked to CD mostly 'solved' by use of a gluten-free diet, but there may be psychological effects too (see here). Gluten is most definitely the 'baddie' when it comes to CD and should not be in the diet of those with CD.The head-to-head piece makes for interesting reading in terms of how in these days of focus on the finances of the National Health Service (NHS), the idea that removing food prescriptions as one way to "reduce costs in the short term" might have some important repercussions in the longer-term. Indeed I was taken by one quote in the 'keep gluten-free food prescriptions' camp: "Would clinical commissioning groups consider this if the treatment for coeliac disease was an immunosuppressive drug and not food?" Food as medicine? I like that sentiment (see here).I have to say however that I did find the viewpoint from James Cave rather appealing in some aspects. Within his various facts and figures he shows how perverse it is that one can go into a supermarket and buy a gluten-free loaf of bread for one price and yet the same loaf is bought by the NHS for prescription for quite a bit more. Sorry to focus on cost and finances but this is salient point in these days of continued austerity and financial/political uncertainty. Cave also adds that gluten-free food prescriptions tend to be restricted to set items, come in bulk and generally need to be collected from a pharmacy. There are additional costs added to the supply of such goods.The two viewpoints do however agree that slight changes could be made to the system to make it both run more efficiently and provide those with coeliac disease a little more 'opportunity' in what they select. As Cave notes: "A national voucher scheme or a personalised health budget could be provided to ensure that patients receive recompense for the extra expense of gluten-free products." As Kurien and colleagues note: "Alternative strategies to prescriptions, such as direct supply schemes from community pharmacies, or voucher allowances, may be a more efficient way of delivering NHS support." A voucher scheme for gluten-free products? Interesting.In these days where areas of England are already seeing changes to gluten-free prescriptions (see here for example) I'm wondering if a voucher scheme might be the [inevitable] way forward, at least for the majority of patients. Not only does this offer more choice to the consumer in terms of what products they buy (and indeed, what they might prefer) but the whole process of the NHS ordering, buying and dispensing such products is also reduced. For those who perhaps do not have access to a full-range of gluten-free products as their local supermarket for example or have mobility issues, exceptions could be made but for the most part, patients are handed choice and a lot more buying power and freedom. A voucher scheme might also 'normalise' the idea of gluten-free products when it comes to CD. By 'normalise' I mean that a young adult diagnosed with CD for example, no longer has to go to their local pharmacy for their 'months supply' but rather can shop - pick and choose - from the growing range of gluten-free products that adorn supermarket shelves these days. Compliance to the gluten-free diet will no doubt benefit when there is more choice and a voucher scheme will bring choice.Change is often difficult when it comes to the NHS and it's been over 50 years since gluten-free products were put on prescription for those with CD so this would be a big change. But gluten-free is everywhere these days and there is seemingly little to hold the NHS back from further empowering those diagnosed with CD in terms of their dietary choices...----------[1] Kurien M. et al. Should gluten-free foods be available on prescription? BMJ 2017: 356.----------Kurien M, Sleet S, Sanders DS, & Cave J (2017). Should gluten-free foods be available on prescription? BMJ (Clinical research ed.), 356 PMID: 28073799... Read more »

Kurien M, Sleet S, Sanders DS, & Cave J. (2017) Should gluten-free foods be available on prescription?. BMJ (Clinical research ed.). PMID: 28073799  

  • January 28, 2017
  • 03:28 AM

When You're Drowsy, Is Your Brain Partly Asleep?

by Neuroskeptic in Neuroskeptic_Discover

When we're feeling very tired, we sometimes remark that we're "half-asleep". But is this more than just a figure of speech? A new paper suggests that parts of our brain may actually 'fall asleep' even while we're still awake.

According to researchers Jeremy D. Slater and colleagues of the University of Texas, "local sleep" occurs throughout the human brain, with each brain region passing into and out of a sleep-like state over time. What's more, local sleep becomes more and more common in... Read more »

Slater JD, Chelaru MI, Hansen BJ, Beaman C, Kalamangalam G, Tandon N, & Dragoi V. (2017) Focal Changes to Human Electrocorticography With Drowsiness: A Novel Measure of Local Sleep. The Journal of Neuropsychiatry and Clinical Neurosciences. PMID: 28121257  

  • January 27, 2017
  • 12:27 PM

Impairment of neurogenesis in ZIKV infected neuronal cells: strain specific ? Asian/American v. African strains

by thelonevirologist in Virology Tidbits

uring the current Zika Virus (ZIKV) outbreaks in the Americas, an increased number of cognitive malformations including but not limited to microcephaly in foetuses and neonates of mothers who had been infected with ZIKV during pregnancy, lead to the conclusion that ZIKV might be neuroteratogenic, a hypothesis that has been supported by findings that various ZIKV strains –including isolates from Asia such ZIKV SZ 01, ZIKV FSS13025 and H/PF/2013 as well as isolates from the Americas such as ZIKV Mex 1-144, ZIKV PRV ABC059 and ZIKV BR Paraiba 2015 or the (original) African isolate ZIKV MR766- not only infect and replicate in neuronal cells in vitro and in vivo, but also induces apoptosis of infected and non-infected cells. These results suggest that ZIKV may cause abnormal neuronal development of the foetal brain by inducing cell death of infected cells via intrinsic apoptosis as well as bystander apoptosis of non-infected cells via the secretion of pro-inflammatory cytokines.
As described before, ZIKV MR766 infected human neuronal progenitor cells (hNPC), not only undergo apoptosis, but also are arrested at G2/M phase of the cell cycle as measured by single parameter flow cytometry, which is supported by findings that in ZIKV Mex 1-144 infected foetal brain tissue of mice a decrease in Ki67 positive and Histone H3-P (Ser-10) positive cells can be observed, suggesting that ZIKV infection arrests infected cells in G2 phase of the cell cycle. Here strain specific differences are discussed. ... Read more »

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

van den Pol AN, Mao G, Yang Y, Ornaghi S, & Davis JN. (2017) Zika virus targeting in the developing brain. The Journal of neuroscience : the official journal of the Society for Neuroscience. PMID: 28123079  

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  

Tang H, Hammack C, Ogden SC, Wen Z, Qian X, Li Y, Yao B, Shin J, Zhang F, Lee EM.... (2016) Zika Virus Infects Human Cortical Neural Progenitors and Attenuates Their Growth. Cell stem cell, 18(5), 587-90. PMID: 26952870  

Garcez PP, Nascimento JM, de Vasconcelos JM, Madeiro da Costa R, Delvecchio R, Trindade P, Loiola EC, Higa LM, Cassoli JS, Vitória G.... (2017) Zika virus disrupts molecular fingerprinting of human neurospheres. Scientific reports, 40780. PMID: 28112162  

Gabriel, E., Ramani, A., Karow, U., Gottardo, M., Natarajan, K., Gooi, L., Goranci-Buzhala, G., Krut, O., Peters, F., Nikolic, M.... (2017) Recent Zika Virus Isolates Induce Premature Differentiation of Neural Progenitors in Human Brain Organoids. Cell Stem Cell. DOI: 10.1016/j.stem.2016.12.005  

Gromley A, Jurczyk A, Sillibourne J, Halilovic E, Mogensen M, Groisman I, Blomberg M, & Doxsey S. (2003) A novel human protein of the maternal centriole is required for the final stages of cytokinesis and entry into S phase. The Journal of cell biology, 161(3), 535-45. PMID: 12732615  

Meitinger F, Anzola JV, Kaulich M, Richardson A, Stender JD, Benner C, Glass CK, Dowdy SF, Desai A, Shiau AK.... (2016) 53BP1 and USP28 mediate p53 activation and G1 arrest after centrosome loss or extended mitotic duration. The Journal of cell biology, 214(2), 155-66. PMID: 27432897  

Souza BS, Sampaio GL, Pereira CS, Campos GS, Sardi SI, Freitas LA, Figueira CP, Paredes BD, Nonaka CK, Azevedo CM.... (2016) Zika virus infection induces mitosis abnormalities and apoptotic cell death of human neural progenitor cells. Scientific reports, 39775. PMID: 28008958  

  • January 27, 2017
  • 05:13 AM

TSC1 expression is affected by VHL alterations and HIF-1α production in clear-cell RCC

by Joana Guedes in BHD Research Blog

VHL genetic alterations do not affect the production of HIF-α in clear-cell renal cell carcinoma (ccRCC). However, their effects on tuberous sclerosis proteins (TSC1/2) and heat shock protein 90 (Hsp90) expression are currently unknown. In a recent study, Damjanovic et al. (2016) evaluated the impact of VHL genetic alterations and HIF-α production on the expression of TSC proteins and Hsp90 in 47 sporadic ccRCCs and corresponding normal tissues.... Read more »

  • January 27, 2017
  • 05:00 AM

Friday Fellow: Black Bread Mold

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Today’s Friday Fellow lives in our houses and our gardens, among our food and our crops. And every time we notice it, we get upset, because it means that something we were supposed to eat is … Continue reading →... Read more »

Hernández-Lauzardo, A., Bautista-Baños, S., Velázquez-del Valle, M., Méndez-Montealvo, M., Sánchez-Rivera, M., & Bello-Pérez, L. (2008) Antifungal effects of chitosan with different molecular weights on in vitro development of Rhizopus stolonifer (Ehrenb.:Fr.) Vuill. Carbohydrate Polymers, 73(4), 541-547. DOI: 10.1016/j.carbpol.2007.12.020  

  • January 27, 2017
  • 03:07 AM

Vitamin D deficiency and risk of dementia

by Paul Whiteley in Questioning Answers

"The results of this systematic review show that low vitamin D levels might contribute to the development of dementia."Whilst slightly off-topic when it comes to the core research material typically included on this blog, I did want to bring to your attention the systematic review and meta-analysis results published by Isolde Sommer and colleagues [1] (open-access) for your perusal. Although unable to "identify a single study investigating the association between sunlight exposure and dementia risk" authors did manage to find "indirect evidence from studies using vitamin D status as a surrogate parameter" where five out of six studies identified ("18,639 participants") suggested a possible correlation. Sunlight by the way, is the primary route of synthesising vitamin D.The sort of 'risk' determined in the Sommer calculations when it comes to vitamin D levels and dementia is not to be sniffed at: "Translated into absolute numbers, 28 (at least 10 but up to 50 more) out of 1000 people with serious vitamin D deficiency would develop dementia compared with 1000 people with sufficient D levels over 18.03 years" despite some cautions around the quality of the studies reviewed.Caveats? Well, examining just one variable (vitamin D status) when it comes to a nebulous condition like dementia has to be kept in mind when interpreting such data and another pet topic of mine - how one assays for vitamin D - is also mentioned: "There is still an ongoing debate regarding the method of choice but a recent comparison between liquid chromatography– tandem mass spectrometry (LC-MS/MS) methods and immunoassays showed variable performance of immunoassays apart from the radioimmunoassay that achieved a performance similar to LC-MS/MS." Discussions on this topic should also mention the epimers of vitamin D too [2]. Then there is the rather important issue of how the genetics of vitamin D formation/metabolism might also be something to look at [3] if one assumes some connection between small genetic 'blips' and possible risk, bearing in mind gene expression over just gene mutation might be important [4].Minus any medical or clinical advice given or intended (something not given on this blog), I do however find data such as that from Sommer et al potentially important and something that can seemingly be acted upon quite easily (at least in terms of correcting any vitamin D deficiency/insufficiency). There is for example, a growing body of evidence potentially linking vitamin D and cognitive functions (see here) and alongside more population-wide advice being handed out by Government (see here), there seems to be some common sense in ensuring adequate sunlight exposure or vitamin intake.Finally, minus any scaremongering or making connections where none might exist, specific groups of people where vitamin D deficiency seems to be 'over-represented' (see here and see here for example) might also be eligible for some enhanced screening for dementia in later life if one assumes a possible longitudinal link...----------[1] Sommer I. et al. Vitamin D deficiency as a risk factor for dementia: a systematic review and meta-analysis. BMC Geriatrics. 2017; 17: 16.[2] Aghajafari F. et al. Plasma 3-Epi-25-Hydroxycholecalciferol Can Alter the Assessment of Vitamin D Status Using the Current Reference Ranges for Pregnant Women and Their Newborns. J Nutr. 2016 Jan;146(1):70-5.[3] Lee YH. et al. Vitamin D receptor polymorphisms and susceptibility to Parkinson's disease and Alzheimer's disease: a meta-analysis. Neurol Sci. 2014 Dec;35(12):1947-53.[4] Delgado-Morales R. & Esteller M. Opening up the DNA methylome of dementia. Mol Psychiatry. 2017 Jan 3.----------Sommer I, Griebler U, Kien C, Auer S, Klerings I, Hammer R, Holzer P, & Gartlehner G (2017). Vitamin D deficiency as a risk factor for dementia: a systematic review and meta-analysis. BMC geriatrics, 17 (1) PMID: 28086755... Read more »

Sommer I, Griebler U, Kien C, Auer S, Klerings I, Hammer R, Holzer P, & Gartlehner G. (2017) Vitamin D deficiency as a risk factor for dementia: a systematic review and meta-analysis. BMC geriatrics, 17(1), 16. PMID: 28086755  

  • January 26, 2017
  • 03:10 AM

Andrew Whitehouse on challenging yet another autism status quo: diagnosis before intervention

by Paul Whiteley in Questioning Answers

"This paper provides an overview of the benefits and drawbacks of the current clinical pathway that places primacy on a diagnostic assessment for triggering the commencement of therapy. The paper then presents an alternative clinical pathway - the identification and provision of therapy to infants at risk of ASD [autism spectrum disorder] - and provides a critical review of current evidence supporting this model."So said the 'lecture paper' by Andrew Whitehouse [1] and, as per the title of this short post, another peer-reviewed critical look at an autism status quo from this author (see here) who does not seem to be afraid to rock the boat (NB. see Cordelia Fine's new book for further discussion on the idea that there probably is no 'male' and female' binary brain differentiation).Bearing in mind this was a paper based on a lecture given at a speech and language conference in Australia, I'm once again intrigued with the sentiments expressed by Prof. Whitehouse, who really does seem to be quite clued into how (a) an autism / autism spectrum diagnosis is for many children, happening 'too late' in terms of the time between when symptoms start manifesting and them getting an 'official' label, and (b) how quite a few children are entering into early intervention programs (for autism) before formal diagnosis is given (see here). I'm not going to go into the possible reasons 'why' the diagnostic pathway seems to be such a long one for so many (although there are clues outside of 'we're just better at recognising autism') but it strikes me as eminently sensible that if a child presents with autistic traits/behaviours, why wait for formal assessment but rather set plans in motion to 'zoom in' on specific areas where intervention might be required. Yes, there will be cost implications - without sounding too conspiracy-like, I've often wondered whether the 'queues' of those waiting for diagnosis at least here in Blighty is partly because the powers-that-be know that there will be cost implications following a diagnosis - but if one assumes that early intervention might have some long-term positive effects (see here) even the bean counters might see some benefits. I might add that whilst behavioural intervention is probably important, this should not be at the expense of other 'types' of intervention for some 'types' of autism (see here) and the value of other screening programs outside of just asking 'is it autism' (see here)?'Nuff said, for now at least but I will be coming to another Whitehouse paper quite soon on this blog...----------[1] Whitehouse AJ. Elizabeth Usher Memorial Lecture: Rethinking the clinical pathway for autism spectrum disorder and challenging the status quo. Int J Speech Lang Pathol. 2017 Jan 13:1-10.----------Whitehouse AJ (2017). Elizabeth Usher Memorial Lecture: Rethinking the clinical pathway for autism spectrum disorder and challenging the status quo. International journal of speech-language pathology, 1-10 PMID: 28084105... Read more »

  • January 25, 2017
  • 08:10 AM

A poo transplant for [some] autism?

by Paul Whiteley in Questioning Answers

I've talked about 'fecal microbial transplants' a.k.a the poo(p) transplant before on this blog (see here). That previous entry was about the more typical (and potentially life-saving) use of a poo transplant - where stool from one person is extracted, 'repackaged' and transferred to another person - albeit with caveats in terms of possible long-term side-effects. Now it appears that poo transplants are being investigated with something rather more central to the typical contents of the blog...The paper by Dae-Wook Kang and colleagues [1] (open-access) has already been picked up by some media (see here) and it seems, also has a following from likely proponents and detractors particularly on social media. Including one James Adams on the authorship list, someone who is quite well-known in autism research circles (see here and see here for examples) alongside some other notable inclusions (Alessio Fasano, Thomas Borody, etc), the authors describe the results of small open-label study - I repeat, a small open-label trial - of 18 participants diagnosed with an autism spectrum disorder (ASD) who underwent a 10-week program characterised by the use of antibiotics, a bowel cleanse and then regular poo transplants for approximately 8 weeks. Additional information about the study and its results can be found here or if you wish, you can see the entry here.Tapping into a growing interest in how the gut (and its contents) might be important for at least some autism (see here for example) the aims of the trial were to "follow gut microbiota in healthy and treated children with ASD longitudinally as well as to evaluate an investigational new treatment, MTT [Microbiota Transfer Therapy], for its effectiveness in children with ASD in treating both GI [gastrointestinal] symptoms (primary outcome) and ASD-related symptoms (secondary outcomes), and to determine the effect of MTT on the gut microbiome."The study included children diagnosed on the autism spectrum - ADI-R diagnosed - aged between 7-16 years old. All presented with moderate to severe functional bowel issues alongside their autism (something not unusual it seems). The authors also report using a control group of "20 age- and gender-matched neurotypical children without GI disorders" who were monitored but not treated as part of their study design.The study first involved the administration of the antibiotic vancomycin for 2 weeks (something that has, on its own, some peer-reviewed research history with autism in mind [2]) used to 'profoundly suppress' pathogenic bacteria. Prilosec, the brand name for omeprazole was also administered towards the end of the bacterial washout phase initiated by the use of vancomycin. Prilosec is a medicine traditionally used to suppress stomach acid secretions and was used to "remove most remaining gut bacteria and vancomycin" and aid the passage and survival of the donor stool to the wider gastrointestinal (GI) tract. I say all that knowing that such medicines can affect the composition of the gut microbiota. Then came the bowel cleanse (Moviprep) complete with a fasting from food day, followed by the main [research] event: oral or rectal administration of donor stool and an initial high dose followed by maintenance doses. I know some people might be slightly uncomfortable with the idea of the rectal administration of medicines but there are some common-sense reasons behind this form of medicines delivery particularly where oral dosage forms (tablets, capsules) might not be well tolerated. As for the initial oral dosage form: "the participants began either oral administration of SHGM [Standardized Human Gut Microbiota] (2.5 × 1012 cells/day) mixed in a chocolate milk, milk substitute, or juice for 2 days (divided into three daily doses)." I have to say that whilst I initially envisaged Austin Powers and his 'tastes a bit nutty' scene, this was very much NOT how things actually were.Alongside the donor stool formulation being trialled predominantly with regards to safety and initial efficacy, researchers also surveyed participants in relation to (i) effects on their gut microbiota (diversity and species present), (ii) the presentation of bowel symptoms/habits and (iii) behavioural outcomes covering autism-specific issues (via the CARS) and more general adaptive behaviours (via the Vineland scales for example). I was also happy to see a section included in their paper labelled 'virome bioinformatics' hat-tipping the idea that gut bacteria are not the only passengers we carry in our deepest, darkest recesses.Results: well something certainly seemed to happen when looking at before, during and after results of this case series trial. First and foremost adverse effects were small and limited (hyperactivity, irritability) meaning that in the short term at least, the poo transplants and pre-poo transplant protocols were tolerated quite well. This is also evident in the 0% study attrition rate (i.e. everyone who started the study stayed in the study).So: "Substantial changes in GI and ASD symptoms were observed. GI symptoms, as assessed by the GSRS [Gastrointestinal Symptom Rating Scale], significantly improved for abdominal pain, indigestion, diarrhea, and constipation." The authors report some significant differences in scores over the course of the intervention period such that: "The average GSRS score dropped 82% from the beginning to end of the treatment and remained improved (77% decrease from baseline) even 8 weeks after treatment stopped." That is a helluva placebo effect! Indeed, only 2 participants from the cohort were classified as 'non-responders' on the basis of their GSRS scores over the course of the study.Also: "Beyond these GI improvements, ASD-related behavior also improved following MTT." The sorts of changes to CARS scores being reported were in the region of a 20% reduction in 'core ASD' symptoms at 8 weeks compared to baseline reports. Further, 8 weeks after the intervention had been completed the behavioural gains ("relative to baseline") were still evident based on CARS scoring. These ratings also did not depend on whether the poo transplant was administered orally or rectally.The authors also discuss some not unexpected changes to gut bacterial profiles in their cohort over the intervention period. At baseline: "gut bacteria were significantly less diverse in children with ASD than neurotypical controls." This finding is in line with other study results from the authors (see here). Bacterial diversity did (slowly) change over the intervention period to a point where at 18 weeks after baseline median richness "was statistically indistinguishable between the ASD and control groups." This was noted in 16 of the 18 participants with ASD.Finally: "Specific genera that significantly changed in their relative abundances with treatment included Bifidobacterium, Prev... Read more »

  • January 25, 2017
  • 08:00 AM

Asthma & Histone Acetylation: an important epigenetic mechanism in allergic diseases

by Daniel Potaczek in EpiBeat

Epigenetic regulation is thought to be one of the most important mechanisms contributing to the development and clinical course of chronic immunological diseases like allergies and asthma. DNA methylation has been extensively studied in this context, which has not been a case of histone modifications such as histone acetylation or methylation.

Early epigenetic studies from our lab conducted in mouse models demonstrated a role for histone acetylation in mediating bacteria-induced protection against asthma.1 Subsequently, apart from the continuation of animal investigations, we also launched human studies. The need of reproducible, quick, and cost-effective methods that allow the analysis of multiple human samples from larger cohorts, led us to the establishment of our own, in-house chromatin immunoprecipitation (ChIP) assay2 that utilizes a relatively low input of cells. Although it was originally optimized for CD4 T-cells, other types of cells can be also studied with small modifications to the protocol.2... Read more »

Harb H, Alashkar Alhamwe B, Garn H, Renz H, & Potaczek DP. (2016) Recent developments in epigenetics of pediatric asthma. Current opinion in pediatrics, 28(6), 754-763. PMID: 27662207  

Harb, H., Amarasekera, M., Ashley, S., Tulic, M., Pfefferle, P., Potaczek, D., Martino, D., Kesper, D., Prescott, S., & Renz, H. (2016) Epigenetic Regulation in Early Childhood: A Miniaturized and Validated Method to Assess Histone Acetylation. International Archives of Allergy and Immunology, 168(3), 173-181. DOI: 10.1159/000442158  

Harb, H., Raedler, D., Ballenberger, N., Böck, A., Kesper, D., Renz, H., & Schaub, B. (2015) Childhood allergic asthma is associated with increased IL-13 and FOXP3 histone acetylation. Journal of Allergy and Clinical Immunology, 136(1), 200-202. DOI: 10.1016/j.jaci.2015.01.027  

Stefanowicz, D., Lee, J., Lee, K., Shaheen, F., Koo, H., Booth, S., Knight, D., & Hackett, T. (2015) Elevated H3K18 acetylation in airway epithelial cells of asthmatic subjects. Respiratory Research, 16(1). DOI: 10.1186/s12931-015-0254-y  

Harb, H., & Renz, H. (2015) Update on epigenetics in allergic disease. Journal of Allergy and Clinical Immunology, 135(1), 15-24. DOI: 10.1016/j.jaci.2014.11.009  

  • January 25, 2017
  • 02:56 AM

Autism and visual impairment reviewed

by Paul Whiteley in Questioning Answers

Of the various autism science journals out there in peer-reviewed (La-La!) land, one journal in particular is really starting to grow on me: [The] Review Journal of Autism and Developmental Disorders.I like this journal because it is basically systematic review and meta-analysis heaven when it comes to the quite voluminous autism research literature and seems to publish some real gems (see here for example).Another paper from this journal caught my eye recently by Maggie Butchart and colleagues [1] (open-access) synthesising the collected research on "the prevalence of visual impairments in children and adults with Autism Spectrum Disorder (ASD), and the similar behavioural traits associated with both visual impairment and autism." Affiliated with the RNIB - Royal National Institute of Blind People - Scotland among other groups, the authors trawled the research literature looking at reported visual impairments in relation to the autism spectrum and provide quite a nice overview of 'where we're at' with regards to "papers published from 2000-2015."The paper is open-access but a few comments are required bearing in mind my relative lack of knowledge on the complexities of visual impairments.First: "Collating the evidence from six of the seven prevalence studies suggests a refractive error rate in the childhood ASD population studied at 22.9–32.7%, which is comparable with general childhood refractive error rates in 6–7 year olds at 29%, and 32.3% in 12–13 year olds." What this means is that a diagnosis of autism does not protect against the presence of refractive errors ('when the shape of the eye prevents light from focusing directly on the retina').Second: "Estimates of childhood strabismus in the UK is 1.5 to 5.3%... but in the evidence collated in this review, the incidence of strabismus amongst autistic participants is higher at 8.3%." Strabismus, where the eyes don't align properly, seems to be a little bit more prevalent when it comes to autism compared with general population statistics. This is a topic that I've talked about before on this blog in relation to correcting such an issue with autism in mind (see here).Finally: "There were no studies examining ophthalmic conditions and adult autistic populations who are more at risk of age-related visual impairments." Bearing in mind the search parameters included in the Butchart paper, I'm kinda dismayed that this is the current state of affairs. You'd have thought with all the money and resources being thrown into autism research that someone, somewhere might have thought more about eye health in adults with autism? Eye-tracking, reading the mind in the eyes test... the word 'eye' or 'eyes' is prominent in autism research but just not in relation to eye health it seems. And bear in mind that issues with eye health probably will affect the results of some of those autism 'eye' studies.Eye or vision issues related to autism have often been a topic of discussion on this blog (see here and see here for examples) and so I'm glad that someone has finally brought a review of this area into the peer-reviewed arena. Screening is important; even if some of those on the autism spectrum may not always be by first sight (pardon the pun) particularly amenable to taking part in an eye exam - adjustments can and should be made.And finally consider this: "Undiagnosed visual impairment is likely to severely impact quality of life. There is a need therefore for education and training that equip autism support practitioners with the awareness and skills to identify potential visual impairment, to refer individuals to optometry professionals if necessary, and to make necessary adjustments to service environments and support practices for individuals identified as having a visual impairment." Not much more to say really is there aside from 'make it so'.----------[1] Butchart M. et al. Autism and Visual Impairment: a Review of the Literature. Review Journal of Autism and Developmental Disorders. 2017. Jan 5.----------Butchart, M., Long, J., Brown, M., McMillan, A., Bain, J., & Karatzias, T. (2017). Autism and Visual Impairment: a Review of the Literature Review Journal of Autism and Developmental Disorders DOI: 10.1007/s40489-016-0101-1... Read more »

Butchart, M., Long, J., Brown, M., McMillan, A., Bain, J., & Karatzias, T. (2017) Autism and Visual Impairment: a Review of the Literature. Review Journal of Autism and Developmental Disorders. DOI: 10.1007/s40489-016-0101-1  

  • January 24, 2017
  • 11:52 AM

Crowdfunding and Tribefunding in Science

by Jalees Rehman in The Next Regeneration

Competition for government research grants to fund scientific research remains fierce in the United States. The budget of the National Institutes of Health (NIH), which constitute the major source of funding for US biological and medical research, has been increased only modestly during the past decade but it is not even keeping up with inflation. This problem is compounded by the fact that more scientists are applying for grants now than one or two decades ago, forcing the NIH to enforce strict cut-offs and only fund the top 10-20% of all submitted research proposals. Such competition ought to be good for the field because it could theoretically improve the quality of science. Unfortunately, it is nearly impossible to discern differences between excellent research grants. For example, if an institute of the NIH has a cut-off at the 13 percentile range, then a grant proposal judged to be in the top 10% would receive funding but a proposal in top 15% would end up not being funded. In an era where universities are also scaling back their financial support for research, an unfunded proposal could ultimately lead to the closure of a research laboratory and the dismissal of several members of a research team. Since the prospective assessment of a research proposal’s scientific merits are somewhat subjective, it is quite possible that the budget constraints are creating cemeteries of brilliant ideas and concepts, a world of scientific what-ifs that are forever lost.... Read more »

Vachelard J, Gambarra-Soares T, Augustini G, Riul P, & Maracaja-Coutinho V. (2016) A Guide to Scientific Crowdfunding. PLoS Biology, 14(2). PMID: 26886064  

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