Did Charles Darwin's thirst for skulls contribute to the near-extinction of the Aboriginal Tasmanian people?
If you believe certain creationists, Darwin sought examples of Tasmanian skulls in order to prove that this unfortunate race was a 'missing link' between humans and apes. However, according to John van Wyhe in a new paper called Darwin's body-snatchers?, this story has zero basis in fact.
As a Darwin scholar, I thought I had heard all the myths concerning Charles Darwin but on... Read more »
A huge of number of people keeps on thinking about the existence of some other intelligent beings in the universe but still we have not met any aliens. Why?
Earth is rare
Earth is special planet
One of the reasons that we have not met aliens is that Earth is rare and there is nothing just like Earth in the universe. In this regard, Paleontologist Peter Ward and astronomer Donald Brownlee presented the Rare Earth Hypothesis about 17 years ago.
According to the Rare Earth Hypothesis, the planets having Earth-like complex (animal) life, according to our knowledge, are very rare in the universe. Moreover, the chains of events that occurred on this planet and that were important for the development of life are so complex that they would not occur anywhere in the universe; thereby, making it highly improbable to meet aliens from other planets.
Picture showing wreckage
Every intelligent life may face some disasters after reaching a sufficiently advanced technology
Even though some alien life exists in the universe, Great Filter Theory suggests that it is probably difficult for the alien or intelligent life in the universe to reach such a technologically advancing stage that they start long-distance space travel or communication.
On the Earth, we know that some natural disasters often occur taking the life many years back; thereby, causing the people to start the life from somewhat beginning. For example, our advancements in nuclear technology could take us to nuclear war finally leading to mass destruction, and loss of advanced technology and many important human beings, i.e. great filter. Similar events, i.e. cataclysmic natural disasters, could also occur on other planets having some alien lives causing them to start their life from zero, and finally, making it almost impossible for them to go somewhere in the universe.
Another similar concept is that of the Medea Hypothesis, noted by paleontologist Peter Ward that suggests the concept of self-destruction. This hypothesis shows that the internal suicidal clock of living beings runs out before making any connection with aliens.
Technology at small scale
Why move outward when inward has much to give?
John Smart’s Transcension Hypothesis suggests that intelligent life in our universe started advancements in an inward direction rather than an outward direction in space. This concept can be compared to the miniaturization concept such as that of computers. Initially, computers were large in size but with the passage of time, their size decreased but power increased. Similarly, intelligent alien life progresses towards more denser and efficient use of space, time, energy, and matter, i.e. STEM. Eventually, the intelligent life in space started living in a black hole that is outside of this space-time continuum. Smart and other such researchers are of opinion that black holes are ideal for computation, energy generation, time travel, and more such processes for any kind of intelligent living beings.
Perhaps Earth is not a super-habitable place…
Science fiction often shows that intelligent alien life was searching for fuel or some other things such as food etc and they found Earth, but reality could be very different from that. May be Earth is not a super-habitable place in the universe. It is quite possible that if aliens are more intelligent than human beings they would not require the resources of Earth. They may think that the Earth and the living beings on this planet are of no use in regards to their highly advanced technologies. Moreover, if we leave the concept of super-habitable worlds, there are more than 8 billion Earth like planets in the universe, and intelligent aliens could go there, if they want.
Perhaps we are living in an artificial universe
Planetarium Hypothesis by Stephen Baxter suggests that we are perhaps living in an “artificial universe” or “virtual reality ‘planetarium’” that is giving us an illusion of empty universe. Supporters of this idea are also of opinion that we are living in a computer simulation that has been designed by some advanced aliens who are able to work on matter and energy on large scale. This is also showing that the intelligent life has not designed the program in such a way that we would be able to find any aliens in the universe.
Perhaps Earth is far far away from other inhabitable planets
Perhaps Earth is at a very large distance from other inhabited planets
Alien life might exist in the universe but still we have not met them, and one of the important reasons is that the Earth is at a very large distance away from them. In this case, Percolation theory suggests that some areas in the universe show large clustered growth, whereas some areas of growth have outlier positions. Other intelligent beings in the universe are perhaps living in that large clustered growth, and the Earth is in the outlier position.
Perhaps aliens have some unknown signals
We are unable to understand their signals
It is quite possible that alien life exists and they are also sending signals to us, but due to the difference in nature of signals we are unable to understand their signals. Perhaps, aliens have completely different senses as compared to human beings. Perhaps they are using the communication methods that are highly advanced in comparison to our communication methods.
As Lord Rees, cosmologist and astrophysicist, noted, “They could be staring us in the face, and we just don’t recognize them. The problem is that we’re looking for something very much like us, assuming that they at least have something like the same mathematics and technology. I suspect there could be life and intelligence out there in forms we can’t conceive.”
Via: John Smart, Montana State University, Robin Hanson, Planetarium Hypothesis, Percolation theory, Medea Hypothesis, ListVerse, Heller, R., & Armstrong, J. (2014). Superhabitable Worlds Astrobiology, 14 (1), 50-66 DOI: 10.1089/ast.2013.1088... Read more »
Time flies! Once again, I'm posting my annual 'state of the science' autism research review, this time covering the particularly unusual year of 2016.With around 300 blog entries to choose from, I'm changing the format this year to list a 'top 5' of areas where I think some scientific progress has been made. The caveat as ever being that there are still mountains to climb in terms of delineating aetiology, nature and importantly, how one can actually improve quality of life for those on the spectrum. At the foot of this post I've also detailed a few 'areas to watch' in the coming months/years too.So, in no particular order, here goes:1. Vitamin D and autism. As per my 'one to watch' prediction from the 2015 end-of-year review, there has been a veritable science feast focused on the sunshine vitamin/hormone in connection to autism (see here). The research discussions in 2016 started with some initial talk about 'clinical improvements' following supplementation with vitamin D (see here). This was accompanied by chatter about the possible use of pregnancy vitamin D affecting risk of offspring autism (see here and see here). Screening for vitamin D levels as and when a diagnosis of autism is received was also discussed (see here). Then, towards the end of the year, things got really interesting as one of the first controlled trials of vitamin D supplementation in autism was published (see here) with the promise of more to come (see here). The findings (double-blind, placebo-controlled) suggested that for some at least, vitamin D over placebo might have the ability to affect the presentation of some aspects of autism. The caveats? Well, larger controlled trials are required and one has to be careful about doses of vitamin D in light of some cautionary tales (see here). What else needs to be done on the topic of vitamin D and autism? Given the number of conditions the sunshine vitamin has been linked to - some labels potentially crossing over with autism - a wider view of any 'effects' outside of those just on core autism symptoms might be useful. This will probably also provide some more potentially information about the possible hows-and-whys of vitamin D action.2. Autism as a plural condition. 'The autisms' is a phrase not unfamiliar to this blog (see here) but this year, a couple of papers really started putting some scientific flesh on to the bones of the argument for why we need to rethink autism. Discussions on the paper by Lynn Waterhouse and colleagues  (see here) set the tone for such a debate and how the label of autism serves a purpose in defining / describing symptoms but seemingly does little else when it comes to a research perspective looking at the hows-and-whys of autism. That autism seemingly appears alongside a long list of other conditions including quite a few of the various inborn errors of metabolism (see here and see here) substantiates the idea that a singular labels says very little about the 'essence' of autism. And speaking of ESSENCE (see here), there was yet more on this important topic. Another part of this 'pluralisation' debate is the fact that the 'autism is a lifelong condition' mantra rolled out again and again and again might not necessarily ring true for everyone who was once diagnosed on the autism spectrum (see here and see here). And to say that these children/adults were 'never autistic in the first place' does a real disservice to them, their parents and loved ones and the professionals who diagnosed them...3. Meta-analysing autism. Mirroring what seems to be apparent in the research literature in general, a whole slew of meta-analyses and systematic reviews on the topic of autism emerged this year. We had reviews on long-term outcome and quality of life (see here), behavioural outcomes following exercise (see here), medication (see here and see here), joint intervention strategies (see here), pregnancy infection and offspring autism risk (see here) and allergic asthma and autism (see here) to name but a few. One of the particularly notable reviews of the collected data was that by Nevill and colleagues  on the topic of parent-mediated interventions for young children with autism. Covering a topic with more than a pinch of media hype this year (see here), the science behind the hype in this area actually turns out to be not that strong at the moment...4. Real-world autism. Although I'm partial to reading quite a bit on the science about autism, one thing I hope I never forget is how that science translates into 'action' when it comes to autism, either in terms of 'hows-and-whys' or impacting on the day-to-day positives and negatives of living with the label. This year I've talked about more research on the topic of 'real world autism' covering various angles including: wandering and autism (see here), parents lived experience of offspring autism diagnosis and beyond (see here and see here), early mortality and autism (... Read more »
Nevill, R., Lecavalier, L., & Stratis, E. (2016) Meta-analysis of parent-mediated interventions for young children with autism spectrum disorder. Autism. DOI: 10.1177/1362361316677838
Thiamine, or vitamin B1, is vital for the survival of all living things. One of the biologically functional forms of thiamine, thiamine pyrophosphate (TPP), is essential for the catalytic activity of several critical metabolic enzymes. For this reason, we must get thiamine from the food that we eat (or the vitamin pills that we swallow). Microbes obtain the vitamin from their surroundings, but they can also make their own thiamine if it's not available.It turns out that the Lyme disease spirochete Borrelia burgdorferi does not need thiamine, as described by Zhang and colleagues in Nature Microbiology. The B. burgdorferi genome lacks the genes encoding the dedicated transporters that bring thiamine into the cell. The genes encoding the enzymes that produce thiamine are also absent. Chemical analysis of B. burgdorferi by HPLC failed to detect thiamine or TPP. Despite lacking the means to make or acquire thiamine, B. burgdorferi grew just fine in culture medium devoid of thiamine.The researchers conducted stringent tests to verify that B. burgdorferi could live without thiamine. To remove all traces of thiamine, they introduced the bcmE gene from Clostridium botulinum into the spirochete. The bcmE gene encodes an enzyme that rapidly breaks down thiamine. In culture, the spirochete grew at the same rate whether or not it had bcmE. The bcmE gene did not affect B. burgdorferi's ability to infect mice or to survive in feeding Ixodes scapularis ticks. The results of these experiments provided strong evidence that B. burgdorferi doesn't need thiamine to infect the tick vector or mouse.How does B. burgdorferi manage to live without thiamine? It can do without most of the enzymes that require the TPP coenzyme, but it's less obvious how B. burgdorferi copes without pyruvate dehydrogenase (PDH), a TPP-dependent enzyme that converts pyruvate to acetyl-CoA (see figure). Acetyl-CoA is an essential precursor to the bacterial cell wall, something that B. burgdorferi obviously needs. The researchers proposed that B. burgdorferi makes acetyl-CoA by an alternative pathway that starts with acetate. B. burgdorferi possesses the enzymes acetate kinase (ACK) and phosphate acetyltransferase (PTA), which convert acetate to acetyl-CoA (see figure).Figure 4 from Zhang et al., 2016. Enzymes in red (PDC, PDH, and POX) require the TPP coenzyme. Metabolic pathways found in other bacteria but missing in B. burgdorferi are shown with dashed lines.B. burgdorferi may not be alone in living without thiamine. The researchers also looked at the genomes of other bacterial pathogens that are transmitted by arthropods. Borrelia hermsii (relapsing fever), Rickettsia prowazekii (epidemic typhus), and R. conorii (Mediterranean spotted fever) were missing the genes for thiamine biosynthesis and the enzymes that use thiamine pyrophosphate as a coenzyme.The presence of the alternative pathway to acetyl-CoA synthesis assumes that acetate is available in the microenvironment surrounding the arthropod-borne pathogen. According to measurements presented in a 2010 paper, acetate is present in the midgut of fed I. scapularis ticks and in mouse blood. The B. burgdorferi protein BBA34 may be a transporter that may brings acetate into the cell.ReferencesZhang K, Bian J, Deng Y, Smith A, Nunez RE, Li MB, Pal U, Yu AM, Qiu W, Ealick SE, & Li C (2016). Lyme disease spirochaete Borrelia burgdorferi does not require thiamin. Nature Microbiology, 2 PMID: 27869793Xu H, Caimano MJ, Lin T, He M, Radolf JD, Norris SJ, Gherardini F, Wolfe AJ, & Yang XF (2010). Role of acetyl-phosphate in activation of the Rrp2-RpoN-RpoS pathway in Borrelia burgdorferi. PLoS pathogens, 6 (9) PMID: 20862323Subba Raju BV, Esteve-Gassent MD, Karna SL, Miller CL, Van Laar TA, & Seshu J (2011). Oligopeptide permease A5 modulates vertebrate host-specific adaptation of Borrelia burgdorferi. Infection and immunity, 79 (8), 3407-20 PMID: 21628523... Read more »
Zhang K, Bian J, Deng Y, Smith A, Nunez RE, Li MB, Pal U, Yu AM, Qiu W, Ealick SE.... (2016) Lyme disease spirochaete Borrelia burgdorferi does not require thiamin. Nature Microbiology, 16213. PMID: 27869793
Xu H, Caimano MJ, Lin T, He M, Radolf JD, Norris SJ, Gherardini F, Wolfe AJ, & Yang XF. (2010) Role of acetyl-phosphate in activation of the Rrp2-RpoN-RpoS pathway in Borrelia burgdorferi. PLoS pathogens, 6(9). PMID: 20862323
Subba Raju BV, Esteve-Gassent MD, Karna SL, Miller CL, Van Laar TA, & Seshu J. (2011) Oligopeptide permease A5 modulates vertebrate host-specific adaptation of Borrelia burgdorferi. Infection and immunity, 79(8), 3407-20. PMID: 21628523
Birt-Hogg-Dubé syndrome is caused by mutations in the FLCN gene. The FLCN protein acts as a tumour suppressor and BHD patients have a high risk of developing renal cell carcinoma (RCC). The mechanisms of tumour formation in BHD have been investigated using mouse models and human RCC tissues. However, in vitro signalling studies of human renal cells with mutant FLCN are still scarce. In a recent study, Furuya et al. (2016) established a new cell line from a BHD patient’s chromophobe RCC. The authors investigated FLCN mutations, chromosome profiles, and cytopathologic characteristics of the cell line to confirm its suitability for functional analysis of the typical phenotype of BHD-associated RCC with impaired FLCN.... Read more »
Furuya, M., Hasumi, H., Baba, M., Tanaka, R., Iribe, Y., Onishi, T., Nagashima, Y., Nakatani, Y., Isono, Y., & Yao, M. (2016) Establishment and characterization of BHD-F59RSVT, an immortalized cell line derived from a renal cell carcinoma in a patient with Birt–Hogg–Dubé syndrome. Laboratory Investigation. DOI: 10.1038/labinvest.2016.137
With the pinnacle of the season of 'jolly' almost upon us, I'd like to make some brief discussion on the findings reported by Denise Rogers and colleagues  and specifically the observation that: "ADHD [attention-deficit hyperactivity disorder] symptoms were significantly greater in the CFS [chronic fatigue syndrome] group than in HC [healthy controls]."With the aim of examining both the prevalence of fatigue in cases of ADHD and the prevalence of ADHD symptoms in adults with CFS (a term 'linked to' the condition called myalgic encephalomyelitis), researchers set about investigating several measures including self-reported (that's 'self-reported') fatigue "across groups of adults with ADHD (N = 243), CFS (N = 86), and healthy controls (HC) (N = 211)." The results were interesting insofar as that previous sentence on ADHD symptoms perhaps not being uncommon in cases of CFS vs. asymptomatic controls but also that: "Fatigue is a common clinical feature of attention deficit hyperactivity disorder (ADHD) in adulthood."Accepting that there may be important implications from the notion that fatigue may be part and parcel of at least some ADHD (see here for example), the idea that ADHD signs and symptoms might be over-represented in cases of CFS is interesting, if not necessarily novel . Minus any sweeping generalisations or psychobabble explanations of hows-and-whys (we've had quite enough of those in relation to CFS), I'd like to think that such an association could shed some light on the possible shared genetics, epigenetics and biochemistry of both conditions. Given also some initial data emerging on the potential usefulness of something like methylphenidate (indicated for cases of ADHD) for cases of CFS (see here) there are also avenues to explore in relation to shared drug targets across both conditions (see here for some discussion on oxidative stress for example). I'd like to see more study on this topic, bearing in mind how broad labels like CFS and ADHD can be. I'm also wondering whether researchers might also one day replace examination of ADHD traits with autistic traits so as to perhaps provide data on whether there may be other important associations to be had...And with that I wish you all a very Merry Christmas and a happy and healthy New Year. I'm not done just yet with this years blogging adventures as my annual 'what was hot in autism research in 2016' post is scheduled sometime next week (if you're interested/bored of turkey/bored of watching Christmas films - delete as appropriate).Music to close and as always at this time of year, it wouldn't be the same without Kirsty and Shane. And please, do try to stay out of the drunk tank this Christmas...---------- Rogers DC. et al. Fatigue in an adult attention deficit hyperactivity disorder population: A trans-diagnostic approach. Br J Clin Psychol. 2016 Dec 5. Sáez-Francàs N. et al. Attention-deficit hyperactivity disorder in chronic fatigue syndrome patients. Psychiatry Res. 2012 Dec 30;200(2-3):748-53.----------Rogers, D., Dittner, A., Rimes, K., & Chalder, T. (2016). Fatigue in an adult attention deficit hyperactivity disorder population: A trans-diagnostic approach British Journal of Clinical Psychology DOI: 10.1111/bjc.12119... Read more »
Rogers, D., Dittner, A., Rimes, K., & Chalder, T. (2016) Fatigue in an adult attention deficit hyperactivity disorder population: A trans-diagnostic approach. British Journal of Clinical Psychology. DOI: 10.1111/bjc.12119
by Piter Kehoma Boll Celebrating Christmas (or whatever you call this time of the year), today’s Friday Fellow is another lichen. And the reason I chose it is because it is known as Christmas wreath lichen due to its red … Continue reading →... Read more »
"Some psychosis cases an 'immune disorder'" went the BBC headline with reference to the paper by Belinda Lennox and colleagues  talking about the detection of antibodies against the N-methyl-D-aspartate receptor (NMDAR) in cases of first-episode psychosis (FEP).Although by no means a universal phenomenon, researchers reported that 3% of their 228 participants diagnosed with FEP who provided a blood sample showed the presence of NMDAR antibodies compared with none of the healthy controls (n=105) included for study. As part of the condition known as anti-NMDAR encephalitis, the presence of NMDAR antibodies can indeed include/induce psychotic features .This is interesting work. For anyone that has come across the book 'Brain on Fire' by Susannah Cahalan, there is a growing interest in how the presentation of psychiatric features can, on occasion, include a significant role for the immune system and particularly, the concept of autoimmunity (where the body's own immune system fails to differentiate between 'self' and 'other'). Some of the authors included on the Lennox paper have previously summarised and discussed the idea that NMDAR antibodies might show a connection to some cases of psychosis and conditions manifesting psychosis such as schizophrenia . The current data tally with their previous conclusion that: "A minority of patients with psychosis are anti-NMDA receptor antibody positive" and onwards the idea that there may be many different 'roads' to psychosis in these days of plural conditions (see here).Where next for this research area I hear you ask? Well, set against the idea that various autoimmune diseases might be over-represented alongside a diagnosis like schizophrenia (see here), one needs to tease out some of the hows-and-whys details. Does, for example, a history of autoimmune disease 'set someone up' for psychosis and/or schizophrenia? Or is the autoimmune element of it something that follows a diagnosis of psychosis and/or schizophrenia? I have some opinions on this based on other findings on how autoimmunity may come about for some (see here for some discussion on HERVs) taking into account other peer-reviewed ideas and data . I don't profess to be right or offer any universal answer but it is interesting that endogenous virus expression does seem to be heightened in a condition like schizophrenia and said elements might be considered important in processes such as molecular mimicry as one mechanism of autoimmunity . There is a research plan to carry out and specifically on the topic of how NMDAR antibodies come about.The other important 'where next' for this area of investigation is the tantalising prospect that 'treating' said autoimmune reaction might have some important effects on the presentation of something like FEP. There are hints out there in the peer-reviewed literature of possible treatment options being available. I might for example, draw your attention to some overlapping work looking at anti-NMDAR encephalitis ('encephalitis' that is) and cases of autism (see here and see here) where intervention options are discussed. With no medical advice given or intended, methylprednisolone seems to have found therapeutic favour for some. Other, more aggressive treatment options have also been reported but further investigations are required.I note the words 'immuno-psychiatry' are mentioned in the media reporting of the Lennox findings and I'm happy to see the profile of this area of research being elevated through such work. The idea that immune function(s) might be doing so much more than just identifying and eradicating foreign bodies to maintain our physical health continues to gather pace...---------- Lennox BR. et al. Prevalence and clinical characteristics of serum neuronal cell surface antibodies in first-episode psychosis: a case-control study. Lancet Psychiatry. 2016. Dec 7. Dalmau J. et al. Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurology. 2011;10(1):63-74. Pollak TA. et al. Prevalence of anti-N-methyl-D-aspartate (NMDA) receptor [corrected] antibodies in patients with schizophrenia and related psychoses: a systematic review and meta-analysis. Psychol Med. 2014 Sep;44(12):2475-87. Slokar G. & Hasler G. Human Endogenous Retroviruses as Pathogenic Factors in the Development of Schizophrenia. Frontiers in Psychiatry. 2015;6:183. Trela M. et al. The role of molecular mimicry and other factors in the association of Human Endogenous Retroviruses and autoimmunity. APMIS. 2016 Jan-Feb;124(1-2):88-104.----------Lennox, B., Palmer-Cooper, E., Pollak, T., Hainsworth, J., Marks, J., Jacobson, L., Lang, B., Fox, H., Ferry, B., Scoriels, L., Crowley, H., Jones, P., Harrison, P., & Vincent, A. (2016). Prevalence and clinical characteristics of serum neuronal cell surface antibodies in first-episode psychosis: a case-control study The Lancet Psychiatry DOI: 10.1016/S2215-0366(16)30375-3... Read more »
Lennox, B., Palmer-Cooper, E., Pollak, T., Hainsworth, J., Marks, J., Jacobson, L., Lang, B., Fox, H., Ferry, B., Scoriels, L.... (2016) Prevalence and clinical characteristics of serum neuronal cell surface antibodies in first-episode psychosis: a case-control study. The Lancet Psychiatry. DOI: 10.1016/S2215-0366(16)30375-3
"New form of autism found" went one of the headlines reporting on the paper by Dora C. Tărlungeanu and colleagues  and findings that "elucidate a neurological syndrome defined by SLC7A5 mutations and support an essential role for the BCAA [branched-chain amino acids] in human brain function." This work continues a rather important research story talking about how one 'type' of autism might have some important roots in relation to the branched-chain amino acids and their metabolism (see here and see here for more information).So, mice were the focus on the paper by Tărlungeanu et al (including one Gaia Novarino on the authorship list) and an extension of the idea that the BCAAs may play an important role in some autism in these days of the plural 'autisms' (see here). SLC7A5 represents a gene that codes for a protein involved in the transport of BCAAs into the brain among other things. Researchers studied mice who were genetically 'edited' to present with a "deletion of Slc7a5 from the endothelial cells of the BBB [blood-brain barrier]." In effect, the area of the body where SLC7A5 serves those important transport duties, a hold-my-hand partner was missing resulting in lower brain levels of the BCAAS. Researchers noted a few important things in those SLC7A5-missing mice; not least in relation to their mouse behaviour(s) and how bearing in mind mice are mice not people, they seemed to present with behavioural issues not a million miles away from that noted in relation to autism. 'Social interaction' was as I understand it, something potentially affected in those SLC7A5-missing mice. Further: "we identified several patients with autistic traits and motor delay carrying deleterious homozygous mutations in the SLC7A5 gene" suggesting that their results might stretch to people too.And then something else that might eventually be important: "we demonstrate that BCAA intracerebroventricular administration ameliorates abnormal behaviors in adult mutant mice." Intracerebroventricular administration basically means an injection straight into the brain. After a few weeks of such injections, researchers noted that mouse behaviours began to change coincidental to the direct administration of those BCAAs.This is interesting research. I know that not everyone on the autism spectrum presents with issues with the BCAAs (as far as we know). But in these days of increasing plurality when it comes to autism coupled to the rise and rise of study on the various inborn errors of metabolism in relation to autism (see here), this could be pertinent to at least one type of autism. I also appreciate that 'brain injections' of something like BCAAs are not exactly a desirable option for anyone so there is still some work to do in terms of how to correct any central BCAA deficiency if and when identified. Talk about a possible relationship between the BBB and autism in the Tărlungeanu paper also continues a theme (see here) where this important barrier separating the brain from the other contents of the body (and indeed, the outside world) might represent something potentially quite important to autism (see here) and indeed, with 'transporters' also in mind (see here).Much more research is implied.---------- Tărlungeanu DC. et al. Impaired Amino Acid Transport at the Blood Brain Barrier Is a Cause of Autism Spectrum Disorder. Cell. 2016. Dec 1.----------Tărlungeanu, D., Deliu, E., Dotter, C., Kara, M., Janiesch, P., Scalise, M., Galluccio, M., Tesulov, M., Morelli, E., Sonmez, F., Bilguvar, K., Ohgaki, R., Kanai, Y., Johansen, A., Esharif, S., Ben-Omran, T., Topcu, M., Schlessinger, A., Indiveri, C., Duncan, K., Caglayan, A., Gunel, M., Gleeson, J., & Novarino, G. (2016). Impaired Amino Acid Transport at the Blood Brain Barrier Is a Cause of Autism Spectrum Disorder Cell, 167 (6), 1481-2147483647 DOI: 10.1016/j.cell.2016.11.013... Read more »
Tărlungeanu, D., Deliu, E., Dotter, C., Kara, M., Janiesch, P., Scalise, M., Galluccio, M., Tesulov, M., Morelli, E., Sonmez, F.... (2016) Impaired Amino Acid Transport at the Blood Brain Barrier Is a Cause of Autism Spectrum Disorder. Cell, 167(6), 1481-2147483647. DOI: 10.1016/j.cell.2016.11.013
There are two major way to label inner proteins, structures or organnelles for live cell imaging. The most common method is fusing the studied protein to a fluorescent protein. A second approach is the addition of labeling agents from outside the … Continue reading →... Read more »
Teng KW, Ishitsuka Y, Ren P, Youn Y, Deng X, Ge P, Belmont AS, & Selvin PR. (2016) Labeling proteins inside living cells using external fluorophores for microscopy. eLife. PMID: 27935478
"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  (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...---------- 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
"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  (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 .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'  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...---------- Fiorentino M. et al. Blood–brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders. Molecular Autism. 2016; 7:49. Simms MD. When Autistic Behavior Suggests a Disease Other than Classic Autism. Pediatr Clin North Am. 2017 Feb;64(1):127-138. 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
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
"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  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.---------- 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 »
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
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 »
Moorcraft SY, Marriott C, Peckitt C, Cunningham D, Chau I, Starling N, Watkins D, & Rao S. (2016) Patients' willingness to participate in clinical trials and their views on aspects of cancer research: results of a prospective patient survey. Trials, 17. PMID: 26745891
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
"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  (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...---------- 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 »
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
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  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...---------- 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 »
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, 52-64. PMID: 27889487
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 »
Offerdahl DK, Dorward DW, Hansen BT, & Bloom ME. (2016) Cytoarchitecture of Zika virus infection in human neuroblastoma and Aedes albopictus cell lines. Virology, 54-62. PMID: 27863275
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
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Gillespie, L., Hoenen, A., Morgan, G., & Mackenzie, J. (2010) The Endoplasmic Reticulum Provides the Membrane Platform for Biogenesis of the Flavivirus Replication Complex. Journal of Virology, 84(20), 10438-10447. DOI: 10.1128/JVI.00986-10
Miorin L, Romero-Brey I, Maiuri P, Hoppe S, Krijnse-Locker J, Bartenschlager R, & Marcello A. (2013) Three-dimensional architecture of tick-borne encephalitis virus replication sites and trafficking of the replicated RNA. Journal of virology, 87(11), 6469-81. PMID: 23552408
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
Liang Q, Luo Z, Zeng J, Chen W, Foo SS, Lee SA, Ge J, Wang S, Goldman SA, Zlokovic BV.... (2016) Zika Virus NS4A and NS4B Proteins Deregulate Akt-mTOR Signaling in Human Fetal Neural Stem Cells to Inhibit Neurogenesis and Induce Autophagy. Cell stem cell, 19(5), 663-671. PMID: 27524440
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Ghouzzi VE, Bianchi FT, Molineris I, Mounce BC, Berto GE, Rak M, Lebon S, Aubry L, Tocco C, Gai M.... (2016) ZIKA virus elicits P53 activation and genotoxic stress in human neural progenitors similar to mutations involved in severe forms of genetic microcephaly and p53. Cell death , 7(10). PMID: 27787521
Shao Q, Herrlinger S, Yang SL, Lai F, Moore JM, Brindley MA, & Chen JF. (2016) Zika virus infection disrupts neurovascular development and results in postnatal microcephaly with brain damage. Development (Cambridge, England), 143(22), 4127-4136. PMID: 27729407
Wu KY, Zuo GL, Li XF, Ye Q, Deng YQ, Huang XY, Cao WC, Qin CF, & Luo ZG. (2016) Vertical transmission of Zika virus targeting the radial glial cells affects cortex development of offspring mice. Cell research, 26(6), 645-54. PMID: 27174054
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
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Yang MR, Lee SR, Oh W, Lee EW, Yeh JY, Nah JJ, Joo YS, Shin J, Lee HW, Pyo S.... (2008) West Nile virus capsid protein induces p53-mediated apoptosis via the sequestration of HDM2 to the nucleolus. Cellular microbiology, 10(1), 165-76. PMID: 17697133
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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
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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
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