Post List

  • October 19, 2014
  • 07:11 PM
  • 17 views

Running Shoes Can Control Motion

by Craig Payne in Running Research Junkie

Running Shoes Can Control Motion... Read more »

  • October 19, 2014
  • 06:39 PM
  • 18 views

Pain is not a "Thing"

by Bronwyn Thompson in Healthskills: Skills for Healthy Living

ResearchBlogging.org
I’m reading some fascinating books at the moment. I’m such a pain geek I take pain books away with me on holiday! Anyway, the two books to hit me between the eyeballs recently are The Pain Chronicles by Melanie Thernstrom (published 2010), and The Story of Pain by Joanna Bourke (published 2014). What makes both of these books fascinating is that these both look at the history of pain and pain management, and explore the “what it is like” to be in pain. Reading them, I’m forcefully reminded that the ways in which we conceptualise pain is an incredibly social process. ... Read more »

Ashton-James, C., Richardson, D., Williams, A., Bianchi-Berthouze, N., & Dekker, P. (2014) Impact of pain behaviors on evaluations of warmth and competence. PAIN®. DOI: 10.1016/j.pain.2014.09.031  

  • October 19, 2014
  • 01:43 PM
  • 25 views

DNA Nanotech: The First Large DNA Crystals

by Gabriel in Lunatic Laboratories

DNA is the stuff of life as we know it, but it is the potential as a programmable material platform that could spawn entire new and revolutionary nanodevices in computer science, microscopy, biology, and more. Researchers have been working to master the ability to coax DNA molecules to self assemble into the precise shapes and sizes needed in order to fully realize these nanotechnology dreams. A dream that been going on for 20 years now and was just realized.... Read more »

Ke, Y., Ong, L., Sun, W., Song, J., Dong, M., Shih, W., & Yin, P. (2014) DNA brick crystals with prescribed depths. Nature Chemistry. DOI: 10.1038/nchem.2083  

  • October 19, 2014
  • 11:00 AM
  • 29 views

Ten years into the making, the HIV-1 mosaic vaccine finally goes into human trial

by EE Giorgi in CHIMERAS

© Bette Korber et al. I hope you will all forgive me if this week I'm gushing over my amazing mentor Bette Korber, as last week she shared some awesome news on Facebook:"A landmark in my life happened yesterday, a major step in a long story. A decade ago I had an idea for making an HIV vaccine that had the potential to work globally. After a struggle (in my first 2 failed proposals, reviewers declared what I proposed was impossible), I got an internal grant from Los Alamos to develop the idea (third time's a charm). With that funding I could bring together a group of computational people to work together on expressing the idea -- a talented guy named Simon Perkins wrote amazing code to make it so, with computational design suggestions from the group, particularly my husband James Theiler. Then James, Will Fischer, Tanmoy Bhattacharya, and I put it through its paces, optimizing running conditions and devising ways to compare mosaics with natural proteins, with additional help from our friends Karina Yusim, Carla Kuiken and Bob Funkhouser. We called it a mosaic vaccine. After so many years of hard work, and with the collaboration of experimentalists at Harvard and at Duke (Drs. Haynes, Letvin, and Barouch), two weeks ago a phase I safety trial finally opened, and an HIV mosaic vaccine went into the arm of a human volunteer for the very first time. "Safety trial" means that this is just the first phase in testing the safety of the vaccine (I explained the three phases of human trials in this post). We will gather immune responses and we are hoping to see the same good results we saw in monkeys [2-5]. If all goes well, HIV mosaics are in the pipeline for 4 more human vaccine studies. I'm so excited about this study and so proud of my mentor.When I explain to people the challenge we are facing when designing an HIV-1 vaccine, I usually make a very simplistic comparison with the flu virus. Influenza evolves from one season to the next, which is why every year we need a new flu shot. So, basically, the flu evolves into a new virus every year. Well, HIV evolves so rapidly that every person has a different virus. In our database alone we have half a million distinct HIV viral sequences: how can you vaccinate people against half a million different viruses? In the past, successful vaccines against diseases like polio or the measles have been made by taking a real virus, inactivating it (for example, you just take one or two of its proteins, but not the whole virus, to ensure it loses its ability to infect cells), and then injecting it into the body. The immune system "sees" the viral proteins and initiates a response. The response is then "saved" into memory cells, which, next time they encounter the pathogen, will remember how to produce the right response that will promptly clear the virus before it can start an active infection. So, as you can see, the problem with HIV is that the viral population is so diverse that no one virus found in nature will protect people from contracting the infection. How to bypass the obstacle, then? Bette's idea is to basically use a computer that mimics HIV's evolutionary mechanisms to create an in-silico virus [1], something I've discussed in this post. The algorithm takes as input a population of, say, 100 different HIV sequences, and then recombines them creating a new population of artificially constructed viral sequences. HIV viruses can naturally recombine when infecting the same cells, and what the algorithm does is mimic this mechanism making sure that after every recombination step the new sequence is still a viable and functional virus. The computer mimics this process, iterates it multiple times and then the best representative is selected as a potential vaccine.The first caveat is: is this new, artificially constructed sequence a real virus? After all, it was never found in nature. It was created by a computer algorithm. It turns out that when reconstructed in a wet lab, the mosaic proteins are functional and viable.The second hurdle was to prove that these artificially constructed sequences are safe to be used in a vaccine and that they do elicit protective responses against not just a few HIV viruses, but many, many HIV viruses -- enough to prevent infection. So, you get an idea of why the mosaic vaccine took 10 years from concept to the first human trial. Animal studies [2-5] demonstrated that mosaic vaccines elicit good immune responses. In one study in particular [3], compared to controls, vaccinated monkeys required many more challenges to get infected (for a risk reduction of 80%), and once infected, they were able to control the viral load and survive the infection. So, as Bette said, we are hopeful. Hopeful and excited![1] Fischer W, Perkins S, Theiler J, Bhattacharya T, Yusim K, Funkhouser R, Kuiken C, Haynes B, Letvin NL, Walker BD, Hahn BH, & Korber BT (2007). Polyvalent vaccines for optimal coverage of potential T-cell epitopes in global HIV-1 variants. Nature medicine, 13 (1), 100-6 PMID: 17187074[2] Nkolola JP, Bricault CA, Cheung A, Shields J, Perry J, Kovacs JM, Giorgi E, van Winsen M, Apetri A, Brinkman-van der Linden EC, Chen B, Korber B, Seaman MS, & Barouch DH (2014). Characterization and immunogenicity of a novel mosaic M HIV-1 gp140 trimer. Journal of virology, 88 (17), 9538-52 PMID: 24965452[3] Barouch DH, Stephenson KE, Borducchi EN, Smith K, Stanley K, McNally AG, Liu J, Abbink P, Maxfield LF, Seaman MS, Dugast AS, Alter G, Ferguson M, Li W, Earl PL, Moss B, Giorgi EE, Szinger JJ, Eller LA, Billings EA, Rao M, Tovanabutra S, Sanders-Buell E, Weijtens M, Pau MG, Schuitemaker H, Robb ML, Kim JH, Korber BT, & Michael NL (2013). Protective efficacy of a global HIV-1 mosaic vaccine against heterologous SHIV challenges in rhesus monkeys. ... Read more »

Fischer W, Perkins S, Theiler J, Bhattacharya T, Yusim K, Funkhouser R, Kuiken C, Haynes B, Letvin NL, Walker BD.... (2007) Polyvalent vaccines for optimal coverage of potential T-cell epitopes in global HIV-1 variants. Nature medicine, 13(1), 100-6. PMID: 17187074  

Nkolola JP, Bricault CA, Cheung A, Shields J, Perry J, Kovacs JM, Giorgi E, van Winsen M, Apetri A, Brinkman-van der Linden EC.... (2014) Characterization and immunogenicity of a novel mosaic M HIV-1 gp140 trimer. Journal of virology, 88(17), 9538-52. PMID: 24965452  

Barouch DH, Stephenson KE, Borducchi EN, Smith K, Stanley K, McNally AG, Liu J, Abbink P, Maxfield LF, Seaman MS.... (2013) Protective efficacy of a global HIV-1 mosaic vaccine against heterologous SHIV challenges in rhesus monkeys. Cell, 155(3), 531-9. PMID: 24243013  

Barouch DH, O'Brien KL, Simmons NL, King SL, Abbink P, Maxfield LF, Sun YH, La Porte A, Riggs AM, Lynch DM.... (2010) Mosaic HIV-1 vaccines expand the breadth and depth of cellular immune responses in rhesus monkeys. Nature medicine, 16(3), 319-23. PMID: 20173752  

  • October 18, 2014
  • 02:55 PM
  • 40 views

New Genetic Test to help Solve Rare Disease Diagnosis

by Gabriel in Lunatic Laboratories

My sister suffers from a rare disease which causes small fiber polyneuropathy, or the killing of nerves in her hands and feet. As it progresses she has trouble standing or using her hands. If that was the worst of it, then it might be liveable given the time between severe attacks is years or more. Unfortunately, it also causes intense and mostly constant pain and burning sensations, pain so bad that conventional narcotic painkillers have trouble controlling it. After some time working with the hospital I narrowed it down to autoimmune mediated. Her Doctors finally agreed, but only after first dismissing it as anything from she was faking it, all the way to lupus.... Read more »

Lee, H., Deignan, J., Dorrani, N., Strom, S., Kantarci, S., Quintero-Rivera, F., Das, K., Toy, T., Harry, B., Yourshaw, M.... (2014) Clinical Exome Sequencing for Genetic Identification of Rare Mendelian Disorders. JAMA. DOI: 10.1001/jama.2014.14604  

  • October 18, 2014
  • 09:45 AM
  • 41 views

Immunoglobulin E: not just a bystander in lupus?

by Aurelie in The Immuno Blog

IgE antibodies are mostly known for their pathophysiological role in allergic reactions and in certain immune deficiencies referred to as hyper-IgE syndromes. In a study published in The Journal of Experimental Medicine in September, Dema et al. find that IgE … Continue reading →... Read more »

Dema B, Charles N, Pellefigues C, Ricks TK, Suzuki R, Jiang C, Scheffel J, Hasni S, Hoffman V, Jablonski M.... (2014) Immunoglobulin E plays an immunoregulatory role in lupus. The Journal of experimental medicine. PMID: 25267791  

  • October 18, 2014
  • 09:34 AM
  • 52 views

Merit’s Liquidity

by nooffensebut in The Unsilenced Science

The latest SAT and ACT data suggest that America’s cognitive elite have been enjoying new geographic mobility, but difficult economic times push them out of the elite strata, contrary to a prediction of The Bell Curve by Richard Herrnstein and Charles Murray.... Read more »

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

  • October 18, 2014
  • 05:30 AM
  • 42 views

More epigenetics, EN-2 and autism... the plot thickens

by Paul Whiteley in Questioning Answers

I don't mind admitting that I was to some extent 'winging it' with my previous post on epigenetics and Engrailed-2 (EN-2) as a consequence of the findings reported by Jill James and colleagues [1] with autism in mind. Although an avid follower of the science of epigenetics when (cautiously) applied to autism, I am by no means any authority on the subject matter particularly when it comes to the nitty-gritty details. You can probably therefore expect similar things in my latest discussions on yet more work from this research group which appeared recently [2].I have only one rule. Everybody fights, no one quits.And so, with that pinch of salt at the ready...The final conclusion made in the most recent James article boils down to the suggestion that "persistent postnatal overexpression of EN-2 suggests that the closing of this programed developmental window may have been missed in some individuals with autism because of epigenetic abnormalities". That being said I think we have quite a way to come before we can substantiate this finding particularly when the main protagonist in the latest article is something called 5-hydroxymethylcytosine (5-hmC) and results which show "that elevated 5-hmC in the EN-2 promoter is associated with a significant decrease in repressive MeCP2 and histone H3K27me3 that appear to over-ride 5-mC hypermethylation". The H3K27me3 bit comes from their previous findings by the way.To most readers that probably sounds as complicated as it first did to me so I will try and explain more.EN-2 as I've talked about in that post on the previous James work, has been linked to cases of autism as per the example of the study by Wang and colleagues [3] linking mutations in this gene to cases of autism. The idea being that mice bred without the gene (the homeobox domain of EN2) show some of the [mouse] signs and symptoms of autism alongside issues with the cerebellum and a reduction in the number of Purkinje cells which have been previously noted in cases of autism [4]. The previous James results in this area reported on hypermethylation of the EN-2 promoter region which would normally equate as gene silencing in epigenetic terms, in line with the more structural genomic issues seen in autism that I've just talked about. But, and it is an important point, when they looked at EN-2 expression and protein levels - function and products of the gene - they actually found that levels were increased in their autism samples despite the methylation mark and its 'stop talking' properties. They noted on that occasion that "transcriptional upregulation by other epigenetic mechanisms predominated over the repressive tendencies of DNA cytosine methylation".Their latest foray into this area sought to further clarify just what might be going on specifically with EN-2 gene-specific DNA hypermethylation previously reported. To do this they focused on both measuring 5-hmC and also 5-methylcytosine (5-mC) among other things based on the same tissue samples (post-mortem cerebellum samples) detailed in their previous study. 5-hmC is apparently an oxidation product of 5-mC mediated via something called TETs.What they found, far from answering the question of a discrepancy between epigenetic gene silencing of EN-2 but increased gene function and products, actually makes the whole thing a lot more complicated. So they observed "a significant increase in both 5-mC and 5-hmC in the autism cerebellum relative to the control samples". Further that there was "a significant increase in 5-hmC content within the upstream EN-2 promoter region" and "a highly significant positive correlation... was found between 5-hmC content and EN-2 gene expression in the 5’ promoter CpG island in autism but not in control samples". They note that: "that 5-hmC accumulation is mechanistically related to gene upregulation" something which I think ties into other work hinting at the demethylating role for 5-hmC [5].Insofar as my mention of MeCP2 and histone H3K27me3 from the latest and previous James reports, I can't really say too much more aside from noting again: "reduced MeCP2-mediated gene repression may have contributed to persistent EN-2 gene overexpression in the autism samples". Actually the authors speculate that MeCP2 binding and histone H3K27 trimethylation might work together in a "repressive" manner but when reduced as they were "may contribute to aberrant overexpression of EN-2 in the autism cerebellum" as per their findings.I have to say that I struggled with getting my head around these findings and I'd quite understand if readers also struggled with my interpretation of them ("If you can't explain something to a six-year-old/granny, you really don't understand it yourself"). I understand that we don't all walk around with our genes stuck in the 'on' or 'off' position and that particularly during foetal and the early post-natal periods, genes are being switched on and off at a surprising rate for many, many different important reasons. I also understand that DNA methylation is an important part of the whole genes switched on or off thing but not the only way that this process can happen as per the authors mention of chromatin and some previous text in this area [6]. With my very limited knowledge of this area, I am however not yet convinced that we have the full story here; specifically in terms of why the original finding of hypermethylation of the EN-2 promotor region (gene silencing) yet increased expression and protein levels were reported. I wonder if indeed we might be able to learn more from a two-hit approach whereby hypermethylation of only one gene allele leaves the other still working?Just before I finish I'd like to also draw your attention to another paper which has started to ask similar questions about 5-hmC and might be contrasted with the recent James paper. Zhubi and colleagues [7] (open-access here) looked at 5-hmC with a couple of other potentially important genes linked to cases of autism (RELN and GAD1) in mind. They reported: "a significant increase in TET1 expression and an enrichment in the level of 5-hmC... at the promoters of GAD1 and RELN in ASD when compared with CON [controls]". Further that their data are: "consistent with the hypothesis that an increase of 5-hmC (relative to 5-mC) at specific gene domains enhances the binding of MeCP2 to 5-hmC and reduces expression of the corresponding target genes... Read more »

  • October 17, 2014
  • 10:29 PM
  • 38 views

Translational Findings: Fruit fly contributions to research in circadian rhythms

by Bethany Christmann in Fly on the Wall

What are circadian rhythms, and why are they important to humans? Over the past century, technological innovations have changed human society dramatically, undeniably for the better. But the advent of jet travel, round-the-clock manufacturing, and internet communication has also had a disruptive effect on our bodies’ circadian rhythms. The word “circadian” comes from the latin […]... Read more »

  • October 17, 2014
  • 04:02 PM
  • 39 views

A look at Air Pollution and Your Body

by Gabriel in Lunatic Laboratories

We have all probably seen stories from China on the horrid air pollution there. Accompanying those reports of course are the statistics for air pollution that deaths have caused. For the record, the World Health Organization estimated that ambient air pollution caused 3.7 million premature deaths (worldwide) in 2012 alone – yet what exactly happens to your body when it encounters pollutants?... Read more »

  • October 17, 2014
  • 11:40 AM
  • 43 views

October 17, 2014

by Erin Campbell in HighMag Blog

For years the prettiest cells to image were flat cells in a dish. Thanks to the tireless work of many, beautiful high-resolution images can now come from tissue in a living organism. Today’s image is from a paper showing improved techniques for imaging fine cellular processes within large volumes, from the lab of recent Nobel prize winner, Eric Betzig. A material’s refractive index refers to how light travels through it; the simplest example being how light bends when passed through water. The refractive index heterogeneities stemming from the many cell types, morphologies, and subdomains within a living organism are a challenge to microscopists. As described in a paper from earlier this year, Wang and colleagues improved on previous techniques for imaging within large volumes. Wang and colleagues use adaptive optics (AO), which corrects for the microscope’s aberrations that limit image resolution, in a mode fast enough to correct for the various aberrations within a large sample, without inducing photodamage or photobleaching. The image above shows a 3D rendering from deep within a living zebrafish brain, with oligodendrocytes (magenta) and neuronal nuclei (green) visible.Wang, K., Milkie, D., Saxena, A., Engerer, P., Misgeld, T., Bronner, M., Mumm, J., & Betzig, E. (2014). Rapid adaptive optical recovery of optimal resolution over large volumes Nature Methods, 11 (6), 625-628 DOI: 10.1038/nmeth.2925Adapted by permission from Macmillan Publishers Ltd, copyright ©2014 ... Read more »

Wang, K., Milkie, D., Saxena, A., Engerer, P., Misgeld, T., Bronner, M., Mumm, J., & Betzig, E. (2014) Rapid adaptive optical recovery of optimal resolution over large volumes. Nature Methods, 11(6), 625-628. DOI: 10.1038/nmeth.2925  

  • October 17, 2014
  • 08:55 AM
  • 48 views

People Are More Swayed by Things That Look Sciencey

by Elizabeth Preston in Inkfish

Anyone who’s paged through a women’s magazine will recognize this strategy: to make a product seem better, surround it with a scientific glow. “Clinical trials show lashes grow up to 400% fuller!” “27% reduction of dark spots in 10 weeks!” “Ceramides!” Does this actually help convince people to hand over their cash? A study using […]The post People Are More Swayed by Things That Look Sciencey appeared first on Inkfish.... Read more »

  • October 17, 2014
  • 06:50 AM
  • 45 views

The Friday Five for 10/17/2014

by Bill Sullivan in The 'Scope

Coolest science news stories of the week: stem cells to treat diabetes, fake testes, erasing memories, more!... Read more »

DeMartini DG, Ghoshal A, Pandolfi E, Weaver AT, Baum M, & Morse DE. (2013) Dynamic biophotonics: female squid exhibit sexually dimorphic tunable leucophores and iridocytes. The Journal of experimental biology, 216(Pt 19), 3733-41. PMID: 24006348  

Pagliuca, F., Millman, J., Gürtler, M., Segel, M., Van Dervort, A., Ryu, J., Peterson, Q., Greiner, D., & Melton, D. (2014) Generation of Functional Human Pancreatic β Cells In Vitro. Cell, 159(2), 428-439. DOI: 10.1016/j.cell.2014.09.040  

  • October 17, 2014
  • 06:13 AM
  • 73 views

Large Sized Men Disadvantaged In Relationships

by Rangina Barakzai in United Academics

For decades men have been diffident and self-doubting about the size of their phallus. Well, luckily for the holders of the pocket rocket, there is a twist.... Read more »

  • October 17, 2014
  • 05:22 AM
  • 53 views

Altered ghrelin levels in boys with autism

by Paul Whiteley in Questioning Answers

"Honey, it's the '90s, remember?"Saudi Arabia and autism research? It must be at least one author from the research tag-team that is Mostafa and Al-Ayadhi.Indeed, in today's post it is Laila Al-Ayadhi featured on the paper by Felwah S. Al-Zaid and colleagues [1] (open-access) who concluded on: "a potential role for the hormone ghrelin in the pathogenesis of autism".Ghrelin, by the way, is often called the 'hunger hormone' as a result of its effects in relation to energy homoeostasis. Alongside another hormone called leptin (which has also been implicated in cases of autism) the long-and-short of food intake regulation seem to be covered by these hormones [2].The Al-Zaid paper is open-access but I'll direct you to a few important points...A case-control study, authors looked at various measures for 31 boys diagnosed with autism compared with 28 age- and sex-matched controls.Alongside various anthropometric measures, plasma and serum levels of "acyl ghrelin (AG), des-acyl ghrelin (DG), total testosterone (TT), free testosterone (FT), leptin and growth hormone (GH)" were measured. These were single spot measures with samples taken "after an overnight fast". Results: the autism group were on average heavier than controls but aside from that, no other physical measure was significantly different (mean height was greater in the autism group but just escaped significance). Both acyl ghrelin and des-acyl ghrelin levels were significantly lower in the autism group. By contrast, leptin levels were higher in the autism group (as per other independent findings) and free and total testosterone levels were significantly elevated compared to controls. Taking into account the effect of weight and it's link to adiposity, authors also showed that an analysis of a smaller subgroup (autism, n=27; controls, n=28) where mean weight was controlled for, found a similar trend in hormone levels (see this link to Table 3 of the paper) bearing in mind how body fat can influence the parameters.Various correlational analyses were completed on the data but given the relatively small participant groups and the use of spot samples I'm not particularly minded to read too much into these findings at this time.The authors conclude that their study: "contributes significantly to the understanding of hormonal dysregulation in the pathophysiology of autism, as it provides baseline data regarding hormonal profiles in autism and substantiates potential clinical interventions".Small participants numbers and a "lack of female subjects with autism" kinda prohibit me from reading too much into these findings as they stand. I've already made mention of the research trend when it comes to elevated leptin levels and autism (see the paper from Rodrigues and colleagues [3] as one example). Likewise, testosterone levels and autism have received quite a bit of autism research attention down the years (see here). Indeed, elevations in testosterone levels not described in-utero with some potential relationship to foetal programming, has been the stuff of controversy in autism research circles [4].Going back to the primary ghrelin findings and the observations of lower levels detected in their autism group, the authors speculate on some of the hows and whys of their findings. Gastrointestinal (GI) issues get a call-out and how some of the variety of GI issues noted in cases of autism "could affect the gastric mucosa and interfere with the normal function of ghrelin-secreting cells". although no particulars about GI issues are included in their descriptions of their cohort. One additional issue that I would perhaps add to the whole inflammation, dysbiosis et al discussions would be how ghrelin seems to play some role in GI motility [5] too. That being said, 'wide-ranging' is perhaps the best way to describe what biological processes ghrelin might impact on [6].I was a touch surprised that the more usual role for ghrelin in terms of hunger and energy homoeostasis was not given more prominence in the Al-Zaid article on autism. Food and feeding patterns are important topics when it comes to autism as per discussions on the extremes sometimes noted in cases of autism (see here) and the increasingly important issue of weight (see here) (which also seemed to be picked up in the authors' findings). One might speculate that hunger and signals linked to hunger might be similarly tied into at least some of the feeding issues reported in autism?As I seem to do in many discussions these days, I'll reiterate that there is quite a bit more to see and do in research terms on the relationship between ghrelin and related hormones and autism. The additional suggestion from Ghanizadeh [7] about the ghrelin being a "promising therapeutic target for co-occurring autism and epilepsy" might also be worthy of greater inspection.Music to close. Iggy Pop and Lust for Life.----------[1] Al-Zaid FS. et al. Altered ghrelin levels in boys with autism: a novel finding associated with hormonal dysregulation. Sci Rep. 2014 Sep 26;4:6478.[2] Klok MD. et al. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007 Jan;8(1):21-34.[3] Rodrigues DH. et al. Changes in Adipokine Levels in Autism Spectrum Disorders. Neuropsychobiology 2014;69:6-10[4] Geier DA. & Geier MR. A prospective assessment of androgen levels in patients with autistic spectrum disorders: biochemical underpinnings and suggested therapies. Neuro Endocrinol Lett. 2007 Oct;28(5):565-73.[5] Greenwood-Van Meerveld B. et al. Ghrelin as a target for gastrointestinal motility disorders. Peptides. 2011 Nov;32(11):2352-6.[6] Delporte C. Structure and physiological actions of ghrelin. Scientifica (Cairo). 2013;2013:518909.[7] Ghanizadeh A. Ghrelin as a promising therapeutic target for co-occurring autism and epilepsy. Epilepsy Behav. 2011 Feb;20(2):420-1.-----------... Read more »

  • October 17, 2014
  • 03:00 AM
  • 48 views

BHD lung cysts are not degenerative, but may cause pneumothorax

by Lizzie Perdeaux in BHD Research Blog

Although 90% of BHD patients develop lung cysts, there is very little information about the natural history of BHD lung cysts. In order to determine how lung cysts change over time, Johannesma et al. (2014a) compared the results of two … Continue reading →... Read more »

Johannesma PC, Houweling AC, van Waesberghe JH, van Moorselaar RJ, Starink TM, Menko FH, & Postmus PE. (2014) The pathogenesis of pneumothorax in Birt-Hogg-Dubé syndrome: A hypothesis. Respirology (Carlton, Vic.), 19(8), 1248-50. PMID: 25302759  

  • October 16, 2014
  • 05:20 PM
  • 71 views

The “New” Roots of our Friends the Mitochondria

by Gabriel in Lunatic Laboratories

Mitochondria, the proverbial “powerhouse” of the cell. Mitochondria are found in virtually all eukaryotic cells, plant or animal and we thought that was pretty much the end of the story. It wasn’t a great explanation but it was Now new research is turning the idea– that our ancestor cells simply “swallowed up” bacterial cells that eventually became mitochondria– on its head.... Read more »

Zhang Wang, & Martin Wu. (2014) Phylogenomic Reconstruction Indicates Mitochondrial Ancestor Was an Energy Parasite . PLoS ONE. info:/10.1371/journal.pone.0110685

  • October 16, 2014
  • 04:18 PM
  • 89 views

Inherited Memories: Too Good To Be True?

by Neuroskeptic in Neuroskeptic_Discover

In December last year, researchers Brian Dias and Kerry Ressler made a splash with a paper seeming to show that memories can be inherited. This article, published in Nature Neuroscience, reported that if adult mice are taught to be afraid of a particular smell, then their children will also fear it. Which is pretty wild. […]The post Inherited Memories: Too Good To Be True? appeared first on Neuroskeptic.... Read more »

  • October 16, 2014
  • 02:19 PM
  • 69 views

Is Axon Guidance by Attraction and Repulsion, or by a Roll of the Dice?

by Wadsworth in Wadsworth Guidance

Attractants and repellants guide axons to their targets.  On its journey, a migrating axon may be confronted with multiple attractive and repulsive guidance cues.  This presents a conundrum. How does the axon avoid a tug-of-war between attractants and repellants?  Does the strongest cue win?  Can one cue negate the effects of another?  Can an axon switch its responsiveness to cues until they all match?   0 0 1 83 474 Robert Wood Johnson Medical School 3 1 556 14.0 Normal 0 false false false EN-US JA X-NONE ... Read more »

Tang, X., & Wadsworth, W. (2014) SAX-3 (Robo) and UNC-40 (DCC) Regulate a Directional Bias for Axon Guidance in Response to Multiple Extracellular Cues. PLoS ONE, 9(10). info:/10.1371/journal.pone.0110031

  • October 16, 2014
  • 01:11 PM
  • 62 views

Deceased & Living Liver Transplant Comparable For Hepatorenal Syndrome

by Cristy at Living Donor 101 in Living Donors Are People Too

30 patients with HRS receiving a live donor liver transplantation (LDLT) and 90 HRS patients (Hepatorenal Syndrome) receiving a full graft deceased donor liver transplantation (DDLT) were compared. No difference was detected between LDLT and DDLT patients regarding graft survival at 1 (80% vs. 82%), at 3 (69% vs. 76%) and 5 years (65% vs. 76%) …
Continue reading »
The post Deceased & Living Liver Transplant Comparable For Hepatorenal Syndrome appeared first on Living Donors Are People Too.
... Read more »

join us!

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

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

Register Now

Research Blogging is powered by SMG Technology.

To learn more, visit seedmediagroup.com.