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  • July 3, 2015
  • 04:05 PM
  • 143 views

Novel DNA repair mechanism brings new horizons

by Dr. Jekyll in Lunatic Laboratories

The DNA molecule is chemically unstable giving rise to DNA lesions of different nature. That is why DNA damage detection, signaling and repair, collectively known as the DNA damage response, are needed. A group of researchers discovered a new mechanism of DNA repair, which opens up new perspectives for the treatment and prevention of neurodegenerative diseases.... Read more »

Nikolay A. Pestov, Nadezhda S. Gerasimova, Olga I. Kulaeva, & Vasily M. Studitsky. (2015) Structure of transcribed chromatin is a sensor of DNA damage. Science Advances. info:/10.1126/sciadv.1500021

  • July 3, 2015
  • 08:15 AM
  • 113 views

Male Kangaroos' Arms Evolved to Pound the Crap out of Each Other

by Elizabeth Preston in Inkfish



When you look at a kangaroo or a wallaby, it's obvious the animal is well built for bouncing around the outback. What may be less obvious is that its arms are built for fighting—if it's male, that is. Males of these species have disproportionately long arm bones. And the more brawling a species does, the more exaggerated the difference between the beefy-armed males and their normal-limbed mates.

To understand this evolutionary quirk, we'll need to review the rules of fighting in wallabies... Read more »

  • July 3, 2015
  • 06:06 AM
  • 184 views

A new tissue-specific FLCN-deficient mouse model of renal tumourigenesis

by Danielle Stevenson in BHD Research Blog

Animal models can be useful for understanding disease pathology and as preclinical models for drug testing. As BHD patients develop renal cell carcinomas (RCCs) of varied histologies, associated with a loss of FLCN, BHD animal models could be used to study of a wide range of renal cancer subtypes. Current BHD mouse models include kidney-specific Flcn-knockouts (Chen et al., 2008, Baba et al., 2008) and ubiquitous knockouts (Hasumi et al., 2009, Hartman et al., 2009, Hudon et al., 2010). The former develop polycystic kidneys and die within three weeks, the latter can only be studied as heterozygotes with tumourigenesis dependent on a “second hit” resulting in variable penetrance and making them less suitable for drug studies.... Read more »

Chen J, Huang D, Rubera I, Futami K, Wang P, Zickert P, Khoo SK, Dykema K, Zhao P, Petillo D.... (2015) Disruption of tubular Flcn expression as a mouse model for renal tumor induction. Kidney international. PMID: 26083655  

  • July 3, 2015
  • 04:56 AM
  • 134 views

Vitamin D metabolic gene variants and risk for autism

by Paul Whiteley in Questioning Answers

I was really rather happy to see the "preliminary evidence" reported by Rebecca Schmidt and colleagues [1] when it came to examining whether selected vitamin D metabolic gene variants might show linkage to autism spectrum disorder (ASD) based on data derived from the CHARGE initiative.For quite a while now I've discussed the various peer-reviewed science on the topic of vitamin D deficiency / insufficiency with autism in mind on this blog (see here and see here for example). Specifically, how a diagnosis of ASD seems to offer little protection against issues with vitamin D appearing and what that could mean for important issues such as bone health (see here) for example.A key component that seemed to be missing from the growing volume of research looking at vitamin D and autism was some discussion about whether the genetics of vitamin production and usage might offer some further clues to how vitamin D might more directly be 'linked' to [some] autism. Schmidt et al have started to put some flesh on to the scientific bones in this area following their previous research discussions on vits and SNPs with autism in mind (see here) .So: "Maternal, paternal, and child DNA samples for 384 (81%) families of children with ASD and 234 (83%) families of TD [typically developing] children were genotyped for: TaqI, BsmI, FokI, and Cdx2 in the vitamin D receptor (VDR) gene, and CYP27B1 rs4646536, GC rs4588, and CYP2R1 rs10741657." In effect, researchers looked for potential genetic 'issues' with the vitamin D receptor (VDR) gene that have previously been linked to various health issues. They found some potentially interesting information including: "Paternal VDR TaqI homozygous variant genotype was significantly associated with ASD in case-control analysis." Homozygous by the way, refers to the concept of zygosity and the fact we have pairs of chromosomes. Further: "A significant association between decreased ASD risk and child CYP2R1 AA-genotype was found in hybrid log-linear analysis."This is early days research insofar as the genetics of vitamin D and autism only being mentioned once before in the research literature as per the report from Yan and colleagues [2]. I'm excited at the Schmidt data but am not going to go all out on this very preliminary inspection of vitamin D receptor gene functioning without further large-scale replication and validation studies being carried out including discussions on things like cognitive ability in light of other recent data [3]. Whilst we are however, on the topic of vitamin D and its potential extra-skeletal activities, I'm minded to also bring in the paper by Kaneko and colleagues [4] and their results implying that "vitamin D affects brain serotonin concentrations" with mention of autism among other labels. Reporting on a particularly interesting enzyme - tryptophan hydroxylase (TPH)2 - which has an important role in serotonin metabolism (see here) I'll be watching closely on how vitamin D research with autism in mind also develops in this area.And then there are the Raftery results [5] to bring to your attention putting further scientific flesh on to the bones about the possibility of a relationship between vitamin D levels and intestinal permeability (see here). Given what has been mentioned about 'leaky gut' and autism in the peer-reviewed literature so far (see here) one might also add this to further investigations in this area...Music: I am the Monarch of the Sea.----------[1] Schmidt RJ. et al. Selected vitamin D metabolic gene variants and risk for autism spectrum disorder in the CHARGE Study. Early Hum Dev. 2015 Jun 11;91(8):483-489.[2] Yan J. et al. Vitamin D receptor variants in 192 patients with schizophrenia and other psychiatric diseases. Neurosci Lett. 2005 May 20-27;380(1-2):37-41.[3] Jorde R. et al. Vitamin D and cognitive function: The Tromsø Study. J Neurol Sci. 2015 Jun 7. pii: S0022-510X(15)00350-0.[4] Kaneko I. et al. 1,25-Dihydroxyvitamin D regulates expression of the tryptophan hydroxylase 2 and leptin genes: implication for behavioral influences of vitamin D. FASEB J. 2015 Jun 12. pii: fj.14-269811.[5] Raftery T. et al. Effects of vitamin D supplementation on intestinal permeability, cathelicidin and disease markers in Crohn's disease: Results from a randomised double-blind placebo-controlled study. United European Gastroenterol J. 2015 Jun;3(3):294-302.----------Schmidt RJ, Hansen RL, Hartiala J, Allayee H, Sconberg JL, Schmidt LC, Volk HE, & Tassone F (2015). Selected vitamin D metabolic gene variants and risk for autism spectrum disorder in the CHARGE Study. Early human development, 91 (8), 483-489 PMID: 26073892... Read more »

Schmidt RJ, Hansen RL, Hartiala J, Allayee H, Sconberg JL, Schmidt LC, Volk HE, & Tassone F. (2015) Selected vitamin D metabolic gene variants and risk for autism spectrum disorder in the CHARGE Study. Early human development, 91(8), 483-489. PMID: 26073892  

  • July 2, 2015
  • 11:57 AM
  • 131 views

Digesting bread and pasta can release biologically active molecules

by Dr. Jekyll in Lunatic Laboratories

Biologically active molecules released by digesting bread and pasta can survive digestion and potentially pass through the gut lining, suggests new research. The study reveals the molecules released when real samples of bread and pasta are digested, providing new information for research into gluten sensitivity.... Read more »

  • July 2, 2015
  • 09:00 AM
  • 85 views

Why Should You Care How Bacteria Fight Viruses?

by Bill Sullivan in The 'Scope

Research into how bacteria fight viruses has spurred a revolution in genetic engineering referred to as "CRISPR". CRISPR provides unprecedented ways to easily modify the genome of any living creature, including humans.... Read more »

Garneau, J., Dupuis, M., Villion, M., Romero, D., Barrangou, R., Boyaval, P., Fremaux, C., Horvath, P., Magadán, A., & Moineau, S. (2010) The CRISPR/Cas bacterial immune system cleaves bacteriophage and plasmid DNA. Nature, 468(7320), 67-71. DOI: 10.1038/nature09523  

Horie, M., Honda, T., Suzuki, Y., Kobayashi, Y., Daito, T., Oshida, T., Ikuta, K., Jern, P., Gojobori, T., Coffin, J.... (2010) Endogenous non-retroviral RNA virus elements in mammalian genomes. Nature, 463(7277), 84-87. DOI: 10.1038/nature08695  

Baltimore, D., Berg, P., Botchan, M., Carroll, D., Charo, R., Church, G., Corn, J., Daley, G., Doudna, J., Fenner, M.... (2015) A prudent path forward for genomic engineering and germline gene modification. Science, 348(6230), 36-38. DOI: 10.1126/science.aab1028  

  • July 2, 2015
  • 02:34 AM
  • 138 views

Acute bipolar depression and immune alterations

by Paul Whiteley in Questioning Answers

"Individuals with acute bipolar depression show immune alterations. Some of the alterations are similar to those found in acute mania."That was the bottom line reported by Faith Dickerson and colleagues [1] following their analysis of blood samples provided by "82 individuals with acute bipolar depression, 147 with acute mania, and 280 controls." Looking for the presence of various antibodies to "human herpesviruses, gliadin, Toxoplasma gondii, and endogenous retroviruses as well as for C-reactive protein (CRP) and pentraxin-3" in said samples, researchers reported a few potentially important findings.So: "The levels of CRP and IgG antibodies to an endogenous retrovirus, Mason-Pfizer monkey virus (MPMV), were significantly elevated in the bipolar depressed group." Further: "Levels of pentraxin-3 were reduced in both psychiatric groups." Researchers also reported that for 32 individuals who were hospitalised (and I assume treated) for bipolar depression, they "showed a significant decrease in the levels of MPMV antibodies, but not a change in the other markers."Looking through the list of antigens included for analysis, without looking at the authorship list, I could have told you that the authors Faith Dickerson and/or Robert Yolken were involved in this study based on what has been discussed before on this blog (see here and see here for example). The work coming out of Johns Hopkins has been particularly interesting with their focus on "the role of infectious and inflammatory processes in complex psychiatric disease such as schizophrenia, bipolar disorder, and autism." Their most recent work on pentraxin-3 looks very interesting indeed (see here) and complements their most recent results.The finding of elevations in the levels of CRP in the "bipolar depressed group" fits in well with the idea of inflammation being somehow involved in psychiatry (see here) and seemingly crossing diagnostic labels (see here). One might reasonable ask whether the research voices are indeed getting stronger for the potential usefulness of 'treating inflammation' when it comes to something like depression (see here) bearing in mind no clinical or medical advice is given or intended.Finally, is that "endogenous retrovirus" finding reported by Dickerson et al. Regular readers of this blog might already know that I'm an avid [amateur] follower of the idea that all those fossil viruses that lurk in our genomes might be some much more than just junk DNA. With schizophrenia in mind (see here), with attention-deficit hyperactivity disorder (ADHD) in mind (see here), with autism in mind (see here), even with chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME) in mind (see here), I've covered the topic a few times on this blog. Although never coming across MPMV before, this is not the first time that antibodies to non-human primate viruses have been talked about with psychiatric / behavioural conditions in mind [2]. Indeed a previous paper from Dickerson and colleagues [3] even went as far as suggesting that as part of suite of inflammatory markers, the presence and elevation of MPMV antibodies is likely derived "from the activation of homologous endogenous retroviruses and to be a reflection of immune activation." Similar sentiments seem to carry over to the most recent results too.Music: Doves - There Goes The Fear.----------[1] Dickerson F. et al. Immune alterations in acute bipolar depression. Acta Psychiatr Scand. 2015 Jun 9.[2] Lillehoj EP. et al. Serum antibodies reactive with non-human primate retroviruses identified in acute onset schizophrenia. J Neurovirol. 2000 Dec;6(6):492-7.[3] Dickerson F. et al. A combined marker of inflammation in individuals with mania. PLoS One. 2013 Sep 3;8(9):e73520.----------Dickerson F, Katsafanas E, Schweinfurth LA, Savage CL, Stallings C, Origoni A, Khushalani S, Lillehoj E, & Yolken R (2015). Immune alterations in acute bipolar depression. Acta psychiatrica Scandinavica PMID: 26061032... Read more »

Dickerson F, Katsafanas E, Schweinfurth LA, Savage CL, Stallings C, Origoni A, Khushalani S, Lillehoj E, & Yolken R. (2015) Immune alterations in acute bipolar depression. Acta psychiatrica Scandinavica. PMID: 26061032  

  • July 1, 2015
  • 02:19 PM
  • 158 views

New epigenetic mechanism revealed in brain cells

by Dr. Jekyll in Lunatic Laboratories

For decades, researchers in the genetics field have theorized that the protein spools around which DNA is wound, histones, remain constant in the brain, never changing after development in the womb. Now, researchers from the Icahn School of Medicine at Mount Sinai have discovered that histones are steadily replaced in brain cells throughout life – a process which helps to switch genes on and off.... Read more »

Maze, I., Wenderski, W., Noh, K., Bagot, R., Tzavaras, N., Purushothaman, I., Elsässer, S., Guo, Y., Ionete, C., Hurd, Y.... (2015) Critical Role of Histone Turnover in Neuronal Transcription and Plasticity. Neuron, 87(1), 77-94. DOI: 10.1016/j.neuron.2015.06.014  

  • July 1, 2015
  • 09:39 AM
  • 104 views

Video Tip of the Week: MorphoGraphX, morphogenesis in 4D

by Mary in OpenHelix

This week’s Video Tip of the Week covers a different aspect of bioinformatics than some of our other tips. But having been trained as a cell biologist, I do consider imaging software as an important part of the crucial software ecosystem. Also, since it’s a holiday week and traffic may be light in the US, […]... Read more »

Barbier de Reuille, P., Routier-Kierzkowska, A., Kierzkowski, D., Bassel, G., Schüpbach, T., Tauriello, G., Bajpai, N., Strauss, S., Weber, A., Kiss, A.... (2015) MorphoGraphX: A platform for quantifying morphogenesis in 4D. eLife. DOI: 10.7554/eLife.05864  

  • July 1, 2015
  • 08:30 AM
  • 107 views

Thinking Asymmetrically About Hormones

by Mark Lasbury in As Many Exceptions As Rules

Your endocrine glands are stimulated or suppressed by hormones. They in turn dump hormones into the blood. Blood goes everywhere equally. So why is your left adrenal gland bigger than your right? And why is the size difference larger in domesticated foxes as opposed to wild foxes? For that matter, why is the size of the right lobe of your thyroid gland depend on which hand you use to write!?... Read more »

Trut LN, Prasolova LA, Kharlamova AV, & Plyusnina IZ. (2002) Directional left-sided asymmetry of adrenals in experimentally domesticated animals. Bulletin of experimental biology and medicine, 133(5), 506-9. PMID: 12420075  

Hojaij, F., Vanderlei, F., Plopper, C., Rodrigues, C., Jácomo, A., Cernea, C., Oliveira, L., Marchi, L., & Brandão, L. (2011) Parathyroid gland anatomical distribution and relation to anthropometric and demographic parameters: a cadaveric study. Anatomical Science International, 86(4), 204-212. DOI: 10.1007/s12565-011-0111-0  

  • July 1, 2015
  • 06:24 AM
  • 146 views

Offspring autism risk and advancing parental age (differences)

by Paul Whiteley in Questioning Answers

Parental age at offspring conception/birth in relation to offspring autism risk has been a recurrent theme in autism research circles for quite a few years now. I've covered it more than once on this blog (see here for example) and the various suggestions that advancing parental age in particular, might elevate the risk of offspring autism.Set in this context, the paper by Sven Sandin and colleagues [1] (open-access) (a name not unfamiliar to this blog) adds to the research evidence based on their analysis of some 5.7 million children born between 1985 - 2004 resident in one of five countries (Denmark, Israel, Norway, Sweden and Western Australia). Including data on some 30,000 children diagnosed with an autism spectrum disorder (ASD): "Parental ages, sex and birth year were obtained from birth or civil registers."After quite a bit of statistical modelling and controlling for various potentially confounding variables, several findings were reported pertinent to the authors' data being "the strongest evidence to date supporting the hypothesis that advanced parental ages at the time of birth are independently associated with risk for ASD in the offspring." Outside of "no support for any modification by the sex of the child" researchers also noted a "combined parental age effect" whereby there "was a joint effect of maternal and paternal age with increasing risk of ASD for couples with increasing differences in parental ages."A few of the finer details of this study have been covered elsewhere (see here). I'll draw your attention to one or two statistics unearthed during the study:"relative to fathers aged 20–29 years, fathers 50 years or older had a statistically significantly increased risk for offspring with ASD (RR=1.66 95% CI:1.49–1.85)","Relative to mothers aged 20–29 years, mothers younger than 20 years had a statistically significantly increased risk for offspring with ASD (RR=1.18 95% CI:1.08–1.29)" and the "lowest risk corresponded to couples that generated the majority of births, specifically, 29–39-year-old fathers and 25–35-year-old mothers." Those estimates of relative risk (RR) statistics translate into an estimated 66% increased risk for offspring autism if a dad was over 50 years old compared with a dad in their 20s, an 18% increased risk for offspring autism for teen mums compared to 20-something mums and the lowest statistical risk of offspring autism being reported when dads conceive in their 30s coupled with a mid-20 to mid-30 year old mum. The authors also note that "Similar patterns of association, but with slightly higher RRs for the highest parental ages, were evident for AD [autistic disorder]" so completing the message about older parental ages at conception and differing parental ages being relevant across the autism spectrum.Accepting that this was a huge study in terms of participant numbers and spanning different geographical locations, the authors rightly offer a few words of caution about their methods and data. So: "we lack information about potentially confounding variables such as SES [socio-economic status] and parental psychiatric history" is something to keep in mind [2]. Further: "We cannot rule out the possibility that other factors associated with parental age (for example, length of marriage or partnership, obstetric complications, gestational age and birth weight) have an important role in explaining our results" and "We did not have individual level information on co-morbid ID [intellectual disability] in ASD cases." I'd also suggest that given the growing emphasis on autism or ASD not existing in some sort of diagnostic vacuum (see here) one might reasonably ask whether other comorbidity outside of ID might also play a role in risk estimates.As to the possible mechanism(s) of effect, well, the authors go through the usual older parents - older sperm and eggs mantra although perhaps bypassing an emerging area outside of just de novo mutations based on the role of epigenetic mechanisms (see here). They do suggest that the 'difference in parental age' factor might suggest "that the increase in risk is not attributable to advancing parental age per se, and that the risk increase cannot be explained solely by an accumulation of point mutations or other genomic alterations in the parents" but say little more on the basis of their collected data.I might be wrong but I also didn't seem too much in the way of discussion of how parental nutrition might impact on offspring autism risk as per the proposed factor from other work by authors on the Sandin paper in relation to the inter-pregnancy interval (IPI) and autism risk (see here and see here). Although the idea that parental age might affect autism offspring risk, I'd be minded to suggest that this is only the first stage in a journey towards elucidating the particular mechanisms of any effect.Music: The Pixies - Gigantic.----------[1] Sandin S. et al. Autism risk associated with parental age and with increasing difference in age between the parents. Mol Psychiatry. 2015 Jun 9.[2] Lehti V. et al. Maternal socio-economic status based on occupation and autism spectrum disorders: A national case-control study. Nord J Psychiatry. 2015 Mar 3:1-8.----------Sandin S, Schendel D, Magnusson P, Hultman C, Surén P, Susser E, Grønborg T, Gissler M, Gunnes N, Gross R, Henning M, Bresnahan M, Sourander A, Hornig M, Carter K, Francis R, Parner E, Leonard H, Rosanoff M, Stoltenberg C, & Reichenberg A (2015). Autism risk associated with parental age and with increasing difference in age between the parents. Molecular psychiatry PMID: 26055426... Read more »

Sandin S, Schendel D, Magnusson P, Hultman C, Surén P, Susser E, Grønborg T, Gissler M, Gunnes N, Gross R.... (2015) Autism risk associated with parental age and with increasing difference in age between the parents. Molecular psychiatry. PMID: 26055426  

  • June 30, 2015
  • 03:28 PM
  • 110 views

Molecular bits of living things with fun names

by Rosin Cerate in Rosin Cerate

Most of the fancy words used by life science folks are dry but effective. However, every once in a while a researcher will discover a new gene or small molecule and decide to gift it with a fun and creative name.The bacterium Photorhabdus luminescens has a gene called makes caterpillars floppy (mcf), which encodes a toxin that causes caterpillars to go all floppy like before it kills them. P. luminescens is a super interesting little bug. It hangs out in the gut of a worm that infects insects, helping the worm to kill and digest its host. It's bioluminescent and may produce antibiotics, and apparently managed to get inside the wounds of soldiers fighting in the American Civil War and make them glow.The bacterium Proteus mirabilis, which can cause urinary tract infections, has a gene named zapA (one of the researchers who found this gene was a Zappa fan). The gene encodes a protein that helps the bacterium change how it moves around, contributing to its ability to cause disease.Tigger, roo, pogo, mariner, gypsy, hobo, and Jordan (discovered in 1993) are specialized pieces of DNA called transposons capable of bouncing/travelling/jumping around the genome of an organism.The cabbage looper, a moth that in its caterpillar form eats several important crops, has a gene named bagheera controlling its eye colour. While adults normally have gray-brown eyes, a mutation in the gene causes them to change to yellow.In 1983, a sheep was born with particularly well defined muscles in its hindquarters. This was subsequently determined to be the result of it possessing a particular variant of a gene named callipyge (from Greek calli-, beautiful; -pyge buttocks).Vertebrates have a gene called Sonic hedgehog (Shh), which is named after the video game character and encodes a protein secreted by cells so they can communicate with one another. The protein is involved in ensuring that we develop properly in the womb (e.g. that our brain is put together the right way). It also regulates angiogenesis and the division and migration of cells in adult bodies, and thus can have a role in cancer development. Sonic hedgehog is related to the hedgehog gene (hh), which was discovered earlier in fruit flies. Altering the hh gene in fly embryos causes them to become covered with small spikes as they develop, such that they look a bit like a really gross tiny hedgehog.Robotnikinin is a small molecule that can bind to Shh protein and disrupt its function. It's named after Dr. Ivo "Eggman" Robotnik, noted foe of Sonic.Pikachurin is a protein found in the retina of the eye. It's named after Pikachu and is necessary for normal vision, having a role in ensuring the proper transfer of rapid electrical signals between the eye and the brain.The stargazer gene in mice encodes a brain protein named stargazin. A mutant version of the gene apparently causes mice to develop a specific form of epilepsy where they stagger around with their heads twitching toward the sky.Beefy meaty peptide (BMP) (aka delicious peptide) is a specific chain of eight amino acids that was at one point thought to be responsible for the taste of red meat. However, BMP was subsequently shown to not be appreciably present in cooked beef and to have a strong acidic and astringent taste. Bummer.Fortunately, there's at least one other food reference to be had. Sushi domains are repeating sequences of amino acids found in some proteins that fold in such a way that they resemble the food (look at figure 8).Diablo, sickle, grim, and reaper are proteins that promote apoptosis, aka programmed cell death.Not sure what Jane Austen would have made of it, but darcin is a protein pheromone found in the urine of male mice that causes females to be sexually attracted to male urinary scent.Finally, there are oodles of silly yet appropriate names for genes found in Arabidopsis plants, fruit flies, and zebrafish. This is largely due to the widespread use of these organisms as models for all sorts of genetic investigations. Some of my favourites:Arabidopsis genesbubble-bath (bub) controls the number of vesicles present within plant cells; plants with certain mutations in this gene have so many vesicles that their cells appear to be full of bubbles (look at J and K of this figure)crabs claw (crc) and knuckles (knu) are involved in flower and silique development; mutations can result in a claw- (compare figure 1 A and C) or knuckle-like (look at C) appearance to their seed capsulespoltergeist helps to maintain stem cell populations in plant roots and shoots; mutations in the gene don't visibly alter plants unless they also have mutations in a second gene (like a ghost, the effects of this gene can't be detected under normal conditions)superman also regulates flower development; mutations can result in flowers with extra stamenskryptonite initiates a pathway by which expression of superman is inhibited by its transformation into clark kent (by DNA methylation)time for coffee contributes to the ability of plants to synchronize their actions with the changing availability of light throughout each 24 hour rotation of the earth, specifically regulating gene expression late at night when coffee would help a person stay awakeFruit fly genesbruchpilot apparently means crash pilot in German; mutants are bad at flyingcouch potato is involved in nervous system development and function; some mutants won't fly unless proddedfuzzy onions mediates the fusion of mitochondria in sperm cells; mutants are sterile and their unfused mitochondria have an onion-like and fuzzy appearance (look at E)ken and barbie mutants don't develop external genitaliamaggie mutants stop developing as larvae, kenny mutants have crappy immune systems and so tend to die youngcheap date mutants are sensitive to alcohol, lush mutants are strongly attracted to alcohol, hangover is required for the development of alcohol tolerance, ether-a-gogo mutants shake their legs when under the effects of etherbagpipe is required for the development of the fly midgut (incidentally, koza and zampogna are related genes found in frogs), concertina and saxophone regulate embryo development such that their mutation causes embryos to develop weirdly and vaguely resemble these instruments (this is totally a guess on my part)arleekin, valient, tungus, and many others are involved with long-term memory (named after Pavlov's dogs)tinman mutants don't grow a heart, the lungs of breathless mutants fail to develop properlyhamlet regulates the development of IIB cells, capulet is involved in the creation of egg cells, malvolio is required for normal sense of taste (mutants, like the Twelfth Night character, "taste with a distempered appetite"), prospero influences the fate of certain developing cellsZebrafish genesdrac... Read more »

  • June 30, 2015
  • 02:56 PM
  • 164 views

Women’s faces get redder at ovulation, but human eyes can’t pick up on it

by Dr. Jekyll in Lunatic Laboratories

Previous studies have shown that men find female faces more attractive when the women are ovulating, but the visual clues that allow this are unclear. Now, new research investigating whether it might be to do with subtle changes in skin colour has shown that women’s faces do increase in redness during ovulation, but the levels of change are just under the detectable range of the human eye.... Read more »

Hannah Rowland, & Robert Burriss. (2015) Women’s faces get redder at ovulation, but human eyes can’t pick up on it. PLOS ONE. info:/

  • June 30, 2015
  • 12:32 PM
  • 122 views

Omega-3 supplements and antioxidants may help with preclinical Alzheimer’s disease

by Dr. Jekyll in Lunatic Laboratories

Here’s more evidence that fish oil supplementation and antioxidants might be beneficial for at least some people facing Alzheimer’s disease. A new report describes the findings of a very small study in which people with mild clinical impairment, such as those in the very early stages of the disease, saw clearance of the hallmark amyloid-beta protein and reduced inflammation in neurological tissues. Although the findings involved just 12 patients over the course of 4 to 17 months, the findings suggest further clinical study of this relatively inexpensive and plentiful supplement should be conducted.... Read more »

Fiala M, Halder RC, Sagong B, Ross O, Sayre J, Porter V, & Bredesen DE. (2015) ω-3 Supplementation increases amyloid-β phagocytosis and resolvin D1 in patients with minor cognitive impairment. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. PMID: 25805829  

  • June 30, 2015
  • 05:06 AM
  • 120 views

Low glycemic index diet reduces symptoms of mouse autism

by Paul Whiteley in Questioning Answers

A quote to begin: "Overall, the manuscript supports the idea that ASD [autism spectrum disorder] results from gene–environment interactions and that in the presence of a genetic predisposition to ASD, diet can make a large difference in the expression of the condition."The manuscript in question was by Antonio Currais and colleagues [1] reporting some rather interesting results based on the 'dangermouse' that is the BTBR mouse model of autism. Researchers from the Salk Institute for Biological Studies showed that "the dietary glycemic index has a significant impact on the ASD phenotype." The dietary glycemic index (GI) by the way, is concerned with how particular foods / foodgroups affect blood glucose levels and the crux of the research was to see what happened to pregnant mice when fed either a high GI or low GI diet in terms of offspring outcomes. Offspring also followed the same diet diet post weaning.To quote from the paper and some associated media: "The two groups of animals consumed the same number of calories and were identical in weight. But mice that ate a high-glycemic index diet showed all of the expected behavioral symptoms of autism. Their social interactions were impaired, they repeated actions that served no apparent purpose, and they groomed extensively."Various other differences were present across the different dieting mice as per the findings that: "diet modulates plasma metabolites, neuroinflammation and brain markers of neurogenesis in a manner that is highly reflective of ASD in humans." This included the finding that "the brains of the high-glycemic index diet mice appeared to have greater numbers of activated microglia, the resident immune cells of the brain" and various inflammation-related genes being more readily expressed in comparison to the low-glycemic index diet mice. Microglia and autism remains a complex topic (see here) but with the advent of recent research findings [2] complete with headlines such as ''Missing link' between brain and immune system discovered' I dare say that we'll be hearing more about this is times to come.The compound doublecortin also receives a mention in the Currais results as per the suggestion that those mice living on the high-glycemic diet had less of the stuff and the significance of this finding given the link between doublecortin and neurogenesis for example [3]. Bearing in mind the BTBR mouse model of autism might already be more prone to reductions in the levels of doublecortin [4] it might be useful to see how this finding pans out when applied to real people in the real world."The new study found that the diet might directly influence the ecosystem of bacteria in the gut." It perhaps goes without saying that any sort of dietary change is likely to affect the composition of those trillions of wee beasties that call our gastrointestinal (GI) tract home. This also applies to mice and probably every other type of animal. "'We were really surprised when we found molecules in the blood that others had reported could only be generated by gut bacteria,' Maher says. 'There were big differences in some of these compounds between the two diets.'" Metabolites of gut bacteria found in general circulation... does this imply intestinal permeability (leaky gut) might be part and parcel of any effect? If so, would that perhaps also tie into the findings reported by Elaine Hsaio and colleagues a while back on leaky mice guts, gut bacteria and autism? Add in also the idea that high glycemic index foods tend to include things like wheat and various other grains and we start to get something looking rather familiar to autism research that may well show some relationship [5]."The group plans to analyze the gut bacteria, and its potential link with features of autism, more directly. They also hope to better understand the role of inflammation in the ability to generate new neurons." I'm very much looking forward to seeing these results, bearing in mind that mice are mice not people [6] and autism (or rather the autisms) is/are [a] very complicated condition(s).Music: The Jesus And Mary Chain - Just Like Honey.----------[1] Currais A. et al. Dietary glycemic index modulates the behavioral and biochemical abnormalities associated with autism spectrum disorder. Molecular Psychiatry. 2015. June 9.[2] Louveau A. et al. Structural and functional features of central nervous system lymphatic vessels. Nature. 2015 Jun 1.[3] Couillard-Despres S. et al. Doublecortin expression levels in adult brain reflect neurogenesis. Eur J Neurosci. 2005 Jan;21(1):1-14.[4] Stephenson DT. et al. Histopathologic characterization of the BTBR mouse model of autistic-like behavior reveals selective changes in neurodevelopmental proteins and adult hippocampal neurogenesis. Mol Autism. 2011 May 16;2(1):7.[5] Lammers KM. et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology. 2008 Jul;135(1):194-204.e3.[6] Wong AH. & Josselyn SA. Caution When Diagnosing Your Mouse with Schizophrenia: The Use and Misuse of Model Animals for Understanding Psychiatric Disorders. Biol Psychiatry. 2015 May 6. pii: S0006-3223(15)00361-3.----------Currais A, Farrokhi C, Dargusch R, Goujon-Svrzic M, & Maher P (2015). Dietary glycemic index modulates the behavioral and biochemical abnormalities associated with autism spectrum disorder. Molecular psychiatry PMID: 26055422... Read more »

  • June 29, 2015
  • 07:55 PM
  • 125 views

You may already be beating cancer

by Angela Reisetter in Steeped in Science

A look at living with disease close at hand, using a couple different papers. Living with Risk.... Read more »

  • June 29, 2015
  • 03:26 PM
  • 160 views

How your brain knows it’s summer

by Dr. Jekyll in Lunatic Laboratories

Researchers led by Toru Takumi at the RIKEN Brain Science Institute in Japan have discovered a key mechanism underlying how animals keep track of the seasons. The study shows how circadian clock machinery in the brain encodes seasonal changes in daylight duration through GABA activity along with changes in the amount of chloride located inside certain neurons.... Read more »

Myung J, Hong S, DeWoskin D, Schutter E, Forger, DB, and Takumi T. (2015) GABA-mediated repulsive coupling between circadian clock neurons in the SCN encodes seasonal time. Proceedings of the National Academy of Sciences. info:/10.1073/pnas.1421200112

  • June 29, 2015
  • 01:51 PM
  • 164 views

The fear you experience playing video games is real, and you enjoy it

by Dr. Jekyll in Lunatic Laboratories

With the advent of video games, a frequently asked question has been whether we get as engrossed in them emotionally as we do when we see a scary movie. The answer is yes and many game players enjoy the fear caused by the zombies, disfigured humans and darkness they often encounter, the researchers found.... Read more »

  • June 29, 2015
  • 04:57 AM
  • 157 views

Fermented foods and social anxiety?

by Paul Whiteley in Questioning Answers

Stumbling across a headline that reads: 'Study Finds Decreased Social Anxiety Among Young Adults Who Eat Fermented Foods' was bound to pique my blogging interest. When I eventually tracked down the source paper behind the headline I became more and more intrigued as today I bring to your attention the study findings reported by Matthew Hilimire and colleagues [1].Implementing "a cross-sectional approach to determine whether consumption of fermented foods likely to contain probiotics interacts with neuroticism to predict social anxiety symptoms" researchers asked over 700 students - psychology students - to self-report on "fermented food consumption, neuroticism, and social anxiety." Fermented foods by the way, cover a range of foods "that contain probiotics" including yogurt and sauerkraut (a particular favourite of mine). Researchers also enquired about various other variables such as fruit and vegetable intake and the amount of exercise taken over the past 30 days.Bearing in mind that this was a study based on self-report and that psychology students might not be entirely representative of the population in general, the results of an "interaction model, controlling for demographics, general consumption of healthful foods, and exercise frequency" did seem to suggest that there may be more to see when it comes fermented food consumption and social anxiety: "Fermented foods should be further investigated as an intervention for social anxiety."I'm not falling hook, line and sinker for these results - correlation is not the same as causation - despite my continuing interest in the science of psychobacteriomics (my word creation) and the idea that those trillions of wee beasties that inhabit our deepest, darkest [gut] recesses might be doing so much more than just helping to digest food and making the odd nutrient or two. I do however think that we need to dedicate quite a few more resources to the idea that psychology and behaviour might not be solely rooted in the grey-pink matter floating in our skull [2] as recent news articles seem to imply.Finally, and without wishing to make too many sweeping generalisations from the Hilimire results, I did think about whether such findings may be particularly 'useful' for certain groups of people where social anxiety might be over-represented. Autism is an obvious label given the suggestion that at least a quarter of those on the autism spectrum might also fulfil the diagnostic criteria for social anxiety disorder (see here). That such anxiety might also have knock-on effects to the presentation of more core autism symptoms (see here) is also noteworthy bearing in mind that a diet rich in fermented foods might not be for everyone and that social anxiety with or without autism is bound to be a very complicated process.We await further research in this area.Music: The Flaming Lips - Do You Realize??----------[1] Hilimire MR. et al. Fermented foods, neuroticism, and social anxiety: An interaction model. Psychiatry Res. 2015; 228: 203-208.[2] Dinan TG. et al. Collective unconscious: how gut microbes shape human behavior. J Psychiatr Res. 2015 Apr;63:1-9.----------Hilimire MR, DeVylder JE, & Forestell CA (2015). Fermented foods, neuroticism, and social anxiety: An interaction model. Psychiatry research, 228 (2), 203-8 PMID: 25998000... Read more »

Hilimire MR, DeVylder JE, & Forestell CA. (2015) Fermented foods, neuroticism, and social anxiety: An interaction model. Psychiatry research, 228(2), 203-8. PMID: 25998000  

  • June 28, 2015
  • 03:10 PM
  • 99 views

Blood & Fog: The Military's Germ Warfare Tests in San Francisco

by Rebecca Kreston in BODY HORRORS

The Nuremberg Code was drafted in 1947 following the appalling revelations of human experimentation committed in Nazi concentration camps. The overarching goal of the Code was to establish a set of rules for the ethical conduct of research using human subjects, guaranteeing that the rights and welfare of such participants would be protected. Two important principles guide and define this Code: the concept of voluntary, informed consent and that no experiment shall be conducted in which "there is... Read more »

WHEAT RP, ZUCKERMAN A, & RANTZ LA. (1951) Infection due to chromobacteria; report of 11 cases. A.M.A. archives of internal medicine, 88(4), 461-6. PMID: 14867953  

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