by TheCellularScale in The Cellular Scale
The auditory brainstem of the boring-old-chicken is actually home to some fascinating neurons.Key West rooster, taken by me.The Nucleus Laminaris (NL) is a group of coincidence-detecting neurons which receive indirect input from both ears and is located in the bird auditory brainstem. NL neurons show a peculiar dendrite pattern. These bipolar neurons fall into the particular category of football shaped cells which have dendrites coming out the top and bottom of their cell body. The cell body (soma) of these neurons are about the same size, but depending on where they are in the NL, the cells have either short, medium or long dendrites. The ones near the midline have a bunch of short stubby little dendrites.Figure 2B from Smith and Rubel, 1979If they are a little further out from the midline, they have longer dendrites.Figure 3B from Smith and Rubel, 1979and finally if they are furthest from the middle, they have fewer and much longer dendrites.Figure 10A Smith and Rubel 1979all together this makes a gradient from short to long dendrites. From Figure6 Smith and Rubel 1979The big question here is "Why?"What is the purpose of having stubby or extended dendrites like this? Well, even in 1979 when Smith and Rubel reconstructed these neurons, they knew that these neurons had a special answer to the "form and function" question. The amazing thing about these neurons is that they are 'tuned' to respond maximally to specific frequencies (sound waves). And just like strings on an instrument, the cells with shorter dendrites respond to higher frequencies and the cells with longer dendrites respond to lower frequencies. Why is this? Dendrites don't actually vibrate like strings, but there must be some reason for a cell with short dendrites to respond to higher frquencies and a cell with long dendrites to respond to low frequencies. The answer lies in what the Nucleus Laminaris actually does. In the next post we'll venture into the wilds of computational neuroscience and explore the reason behind this strange connection between dendrite shape and cell function. © TheCellularScaleSmith DJ, & Rubel EW (1979). Organization and development of brain stem auditory nuclei of the chicken: dendritic gradients in nucleus laminaris. The Journal of comparative neurology, 186 (2), 213-39 PMID: 447882... Read more »
Smith DJ, & Rubel EW. (1979) Organization and development of brain stem auditory nuclei of the chicken: dendritic gradients in nucleus laminaris. The Journal of comparative neurology, 186(2), 213-39. PMID: 447882
From [1]:"Until relatively recently, the [genetic] code was thought to be invariable, frozen, in all organisms, because of the way in which any change would produce widespread alteration in the amino acid sequences of proteins. The universality of the genetic code was first challenged in 1979, when mammalian mitochondria were found to use a code that deviated somewhat from the universal."A brief refresher: proteins are chains of amino acids. They are made from messenger RNA by assigning each triplet of RNA nucleotides (a codon) to one amino acid. For example, in the sequence AUGCCCAAGCUG each triplet codes an amino acid: AUG becomes M, CCC becomes P, AAG becomes K, and CUG becomes L. All together: AUG|CCC|AAG|CUG - MPKL.So, what does "universal" mean in the above quote? It means that the above sequence gets translated into the same amino acids in every organism, from bacteria to humans. Is this true? Not always.Take a stop codon, for example. A stop codon is a triplet of RNA nucleotides that end the translation. Think of it as a flag that says, "The protein code ends here." If the genetic code were a universal one, a stop codon would always be a stop codon, in all organisms. The first exception to this was discovered in 1985, when the stop codon UGA was found to be actually coding an amino acid in the bacteria Mycoplasma capricolum. More exceptions to the "universal" conception (other triplets that coded different amino acids instead of always the same one) were later found in other organisms and in mitochondrial DNA as well. A more realistic theory is that, being DNA dynamical, when codons "disappear" the old codons can undergo reassignments and take on a new meaning.The "universal" view has prevailed for many years on the basis that present time proteins are so evolved that changes would most likely be lethal. The first deviations from universality were found in the late 'seventies in mitochondrial DNA. It was argued that mtDNA is considerably smaller than nuclear DNA and hence it had a better tolerance to changes. In [1], Ohama et al. list various code changes reported in the nuclear DNA in the past three decades, and then discuss the origin of the genetic code:"The theories to explain the early evolution of the genetic code are numerous, all of which include speculations that the coding system arose with one or a limited number of amino acids, and that others were added until a total of 20 was reached. Most of these theories are aesthetically pleasing but cannot be verified."They assume that the most ancient genetic code had to have a minimum number of codons made of all 20 amino acids and a minimum number of corresponding tRNAs -- transfer RNA molecules that act as mediators between the mRNA and the amino acids. This first genetic code had to have very little tolerance for change. However, with the time, the development of synonymous codons (different triplets code the same amino acid), allowed for flexibility and therefore resulted in an advantageous addition. Finally, they conclude:"It should be stressed however that there are no organisms which use the genetic code system for more than, or less than, 20 amino acids. What were frozen are 20 amino acids (magic 20!) and not the genetic code that assigns them. Thus the genetic code is still in the state of evolution."I'm including below a second reference [2] that goes a bit more in depth on how these codon reassignments happen, for those of you who might be interested. In this case, the authors looked at the evolution of the genetic code in yeast.[1] Ohama T, Inagaki Y, Bessho Y, & Osawa S (2008). Evolving genetic code. Proceedings of the Japan Academy. Series B, Physical and biological sciences, 84 (2), 58-74 PMID: 18941287[2] Miranda, I., Silva, R., & Santos, M. (2006). Evolution of the genetic code in yeasts Yeast, 23 (3), 203-213 DOI: 10.1002/yea.1350... Read more »
Ohama T, Inagaki Y, Bessho Y, & Osawa S. (2008) Evolving genetic code. Proceedings of the Japan Academy. Series B, Physical and biological sciences, 84(2), 58-74. PMID: 18941287
by Sean Roberts in A Replicated Typo 2.0
This new documentary about animal intelligence shares some of these elements (sandy beaches, far flung destinations), but crucially, Liz Bonnin is more than an enthusiastic observer – she is not just an engaging television presenter, but a REAL SCIENTIST.... Read more »
Pilley, J., & Reid, A. (2011) Border collie comprehends object names as verbal referents. Behavioural Processes, 86(2), 184-195. DOI: 10.1016/j.beproc.2010.11.007
by Erin Campbell in HighMag Blog
Our nervous system would be in trouble without myelin sheaths and nodes of Ranvier. No, those two things do not refer to some kind of Lord of the Rings-type silliness. They are very important components of our nervous system that ensure fast and efficient signal conduction.Myelin sheaths are membranes that insulate the axons of many neurons. Myelin sheaths have distinct domains of ion channels and proteins, such as the nodes of Ranvier, along the axon that are required for the high speed and efficiency of signal conduction along the axon. The nodes of Ranvier, for example, are especially important for swift movement of an axon’s action potential, which jumps from node to node in a process termed staltatory conduction. A recent paper describes the importance of a cytoskeletal adaptor protein called 4.1G in regulating the localization of proteins along the axon-sheath interface. Ivanovic and colleagues found that in mice without 4.1G, adhesion proteins and neuronal proteins were mislocalized. Images above show localization of 4.1G at the same sites as two other periaxonal membrane proteins (MAG on left, Necl4 on right) in adult mouse sciatic nerves.Ivanovic, A., Horresh, I., Golan, N., Spiegel, I., Sabanay, H., Frechter, S., Ohno, S., Terada, N., Mobius, W., Rosenbluth, J., Brose, N., & Peles, E. (2012). The cytoskeletal adapter protein 4.1G organizes the internodes in peripheral myelinated nerves originally published in the Journal of Cell Biology, 196 (3), 337-344 DOI: 10.1083/jcb.201111127... Read more »
Ivanovic, A., Horresh, I., Golan, N., Spiegel, I., Sabanay, H., Frechter, S., Ohno, S., Terada, N., Mobius, W., Rosenbluth, J.... (2012) The cytoskeletal adapter protein 4.1G organizes the internodes in peripheral myelinated nerves. originally published in the Journal of Cell Biology, 196(3), 337-344. DOI: 10.1083/jcb.201111127
by The Neurocritic in The Neurocritic
Are you having trouble sleeping? But you're not feeling that 19th century retro hipster insomniac vibe? Try some of these behavioral remedies recommended by the finest scientific and medical journals of today.What a Difference a Day MakesIs Intensive Sleep Retraining (ISR) a new overnight treatment for chronic insomnia (Harris et al., 2012)? ISR is conducted in one 25 hr session at a sleep lab, where the insomniac sleeps a maximum of 3 min every 30 min for a period of 25 hrs. Instant cure! (supposedly). The basic idea is that the person will learn they can fall asleep fairly quickly and easily, and this will translate directly to real life sleeping patterns.In a commentary accompanying the main article in Sleep, Spielman and Glovinsky (2012) describe it as:...a novel insomnia treatment that while radical in procedure is grounded in learning theory, a long-established conceptual framework for understanding insomnia. ISR combines two familiar components of sleep research—sleep deprivation and the polysomnographic recording of sleep onset—to yield an entirely new therapeutic procedure: repeated practice in falling asleep quickly. Massed practice in achieving sleep is here shown to possess a therapeutic value rivaling that of stimulus control therapy (SCT), that mainstay of behavioral sleep medicine, as well as offering a possible additive effect when administered in conjunction with SCT.ISR employs sleep laboratory technology to measure the speed of sleep onset, limit the duration of sleep, and allow immediate feedback to subjects as to whether objectively recorded sleep has occurred. It typically provides dozens of successful entries to sleep over the course of a single night and day. Then it is over, handing off responsibility for good sleep management to sleep hygiene recommendations.In contrast to ISR, there is already strong research support for stimulus control therapy (SCT), which is designed to:...reduce the anxiety or conditioned arousal individuals may feel when attempting to go to bed. Specifically, a set of instructions designed to reassociate the bed/bedroom with sleep and to re-establish a consistent sleep schedule are implimented. These include: 1) Going to bed only when sleepy; 2) Getting out of bed when unable to sleep; 3) Using the bed/bedroom only for sleep and sex (i.e., no reading, watching TV, etc); 4) Arising at the same time every morning; and 5) Avoiding naps.One question, then, is whether ISR is better than SCT, an accepted behavioral therapy for insomnia. Eighty participants in the study of Harris et al. were randomized into one of four groups: (1) ISR + sleep hygeine instruction (SH); (2) SCT + SH; (3) ISR + SCT; (4) SH alone, which served as the control condition. All participants kept a sleep diary, answered questionnaires, and wore an actigraph to measure motor activity. Those in the ISR groups slept no more than 5 hrs the night before they came to the lab.The highly intrusive ISR procedure involved arriving at 21:00.Following an explanation, the signing of an informed consent form, electrode application, and a quiet settling period, treatment began at 22:30. Treatment trials were conducted every half hour, finishing after 23:00 on night 2. Thereby, the ISR treatment routine allowed a series of 50 half-hourly sleep onset opportunities. ... Within each treatment trial, the opportunity for sleep onset was limited to a 20-min period, with the trial stopping if sleep onset had not occurred by this time. For those trials in which sleep was initiated, 3 consecutive minutes of sleep were permitted, prior to being awoken [the method of awakening was not described]. Upon awakening, treatment participants first rated their perception of whether sleep onset had occurred (on a Likert scale of 1 “No, definitely not” to 7 “Yes, definitely”). Following this response, participants were provided with information as to whether sleep onset had or had not occurred.Then they got out of bed to read or watch DVDs. After 10 trials of this nonsense, people were falling asleep in 5 min or less.Ultimately, did this punitive procedure work? Yes. But it wasn't significantly better than SCT for most of the subjective sleep measures used. All three active treatment conditions produced improvements in self-reported duration and efficiency of sleep, relative to the SH control. Of the 16 or so analyses at 2 of 7 selected time points (which did not seem to be corrected for multiple comparisons), there were some instances where ISR or the combined ISR + SCT treatment was better than stimulus control therapy (see below), but nothing earth shattering.In another graph (Fig. 5 - Mean sleep diary wake time after sleep onset), the SCT groups were superior to ISR at Week 1 and Post-Treatment.What about the objective sleep measures obtained by actigraphy?The actigraphy data failed to support significant changes in sleep, despite using an adjusted manual scoring method and a sensitivity setting in the scoring algorithm that calibrated actigraphy TST [total sleep time] to PSG [polysomnography] TST. Actigraphy has similarly failed to mirror subjective sleep changes in other treatment studies in insomnia, and objective measures (i.e., EEG) fail to replicate the extent of subjective sleep changes in clinical insomnia treatment studies.The authors concluded that actigraphy is useless and that subjective sleep report is the only thing that matters (basically).So what's next? Intensive Sleep Retraining is costly and available only from highly specialized centers.1 But the possibility of self-administered ISR is on the horizon, using portable EEG headsets, actigraphs, and vibrating alarms. Is there an app for that?Footnote1 I'm not sure that it's even being offered as a clinical treatment. The RCT was conducted in Australia.References... Read more »
Harris, J., Lack, L., Kemp, K., Wright, H., & Bootzin, R. (2012) A Randomized Controlled Trial of Intensive Sleep Retraining (ISR): A Brief Conditioning Treatment for Chronic Insomnia. SLEEP. DOI: 10.5665/sleep.1584
Spielman, A., & Glovinsky, P. (2012) What a Difference a Day Makes. SLEEP. DOI: 10.5665/sleep.1574
by Connor Bamford in The Rule of 6ix
Still-born lamb after Schmallenberg infection. http://www.augsburger-allgemeine.de/i
Europe is currently experiencing an incredibly worrying outbreak of disease across hundreds of farms in the North-West and it has finally popped up in the UK. The disease - caused by a previously unknown virus - has been causing a large number of still births in cows, goats and sheep after it was initially found in the Netherlands and Germany. What is worrying about this is our economic dependance on this kind of agriculture - but should we really be worried?
Following this initial outbreak in Germany/Netherlands it was rapidly discovered to be
present in Belgium, France and the South-East of England where it was most likely spread by the movements of infected midge flies. And even now, Russia has begun to close off it's importing of Dutch meat and animals. The rest of the UK is even bracing itself for further spread of the virus and now the UK's veterinary labs have weighed in on the research. But a number of questions still need answered before we can really do anything about it, which is why so much interest has been generated over the last couple of weeks, especially as we have probably only seen the tip of the iceberg.
Named after the German town where it was initially found, Schmallenberg virus has been a cause for concern ever since it appeared during the end of last year. Looking back we can tell that it initially emerged into farm animals during last summer when Dutch and German farmers noticed that some of their animals (many of which would be pregnant) were coming down with a fever and having low yields of milk, although no deaths were noticed. Something was clearly not right and this set off alarm bells across the national labs in Europe but it was only going to get worse: as we came into lambing season the farmers started to notice the devastating effect of the virus on their farms.
After exhaustive tests for all the usual suspects, the German scientists were forced to get creative and using next generation sequencing technologies they were able to find the culprit: a new RNA virus called an orthobunyavirus. The only closest relatives were a group of viruses found across Asia known as the 'Simbu group' of viruses.
Initial cases in Germany
As the recent paper reports:
Members of this genus within the family Bunyaviridae are widely distributed in Asia, Africa, and Oceania; transmission occurs predominantly through biting midges, mainly Culicoides
spp. and mosquitoes. Especially the Simbu serogroup, which includes
Akabane, Aino, and Shamonda viruses, can play a role as pathogens of
ruminants. However, to our knowledge, viruses of this serogroup have not
previously been detected in Europe (6). Because of the origin of the first positive samples, the virus was provisionally named Schmallenberg virus.
Now we aren't completely sure how this virus is spread from one infected animal to another - or even how it moves between countries (infected flies or infected farm animals?) but as you can see above, we are basing this on how closely related viruses behave. However, it was predicted that if the virus was spread by midges it would most likely initially effect the South-East of England based on the patterns of wind dispersal - this turned out to be a correct prediction. Where these midges help to move the virus very efficiently during the summer, with the cold snap across Europe worsening it is unlikely that these insects would survive the winter. But the question whether the virus could survive the winter through the infected animals is to be seen - and this may not be true.
A bunyavirus, from Overby et al (2007)
The bunyaviruses are one of a couple of the groups of RNA viruses (negative sense RNA viruses to precise). They are spherical viruses (see above) whose genomes are shared across three chromosomes composed of RNA and protein (gold in the picture): they have a large (L) segment, a medium one (M) and a small one (S). This is much like influenza which has eight different genetic segments but the more parts a virus has the more worried we get: with this comes the chance for mixing up of the different genes which can result in very rapid evolution. These viruses are one of the most successful pathogens out there and a number of them even cause serious disease in humans. For example: Crimean-Congo hemorrhagic fever virus, spread by ticks, causes serious bleeding, respiratory problems and neurological dysfunction. And just in 2009, a Chinese group discovered that one of these viruses was the cause behind the deadly "Severe fever with thrombocytopenia syndrome".
The scientists stress that the risk of Schmallenberg to humans is
minimal as none of the closely related bunyaviruses are able to infect
us. But still they suggest that farmers and vets use appropriate hygiene
measures when dealing with infected animals. Although, to date nobody has
reported being infected but then nobody has looked so as we develop
appropriate tests we may detect that many farmers have actually been
infected.
Virus movement from NW-Europe continent to UK. Where else will it appear?
Because we are following this outbreak of disease in real-time we currently have very little information on how this is going to play out over the next couple of months,we do have a lot of speculation however.
Of the important questions that need answered are: how come this virus
is only appearing now? Where was it before this? Ho... Read more »
Hoffmann, B., Scheuch, M., Höper, D., Jungblut, R., Holsteg, M., Schirrmeier, H., Eschbaumer, M., Goller, K., Wernike, K., Fischer, M.... (2012) Novel Orthobunyavirus in Cattle, Europe, 2011. Emerging Infectious Diseases, 18(3), 469-472. DOI: 10.3201/eid1803.111905
by Sathishk in neuro JC
This study illustrates the requirement of training and exercise in executing successful fine motor skills in the invertebrates.Fruit fly Drosophila groups reared and grown in two different fly chambers ,one allows free flight movement and other restricted flight movement were tested for various flight kinematics in free flight arena and tethered flight simulator.Overall performance [...]... Read more »
Hesselberg, T., & Lehmann, F. (2009) The role of experience in flight behaviour of Drosophila. Journal of Experimental Biology, 212(20), 3377-3386. DOI: 10.1242/jeb.025221
by Colin Beale in Safari Ecology
Sometimes scientists suggest the mostabsurd things. In the news last week (with thanks to an Australianfriend for tipping me off) was a paper published in the prestigiousjournal Nature that suggested in the text and headline that Australiashould introduce elephants to control an invasive grass thatoriginally came from Africa: Gamba grass, Andropogon guyanus. Theauthor made a number of sound observations: Australia (like too muchof the world) is riddled with invasive species, has suffered amassive extinction of it's native mammal population and has had somepretty nasty wildfires in the last few years. But how you get fromthose observations to suggesting elephants (and even rhinos) shouldbe introduced to the savannas of Australia is a story worth lookinginto.Invasive species can be extremelydamaging to biodiversity, farmers and even human health. Here inAfrica we have our own set of problem species, highest priority inEast Africa at the moment is surely Parthenium hysterophorus, a weednative to the American tropics that is currently invading savannah habitats acrossEast Africa, after introduction for the cut flower trade. InEthiopia, where the species is already established, the grazingpotential of rangelands has already been reduced by 30% as the weed is toxic tomost mammals. It's also causing unknown damage to human health, asmany (most?) people coming into regular contact with the plantdevelop allergic reactions to the pollen and sap. In South Africa it is estimated that invasiveweeks cost the economy around 6.5billion Rand ($800Million) per year. Soinvasive weeds can certainly be a major problem. Most scientistsrecognize that these plants, which may be perfectly innocuous intheir own environment, become serious pests in the areas they're areintroduced, because they are freed from their natural predators thathelp keep the populations in check in the native range. One of thebest solutions, therefore, is the introduction of a suitable plantpredator, to keep the population under control. Some great examplesof this exist: the Prickly Pear (Opuntia) cactus, for example, is native in theAmericas but a weed across Africa and Australia. A moth was identified that is a specific herbivore of the prickly pearand has been introduced in Australia and parts of Africa with oftendramatic success. After introduction to Australia, the moth (Cactoblastis - the perfect name for an effective cactus eradication agent!) rapidlyinfested many of the cactus plants with the effect that today the infestation has beeneliminated. Prickly pear is no-longer considered a serious threat inAustralia.Biological control, however, is not astraightforward option – to deliberately introduce one species tocontrol the population of another species is a rather risky option.You don't want to end up like the old woman who swallowed a fly, thena spider to catch the fly, then a bird, then a cat, etc., etc. Manyexamples of apparently good ideas have gone horribly wrong, a favorite example of mine being the introduction of predatory snailsto eat the introduced giant land snail on Tahiti where, onceintroduced, the predatory snail decided the native snail populationswere far tastier than than invasive species, and rapidly drove thenative species to extinction in the wild (happily a few were savedand are bred in captivity to be, hopefully, reintroduced once thepredator has been dealt with. Somehow...). Recognising this,conservation organisations got together to come up with a list ofguidelines for the introduction of species under the umbrella ofIUCN, the World Conservation Union. These guys propose a number ofquestions and guidelines that governments should consider beforemaking introductions: “What is the probability that the species tobe introduced will threaten the continued existence or stability ofpopulations of native species, whether as a predator, competitor torfood, cover, breeding sites or in any other way? If the introducedspecies is a carnivore, parasite or specialised herbivore, it shouldnot be introduced if its food includes rare native species that could beadversely affected.” Etc. (Note the implication that you'd only beconsidering introducing a specialised herbivore!)They note that “No introductionshould be made for which a control does not exist or is not possible.A risk-and-threat analysis should be undertaken includinginvestigation of the availability of methods for the control of theintroduction should it expand in a way not predicted or haveunpredicted undesirable effects, and the methods of control should besocially acceptable, efficient, should not damage vegetation and fauna,man, his domestic animals or cultivars.”In this paper David Bowman suggeststhat the ideal control method for gamba grass is the introduction ofelephants. (He further suggests that introduced grasses such as thisspecies, by leading to a build-up of fuel, are responsible for thefires that have killed so many in Australia. This notion is so absurdI don't think it's worth going into: the grasses in question are inthe savanna zone of northern Australia, the worst fires in the south.As with all savannas globally, there are and always have been firesin the savanna belt – to remove them would be to cause untilddamage to these savanna habitats, etc., etc.) He suggests that othermammals in Australia, such as Asian water buffalo Bubalus bubalis, cattleand the rest are too small to eat the exotic grass, but states that“gamba grass is a great meal for elephants or rhinoceroses”. So,how would this proposal fit the IUCN guidelines? Well, the firstthing to do would be to find out if elephants and rhinos really doeat gamba grass. It took me about 10 minutes online to discover thatelephants do eat gamba grass, but they certainly don't select it overother species but rather eat it in proportion to it's abundanceduring the wet season (and not at all during the dry season). RhinosI could find less details of: black rhinos are browsers, so we canignore them for now and look at white rhinos. Contrary to Bowman'sassertion, I certainly couldn't find any evidence suggesting gambagrass is a great meal for them, but I did find evidence that theydon't like it, with areas covered in gamba grass consideredunsuitable habitat for white rhino reintroductions. What's more, as anyone who's studiedelephant diets would have been able to tell the author, elephantshave a mixed feeding strategy – being predominantly grazers in thewet season, and predominantly browsers in the dry season. Evenassuming they could be persuaded to eat gamba grass in the Australianwet season, what will they eat in the dry season? If they findsomething they like, their impacts can be very serious indeed (and ifthey don't what hope can their introduction have of success?). What'smore, if they start having unintended consequences and people wantedto wind the introduction back, I can't see a cost effective method ofcontrol ever fitting the “socially acceptable” criterion. Livetrapping would be incredibly expensive, and even if possible, wherecould you put several thousand elephants to live out their lives?!So, it seems to me that introduction ofelephants to Australia could never reduce the fuel loads in southernAustralia (particularly not around habitation, where fires are mostdangerous). Nor is it likely the animals would even do the jobthey're being promoted for. There's no way the introductions couldever come close to meeting the IUCN guidelines. And it would be atotally crazy thing to do, as anyone with a bit of knowledge ofelephants and rhinos could tell you. So why did this get written? Andthen why did it get published? Sometimes I wonder about mycolleagues...Main reference:... Read more »
Bowman, D. (2012) Conservation: Bring elephants to Australia?. Nature, 482(7383), 30-30. DOI: 10.1038/482030a
by Lab Rat in Lab Rat Blog
The bacteria that causes Tuberculosis is a nasty little beast. The white blood cells that clear infection in your body work by ingesting bacteria and then breaking them up, and the TB escapes this by letting itself get ingested and then sitting inside your white blood cells. They don’t sit passively, however, they burst out of the cell and recruit a whole host of other blood cells which surround the infection and form what’s called a granuloma. The bacteria stay inside the granuloma and become dormant, but if they escape they can set up other sites of infection throughout the body.... Read more »
Simeone R, Bobard A, Lippmann J, Bitter W, Majlessi L, Brosch R, & Enninga J. (2012) Phagosomal Rupture by Mycobacterium tuberculosis Results in Toxicity and Host Cell Death. PLoS pathogens, 8(2). PMID: 22319448
by Mauro Mandrioli in The aphid room
It is frequently difficult to distinguish aphid species and considering that a same species could be present on different host plants, numerous cryptic species could exist in aphids. Furthermore, the split of aphids of the same species into two distinct species due to the presence of environmentally induced differences is also present making more and [...]... Read more »
R.G. Foottit, H.E.L. Maw, K.S. Pike, R.H. Miller. (2010) The identity of Pentalonia nigronervosa Coquerel and P. caladii van der Goot (Hemiptera: Aphididae) based on molecular and morphometric analysis . Zootaxa, 25-38. info:/
by dragonflywoman in The Dragonfly Woman
Aquatic insects and other invertebrates have been used as indicators of water quality for about 40 years. Insects can be found in a huge variety of freshwater habitats year round and can tell scientists and water resource managers a great … Continue reading →... Read more »
Silva, D., De Marco, P., & Resende, D. (2010) Adult odonate abundance and community assemblage measures as indicators of stream ecological integrity: A case study. Ecological Indicators, 10(3), 744-752. DOI: 10.1016/j.ecolind.2009.12.004
by Mutant Dragon in Puff the Mutant Dragon
For those unfortunate enough to inherit it, sickle cell anemia is a devastating disease. Victims suffer from symptoms like frequent infections, persistent fatigue and bouts of crippling pain. It’s a little surprising to realize all this havoc stems from a single and seemingly minor change in the hemoglobin protein — exchanging one amino acid called glutamate for another called valine. That swap creates a pocket on the surface of the protein that can bind other hemoglobin molecules when oxygen is in short supply.... Read more »
Tackett, A. (2002) Non-Watson-Crick interactions between PNA and DNA inhibit the ATPase activity of bacteriophage T4 Dda helicase. Nucleic Acids Research, 30(4), 950-957. DOI: 10.1093/nar/30.4.950
by Iddo Friedberg in Byte Size Biology
Continuing with rather philosophical musings about life, Ed Trifonov has recently suggested a new approach to defining life: let’s just vote on the definition.
So how does that work? And why should it work in the first place?... Read more »
Trifonov EN. (2011) Vocabulary of definitions of life suggests a definition. Journal of biomolecular structure , 29(2), 259-66. PMID: 21875147
by Shermin de Silva in Elephants of Uda Walawe
A side-by-side comparison of Asian and African elephant societies shows that the two species are not as similar as one might think, overturning decades of popular depictions of elephants which paint the two species as identical.... Read more »
Eggert, L., Rasner, C., & Woodruff, D. (2002) The evolution and phylogeography of the African elephant inferred from mitochondrial DNA sequence and nuclear microsatellite markers. Proceedings of the Royal Society B: Biological Sciences, 269(1504), 1993-2006. DOI: 10.1098/rspb.2002.2070
Wildman, D. (2003) Implications of natural selection in shaping 99.4% nonsynonymous DNA identity between humans and chimpanzees: Enlarging genus Homo. Proceedings of the National Academy of Sciences, 100(12), 7181-7188. DOI: 10.1073/pnas.1232172100
de Silva, S., Ranjeewa, A., & Kryazhimskiy, S. (2011) The dynamics of social networks among female Asian elephants. BMC Ecology, 11(1), 17. DOI: 10.1186/1472-6785-11-17
de Silva, S., & Wittemyer, G. (2012) A Comparison of Social Organization in Asian Elephants and African Savannah Elephants. International Journal of Primatology. DOI: 10.1007/s10764-011-9564-1
Coots are the odd ones out in their family. Unlike other rails, they are bold, noisy and aggressive birds. Instead of searching for cover, they are all out, even their nests are usually placed in the open water and they are as prominent that you cannot miss them. Their squabbles amongst themselves and with other birds may carry out through the winter, as some birds keep their territorial behaviour year round. Coots have ashy-black bodies and black heads where a strikingly contrasting white frontal shield and beak is one of their most distinctive features. Unlike the long, thin toes of the Moorhen, coots have lobulated toes with side extensions - similar to a Grebe's - that allow them to dive in search of the algae and underwater plants that form a good portion of their diet.The Coot "flippers"But lets go back to the frontal shield. The size of the shield changes through the year depending on the bird reproductive status. Both males and females have frontal shields although the males' are larger, but both change in parallel, getting bigger in size as the start of the reproductive season approaches, and peaking in February -March.(from Visser 1988)Birds holding a territory have thicker and larger shields than birds not defending one. Experiments on the American Coot, a close relative of the Eurasian Coot, showed that frontal shields enlarged when coots were injected with testosterone pellets, while they become smaller when injected with estradiol. At the same time, the birds climbed up in the pecking order when injected with testosterone due to an increasingly "pugnacious attitude" in the words of Gordon Gullion. The size of the frontal shield in European coots is also correlated with gonadal size. The frontal shield is apparently used for individual recognition and it is an important in territorial disputes or fights. When an intruder enters a territory, the resident bird will lower its head, raise its wings and prominently displaying their shield to the intruder. Like so...A typical posture of an aggressive cootI have much more on stock on Coots, but this will have to do for today.More informationVisser, J. (1988). Seasonal changes in shield size in the Coot Ardea, 76, 56-63Gordon W. Gullion (1951). The Frontal Shield of the American Coot The Wilson Bulletin, 63, 157-166... Read more »
Visser, J. (1988) Seasonal changes in shield size in the Coot. Ardea, 56-63. info:/
Over 300 million years ago, long before the time of the dinosaurs, giant amphibians hopped along the sandy shores of Pennsylvania. At least, that was what Pittsburgh Post-Gazette reporter James Ross explained to readers of the newspaper’s November 28th, 1948 issue. The inspiration for the report was a set of strange tracks found in the [...]... Read more »
Niedźwiedzki, G., Szrek, P., Narkiewicz, K., Narkiewicz, M., & Ahlberg, P. (2010) Tetrapod trackways from the early Middle Devonian period of Poland. Nature, 463(7277), 43-48. DOI: 10.1038/nature08623
by Sally Church in Pharma Strategy Blog
This week I have been in Orlando for the American Association for Cancer Research (AACR) Special Conference on prostate cancer chaired by Drs Arul Chinnaiyan (U. of Michigan) and Charles Sawyers (MSKCC). It was a superb meeting, probably one of … Continue reading →
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Hu, R., Dawood, S., Holmes, M., Collins, L., Schnitt, S., Cole, K., Marotti, J., Hankinson, S., Colditz, G., & Tamimi, R. (2011) Androgen Receptor Expression and Breast Cancer Survival in Postmenopausal Women. Clinical Cancer Research, 17(7), 1867-1874. DOI: 10.1158/1078-0432.CCR-10-2021
by Erin Campbell in the Node
A fully differentiated cell took a fascinating journey to become its present self. For every cell, a precursor cell existed that gave rise to it. And for every precursor cell, a stem cell existed that gave rise to it. Understanding precursor cells is an important part in understanding stem cell biology. Today’s image is from [...]... Read more »
Mairet-Coello, G., Tury, A., Van Buskirk, E., Robinson, K., Genestine, M., & DiCicco-Bloom, E. (2012) p57KIP2 regulates radial glia and intermediate precursor cell cycle dynamics and lower layer neurogenesis in developing cerebral cortex. Development, 139(3), 475-487. DOI: 10.1242/dev.067314
by Austin Bouck in Animal Science Review
Generally not small talk, though I imagine they might be interested in the projections for this year's salmon run (pause for polite awkward laughter). A new article from PLoS ONE has been discussed, implying that, while direct contact may not be routine, exchange of disease between domesticated and wild cats may be fairly common.... Read more »
Sarah N. Bevins1*, Scott Carver2, Erin E. Boydston, Lisa M. Lyren, Mat Alldredge, Kenneth A. Logan, Seth P. D. Riley, Robert N. Fisher, T. Winston Vickers, Walter Boyce, Mo Salman, Michael R. Lappin.... (2012) Three Pathogens in Sympatric Populations of Pumas, Bobcats, and Domestic Cats: Implications for Infectious Disease Transmission. PLoS ONE. info:/
by Elizabeth Preston in Inkfish
Does your dog understand you when you point at something? If so, this may be one of the few pop intelligence quizzes on which it can outscore a chimpanzee.
Previous studies had shown that dogs can pass a test in which a human points to a container and the dog must look inside it to find food. Human one-year-olds can pass this kind of test too. But chimpanzees have a hard time with it. Researchers at the Max Planck Institute for Evolutionary Anthropology in Germany wondered if these previous tests were unfair to chimpanzees. Would changing the setup of the experiment prove that chimps really do understand our gesturing?
In previous versions of the experiment, chimpanzees had been seated behind a barrier, while dogs were in the same room as the humans. Additionally, the objects that the animals were asked to choose between usually sat between the human experimenter and the chimpanzee--so the human didn't actually need the chimps' help to lift a container and get the food underneath. Perhaps the chimpanzees understood just fine when the human experimenter pointed to a cup, but thought, "Get it yourself, big-brain."
So the German researchers leveled the playing field between the two non-human species. They added a barrier between human and dog to make their setup more like the chimps'. They put the objects they were pointing to on the far side of their animal subjects, so the humans really couldn't reach the objects themselves. They also replaced containers and hidden food with boring, inedible objects, such as a rope or a sponge. Then they gathered 32 dogs and 20 chimps. ("For practical reasons," the authors write, "the studies of the chimpanzees and the dogs were conducted separately.")
First came a warm-up phase in which the experimenter encouraged the animal to fetch a single object (in exchange for a treat) by saying "Give it to me!" This taught the animals to associate the voice command with retrieving an object. But the experimenter didn't point or look at the object she wanted.
For the experiment itself, there were two objects in the room instead of one. The experimenter pointed to the one she wanted and repeated the "Give it to me!" command, moving her eyes between the animal and the desired object to make her point clearer. The dog or chimp had to turn around, retrieve the correct object, and bring it back to the experimenter to get a treat.
The chimpanzees flunked the test. While they consistently picked up one of the two objects and brought it back to the researcher, they only picked the correct object half the time. But the dogs, as a group, performed significantly better than if they were guessing. (And they did even better when the barrier between them and the human experimenter was removed.)
It's not that chimpanzees don't follow other animals' gazes. Previous studies found that great apes will look where a human is looking to check for anything of interest. But they don't seem to understand that gaze as a form of communication. And pointing with a finger--which is really just an exaggerated way to show where you're looking--doesn't help them.
Dogs, on the other hand, have evolved to be highly attuned to what humans want. As long as they pee outside and perform the duties we assign them (sheep herding, duck retrieving, company keeping) we give them food and warm place to stay.
Of course, dogs' understanding of human gestures will depend somewhat on their personal experiences with their owners. In this study, many of the individual dogs did not perform any better than chance. But earlier studies have shown that young puppies can understand human finger-pointing, while young wolves don't understand it as well.
The fact that chimps don't understand pointing as a form of communication suggests this isn't a universal ape gesture. They can follow a gaze and understand that other individuals have different perspectives; and the captive chimps in this study should have been especially used to communicating with people. But, fittingly enough, the gesture that says "go and fetch that thing for me" seems to be specifically human.
Kirchhofer, K., Zimmermann, F., Kaminski, J., & Tomasello, M. (2012). Dogs (Canis familiaris), but Not Chimpanzees (Pan troglodytes), Understand Imperative Pointing PLoS ONE, 7 (2) DOI: 10.1371/journal.pone.0030913
Photo: by me.
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Kirchhofer, K., Zimmermann, F., Kaminski, J., & Tomasello, M. (2012) Dogs (Canis familiaris), but Not Chimpanzees (Pan troglodytes), Understand Imperative Pointing. PLoS ONE, 7(2). DOI: 10.1371/journal.pone.0030913
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