by Usman Paracha in SayPeople
Main Point:
Researchers have found that N400 can work as an effective neural marker of deception or telling a lie.
Journal:
PLoS ONE
Study Further:
Researchers found that when someone lies Autonomic nervous system activates catecholaminic response resulting in brain arousal level. This system also results in other bodily changes such as voice changes, pupil dilation and change in skin responses. Usually, polygraph (or lie detector) is used to catch the lies using these changes.
In the new study, researchers presented a total of 296 questions including neutral and affective questions, which included sexual, shameful or disgusting topics, to the 25 subjects while recording Event-Related Potentials (ERPs) from 128 scalp sites. Participants were asked to tell the truth in half of the questions and to tell the life in the other half.
Researchers found increased use of executive control functions, such as working memory, inhibition and task switching processes, during false or deceptive actions. They also found higher “negative N400 (that peaks around 400 milliseconds post-stimulus onset) over the prefrontal areas and a smaller late positivity (LP 550–750 ms) over the prefrontal and frontal areas”. Researchers found a later LP deflection as a symbol for truthfulness for neutral questions while emotional or affective questions showed reduced LP amplitudes.
Isocolour topographic maps (top left view) of brain voltage recorded in between 340–390 ms of latency (N400 peak) during the lie (Bottom) vs. tell the truth condition (Top) as a function of question affective value (Left = affective; Right = neutral) (Credit: PLoS ONE)
Moreover, elevation of superior, medial, middle and inferior frontal gyri (BA9, 11, 47) and the anterior cingulate cortex was also found during deceptive responses.
“The LP amplitude is not a reliable marker for deception. However, the N400 is a reliable marker of lying that is not affected by emotional factors,” Researchers wrote.
Reference:
Proverbio, A., Vanutelli, M., & Adorni, R. (2013). Can You Catch a Liar? How Negative Emotions Affect Brain Responses when Lying or Telling the Truth PLoS ONE, 8 (3) DOI: 10.1371/journal.pone.0059383... Read more »
Proverbio, A., Vanutelli, M., & Adorni, R. (2013) Can You Catch a Liar? How Negative Emotions Affect Brain Responses when Lying or Telling the Truth. PLoS ONE, 8(3). DOI: 10.1371/journal.pone.0059383
by Neuroskeptic in Neuroskeptic_Discover
I’m currently researching a piece on politics and neurosurgery, and I just came across this amusing snippet. David McKalip MD is a brain surgeon from Florida. He attained 15 minutes of infamy in 2009 when he deemed a virulently racially insensitive of Barack Obama to be “funny stuff” and emailed it to some Tea Party [...]... Read more »
McKalip D. (2013) Letter to the editor: shaving. Journal of neurosurgery, 118(3), 701-2. PMID: 23259824
by beredim in Stem Cells Freak
Researchers at Lund University in Sweden published a few days ago a study in which they successfully rejuvenated the blood of old mice, by reprogramming their blood-forming stem cells using iPSCs technology.Full Story... Read more »
Wahlestedt, M., Norddahl, G., Sten, G., Ugale, A., Micha Frisk, M., Mattsson, R., Deierborg, T., Sigvardsson, M., & Bryder, D. (2013) An epigenetic component of hematopoietic stem cell aging amenable to reprogramming into a young state. Blood. DOI: 10.1182/blood-2012-11-469080
by Paul Whiteley in Questioning Answers
I've hinted before on this blog and its sister blog about how one of the most unappealing of interventions - fecal bacteriotherapy - is starting to make some waves in managing various conditions. I know its not everyone's cup of tea but the concept of transplanting whole stools or specific types of enteric bacteria from one person to another is actually providing some well needed relief for quite a few people.Insert here.... @ Wikipedia If it sounds like an undesirable treatment option, put yourself in the shoes of someone who for example is suffering as result of infection due to C. difficile and the potential consequences that this can entail after other treatment options have been exhausted and then wonder again. Better still, have a look at that probiotic yoghurt drink that is sitting in your fridge and ponder the question: where did the 'special' bacteria included in this drink originally come from? (hint: 'donor zero' is probably smiling at all of us).Whilst fecal bacteriotherapy is moving into more mainstream medicine circles for conditions linked to things like C.diff, various other states and diseases are also starting to be discussed with the s--t transplant in mind. One person in particular is leading these discussions, Dr Thomas Borody, following his groundbreaking work on triple therapy for H.pylori infection (see here), and some discussions on 'emerging' applications* (no pun intended). Indeed Dr Borody is quite the leading light when it comes to fecal bacteriotherapy.I was particularly interested to read the paper by Borody and colleagues** looking at the potential application of bacteriotherapy to cases of chronic fatigue syndrome (CFS). Regular readers might already know of my tendency to stray into the research domain of CFS (and ME) on this blog and beyond not least because quite a bit of the research there seems to overlap with what I talk about with autism in mind (e.g. immune function, mitochondrial issues, even HERVs..).Anyhow, with many thanks to Sarah Finlayson, one of Dr Borody's co-authors, for sending me a copy of their paper, a few points are worth noting:This is a paper which kills two birds with one stone. On the one hand, there is quite a nice summary of CFS and the gut microbiome (hopefully this link still works for non-members). On the other hand, the paper describes the experiences of 60 patients with CFS attending Dr Borody's clinic some time in the mid-1990s and in receipt of transcolonoscopic (TC) and rectal infusions of "anaerobic bacterial culture". Distinct from the 'full works' of of a stool transplant or 'fecal microbiota transplantation (FMT)', bacteriotherapy involves the 'fusion of a mixture of 13 non-pathogenic enteric bacteria" which include those of the Bacteroidetes, Clostridia and E.coli families/phyla/species.Every participant received at least one TC infusion; most also received a second rectal infusion (n=52); a small number received two days of additional rectal infusion (n=3). Actually, as you'll see in a minute, there was a bit more to this than what is mentioned in the methods section of the paper.Results: it is slightly difficult to gauge what specific results were achieved from this trial given that participants were judged to be responders or non-responders at 4 weeks based on some fairly nebulous criteria. So for example, responders signified "a resolution of CFS symptoms (sleep deprivation, lethary/fatigue)" but without the paper actually saying how these outcomes were measured or what tools were used. I'd hazard a guess that it was a case of participant interview or questionnaire but I can't confirm this. On the basis of this responder / non-responder coding, 35 (58%) were judged responders to bacteriotherapy. This figure improved when initial non-responders (n=15) were given a second TC infusion "followed by rectal infusion (n=4) or an oral course of cultured bacteria (n=6)"; up to 42 / 60 (70%) responders.Gastrointestinal (GI) symptoms were reported to be resolved in 37 of the 42 final responders.Follow-up of participants some 15-20 years later (12 of the original cohort) suggested that over half of them remained free of their CFS symptoms; although importantly, some relapsed (5/12) between 18-36 months post-bacteriotherapy.I probably don't need to highlight the fact that this was very much an observational case-series study over anything like a clinical trial. My initial excitement at reading this paper was very slightly dampened by the way results were reported and those all-important missing details regarding how the authors measured change over the period of baseline vs. bacteriotherapy. Even the reported resolution of GI symptoms leaves me asking questions like: what GI symptoms, how were they measured and who did the measuring? There are gaps in this work, make no mistake of that. Bear however in mind issues such as when this study was initially carried out and how the diagnostic criteria of CFS might not necessarily have been as well-defined as they are today. Just sayin.I can also imagine some people are reading this post and thinking what the .... ! How can a condition like CFS be sensitive to a bacterial transplant, and what about those methods used to introduce such a therapy... yeah right. Bear in mind however that our nether regions are actually quite good routes of drug administration bypassing for example, hostile environments like the stomach and onward the first-pass effect. Indeed the question should be: would you prefer this to the insertion of a naso-gastric tube as is the other option when delivering bacteria to where it is needed? Your choice...Having said all that I am still interested in this line of inquiry. The authors for example, suggest a possible link between "the resolution of gastrointestinal and CFS symptoms" and how this "supports the theory of a possible gastrointestinal-associated etiology, potentially arising from alterations to the bowel flora". I kinda speculated about the many faces (Man-E-Faces?) of CFS in a previous post on HERVs and ME (see here) and how the spectrum of CFS/ME might be just that, a spectrum. It strikes me that one could very easily investigate this possible sub-types issue within a well-defined population.There is obviously more to do in this area of endeavour. As per ... Read more »
Thomas Borody, Anna Nowak, & Sarah Finlayson. (2012) The GI microbiome and its role in Chronic Fatigue Syndrome: A summary of bacteriotherapy. Journal of the Australasian College of Nutritional and Environmental Medicine, 31(3). info:/
by beredim in Stem Cells Freak
In a new study funded by the Great Ormond Street Hospital Children's Charity researchers from the UCL Institute of Child Health have successfully used stem cells derived from amniotic fluid to treat necrotizing enterocolitis in a rodent model. The researchers believe that their study paves the way for new, cell-based therapies for treating this, many times lethal, condition.Full Story... Read more »
Zani, A., Cananzi, M., Fascetti-Leon, F., Lauriti, G., Smith, V., Bollini, S., Ghionzoli, M., D'Arrigo, A., Pozzobon, M., Piccoli, M.... (2013) Amniotic fluid stem cells improve survival and enhance repair of damaged intestine in necrotising enterocolitis via a COX-2 dependent mechanism. Gut. DOI: 10.1136/gutjnl-2012-303735
by Shelly Fan in Neurorexia
WARNING: Wall of text on the yummy neuroprotective effect of ketosis from a molecular neuroscience point of view. Proceed with caution. Remember when your high school biology teacher said that the brain absolutely NEEDS glucose to function? Well, that’s not entirely true. Under severe carbohydrate restriction, the brain can adapt and start burning ketones as [...]... Read more »
Hallböök T, Ji S, Maudsley S, & Martin B. (2012) The effects of the ketogenic diet on behavior and cognition. Epilepsy research, 100(3), 304-9. PMID: 21872440
Rho, J., & Sankar, R. (2008) The ketogenic diet in a pill: Is this possible?. Epilepsia, 127-133. DOI: 10.1111/j.1528-1167.2008.01857.x
Phelps, J., Siemers, S., & El-Mallakh, R. (2012) The ketogenic diet for type II bipolar disorder. Neurocase, 1-4. DOI: 10.1080/13554794.2012.690421
Ruskin DN, Ross JL, Kawamura M Jr, Ruiz TL, Geiger JD, & Masino SA. (2011) A ketogenic diet delays weight loss and does not impair working memory or motor function in the R6/2 1J mouse model of Huntington's disease. Physiology , 103(5), 501-7. PMID: 21501628
Krikorian R, Shidler MD, Dangelo K, Couch SC, Benoit SC, & Clegg DJ. (2012) Dietary ketosis enhances memory in mild cognitive impairment. Neurobiology of aging, 33(2), 2147483647-27. PMID: 21130529
Denke, M. (2001) Metabolic effects of high-protein, low-carbohydrate diets. The American Journal of Cardiology, 88(1), 59-61. DOI: 10.1016/S0002-9149(01)01586-7
by Tetyana Pekar in Science of Eating Disorders
I see this on an daily basis: patients with subtreshold eating disorders feeling invalidated and “not sick enough.” They are struggling so much, but maybe they still have their periods, or maybe their weight isn’t quite low enough, and so they often (but not always, thankfully) get dismissed by doctors, other healthcare professionals, and insurance companies. Do you think you really need this treatment, maybe you can just focus on eating healthier? You know you are not fat, you are perfectly healthy! Just be happy! Or, Sorry, we can’t cover this psychological treatment because you don’t fit the full diagnostic criteria.
Why do we draw a line between ‘threshold’ and ‘subthreshold’ at arbitrary numerical criteria? Sure numbers are important for medical treatment–for example, someone with a very low BMI might have considerably more physical complications that need to be taken into account during treatment than someone with a not-so-low BMI–but do these arbitrary weight and numerical criteria really say as much as we think they say? Is BMI or menstruation really a valid way of demarcating between severe (or …
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Le Grange, D., Crosby, R., Engel, S., Cao, L., Ndungu, A., Crow, S., Peterson, C., Mitchell, J., & Wonderlich, S. (2013) DSM-IV-Defined Anorexia Nervosa Versus Subthreshold Anorexia Nervosa (EDNOS-AN). European Eating Disorders Review, 21(1), 1-7. DOI: 10.1002/erv.2192
by Stephen Thomas in Sports Medicine Research (SMR): In the Lab & In the Field
Take Home Message: Over one year, high school baseball players had no bony changes (humeral retroversion) in their dominant arm’s humerus but had decreased shoulder internal rotation.
Unilateral overhead sports cause several bony and soft tissue adaptations on the dominant arm due to the large amounts of mechanical stress. However, it is unknown when bony adaptations (e.g., humeral retroversion) occur during skeletal development. Therefore, the authors examined the longitudinal change of humeral retroversion and glenohumeral range of motion in 138 high school baseball players between the start of 2 consecutive seasons.... Read more »
Oyama S, Hibberd EE, & Myers JB. (2013) Changes in humeral torsion and shoulder rotation range of motion in high school baseball players over a 1-year period. Clinical Biomechanics (Bristol, Avon). PMID: 23434341
by Heather Buschman, Ph.D. in Beaker
Researchers discover that the extra chromosome inherited in Down syndrome impairs learning and memory because it leads to low levels of SNX27 protein in the brain.... Read more »
Wang, X., Zhao, Y., Zhang, X., Badie, H., Zhou, Y., Mu, Y., Loo, L., Cai, L., Thompson, R., Yang, B.... (2013) Loss of sorting nexin 27 contributes to excitatory synaptic dysfunction by modulating glutamate receptor recycling in Down's syndrome. Nature Medicine. DOI: 10.1038/nm.3117
by Craig Payne in Running Research Junkie
We have all seen the claims on blogs, in articles and on places like You Tube that running shoes weaken muscles and that is why we should not be using the big bulky motion controlling running shoes. The claims are made quite regularly and with a certain amount of assertiveness that you would have to believe that those making the claims actually have some evidence to back up the claims, but they don’t.... Read more »
Goldmann, J., Potthast, W., & Brüggemann, G. (2013) Athletic training with minimal footwear strengthens toe flexor muscles. Footwear Science, 5(1), 19-25. DOI: 10.1080/19424280.2012.744361
by beredim in Stem Cells Freak
Medistem, announced today via a press release that it has updated the paper regarding its Phase II clinical trial on patients with heart failure. Purpose of the trial is to assess the safety and efficacy of Medistem's proprietary type of stem cell called "Endometrial Regenerative Cell" (ERC).Full Story... Read more »
Bockeria, L., Bogin, V., Bockeria, O., Le, T., Alekyan, B., Woods, E., Brown, A., Ichim, T., & Patel, A. (2013) Endometrial regenerative cells for treatment of heart failure: a new stem cell enters the clinic. Journal of Translational Medicine, 11(1), 56. DOI: 10.1186/1479-5876-11-56
by beredim in Stem Cells Freak
A team of researchers from the Weill Medical College of Cornell University and the Memorial-Sloan Kettering Cancer Center has developed a new method to greatly expand, in the laboratory, the numbers of hematopoietic stem cells (HSCs) after they have been extracted from bone marrow tissue. The researchers say that their method is of great importance as it allows, like no other previously described, the mass production of MSCs for clinical use.Full Story... Read more »
Lee, J., Shieh, J., Zhang, J., Liu, L., Zhang, Y., Eom, J., Morrone, G., Moore, M., & Zhou, P. (2013) Improved ex vivo expansion of adult hematopoietic stem cells by overcoming CUL4-mediated degradation of HOXB4. Blood. DOI: 10.1182/blood-2012-09-455204
by Rogue Medic in Rogue Medic
In the comments to what I wrote yesterday about seizures and a study comparing lorazepam (Ativan), diazepam (Valium), and placebo,[1] Brooks Walsh had the following comment –
"Although I’ve read the study before, I am only wondering now how the IRB for Alldredge 2001 thought there was 'equipoise' between placebo and benzos."... Read more »
Alldredge BK, Gelb AM, Isaacs SM, Corry MD, Allen F, Ulrich S, Gottwald MD, O’Neil N, Neuhaus JM, Segal MR, Lowenstein DH. (2001) A Comparison of Lorazepam, Diazepam, and Placebo for the Treatment of Out-of-Hospital Status Epilepticus. New England Journal of Medicine, 345(25), 1860-1860. DOI: 10.1056/NEJM200112203452521
Callaway, C. (2012) Questioning the Use of Epinephrine to Treat Cardiac Arrest. JAMA: The Journal of the American Medical Association, 307(11), 1198. DOI: 10.1001/jama.2012.313
Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S. (2012) Prehospital Epinephrine Use and Survival Among Patients With Out-of-Hospital Cardiac Arrest. JAMA: The Journal of the American Medical Association, 307(11), 1161. DOI: 10.1001/jama.2012.294
by Paul Whiteley in Questioning Answers
The paper by Emma Frans and colleagues* looking at autism risk across the generations is the focus of this post. Published in the journal JAMA Psychiatry alongside a provocative article by Andrea Roberts and colleagues** on maternal exposure to child abuse being "associated" with elevated risk for offspring autism (see here and here), the theme is transgenerational effects and quote: "that your father's and grandfather's lifestyle choices can affect you" as per some of media on this paper.Ο Κακός Εγγονός @ Wikipedia I'm not going to head too heavily into the Frans study because others have already discussed it far better than I ever could (see here and here). Indeed NHS Choices carries a particularly good run-down of the study which is well worth a read (see here).The main details were that based on an analysis of nearly 6000 cases of autism spectrum disorder (ASD) in Sweden, grandfathers who had fathered their daughter when aged 50 or above were 1.79 times more likely to have a grandchild diagnosed with autism than younger fathering grandfathers.If grandfathers fathered a son when aged 50 or above, they were 1.67 times more likely to have a grandchild diagnosed with autism (again compared to grandfathers having children when they were younger).The magic word 'epigenetics' is also mentioned to potentially account for results alongside the mutation side of things. I should also point out that Frans has published on similar things before with schizophrenia in mind***.I'm interested in studies like the current Frans one despite their reliance on association and relatively limited increased risk of autism. Interested because alongside the 'older dads and autism risk' research (see here), I have actually talked about grandparents and risk of autism and schizophrenia previously on this blog (see here) based partly on some interesting data derived from ALSPAC published by Jean Golding and colleagues**** (open-access) and also that 2011 Frans study. In particular was the emphasis on the Golding 3M - meiotic mismatch methylation - hypothesis used to account for their results on grandmother's age as potentially being relevant to grandchild autism risk (please read the Golding article for more information on 3M complete with nice diagram).I know it might sound a little far-fetched that the lives of our grandparents might so profoundly be able to affect the lives of subsequent generations but before we put this down to mere coincidence, let me draw your attention to some work that was done on a dark period of quite recent history: the Hongerwinter. The basics: the Dutch famine of 1944, where a Nazi blockade led to the deaths of thousands. As per the often cruel twists of fate, science actually learned something from the suffering of the Dutch people in these dark days. Not only the confirmation that wheat was tied into coeliac (celiac) disease but also the suggestion that famine exposure during a critical period of gestation *might* potentially affect offspring physical and mental health. I've kinda talked about something similar before with 'thin-fat bodies' and David Barker in mind (see here).Granted in the current Frans study we are heading back even further through the germline as potentially hosting some effect, but to all intents and purposes, the theory is the same as per the intergenerational effects noted in other conditions like depression*****. I suppose one could ask whether specific types of autism might be more related to this grandparental age hypothesis over others. So for example, older grandparents at time of fathering or mothering impacting on the genome of their offspring - themselves then expressing certain traits associated with autism or the broader phenotype (not necessarily hitting the diagnostic threshold) - which are then transmitted (amplified?) to the next generation. Perhaps even some link to things like assortative mating theory too? I'm not saying that this is the only scenario and such 'transmission' works on its own to elevate risk of an autism diagnosis but the theory is an interesting one; even more so if we assume for example, that the autism and schizophrenia spectrums might not necessarily be poles apart (see here).By the same token one might also extend such a hypothesis to include other variables other than just parental age at offspring conception. The availability of and exposure to certain food in these 'olden days', exposure events to pollutants, pharmaceuticals (yes, we did have them then) or lifestyle factors such as smoking and drinking habits, various psychological and somatic stressors; the list is seemingly endless. In at least some of these factors, there are subtle clues to potential future directions for autism research and beyond already being examined (see here and here). Assuming also that epigenetics might be tied into all of this, we also open up the concept of epigenetic reprogramming of the germline as per the very interesting article by Petra Hajkova****** (open-access); something which I think might be/have been discussed at the recent Environmental Epigenetics symposium hosted by the MIND Institute.But let's not get too carried away with this area of inquiry or where it potentially leads in terms of the autism 'blame game'. Although I've not been able to find specific figures, I assume the actual numbers of grandfathers who fathered their children aged 50+ years is probably not going to be all that frequent if more current rates, at least here in the UK, are anything to go by (see this paper by Bray and colleagues*******). And then we have to wonder whether other variables might come into play such as the effect of paternal age at conception on birth factors such as birth weight or time of gestation even fecundity itself and how that might relate to autism risk.Such transgenerational effects whilst interesting, should also not detract research attention away from other more here-and-now possibilities which might affect autism risk as per the recent ... Read more »
Frans, E. (2013) Autism Risk Across GenerationsA Population-Based Study of Advancing Grandpaternal and Paternal AgeAutism Risk. JAMA Psychiatry, 1. DOI: 10.1001/jamapsychiatry.2013.1180
by Stephen Stache in Sports Medicine Research (SMR): In the Lab & In the Field
Take Home Message: Preseason neck pain and headache may be predictors for in season concussion among male youth hockey players.
Over the last few years, concussion has become one of the most common injuries among youth hockey players. Athletes have reported preseason neck pain, headache, and dizziness in recent concussion research, but it remains unclear if these symptoms predict who may be at risk for concussion. Consequently, in this prospective cohort study, Schneider et al. sought to determine the risk of concussion among youth male hockey players with and without preseason complaints of neck pain, headaches, or dizziness.... Read more »
Schneider KJ, Meeuwisse WH, Kang J, Schneider GM, & Emery CA. (2013) Preseason Reports of Neck Pain, Dizziness, and Headache as Risk Factors for Concussion in Male Youth Ice Hockey Players. Clinical Journal of Sport Medicine. PMID: 23391986
by Shelly Fan in Science of Eating Disorders
In my previous post, I looked at two hormones released during the cephalic phase (gastric secretion that occurs before food is eaten), ghrelin and obestatin, and how they may contribute to runaway eating behavior. Today I’m going to be looking at insulin release during chew and spit (CHSP), a fairly common symptom in eating disorders where the food is tasted, chewed and spit out. Insulin is a small peptide hormone that acts as a key regulator of metabolism; deregulation of insulin signalling plays a role in illnesses such as diabetes and metabolic syndrome. Some people have theorized that CHSP behavior may influence insulin regulation. In fact, there are a number of individuals stating on internet forums that chronic CHSP could lead to insulin resistance, potentially promoting diabetes. As interesting as these theories are, recent data have shown that they are probably not true.
INSULIN RELEASE DURING THE CEPHALIC RESPONSE
The taste of food activates the vagus nerve, a part of the peripheral nervous system that sends signals to the pancreas. In response, the pancreas releases insulin (as well as other …
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Broberg DJ, & Bernstein IL. (1989) Cephalic insulin release in anorexic women. Physiology , 45(5), 871-4. PMID: 2675143
Moyer A, Rodin J, & Cummings N. (1993) Cephalic phase insulin release in bulimia. The International journal of eating disorders, 14(3), 331-9. PMID: 8275069
Teff KL, & Engelman K. (1996) Palatability and dietary restraint: effect on cephalic phase insulin release in women. Physiology , 60(2), 567-73. PMID: 8840920
Teff KL. (2011) How neural mediation of anticipatory and compensatory insulin release helps us tolerate food. Physiology , 103(1), 44-50. PMID: 21256146
by Christen Rune Stensvold in Blastocystis Parasite Blog
Over the past few years nucleic acid based methods have revolutionised parasite diagnostics in modern clinical microbiology (CM) labs. Real-time PCR is really gaining a foothold in CM labs, but despite the opportunity for plexing, mostly only up to 6 DNA targets can be included in each assay (due to the number of available channels). LUMINEX xMAP technology is appealing due increasing opportunities but is still limited by probe-based detection.... Read more »
Dunbar SA. (2006) Applications of Luminex xMAP technology for rapid, high-throughput multiplexed nucleic acid detection. Clinica chimica acta; international journal of clinical chemistry, 363(1-2), 71-82. PMID: 16102740
Santos HL, Bandyopadhyay K, Bandea R, Peralta RH, Peralta JM, & Da Silva AJ. (2013) LUMINEX(R): a new technology for the simultaneous identification of five Entamoeba spp. commonly found in human stools. Parasites , 6(1), 69. PMID: 23497666
Stensvold CR, Lebbad M, & Verweij JJ. (2011) The impact of genetic diversity in protozoa on molecular diagnostics. Trends in parasitology, 27(2), 53-8. PMID: 21168365
Stensvold CR, Lebbad M, Victory EL, Verweij JJ, Tannich E, Alfellani M, Legarraga P, & Clark CG. (2011) Increased sampling reveals novel lineages of Entamoeba: consequences of genetic diversity and host specificity for taxonomy and molecular detection. Protist, 162(3), 525-41. PMID: 21295520
Taniuchi M, Verweij JJ, Sethabutr O, Bodhidatta L, Garcia L, Maro A, Kumburu H, Gratz J, Kibiki G, & Houpt ER. (2011) Multiplex polymerase chain reaction method to detect Cyclospora, Cystoisospora, and Microsporidia in stool samples. Diagnostic microbiology and infectious disease, 71(4), 386-90. PMID: 21982218
by beredim in Stem Cells Freak
A team of researchers, led by Dan Kaufman, released a study today in which they describe a new method for producing anti-cancer natural killer cells from embryonic and induced pluripotent stem cells. Although this has been achieved in the past, the researchers say that their method produces way more cells than any other technique previously described.Full Story... Read more »
Knorr, D., Ni, Z., Hermanson, D., Hexum, M., Bendzick, L., Cooper, L., Lee, D., & Kaufman, D. (2013) Clinical-Scale Derivation of Natural Killer Cells From Human Pluripotent Stem Cells for Cancer Therapy. Stem Cells Translational Medicine. DOI: 10.5966/sctm.2012-0084
by beredim in Stem Cells Freak
Researchers at Moffitt Cancer Center just announced the results of a phase II clinical trial on patients with with higher-risk myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia, or acute myeloid leukaemia arising from MDS, who had previously failed to respond to conventional treatment (azanucleosides). Purpose of the trial was to assess the safety and efficacy of dasatinib in treating these conditions. The researchers say that although the drug won't help all patients, it does help the ones with the trisomy 8 chromosomal disorder.Full Story... Read more »
Duong, V., Jaglal, M., Zhang, L., Kale, V., Lancet, J., Komrokji, R., & List, A. (2013) Phase II pilot study of oral dasatinib in patients with higher-risk myelodysplastic syndrome (MDS) who failed conventional therapy. Leukemia Research, 37(3), 300-304. DOI: 10.1016/j.leukres.2012.11.001
by Dorothy Bishop in bishopblog
In a previous blogpost, I criticized a recent paper claiming that playing action video games improved reading in dyslexics. In a series of comments below the blogpost, two of the authors have responded to my criticisms. I thank them for taking the trouble to spell out their views and giving readers the opportunity to see another point of view. I am, however, not persuaded by their arguments, which make two main points. First, that their study was not methodologically weak and so Current Biology was right to publish it, and second, that it is unfair, and indeed unethical, to criticize a scientific paper in a blog, rather than through the regular scientific channels.... Read more »
Ioannidis JP, Pereira TV, & Horwitz RI. (2013) Emergence of large treatment effects from small trials--reply. JAMA : the journal of the American Medical Association, 309(8), 768-9. PMID: 23443435
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