Welcome to the latest Naturally Speaking blog post. This post was written by Research Associate Caroline Millins a qualified veterinary pathologist and researcher in wildlife disease epidemiology. Here Caroline describes work that was featured in her most recent research paper, but also gives the broader story to becoming involved in wildlife pathology. Silent witnesses: investigating wildlife crime in Scotland Seeing wildlife […]
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Millins, C., Howie, F., Everitt, C., Shand, M., & Lamm, C. (2014) Analysis of suspected wildlife crimes submitted for forensic examinations in Scotland. Forensic Science, Medicine, and Pathology, 10(3), 357-362. DOI: 10.1007/s12024-014-9568-1
The paper by T. Peter Stein and colleagues  suggesting an "association" between BPA (Bisphenol-A) and autism spectrum disorder (ASD) was always bound to create some interest. Reporting results based on the analysis of urine samples from a group of children diagnosed with an autism spectrum disorder (ASD) (n=46) compared to controls (n=52), authors concluded that: "there is an association between BPA and ASD." Association... note that word.C'mon. Let's go see how much we're going for on eBayBPA has been around for quite a few years. An important chemical in the production of certain plastics and resins, in more recent times quite a volume of science has suggested that caution should be applied to the use of and exposure to BPA particularly with reference to its potential estrogenic properties . As with everything in life, the effects or not of BPA continue to be the source of some discussion, with concerns even been raised about the alternatives to BPA (see here) being put forward. In short, it's very, very complicated.Stein and colleagues started from the premise that: "The major pathway for BPA metabolism and excretion is via glucuronidation." Glucuronidation involves the addition of glucuronic acid to a particular metabolite thus aiding the removal of said metabolite from the body. Those of you who have come across the whole sulphation and autism story might remember how glucuronidation and sulphation share some history with [some] autism in mind as per papers like the one from Alberti and colleagues . Stein et al have some research form when it comes to glucuronidation and autism as per papers such as this one  (open-access) that concluded that: "The glucuronidation pathway may differ in some children with ASD." They reported lower levels of glucuronidation which impacted on the metabolism of phthalates among other things (see here).Anyhow, the analytical weapon of choice in the BPA-autism study by Stein et al was mass spectrometry (MS). Again, this research group have some interest/experience in this area as per other research of theirs which has crossed my blogging path (see here). Looking at those urine samples from participants with ASD vs asymptomatic controls, researchers reported a few important details including that: "about 20% of the ASD children had BPA levels beyond the 90th percentile (>50 ng/mL) of the frequency distribution for the total sample of 98 children." They also reported "significant differences (P < 0.05) between the groups in total and % bound BPA" (bound BPA referring to BPA glucuronide). Reiterating their conclusion: "The results suggest there is an association between BPA and ASD."Bearing in mind how the word 'chemical' has been mis-represented down the years, there is quite a body of work emerging suggestive that there is quite a bit more to do when it comes to environmental exposures potentially linking into at least some cases of autism. This is not the first time that BPA has been examined with autism in mind as per discussions like the one from de Cock and colleagues  and some animal model work such as that from Wolstenholme et al . The paper from Kaur and colleagues  suggesting that: "BPA may act as an environmental risk factor for autism in genetically susceptible children by inducing oxidative stress and mitochondrial dysfunction" offers some tantalising areas of further research tallying with other non-autism research . I might also bring your attention to the paper by Lichtensteiger and colleagues  (thanks to @autismepi) perhaps providing another important area for further research.Further study is of course implied from the Stein work and other research in this area. That and quite a bit more investigation of the biological systems implicated in any effect from BPA on cases of autism brings the focus back to a model of genes and environment [variably] interacting on the very wide autism spectrum...Music: Madonna - Papa Don't Preach. Well, preaching is what we do best!---------- Stein TP. et al. Bisphenol A Exposure in Children With Autism Spectrum Disorders. Autism Research. 2015. Jan 13. Sharpe RM. Is it time to end concerns over the estrogenic effects of bisphenol A? Toxicol Sci. 2010 Mar;114(1):1-4. Alberti A. et al. Sulphation deficit in "low-functioning" autistic children: a pilot study. Biol Psychiatry. 1999 Aug 1;46(3):420-4. Stein TP. et al. Autism and Phthalate Metabolite Glucuronidation. J Autism Dev Disord. Nov 2013; 43(11): 2677–2685. de Cock M. et al. Does perinatal exposure to endocrine disruptors induce autism spectrum and attention deficit hyperactivity disorders? Review. Acta Paediatr. 2012 Aug;101(8):811-8. Wolstenholme JT. et al. Gestational exposure to low dose bisphenol A alters social behavior in juvenile mice. PLoS One. 2011;6(9):e25448. Kaur K. et al. Bisphenol A induces oxidative stress and mitochondrial dysfunction in lymphoblasts from children with autism and unaffected siblings. Free Radic Biol Med. 2014 Nov;76:25-33. Veiga-Lopez A. et al. Impact of Gestational Bisphenol A on Oxidative Stress and Free Fatty Acids: Human Association and Interspecies Animal Testing Studies. Endocrinology. 2015. Jan 20. Lichtensteiger W. et al. Differential Gene Expression Patterns in Developing Sexually Dimorphic Rat Brain Regions Exposed to Anti-androgenic, Estrogenic, or Complex Endocrine Disruptor Mixtures: Glutamatergic Synapses as Target. Endocrinology. 2015 Jan 21: en20141504.----------Stein, T., Schluter, M., Steer, R., Guo, L., & Ming, X. (2015). Bisphenol A Exposure ... Read more »
Stein, T., Schluter, M., Steer, R., Guo, L., & Ming, X. (2015) Bisphenol A Exposure in Children With Autism Spectrum Disorders. Autism Research. DOI: 10.1002/aur.1444
Let’s be honest, we’ve been getting a little fancy with the antibiotics, creating new and more relevant versions of old favorites like penicillin. Truthfully, we are the problem, how many times do we have to drive home the idea that antibiotics are for bacteria, not viruses. It is not all the consumers fault, the Doctors used to hand out antibiotics to placate angry parents of sick children.... Read more »
WHO. (2014) Antimicrobial resistance. World Health Organization . info:other/
Lewis NE, Hixson KK, Conrad TM, Lerman JA, Charusanti P, Polpitiya AD, Adkins JN, Schramm G, Purvine SO, Lopez-Ferrer D.... (2010) Omic data from evolved E. coli are consistent with computed optimal growth from genome-scale models. Molecular systems biology, 390. PMID: 20664636
Solomon SL, & Oliver KB. (2014) Antibiotic resistance threats in the United States: stepping back from the brink. American family physician, 89(12), 938-41. PMID: 25162160
Tellería-Orriols JJ, García-Salido A, Varillas D, Serrano-González A, & Casado-Flores J. (2014) TLR2-TLR4/CD14 polymorphisms and predisposition to severe invasive infections by Neisseria meningitidis and Streptococcus pneumoniae. Medicina intensiva / Sociedad Espanola de Medicina Intensiva y Unidades Coronarias, 38(6), 356-62. PMID: 24144680
Corie Lok. (2001) Antibiotic resistance switched off. Nature. info:/10.1038/news010322-4
Cobb RE, Wang Y, & Zhao H. (2014) High-Efficiency Multiplex Genome Editing of Streptomyces Species Using an Engineered CRISPR/Cas System. ACS synthetic biology. PMID: 25458909
Fancy some weekend reading? Well, you could do a lot worse than having a gander through the paper by Jane Naviaux and colleagues  (open-access) discussing the results of a whole host of analyses following the use of the antipurinergic agent suramin on a mouse model of Fragile X syndrome.Overprotective mother, forbidden road trip...Regular readers might remember some previous discussions about suramin - a pharmaceutic designed to treat African sleeping sickness - and autism which have graced this blog (see here and see here). Following a series of studies which looked at the physiological and behavioural effects of suramin administration on a mouse model trying to recreate conditions of maternal immune activation (MIA (which itself has some autism research history), authors this time turned their attention to a mouse model of Fragile X syndrome, a condition which can in humans manifest with autistic traits (sometimes).The Naviaux paper is a whopper in terms of data accumulated and results so I'm not going to even try and summarise the findings aside from quoting the authors that their: "results support the novel conclusion that antipurinergic therapy is operating by a mechanism that lies close to the root cause of the core behaviors and development in both the environmental MIA, and the genetic Fragile X models of ASD [autism spectrum disorder]. This mechanism appears to be traceable to mitochondria and regulated by purinergic signaling." Both mitochondrial and purinergic issues have featured in the autism research historical tapestry before (see here and see here respectively).Just before anyone makes a run on suramin, I might however point out a few things: (a) the current and previous results are based on mouse studies and mice are mice not humans, and (b) suramin, whilst indicated for sleeping sickness, is not without the possibility of some pretty important side-effects (see here).Still, this latest paper again potentially opens up a number of promising lines of inquiry in need of further investigation. And the added bonus is to see some more metabolomics included in their results!To close: INXS and Mystify.---------- Naviaux JC. et al. Antipurinergic therapy corrects the autism-like features in the fragile X (Fmr1 knockout) mouse model. Molecular Autism 2015, 6:1----------Jane C Naviaux, Lin Wang, Kefeng Li, A Taylor Bright, William A Alaynick, Kenneth R Williams, Susan B Powell, & Robert K Naviaux (2015). Antipurinergic therapy corrects the autism-like features in the fragile X (Fmr1 knockout) mouse model Molecular Autism : 1186/2040-2392-6-1... Read more »
Jane C Naviaux, Lin Wang, Kefeng Li, A Taylor Bright, William A Alaynick, Kenneth R Williams, Susan B Powell, & Robert K Naviaux. (2015) Antipurinergic therapy corrects the autism-like features in the fragile X (Fmr1 knockout) mouse model. Molecular Autism. info:/1186/2040-2392-6-1
Studies of stress and its effects on health have typically focused on the worries of an individual: money, love, health, work. When we turn our attention on relationship stress, the focus is generally on your typical couple. However, new research studies how minority stress -- which results from being stigmatized and disadvantaged in society -- affects same-sex couples' stress levels and overall health.... Read more »
LeBlanc, A., Frost, D., & Wight, R. (2015) Minority Stress and Stress Proliferation Among Same-Sex and Other Marginalized Couples. Journal of Marriage and Family, 77(1), 40-59. DOI: 10.1111/jomf.12160
"Findings confirm the heterogeneous nature of developmental trajectories in ASD [autism spectrum disorder]." That was the bottom line of the study by Peter Szatmari and colleagues  (open-access) tracking the developmental trajectory - autistic symptom severity and adaptive functioning - for a sample of "421 newly diagnosed preschool children with ASD 2 to 4 years old." Some accompanying media for the study can be found here.The Szatmari paper is open-access so it doesn't need any grand details from me... OK, well just a few:"Prospective data collected at 4 points from time of diagnosis to age 6 years were used to track the developmental trajectories of children." Old reliable ADOS (Autism Diagnostic Observation Schedule) was used "to index the developmental trajectories of autistic symptom severity" alongside the VABS (Vineland Adaptive Behavior Scales) which "assesses child adaptive behavior in the communication, socialization, daily living skills, and motor domains." The immediate difference between these schedules outside of looking at autism symptoms and adaptive behaviours is the reliance on observer scores and parent/caregiver report respectively. Just in case you were worried, the timing gaps between ADOS sessions for example, were probably large enough so as not to lead to any so-called practice effects impacting results. Other psychometric tools were also used to gauge 'trajectory prediction and outcome' including the ADI (Autism Diagnostic Interview) among other things.Results: outside of the heterogeneity of symptom presentations, a few key points were noted. So: "Individual children with ASD differ from each other in terms of autistic symptom severity and adaptive functioning from the time of diagnosis in the preschool years, and some of these differences appear to increase by age 6 years." Interesting but not exactly a novel finding as per other discussions in this area (see here)."Moreover, change in one domain is not necessarily associated with change in another." In other words, about 20% of their sample showed changes in "adaptive functioning trajectories" indicative of improvement. But that doesn't necessarily translate into similar changes in autistic presentation which were reported to be "more stable" although in about 10% of cases showing "a decrease in symptom severity from baseline to age 6 years."In all, the authors report two distinct trajectory groups based on autism severity and three groups for adaptive functioning. Caveats? Well, this was a multi-site study in Canada but following diagnosis, participants were not just left without intervention. The Hanen More Than Words® intervention is mentioned as being offered at one site. Indeed the authors note: "the present analysis did not investigate the possible effect of services or opportunities to learn adaptive functioning skills on the developmental trajectories of children with ASD" so one has to be mindful that the results reported might be affected by this variable. Indeed, one would expect trajectory to be potentially affected by such early intervention...This is interesting work particularly from the perspective of being a longitudinal study which relied on some of the gold-standard tools available to autism psychometric research. I'm really interested in developmental trajectory and autism in light of this area of research highlighting how autism is perhaps better described as the more plural 'autisms' and the breaking down of some sweeping generalisations and dogma which have pervaded autism understanding. That also one or more trajectory might come under the label of 'optimal outcome' (see here), that is moving outside of the diagnostic boundaries of the clinical description of autism, is another important part of this work. Oh, and just in case you think such ideas are bound to just children, think again (see here).Gender (sex) is also mentioned in the Szatmari paper and the idea that "sex was the only significant predictor of autistic symptom group trajectory membership." The authors continue: "Boys were more likely to be in the group with more severe symptoms and a stable trajectory than girls, who were more likely to be in the group with less severe symptoms and an improving trajectory (controlling for age at diagnosis, cognitive and language scores, and site)." This is really quite an interesting observation and perhaps ties into the idea of sex differences in the presentation of autism (see here) among other things. I'd be interested to see how the gender splits pan out when it comes to those optimal outcomers too as and when larger participant numbers are eventually meta-analysed by someone.Finally: "earlier age at diagnosis was more likely associated with membership in a group with higher functioning and improving." Going back to my previous point about a possible role for early intervention in developmental trajectory, the idea that earlier diagnosis can make a difference through the use of earlier intervention also potentially gains ground from such observations. Early diagnosis is a primary endpoint for quite a lot of autism research (see here) although with still quite a bit to do in this area (see here).The Hurdy Gurdy Man to close from The "B.H. Surfers".---------- Szatmari P. et al. Developmental Trajectories of Symptom Severity and Adaptive Functioning in an Inception Cohort of Preschool Children With Autism Spectrum Disorder. JAMA Psychiatry. 2015. Jan 28.----------Szatmari, P., Georgiades, S., Duku, E., Bennett, T., Bryson, S., Fombonne, E., Mirenda, P., Roberts, W., Smith, I., Vaillancourt, T., Volden, J., Waddell, C., Zwaigenbaum, L., Elsabbagh, M., & Thompson, A. (2015)... Read more »
Szatmari, P., Georgiades, S., Duku, E., Bennett, T., Bryson, S., Fombonne, E., Mirenda, P., Roberts, W., Smith, I., Vaillancourt, T.... (2015) Developmental Trajectories of Symptom Severity and Adaptive Functioning in an Inception Cohort of Preschool Children With Autism Spectrum Disorder. JAMA Psychiatry. DOI: 10.1001/jamapsychiatry.2014.2463
Growing with time and becoming old is a common phenomenon. Every person grows older with time, but some people may have the wish to grow old faster. So, this article is for those people. On the contrary, if you want to feel young and good, do the opposite as mentioned in this article.
Think that you are old
It has been found that self-perceived age is strongly related to cardiovascular health. It is important to think that you are older. Researchers have found that older people, who think that they are older than their actual age, have more chances of worsening the condition and increasing rates of death. If you feel that you are three or more years younger than actual age, it would be good for you and can decrease the death rate.
Move to a society with lower value for older people
If someone wants to become older and worsen his or her condition, he or she has to think that he or she is “old”. Researchers have found that this thinking can worsen the condition of health, especially in those societies, where older people are considered to have little value as compared to younger people. On the other hand, if someone wants to grow older with good condition, he or she has to move away from the society, where older people have higher values as compared to younger people.
Don’t exercise and try to decrease physical activity
Exercise can improve the quality of life and independence, especially in older people. It can also decrease the social isolation. So, it is important that you have not to exercise, so that there would be no improvement in long-term health or wellbeing.
Increased physical activity can help in maintaining proper weight and function of the body. So, try to reduce physical activity.
Don’t use vitamin D and other vitamins
Vitamin D can help in improving the immunity. It can also help in absorbing calcium that is important for bones and skeletal system. So, if someone wants to grow older and worsen the condition, he or she has to stop taking vitamin D. It is also important to not to expose yourself to the direct sunlight as it can help in producing vitamin D in the body.
Start cynical distrust
If you want to feel worse, start cynical distrust. It is the belief that people have selfish concerns in their tasks. Researchers have found that people with high level of cynical distrust have more chances of developing health and psychology related problems such as heart disease and dementia. If you want to feel worse, keep on thinking like this – “It is safer to trust nobody”, "I think most people would lie to get ahead" and “People use unfair reasons to gain profit or advantage.” These types of thinking belong to cynical distrust.
Nobody is trustworthy - cynical distrust (Credit: Pixabay/ PublicDomainPictures)
Nobody is trustworthy - cynical distrust (Credit: Pixabay/ PublicDomainPictures)
Don’t take proper sleep
Sleep disturbances (non-restorative sleep) can help in increasing the chances of widespread pain especially in older people.
Use more medicines such as statin
Statins belong to that class of medicine that are used to lower cholesterol. Nearly 33% of older people in America use statins to control their cholesterol problems. It has been found the use of statin is related to decrease physical activity. It is clear that with less physical activity, your chances of getting worse increase. Moreover, if a person has started taking statin recently, he may show the largest decrease in physical activity as compared to older statin users.
…. And the ideas to feel old and/or worse keep on going. Fortunately or unfortunately, many of us are already following those ideas.
Laird, H. McNulty, M. Ward, L. Hoey, E. McSorley, J. M. W. Wallace, . . . J. J. Strain. (2014). Vitamin D Deficiency Is Associated With Inflammation in Older Irish Adults. Journal of Clinical Endocrinology & Metabolism.
Lee, D. S., Markwardt, S., Goeres, L., Lee, C. G., Eckstrom, E., Williams, C., . . . Nielson, C. M. (2014). Statins and physical activity in older men: the osteoporotic fractures in men study. [Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't]. JAMA Intern Med, 174(8), 1263-1270. doi: 10.1001/jamainternmed.2014.2266
Marques, S., Swift, H. J., Vauclair, C. M., Lima, M. L., Bratt, C., & Abrams, D. (2014). 'Being old and ill' across different countries: Social status, age identification and older people's subjective health. Psychol Health, 1-16. doi: 10.1080/08870446.2014.938742
McBeth, J., Lacey, R. J., & Wilkie, R. (2014). Predictors of new-onset widespread pain in older adults: results from a population-based prospective cohort study in the UK. [Research Support, Non-U.S. Gov't]. Arthritis Rheumatol, 66(3), 757-767. doi: 10.1002/art.38284
Neuvonen, E., Rusanen, M., Solomon, A., Ngandu, T., Laatikainen, T., Soininen, H., . . . Tolppanen, A. M. (2014). Late-life cynical distrust, risk of incident dementia, and mortality in a population-based cohort. [Research Support, Non-U.S. Gov't]. Neurology, 82(24), 2205-2212. doi: 10.1212/WNL.0000000000000528
Rippon, I., & Steptoe, A. (2014). Feeling Old vs Being Old JAMA Internal Medicine DOI: 10.1001/jamainternmed.2014.6580
Wallace, R., Lees, C., Minou, M., Singleton, D., & Stratton, G. (2014). Effects of a 12-week community exercise programme on older people. Nurs Older People, 26(1), 20-26. doi: 10.7748/nop2014.02.26.1.20.e508... Read more »
It’s more socially acceptable to talk about mental illness, which is important since the number of people who have it — or should we say, are getting treatment for mental illness — has steadily increased over the years. While it still may be taboo to talk about, mental illness is a very real thing needing very real treatment, however new research now shows that texting may be a more suitable treatment aid for those with mental illness than mobile applications.... Read more »
Campbell, B., Caine, K., Connelly, K., Doub, T., & Bragg, A. (2014) Cell phone ownership and use among mental health outpatients in the USA. Personal and Ubiquitous Computing, 19(2), 367-378. DOI: 10.1007/s00779-014-0822-z
In a study published in the Proceedings of the National Academy of Sciences, Anne-Marie Chang and her colleagues found that reading on light-emitting eReaders before bed negatively affected sleep by altering levels of melatonin. The researchers recruited 12 participants and randomly assigned them to one of two groups: one group read printed books for four hours before bed every day for five consecutive days while the other group used eReaders. After five days, the participants switched to reading on the other device. This study design allowed researchers to compare sleep-related metrics from the same individual when they were reading a printed book to when they were reading an eReader. The eReaders used in this study were iPads set to maximum brightness.... Read more »
Chang, A., Aeschbach, D., Duffy, J., & Czeisler, C. (2015) Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness. Proceedings of the National Academy of Sciences, 112(4), 1232-1237. DOI: 10.1073/pnas.1418490112
I was not surprised to read the findings of the paper from Marie Moore Channell and colleagues  (open-access) who "identified patterns of ASD [autism spectrum disorder] symptomatology, measured by the SRS [Social Responsiveness Scale], in individuals with DS [Down syndrome] who do not have comorbid ASD."You're not going Turbo, are you?Harking back to the paper by Georgina Warner and colleagues  discussed not-so-long-ago on this blog (see here), the idea that various autistic traits might also overlap into other conditions including that of Down's syndrome, is gaining some research momentum at the moment. Whether such overlap will yield further clues regarding the aetiology of [some] autism or feed into the various discussions about the changing autism numbers game are discussions to be had in future times.Channell et al report results for a small group of children/young adults diagnosed with DS. Their participant cohort originally started at 54 individuals with DS who met various study criteria. This was subsequently boiled down to 46 participants given that: "Eight participants scored above our predetermined cutoff" based on scores on the Social Communication Questionnaire (SCQ) "and were determined to be at risk for a comorbid ASD diagnosis, and they were referred for a full diagnostic evaluation." The authors importantly add that: "this number should not be used as a prevalence estimate of ASD risk in DS." Not yet at least.The SRS was the primary assessment tool, a parent/caregiver reporting schedule "that asks caregivers about their child’s behavior over the past 6 months" specifically looking at reciprocal social behaviours. As part of the autism screening arsenal, the SRS is doing pretty well by all accounts . That being said, it has it limitations as was recently mentioned  following it's use in that broccoli sprout - autism trial (see here).Anyhow, the results: "In general, scores were elevated relative to the available normative data on typically developing children and adolescents, suggesting the need for normative data on the SRS for syndrome-specific samples such as those with DS." Indeed, the authors go on to suggest that as more is done in this area looking at any overlap between autism and DS: "It is likely that some of the currently used diagnostic measures also will require modification for ease of use and interpretation in the DS population." Too true although I would perhaps stress the idea that something like issues with social reciprocity might be something in need of further investigation in some cases of DS.I've got little more to say on this issue over and above what has already been said. I'd like to think that once science has progressed a little further in this specific area, it might also turn its attention to the preliminary data reported by Worley and colleagues  and further testing of the concept of 'Down Syndrome Disintegrative Disorder' (see here) as one among other potential links between DS and the presentation of autism.Music, music, music to close: Limahl - Never Ending Story. Sing it with passion...---------- Channell MM. et al. Patterns of autism spectrum symptomatology in individuals with Downsyndrome without comorbid autism spectrum disorder. Journal of Neurodevelopmental Disorders 2015, 7:5. Warner G. et al. Autism Characteristics and Behavioural Disturbances in ∼ 500 Children with Down's Syndrome in England and Wales. Autism Res. 2014. March 24. 10.1002/aur.1371 Duvekot J. et al. The Screening Accuracy of the Parent and Teacher-Reported Social Responsiveness Scale (SRS): Comparison with the 3Di and ADOS. J Autism Dev Disord. 2014 Nov 28. Scahill L. Uncommon use of common measures in sulforaphane trial. PNAS. 2015. Jan 13. Worley G. et al. Down Syndrome Disintegrative Disorder: New-Onset Autistic Regression, Dementia, and Insomnia in Older Children and Adolescents With Down Syndrome. J Child Neurol. 2014 Nov 3. pii: 0883073814554654.----------Marie Moore Channell, B Allyson Phillips, Susan J Loveall, Frances A Conners, Paige M Bussanich, & Laura Grofer Klinger (2015). Patterns of autism spectrum symptomatology in individuals with Down syndrome without comorbid autism spectrum disorder Journal of Neurodevelopmental Disorders : 10.1186/1866-1955-7-5... Read more »
Marie Moore Channell, B Allyson Phillips, Susan J Loveall, Frances A Conners, Paige M Bussanich, & Laura Grofer Klinger. (2015) Patterns of autism spectrum symptomatology in individuals with Down syndrome without comorbid autism spectrum disorder. Journal of Neurodevelopmental Disorders. info:/10.1186/1866-1955-7-5
MedicalResearch.com Medical Research Interviews and News
MedicalResearch.com Interview with: Dr Maddy Greville-Harris Research Fellow University of Southampton Medical Research: What is the background for this study? What are the main findings? Dr. Greville-Harris: Our research looks at the effects of non-understanding feedback (‘invalidation’) and discusses … Continue reading →
The post Negative Patient-Doctor Communication More Powerful Than Positive Interaction appeared first on MedicalResearch.com Medical Research Interviews and News .
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MedicalResearch.com Interview with, Dr Maddy Greville-Harris, Research Fellow, & University of Southampton. (2015) Negative Patient-Doctor Communication More Powerful Than Positive Communication . MedicalResearch.com. info:/
Seems like everything is killing us these days. Well ladies, you have one more thing that is causing you problems. New research has shown that women whose bodies have high levels of chemicals found in plastics, personal-care products, common household items and the environment experience menopause two to four years earlier than women with lower levels of these chemicals.... Read more »
Grindler, N., Allsworth, J., Macones, G., Kannan, K., Roehl, K., & Cooper, A. (2015) Persistent Organic Pollutants and Early Menopause in U.S. Women. PLOS ONE, 10(1). DOI: 10.1371/journal.pone.0116057
Nematodes cause horrible diseases, but they way they reproduce is the most fascinating thing about them. Their sperm aren’t shaped like typical animal male gametes. They crawl instead of swimming, and they have a type of cytoskeleton not seen in any other cell type on Earth. Yet, the nematode is the most numerous type of animal on Earth.... Read more »
H. Ferris. (2009) The beer mat nematode, Panagrellus The beer mat nematode, Panagrellus redivivus: A study of the connectedness of scientific discovery . J. Nematode Morphol. Syst., 12(1), 19-25. info:/
McKnight, K., Hoang, H., Prasain, J., Brown, N., Vibbert, J., Hollister, K., Moore, R., Ragains, J., Reese, J., & Miller, M. (2014) Neurosensory Perception of Environmental Cues Modulates Sperm Motility Critical for Fertilization. Science, 344(6185), 754-757. DOI: 10.1126/science.1250598
Morgan, E., Azam, D., & Pegler, K. (2013) Quantifying sources of environmental contamination with Toxocara spp. eggs. Veterinary Parasitology, 193(4), 390-397. DOI: 10.1016/j.vetpar.2012.12.034
Sepsenwol S, Ris H, & Roberts TM. (1989) A unique cytoskeleton associated with crawling in the amoeboid sperm of the nematode, Ascaris suum. The Journal of cell biology, 108(1), 55-66. PMID: 2910878
The paper by Muneko Nishijo and colleagues  (open-access) caught my eye recently and their continuing investigations into the potential effects of perinatal dioxin exposure on offspring neurodevelopmental outcomes. For a bit of background on this initiative based in Vietnam, I would refer readers to a previous post on this blog (see here).Your weakness is copper? Y-you're kidding right?In case you can't be bothered to follow that previous link, the idea was that exposure to TCDD [2,3,7,8-tetrachlorodibenzo-p-dioxin], a particularly hazardous chemical which contaminated the compound known as Agent Orange quite extensively used in Vietnam a few years back, might have some important links to infants exposed to said compound, particularly in relation to the expression of autistic traits. As an aside, I note that dioxin and Agent Orange continues to generate headlines and debate as per news items such as this one suggesting that the legacy of the Vietnam war continues even today.The latest paper from Nishijo et al sought to look at urinary amino acid profiles of groups (N=26) exposed or not to various combinations of "high total dioxin toxic equivalent (TEQ-PCDDs/Fs)" and/or TCDD. The analytical weapon of choice was gas chromatography-mass spectrometry (GC-MS), and alongside the examination of urine samples, researchers also took into account breast milk concentrations of "PCDD and PCDF congeners (PCDDs/Fs)" as well as variables such as body size, food intake and neurodevelopmental measures based on scores from the "Bayley Scales of Infant and Toddler Development, Ver. 3 (Bayley III)."Results: "The present study demonstrated that perinatal dioxin exposure to TCDD and TEQ-PCDDs/Fs, as indicated by levels in breast milk, significantly decreased urinary excretion of histidine and tryptophan in 3-year-old Vietnamese children with lower neurodevelopmental scores in dioxin contamination hot spots." As per the title of this post: "urinary levels of histidine were decreased in 3-year-old Vietnamese children who had been exposed to high dioxin levels." Histidine also features quite a bit in the discussion of the study results as per one section labelled: Histidine and brain function.There is obviously a lot more work to do in this area to further enlighten the research path about the hows, whys and wherefores of dioxin exposure affecting both psychological and biological functions in children. Not least is the need for further prospective study methods to get around the use of breast milk levels of these compounds as a marker of perinatal dioxin exposure. I might also add that decreased levels of urinary histidine have been reported previously with autism in mind  (see here for some discussion) so suggesting that dioxin levels might be the only correlate of the group in question might be a step too far at the moment.With my autism research blogging hat on, I continue to be interested in the chemical exposure link postulated with the expression of 'some' autism and the roads where this might lead autism research. The paper from Peter Stein and colleagues  who just featured in that that other paper on urinary histidine among other things , suggesting that there may be more to see with regards to Bisphenol-A (BPA) and autism (which I will be blogging about soon) adds to interest in this area, albeit with again the need for further independent verification and more data on the hows and whys.Music. In memory of Demis... and with the hopes and dreams of Greece and the Greek nation in mind.---------- Nishijo M. et al. Urinary Amino Acid Alterations in 3-Year-Old Children with Neurodevelopmental Effects due to Perinatal Dioxin Exposure in Vietnam: A Nested Case-Control Study for Neurobiomarker Discovery. PLoS ONE. 2015; 10(1): e0116778. Ming X. et al. Metabolic perturbance in autism spectrum disorders: a metabolomics study. J Proteome Res. 2012 Dec 7;11(12):5856-62. Stein TP. et al. Bisphenol A Exposure in Children With Autism Spectrum Disorders. Autism Research. 2015. Jan 13.----------Nishijo M, Tai PT, Anh NT, Nghi TN, Nakagawa H, Van Luong H, Anh TH, Morikawa Y, Waseda T, Kido T, & Nishijo H (2015). Urinary Amino Acid Alterations in 3-Year-Old Children with Neurodevelopmental Effects due to Perinatal Dioxin Exposure in Vietnam: A Nested Case-Control Study for Neurobiomarker Discovery. PloS one, 10 (1) PMID: 25584822... Read more »
Nishijo M, Tai PT, Anh NT, Nghi TN, Nakagawa H, Van Luong H, Anh TH, Morikawa Y, Waseda T, Kido T.... (2015) Urinary Amino Acid Alterations in 3-Year-Old Children with Neurodevelopmental Effects due to Perinatal Dioxin Exposure in Vietnam: A Nested Case-Control Study for Neurobiomarker Discovery. PloS one, 10(1). PMID: 25584822
Your brain might just be killing you slowly. Atherosclerosis — or hardening and narrowing of the arteries — can be caused by fat buildup that causes plaque deposits, and is one of the main causes of cardiovascular disease. What does that have to do with the brain? Well new research has shown a link between how the brain regulates fat metabolism, which has the potential of stopping the development of this disease risk factor in obesity and diabetes.... Read more »
Yue JT, Abraham MA, LaPierre MP, Mighiu PI, Light PE, Filippi BM, & Lam TK. (2015) A fatty acid-dependent hypothalamic-DVC neurocircuitry that regulates hepatic secretion of triglyceride-rich lipoproteins. Nature communications. PMID: 25580573
Ginsberg, H. (2002) New Perspectives on Atherogenesis: Role of Abnormal Triglyceride-Rich Lipoprotein Metabolism. Circulation, 106(16), 2137-2142. DOI: 10.1161/01.CIR.0000035280.64322.31
Duez, H., Lamarche, B., Valero, R., Pavlic, M., Proctor, S., Xiao, C., Szeto, L., Patterson, B., & Lewis, G. (2008) Both Intestinal and Hepatic Lipoprotein Production Are Stimulated by an Acute Elevation of Plasma Free Fatty Acids in Humans. Circulation, 117(18), 2369-2376. DOI: 10.1161/CIRCULATIONAHA.107.739888
Star Trek celebrates its 50th anniversary in 2016. In preparation for the celebrations, we’re checking in on how close we are to making Star Trek technology a reality. The replicator made food and recycled trash, and later was used to make parts for the Enterprise. A machine fabricated what they needed on the spot. We have that now on the space station! Do you know how 3-D printing works and how we print parts, food, and even living tissue? Here’s how.... Read more »
Yu, A., & Khan, M. (2015) On-demand three-dimensional printing of surgical supplies in conflict zones. Journal of Trauma and Acute Care Surgery, 78(1), 201-203. DOI: 10.1097/TA.0000000000000481
Kolesky, D., Truby, R., Gladman, A., Busbee, T., Homan, K., & Lewis, J. (2014) Bioprinting: 3D Bioprinting of Vascularized, Heterogeneous Cell-Laden Tissue Constructs (Adv. Mater. 19/2014). Advanced Materials, 26(19), 2966-2966. DOI: 10.1002/adma.201470124
The paper by Ryan Yuen and colleagues  suggesting that most siblings with autism do not share the same genetic variations thought to contribute to the condition has garnered quite a few media headlines of late (see here and see here).Applying the concept of whole-genome sequencing whereby the complete genetic blueprint of a person is mapped to provide "the most comprehensive collection of an individual's genetic variation" , 340 genomes from 85 families with two children with a diagnosis of autism or autism spectrum disorder (ASD) were analysed. Yuen et al reported that examination of de novo and rare inherited SNPs previously linked to cases of autism were not present in some 70% of their "affected siblings" group. Further, that less than a third of siblings shared the same autism-related gene changes, potentially over-turning the idea that most affected siblings (with the same parentage) share the same genetic issues as being related to their autistic symptoms and label. That all being said, the authors did report that: "Brothers and sisters who shared autism-related mutations displayed more similar symptoms than those who did not".This is a significant paper in quite a few ways although there are caveats. The results only covered 85 sibling-pairs and the number of autism-related genetic variations inspected was relatively limited. One therefore needs to be a little cautious about sweeping generalisations to the very wide autism spectrum, heterogeneity, comorbidity and all. “The findings suggest that there is significant genetic diversity among people which autism” was one of the commentaries on the Yuen study which I would definitely second (see here). The 'people with autism are like snowflakes' analogy has also been banded around to illustrate that idea of diversity; something that I would also agree with, although perhaps preferring the slightly more scientific idea that 'autism' should perhaps be replaced by the more plural idea: the autisms. Exactly how many 'autisms' there are, remains to be seen as it does in other areas of psychiatry.Ways forward following the Yuen study? Well, I might suggest that alongside replicating the work in a larger cohort, one might also entertain the idea that structural issues associated with the genome might also be complemented by a little more focus on gene functions and that rising star discipline called epigenetics (see here). The idea for example, that even identical twins might vary in their 'methylomic' profile (see here) is gaining traction in autism research circles to potentially account for some of the missing heritability which has been reported in recent years (see here). I'm not saying that the significant resources ploughed into the genetic roots of autism is all bunk; merely that the idea that genes and environment might synergistically [and variably] act on autism risk should be given a lot more credence, alongside the role that common variants might play in [some] autism (see here). Air pollution is one environmental example perhaps requiring a little more study (see here), although I hasten to stress not the only variable which might need further investigation.Finally, as part of the Google - Autism Speaks MSSNG initiative (see here), the 'de-identified' data from the Yuen study has been uploaded to the 'cloud' for other researchers to utilise in further investigations. Again, a very good idea for those interested in this branch of autism research but again with the proviso that autism is a very, very heterogeneous condition often including quite a bit of enhanced risk for various comorbidity...---------- Yuen RKC. et al. Whole-genome sequencing of quartet families with autism spectrum disorder. Nature Medicine. 2015. Jan 26. Ng PC. & Kirkness EF. Whole genome sequencing. Methods Mol Biol. 2010;628:215-26.----------Yuen, R., Thiruvahindrapuram, B., Merico, D., Walker, S., Tammimies, K., Hoang, N., Chrysler, C., Nalpathamkalam, T., Pellecchia, G., Liu, Y., Gazzellone, M., D'Abate, L., Deneault, E., Howe, J., Liu, R., Thompson, A., Zarrei, M., Uddin, M., Marshall, C., Ring, R., Zwaigenbaum, L., Ray, P., Weksberg, R., Carter, M., Fernandez, B., Roberts, W., Szatmari, P., & Scherer, S. (2015). Whole-genome sequencing of quartet families with autism spectrum disorder Nature Medicine DOI: 10.1038/nm.3792... Read more »
Yuen, R., Thiruvahindrapuram, B., Merico, D., Walker, S., Tammimies, K., Hoang, N., Chrysler, C., Nalpathamkalam, T., Pellecchia, G., Liu, Y.... (2015) Whole-genome sequencing of quartet families with autism spectrum disorder. Nature Medicine. DOI: 10.1038/nm.3792
Acute kidney injury often arises after major surgery because the kidneys can be deprived of normal blood flow during the procedure. The use of contrast media, or dyes, can contribute to this problem. In patients undergoing coronary angiography or percutaneous coronary intervention, which are heart procedures that use dyes to help surgeons visualize the arteries, a high dose of the statin atorvastatin was linked with a reduction in blood levels of creatinine, a marker of kidney injury, as well as a lower incidence of acute kidney injury compared with a low dose of the statin.... Read more »
Wu, H., Li, D., Fang, M., Han, H., & Wang, H. (2015) Meta-analysis of short-term high versus low doses of atorvastatin preventing contrast-induced acute kidney injury in patients undergoing coronary angiography/percutaneous coronary intervention. The Journal of Clinical Pharmacology, 55(2), 123-131. DOI: 10.1002/jcph.411
There is a saying, “you can’t unboil an egg.” Usually this is just illustrating cause and effect; you can’t turn back time, or what’s done is done. Well now scientists have successfully unboiled an egg, so suck it thermodynamics. An international team of chemists have accomplished this feat – an innovation that could dramatically reduce costs for cancer treatments, food production and other segments of the $160 billion global biotechnology industry, according to the findings.... Read more »
Yuan, T., Ormonde, C., Kudlacek, S., Kunche, S., Smith, J., Brown, W., Pugliese, K., Olsen, T., Iftikhar, M., Raston, C.... (2015) Shear-Stress-Mediated Refolding of Proteins from Aggregates and Inclusion Bodies. ChemBioChem. DOI: 10.1002/cbic.201402427
If you had the choice, would you like to live until you’re 130 years old? New research in fruit flies shows that manipulating a single gene can extend their lifespan up to 60%, suggesting that living well into your hundreds might become a reality in the foreseeable future.Dying of old age is a strange thing. Why does our health decline just because we’re old? Although the answer might at first seem obvious or simple, it really isn’t. There are countless theories of ageing, a few popular even outside the scientific community. Take ‘superfoods’, for example. The miracle properties credited to these antioxidant-rich foods stem from the free radical theory of ageing—older cells produce more of a toxic form of oxygen that gradually poisons them. Antioxidants like vitamin C or D counteract this deleterious effect and prevent ageing (and the appearance of wrinkles), superfood advocates claim.A common denominator in these theories is that we age—and ultimately die—because our cells deteriorate with time (for whatever reason). As tissues and organs mount up more and more of these damaged cells, they begin to malfunction and eventually stop working. This raises an interesting assumption. What if we could get rid of these unfit cells and keep only the healthy ones? Would we live longer? Jeanne Louise Calment had the longest confirmed human lifespan on record (122 years and 164 days).It’s well known that sick cells such as cancerous cells, are eliminated by our bodies, either by immune cells or by committing suicide. However, our ‘old’ unfit cells are still healthy enough to bypass this quality-control checkpoint. Or so it was thought. A few years ago, Eduardo Moreno and colleagues at the University of Bern, Switzerland, showed that healthy but less fit cells are also culled from tissues, by a mechanism they called “fitness fingerprints”. Each cell has a molecular fingerprint on its surface that tells its neighbours how healthy it is. When a given cell has a fingerprint that is worse than its neighbours', it kills itself. But the researchers didn’t know the importance of this cell elimination process for the organism. For example, would we age faster if those cells could not kill themselves? To answer these questions, Moreno’s team genetically engineered fruit flies to control a newly found gene essential for marking unfit cells for culling. “If you put an extra copy of this gene you have better selection of the [unfit] cells, they are eliminated faster and therefore the animals can live longer”, says Moreno.When the gene, which Moreno named azot, was removed from flies, they became sick and died prematurely. On the other hand, flies with an extra copy of the azot gene lived up to 60% longer. Previously, only caloric restriction had been shown to prolong lifespan to such an extent in flies. In fact, reducing the amount of daily calorie input increases longevity in flies, nematodes, fish, mice and rats (data from studies with primates remain controversial). Could it be then, that starved flies with an extra copy of the azot gene live even longer? Indeed, these flies lived about 80% longer, Moreno’s team showed. In human time this would be equivalent to living up to 150 years! The question remains whether these findings could be relevant for our species. Humans have the azotgene, in fact most organisms do, so potentially it should be possible to increase life expectancy in people by altering azot protein levels.“You could start thinking of how to manipulate these mechanisms with drugs, for example, to treat ageing or diseases like neurodegeneration or myocardial infarction,” says Moreno, “I’m totally convinced it will be possible to delay aging and prolong lifespan in humans.” Would we want to live longer though, if we spend most of our life old and sick? “Our long-term challenge will be to understand the biology of aging to address problems associated with steadily increasing life expectancy, such as metabolic disease and neurodegeneration”, says Martin Denzel, a researcher at the Max Planck Institute for Biology of Ageing in Cologne, Germany. With this in mind, Moreno’s team tested whether the long-living azot flies remained healthy as they aged. When the researchers looked in these flies’ brains, they found that their neurons accumulated fewer ageing cellular markers. Azot not only prolongs lifespan, but it also delays ageing. In the future the team wants to understand what azot is actually doing. This gene encodes for a protein of unknown function, but the researchers know that when “the azot gene is activated, it triggers the normal cell death apoptosis pathway”, Moreno concludes. The team will also investigate the function of azot in mice, and collaborate with medical doctors to see if the azot-dependent cell elimination pathways are present in ageing-related diseases like Alzheimers. “I have high hopes that eventually basic research into the aging process will yield treatments that extend the span of healthy living and that improve the quality of life in advanced age”, Denzel explains. “However, it will take a lot of additional work to investigate if this mechanism might be beneficial in mammals.”Reference:... Read more »
Merino Marisa M., Jesus M. Lopez-Gay, David Buechel, Barbara Hauert, & Eduardo Moreno. (2015) Elimination of Unfit Cells Maintains Tissue Health and Prolongs Lifespan. Cell. DOI: http://dx.doi.org/10.1016/j.cell.2014.12.017
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