So we all know smoking is bad for us – we were told when we were kids, and even the packets have warning messages and gruesome pictures to try and help us kick the habit! So why do people still smoke?
As most of you will already know, it’s the nicotine in cigarettes that is the primary cause of smoking addiction. The nicotine is absorbed when cigarette smoke is inhaled and goes on to affect normal body functions, as well as mood and cognition – this is because it binds to receptors in the body called nicotinic acetylcholine receptors (nAChs). These are usually activated by the neurotransmitter acetylcholine, but they are also sensitive to nicotine, and it’s this sensitivity that underlies nicotine addiction. Nicotine can induce mild euphoria, can stimulate attention focus, decrease appetite and relieve anxiety.
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D'Souza MS, & Markou A. (2011) Neuronal mechanisms underlying development of nicotine dependence: implications for novel smoking-cessation treatments. Addiction science , 6(1), 4-16. PMID: 22003417
George O, Ghozland S, Azar MR, Cottone P, Zorrilla EP, Parsons LH, O'Dell LE, Richardson HN, & Koob GF. (2007) CRF-CRF1 system activation mediates withdrawal-induced increases in nicotine self-administration in nicotine-dependent rats. Proceedings of the National Academy of Sciences of the United States of America, 104(43), 17198-203. PMID: 17921249
Increased levels of leptin in cases of autism was a primary finding described in the paper by Rodrigues and colleagues  as part of their analysis of the adipokines, the cell signalling molecules secreted by fat (adipose tissue) (see this paper by Trayhurn and colleagues  for quite a good overview). Not for the first time I might add, that elevations in levels of leptin have been talked about with autism in mind . Indeed if you want even more evidence of a possible link, see also the paper by Blardi and colleagues  and their findings in relation to cases of Rett syndrome . Oh and elevations in leptin in cases of autism crosses countries too.Have parasol will travel @ WikipediaFrom the beginning, leptin is an adipokine which are cytokines. There is quite a bit of chatter about leptin being more of a proinflammatory cytokine and in particular, it's similarity to another inflammatory-related cytokine, IL-6 (see here for a previous post on this molecule). It's also worthwhile noting that leptin has an emerging role in the shift in immune function toward a T-helper1(Th1) response (see here for some background on Th1 and Th2 responses) which potentially brings into play an autoimmune element. I've actually talked about leptin before on this blog and some preliminary findings correlating leptin levels and fatigue scores in cases of Chronic Fatigue Syndrome (CFS).Quite a lot of discussion has focused on the role that leptin also plays in regulating dietary intake and its suggested link with body weight and obesity; circulating leptin levels correlating well with the proportion of body fat. It's well beyond the scope of this post or indeed my very rudimentary knowledge of this area, but there is quite a lot of evidence to suggest that deficiencies in leptin lead to severe obesity as a function of it's role in the activation of satiety mechanisms. That being said it's not all plain scientific sailing as per the review by Paracchini and colleagues  (open-access) on the genetics of leptin and obesity. Obese people generally have high leptin levels, as a function of having more fat, which has led to some speculation about the notion of leptin resistance (see the paper from Myers and colleagues  for more information).That energy homeostasis role aside - which may nevertheless be important when it comes to medication-induced weight gain in autism  - the elevations in plasma leptin levels reported by Rodrigues et al (and other authors) may be important. As per the Stringer paper  which was the source material for my leptin-CFS post: "Multiple studies have demonstrated elevated levels of circulating leptin in chronic inflammatory conditions". A quick trawl of PubMed leads me to believe that there may be indeed be an important role for leptin in the process of inflammation as per articles like this one and this one. That also quite a nice correlation between leptin and more traditional markers of inflammation, such as C-reactive protein (CRP) have been discussed  is added fodder for this assertion. Oh, and just in case you're wondering, CRP has also been examined with autism in mind (see this post and this post).The implication therefore is that elevated levels of leptin present in cases of autism might be an important sign of immune processes, particularly those related to inflammation. I can't say whether this means autism per se is 'inflammatory' in those cases of elevations or whether we're talking about some inflammatory-mediated comorbidity for example. Nonetheless, there is a growing consistency in the results obtained so far which is crying out for more detailed investigation controlling for weight, body fat and body mass index (BMI). This call likewise resonates with other conditions too including bipolar disorder and schizophrenia albeit without over-generalising and again taking into account the important effect of medication.And just in case you're wondering about possible ways and means to reduce leptin levels, well without any medical or clinical advice being given, how about a spot of exercise for starters?To close, having recently watched the excellent Dave Grohl documentary about Sound City (UK viewers if they're quick, can catch it on the BBC iPlayer), a song about someone's wife calling?----------- Rodrigues DH. et al. Changes in Adipokine Levels in Autism Spectrum Disorders. Neuropsychobiology 2014;69:6-10 Trayhurn P. et al. Adipose Tissue and Adipokines—Energy Regulation from the Human Perspective. J Nutr. 2006; 136: 19355-19395. Ashwood P. et al. Brief report: plasma leptin levels are elevated in autism: association with early onset phenotype? J Autism Dev Disord. 2008 Jan;38(1):169-75. Blardi P. et al. Variations of plasma leptin and adiponectin levels in autistic patients. Neurosci Lett. 2010 Jul 19;479(1):54-7. Blardi P. et al. Long-term plasma levels of leptin and adiponectin in Rett syndrome. Clin Endocrinol (Oxf). 2009 May;70(5):706-9. Paracchini V. et al. Genetics of Leptin and Obesity: A HuGE Review. Am. J. Epidemiol. 2005; 162: 101-114. Myers MG. et al. Obesity and Leptin Resistance: Distinguishing Cause from Effect. Trends Endocrinol Metab. 2010 November; 21(11): 643–651. Nurmi EL. et al. Moderation of antipsychotic-induced weight gain by energy balance gene variants in the RUPP autism network risperidone studies. Transl Psychiatry. 2013 Jun 25;3:e274. Stringer EA. et al. Daily cytokine fluctuations, driven by leptin, are associated with fatigue severity in chronic fatigue syndrome: evidence of inflammatory pathology. Journal of Translational Medicine 2013, 11:93 Shamsuzzaman ASM. et al. Independent Association Between Plasma Leptin and C-Reactive Protein in Healthy Humans. Circulation. 2004... Read more »
Rodrigues D.H, Rocha N.P, Sousa L.F.C, Barbosa I.G, Kummer A, & Teixeira A.L. (2013) Changes in Adipokine Levels in Autism Spectrum Disorders. Neuropsychobiology. info:/
Research projects evolve in a fortuitous manner, often guided by a convergence of novel observations, intuition, helpful colleagues and unique personal circumstances. It is precisely this constellation that prompted two cardiologists to study the mitochondrial networks in lung cancer cells.... Read more »
Jalees Rehman, Hannah J. Zhang, Peter T. Toth, Yanmin Zhang, Glenn Marsboom, Zhigang Hong, Ravi Salgia, Aliya N. Husain, Christian Wietholt, & Stephen L. Archer. (2012) Inhibition of mitochondrial fission prevents cell cycle progression in lung cancer. FASEB Journal. DOI: 10.1096/fj.11-196543
Using a novel 3D culture method, Boston researchers were able to prod bronchioalveolar stem cells to produce colonies containing airway (bronchiolar) epithelial cells, alveolar epithelial cells or both cell types.Credit: Joo-hyeon Lee, Boston Children's HospitalOne day it may be possible to treat a wide range of lung diseases using proteins that direct lung stem cells to grow specific cell types needed to repair the lung injuries involved in the conditions, according to a new study by researchers at the Boston Children's Hospital.Appearing January 30th issue of Cell, researchers led by Carla Kim, PhD, and Joo-Hyeon Lee, PhD, of the Stem Cell Research Program at Boston Children's, describe a new pathway in the lung, activated by injury, that directs stem cells to transform into specific types of cells.By enhancing this natural pathway in a mouse model, they successfully increased production of alveolar epithelial cells, which line the small sacs (alveoli) where gas exchange takes place. These cells are irreversibly damaged in diseases like pulmonary fibrosis and emphysema.By inhibiting the same pathway, the researchers ramped up production of airway epithelial cells, which become damaged in diseases affecting the lung's airways, such as asthma and bronchiolitis obliterans.Read More... Read more »
Joo-Hyeon Lee, Dong Ha Bhang, Alexander Beede, Tian Lian Huang, Barry R. Stripp, Kenneth D. Bloch, Amy J. Wagers, Yu-Hua Tseng, Sandra Ryeom, Carla F. Kim. (2013) Lung Stem Cell Differentiation in Mice Directed by Endothelial Cells via a BMP4-NFATc1-Thrombospondin-1 Axis. Cell. info:/10.1016/j.cell.2013.12.039
Dichlordiphenyltrichloroethane, also known as DDT, emerged during World War II as something of a miracle chemical. The war had left cities across Europe devastated and struggling to cope with (among other things) poor sanitation, which created a fertile environment for the spread of disease. When Allied forces entered Naples soon after the Germans retreated, they discovered a typhus epidemic that was killing 25% of those infected; the number of infected was into the thousands. The Germans, before leaving, had laid waste to Naples’ water and sewer system, with the hopes of bringing about some sort of humanitarian crisis as punishment for Naples’ uprising against occupying German forces. They had succeeded.The typhus epidemic in Naples was spread by lice, and so Allied forces needed a way to rid the city of the disease-carrying parasites. If you’ve ever had the misfortune of having to deal with a lice infestation of your own, you can imagine the difficulty of trying to accomplish this on a city-wide scale. Fortunately, the Marines had recently contracted DuPont Chemical to produce tons of DDT for them to reduce malaria rates among soldiers (by spraying to kill mosquitos). They sprayed Neapolitan citizens with DDT in an assembly-line fashion, and the epidemic was over within a month.DDT was used in the late 1940s and 1950s to reduce malaria rates in many areas of the world. In 1948 the discoverer of DDT’s insecticide properties, Paul H. Muller, won a Nobel Prize in Medicine. However, as DDT use increased over these decades, there was a growing murmur about negative health effects that might be associated with DDT. This murmur grew to a roar in 1962 with the publication of scientist and author Rachel Carson’s book Silent Spring, which implicated pesticides like DDT in endangering the environment, wildlife, and humans. Carson’s book sparked the environmentalist movement in the United States, which precipitated a ban on DDT use in the U.S. in 1972, except in cases where it was necessary for public health (e.g. curbing epidemics). Most countries in the world have now signed on to a similar ban of DDT use.You would expect that, because the ban was put into effect in the early 1970s, any health effects associated with DDT in the U.S. would have disappeared by now. But DDT is highly resistant to degradation, as are the products it primarily breaks down into: DDE and DDD. The half-life of DDT in soil can be up to 15 years, and in water it may extend up to 150 years. In the human body, DDT’s half-life is around 6 years; DDE's is 10 years. Because DDT and its breakdown products remain in the environment for a long period of time, and because they persist in the human body for years after exposure, most of us have some level of these chemicals in our blood today. The unanswered question, however, is: are those levels affecting our health?In an attempt to answer that question, Richardson et al. published a study this week in The Journal of the American Medical Association that compared levels of DDE in patients with Alzheimer’s disease (AD) to levels in control patients who didn’t have the disease. The authors found levels of DDE in AD patients that were 3.8 times higher than the levels found in their control group. They determined that the participants in the top ⅓ of their sample in terms of high DDE levels had more than 4 times the risk of developing AD than those with lower blood DDE levels. Participants in the ⅓ with the highest DDE blood levels also had the lowest scores in a questionnaire that assesses cognitive impairment. The researchers also looked at the participants who possessed a form of a gene called Apolipoprotein E4 (ApoE 4), which is known to increase AD risk. They found that those who had the ApoE 4 variant (as opposed to ApoE 3, which doesn’t suggest AD risk) had the lowest cognitive scores in the sample, suggesting that this population might be most susceptible to any effect DDT might have on increasing AD risk.This study by Richardson et al. is what is known as a case-control study, meaning that DDE levels were compared between participants known to have the disease and those without it. A case-control study, however, does not have the ability to determine a causal link between an exposure and a disease due to a number of inherent limitations to the design (such as the fact that there could have been a variety of other influences on the participants’ development of AD). However, the Richardson et al. study provides a basis for further investigation into a link between DDT and AD.... Read more »
Richardson JR, Roy A, Shalat SL, von Stein RT, Hossain MM, Buckley B, Gearing M, Levey AI, & German DC. (2014) Elevated Serum Pesticide Levels and Risk for Alzheimer Disease. JAMA neurology. PMID: 24473795
Thin layer chromatography, or TLC, is a technique used for the separation and analysis of molecules in a sample (Note- NOT DNA!). It can be used on amino acids1, although in my lab it has been used to analyze the degradation (or lack of!) of large polymeric sugars by whole metabolically inactivated cells or by simple enzymes. Because of this, I’ll be focusing on the analysis of saccharides (sugars).
So far, good stuff! But! How does it work, and what the HELL do these results mean!?!... Read more »
Bhawani SA, Albishri HM, Khan ZA, Mohamad Ibrahim MN, & Mohammad A. (2013) Surfactant Modified/Mediated Thin-Layer Chromatographic Systems for the Analysis of Amino Acids. Journal of analytical methods in chemistry, 973280. PMID: 24455427
Anaesthesia and Intensive Care (AIC) is an Australian medical journal. The latest issue, just published online, contains a remarkable – and possibly even unique – pair of Letters. These letters take the form of apologies for the distress caused by the publication of an article – I do not know of any similar cases in […]The post Medical Journal Apologizes “For The Distress Caused” By A Paper appeared first on Neuroskeptic.... Read more »
Simpson RS, & Van K. (2013) Fatal rhabdomyolysis following volatile induction in a six-year-old boy with Duchenne Muscular Dystrophy. Anaesthesia and intensive care, 41(6), 805-7. PMID: 24180726
Gibbs N. (2014) Apology for distress caused by the publication of recent correspondence describing fatal rhabdomyolysis in a patient with Duchenne muscular dystrophy. Anaesthesia and intensive care, 42(1), 134. PMID: 24471672
Simpson R, & Van K. (2014) Apology in relation to our recent letter describing a case of fatal rhabdomyolysis in a patient with Duchenne muscular dystrophy. Anaesthesia and intensive care, 42(1), 134. PMID: 24471673
“RAF inhibitors (vemurafenib and dabrafenib) have profound clinical activity in patients with BRAF-mutant melanoma, but their therapeutic effects are limited…
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Solit DB, & Rosen N. (2014) Towards a Unified Model of RAF Inhibitor Resistance. Cancer discovery, 4(1), 27-30. PMID: 24402945
Shi H, Hugo W, Kong X, Hong A, Koya RC, Moriceau G, Chodon T, Guo R, Johnson DB, Dahlman KB.... (2014) Acquired Resistance and Clonal Evolution in Melanoma during BRAF Inhibitor Therapy. Cancer discovery, 4(1), 80-93. PMID: 24265155
Van Allen EM, Wagle N, Sucker A, Treacy DJ, Johannessen CM, Goetz EM, Place CS, Taylor-Weiner A, Whittaker S, Kryukov GV.... (2014) The Genetic Landscape of Clinical Resistance to RAF Inhibition in Metastatic Melanoma. Cancer discovery, 4(1), 94-109. PMID: 24265153
Wagle N, Van Allen EM, Treacy DJ, Frederick DT, Cooper ZA, Taylor-Weiner A, Rosenberg M, Goetz EM, Sullivan RJ, Farlow DN.... (2014) MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition. Cancer discovery, 4(1), 61-8. PMID: 24265154
Das Thakur M, Salangsang F, Landman AS, Sellers WR, Pryer NK, Levesque MP, Dummer R, McMahon M, & Stuart DD. (2013) Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistance. Nature, 494(7436), 251-5. PMID: 23302800
Also known as "halfsiders" or tetragametic chimæras, these unusual birds are actually two genetically distinct individuals -- twins -- fused into one being. ... Read more »
Zhao D., McBride D., Nandi S., McQueen H. A., McGrew M. J., Hocking P. M., Lewis P. D., Sang H. M., & Clinton M. (2010) Somatic sex identity is cell autonomous in the chicken. Nature, 464(7286), 237-242. DOI: 10.1038/nature08852
Agate R. J., Grisham W., Wade J., Mann S., Wingfield J., Schanen C., Palotie A., & Arnold A. P. (2003) Neural, not gonadal, origin of brain sex differences in a gynandromorphic finch. Proceedings of the National Academy of Sciences, 100(8), 4873-4878. DOI: 10.1073/pnas.0636925100
Arnold A. P. (2003) Minireview: Sex Chromosomes and Brain Sexual Differentiation. Endocrinology, 145(3), 1057-1062. DOI: 10.1210/en.2003-1491
Chue Justin, & Smith Craig A. (2011) Sex determination and sexual differentiation in the avian model. FEBS Journal, 278(7), 1027-1034. DOI: 10.1111/j.1742-4658.2011.08032.x
Johnson Phyllis T., & Otto Sara V. (1981) Histology of a Bilateral Gynandromorph of the Blue Crab, Callinectes sapidus Rathbun (Decapoda: Portunidae). Biological Bulletin, 161(2), 236. DOI: 10.2307/1540801
Boklage C. E. (2005) Embryogenesis of chimeras, twins and anterior midline asymmetries. Human Reproduction, 21(3), 579-591. DOI: 10.1093/humrep/dei370
by Jackie in Science of Eating Disorders
I recently had a total Aha! moment (or a why-didn’t-I-ever-think-of-it moment) when I had chanced upon a recently published article titled “Eating Expectancies in Relation to Eating Disorder Recovery” by Fitzsimmons-Craft and colleagues. The title caught my attention because I had never come across any research tying eating expectancies to eating disorders, though I was familiar with the concept from the health psychology and obesity literature. Eating, as a behaviour and as a mechanism, is incredibly complex, with many factors contributing to why and how we eat; eating expectancies are one such factor.
Expectancy theory, first proposed by Tolman (1932), suggests that expectancies, or assumptions about the consequences of various behaviours, develop as a result of one’s learning history (Smith et al., 2007). Such expectancies are thought to influence subsequent behavioural choices, with one acting to either increase the likelihood of reward or decrease the likelihood of punishment. Essentially, expectancies are cognitive mechanisms that drive future behaviours.
With respect to eating, expectancies represent the culmination of one’s learning history as related to eating and act …
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Bohon C, Stice E, & Burton E. (2009) Maintenance factors for persistence of bulimic pathology: a prospective natural history study. International Journal of Eating Disorders, 42(2), 173-8. PMID: 18951457
Fitzsimmons-Craft EE, Keatts DA, & Bardone-Cone AM. (2013) Eating Expectancies in Relation to Eating Disorder Recovery. Cognitive Therapy and Research, 37(5), 104. PMID: 24089581
Smith GT, Simmons JR, Flory K, Annus AM, & Hill KK. (2007) Thinness and eating expectancies predict subsequent binge-eating and purging behavior among adolescent girls. Journal of abnormal psychology, 116(1), 188-97. PMID: 17324029
Evidence based de-implementation. Should we stop some of what we are doing? Over the past few months, I have made a real effort to read the general literature on evidence based care. I came across this very interesting paper concerned with the re-evaluation of the evidence underpinning established clinical practice. It was written by Vinay […]The post Evidence based de-implementation in orthodontics. Should we stop some of what we are doing? appeared first on Kevin O'Brien's Orthodontic Blog.... Read more »
Vinay Prasad, & John Ioannidis. (2014) Evidence based de-implementation for contradicted, unproven and aspiring healthcare practices. Implementation Science, 9(1). DOI: 10.1186/1748-5908-9-1
STAP cells generated entire fetus body.An unusual reprogramming phenomenon by which the fate of somatic cells can be drastically altered through changes to the external environment is described in two new papers appearing in this week's Nature.Postnatal somatic cells committed to a specific lineage are shown to be converted into a pluripotent state (capable of differentiating into almost all types of cells) when exposed to an environmental stress, in this case short exposure to low pH.This reprogramming process does not need nuclear manipulation or the introduction of transcription factors ( previously thought to be necessary to induce pluripotency) so the work may have important implications for regenerative medicine.Read More... Read more »
Haruko Obokata, Teruhiko Wakayama, Yoshiki Sasai, Koji Kojima, Martin P. Vacanti, Hitoshi Niwa, Masayuki Yamato, Charles A. Vacanti. (2013) Stimulus-triggered fate conversion of somatic cells into pluripotency. Nature. DOI: 10.1038/nature12968
Haruko Obokata, Yoshiki Sasai, Hitoshi Niwa, Mitsutaka Kadota, Munazah Andrabi, Nozomu Takata, Mikiko Tokoro, Yukari Terashita, Shigenobu Yonemura, Charles A. Vacanti, Teruhiko Wakayama. (2013) Bidirectional developmental potential in reprogrammed cells with acquired pluripotency. Nature. DOI: 10.1038/nature12969
Air pollution is a significant determinant of human health. Over the past decades, studies conducted in various parts of the world documented a number of hazardous effects of ambient air pollution on health.
The adverse effects of particulate matter (PM) on health are especially well documented. However, while there is no evident and appropriate safe level of exposure, ...... Read more »
Cesaroni G, Forastiere F, Stafoggia M, Andersen ZJ, Badaloni C, Beelen R, Caracciolo B, de Faire U, Erbel R, Eriksen KT.... (2014) Long term exposure to ambient air pollution and incidence of acute coronary events: prospective cohort study and meta-analysis in 11 European cohorts from the ESCAPE Project. BMJ (Clinical research ed.). PMID: 24452269
What are the tastes humans sense? Sweet salt, sour, and bitter – don’t forget umami. Even though it has been around since 1908, umami as a concept has hit it big in just the past decade or so. This makes one wonder, are there more tastes out there? How about fat. New research shows that there are fatty acid receptors in the oral cavity, and they do induce specific physiologic responses. Is this the same as tasting?
Fatty acid receptors may turn out to be especially important for obesity research. People with less active or fewer fatty acid receptors tend to eat more, as their hormonal balance tips toward hunger. It may be that inducing expression of these receptors could lead to more satiety and less overeating.
How about water, do we taste water? We definitely have receptors for water – they help us swallow. And just to confuse things more – new research shows that being in love can make water taste sweeter.
... Read more »
Newman L, Haryono R, & Keast R. (2013) Functionality of fatty acid chemoreception: a potential factor in the development of obesity?. Nutrients, 5(4), 1287-300. PMID: 23595136
Pepino MY, Love-Gregory L, Klein S, & Abumrad NA. (2012) The fatty acid translocase gene CD36 and lingual lipase influence oral sensitivity to fat in obese subjects. Journal of lipid research, 53(3), 561-6. PMID: 22210925
Keller KL, Liang LC, Sakimura J, May D, van Belle C, Breen C, Driggin E, Tepper BJ, Lanzano PC, Deng L.... (2012) Common variants in the CD36 gene are associated with oral fat perception, fat preferences, and obesity in African Americans. Obesity (Silver Spring, Md.), 20(5), 1066-73. PMID: 22240721
MacDonald CJ, Meck WH, & Simon SA. (2012) Distinct neural ensembles in the rat gustatory cortex encode salt and water tastes. The Journal of physiology, 590(Pt 13), 3169-84. PMID: 22570382
I am so sorry dear readers for the dreadful pun used in the title of this post. It comes from years of reading books about 'knock-knock' jokes and the ever versatile 'the boy stood on the burning deck' ditties. More so in recent times with the advent of one of my brood starting to use the old 'Dr Who' version of the knock-knock joke. Having said all that I'm sure some people might think I am joking when it comes to talking about camel milk as a potential intervention for autism (some autism).Send in the camel corp @ Wikipedia But I assure you readers that I am quite serious...The primary fodder for this post comes in the shape of the trial results reported by Bashir and Al-Ayadhi  and their assertion that "camel milk administered for 2 weeks significantly improved clinical measurements of autism severity". The results are based on a small sample of children diagnosed with an autism spectrum condition and who were randomly assigned to one of three conditions: (a) boiled camel milk (CM), (b) raw camel milk and (c) normal cows milk (acting as a placebo). Alongside plotting responses to group assignment based on the CARS, the authors also reported on serum levels of Thymus and Activation-Regulated Chemokine (TARC) otherwise known as CCL17.The results: well bearing in mind this was a small study looking at intervention over the course of only 2 weeks "significant improvements were observed in CARS score (p=0.04) in raw CM group only". That and levels of TARC also being reported to have dropped significantly in both the CM groups but not the placebo group.I would echo the sentiments of the authors in their desire to see further more methodologically strong trials on whether CM might indeed have some potentially important effects for at least some people on the autism spectrum. One might argue that use of cows milk as a placebo may be problematic or indeed that the study may have benefited from a milk exclusion or non-mammalian milk source group as part of the trial. But it didn't.This is also not the first time that the words 'camel milk and autism' have appeared together in a research sense as per the study by Al-Ayadhi & Elamin  (open-access here) looking at what happened to antioxidant biomarkers as a function of adopting camel milk including that very important compound, glutathione (see here). That and some research write-up of a case study of camel milk use in one child with autism  (open-access here). Don't underestimate the value of the N=1 when it comes to autism... 'if you've met one person with autism' and all that.As for the hows and whys of camel milk potentially affecting the presentation of autism, well, outside of the possible immunological effects as per other research from some of the same authors  I'm inclined to suggest a few areas which might be important:Lactose, the sugar in milk, has previously appeared on the autism research radar as per the Kushak findings a few years back (see here). Although I'm no expert on the chemical composition of camel milk, there is some evidence to suggest that some of those with a lactose intolerance might be able to better 'tolerate' camel milk . One might envisage similar things where lactose intolerance / lactase deficiency is present in cases of autism too.Milk protein structure is another area of possible inquiry. Harking back to some elements of the opioid-excess hypothesis of autism  the suggestion is that not all milk protein derived from various mammals is the same. Indeed, even within the same species, milk protein composition might not necessarily be the same . So, would the subtle changes in milk protein (and subsequent peptide formation) be different in camel milk vs. cows milk?Interestingly, camel milk is nutritionally different from other forms of milk . When we're talking about higher levels of things like iron or zinc being present in comparison to more typical bovine milk samples, there's always the possibility that this might also have an effect. Having said that iron and calcium for example, aren't necessarily good bed-fellows...The very interesting paper by Yang and colleagues  describing the proteomic analysis of various types of milk, placed camel milk in its very own category when it came to the expression of proteins distinct from every other animal milk investigated (cow, goat, buffalo, yak). I might be making mountains out of molehills here but this could be potentially important. I could spend all night listing the correlations being made from GABA to phospholipids. Take yer pick... Oh, and on the topic of GABA, I'll also direct you some other recent preliminary research from some of the authors of the camel milk trial (see here).Science is science, and whether or not you believe that camel milk or any other alternative to regular cow milk might be able to exert an effect on at least some cases of autism, this is nevertheless a potentially interesting area of autism research. Complimentary perhaps to some of the other dietary intervention research that has been done (see here) but with the added bonus that, if found to be effective in larger scientific trials, exclusion of milk may not be as daunting a prospect as it is currently for many people with autism.So the question remains, one hump or two?And since we're on the topic of camels and the very soft connection with Egypt, I leave you with a song about walking [like an .....] by the Bangles.---------- Bashir S. & Al-Ayadhi L. Effect of camel milk on Thymus and Activation-Regulated Chemokine (TARC) in autistic children: double blind study. Pediatr Res. 2013 Dec 27. doi: 10.1038/pr.2013.248. Al-Ayadhi LY & Elamin NE. Camel Milk as a Potential Therapy as an Antioxidant in Autism Spectrum Disorder (ASD). Evid Based Complement Alternat Med. 2013;2013:602834. Adams CM. Patient report: autism spectrum disorder treated with camel milk. Glob Adv Health Med. 2013 Nov;2(6):78-80. Al-Ayadhi LY. & Mostafa GA. Elevated serum levels of macrophage-derived chemokine and thymus and activation-regulated chemokine in autistic children. J Neuroinflammation. 2013; 10: 72. Cardoso RR. et al. Consumption of camel's milk by patients intolerant to lactose. A preliminary study. Rev Alerg Mex. 2010 Jan-Feb;57(1):26-32. Shattock P. & Whiteley P. Biochemical aspects in autism spectrum disorders: updating the opioi... Read more »
Bashir S, & Al-Ayadhi L. (2013) Effect of camel milk on Thymus and Activation-Regulated Chemokine (TARC) in autistic children: double blind study. Pediatric research. PMID: 24375082
A lack of consistency was found in pediatric concussion diagnosis and management in one emergency department over a year. Most patients did not receive restriction upon their physical activity or instructions as to when to return to play. ... Read more »
De Maio VJ, Joseph DO, Tibbo-Valeriote H, Cabanas JG, Lanier B, Mann CH, & Register-Mihalik J. (2014) Variability in Discharge Instructions and Activity Restrictions for Patients in a Children's ED Postconcussion. Pediatric Emergency Care, 30(1), 20-5. PMID: 24365726
Hair shafts (arrows) formed by induced pluripotent stem cell-derived epithelial stem cells.If the content of many a situation comedy, not to mention late-night TV advertisements, is to be believed, there's an epidemic of balding men along with an intense desire to fix their follicular deficiencies.One potential approach to reversing hair loss is using stem cells to regenerate the missing or dying hair follicles. As of now, it hasn't been possible to generate sufficient number of hair-follicle-generating stem cells.Now, a new study by Xiaowei "George" Xu, MD, PhD, associate professor of Pathology and Laboratory Medicine and Dermatology at the Perelman School of Medicine, University of Pennsylvania, and colleagues published in Nature Communications shows a method for converting adult cells into epithelial stem cells (EpSCs), the first time anyone has achieved this in either humans or mice.Read More... Read more »
Ruifeng Yang, Ying Zheng, Michelle Burrows, Shujing Liu, Zhi Wei, Arben Nace, Wei Guo,Suresh Kumar, George Cotsarelis, Xiaowei Xu. (2013) Generation of folliculogenic human epithelial stem cells from induced pluripotent stem cells. Nature Communications. DOI: 10.1038/ncomms4071
Researchers at the Genome Institute of Singapore (GIS) in A*STAR announced today that they have developed a new method of directing human pluripotent stem cells (hPSCs) into highly pure populations of endoderm, a valuable cell type that gives rise to organs including the liver and pancreas.These cells are highly sought-after for therapeutic and biotechnological purposes, but have been historically difficult to attain from hPSCs. The ability to generate pure endoderm at higher yields from hPSCs is a key and important step towards the use of stem cells in clinical applications.Read More... Read more »
Loh KM, Ang LT, Zhang J, Kumar V, Ang J, Auyeong JQ, Lee KL, Choo SH, Lim CY, Nichane M.... (2014) Efficient Endoderm Induction from Human Pluripotent Stem Cells by Logically Directing Signals Controlling Lineage Bifurcations. Cell stem cell. PMID: 24412311
Drug that destroy HIV carrying lymphocytes; can impart complete treatment so that patient will not have to take antiretroviral drugs through out life as after certain period after attaining nill HIV count discontinuation of antiretroviral drug therapy there will be no hidden HIV virus in human body cells lymphocytes that relapse HIV infection and reproduce HIV count. ... Read more »
B V Waghmare. (2014) Drug that destroy HIV carrying lymphocytes; will result in complete treatment that will not require to taking antiretroviral drugs through out life. . http://bvwaghmare.blogspot.com. info:/
Karl Tryggvason (left)and Outi HovattaCreditResearchers at the Karolinska Institutet just announced that they have developed a new method which allows the large-scale production of human embryonic stem cells of high clinical quality, without destroying any human embryos. The discovery is a big step forward for stem cell research and for the high hopes for replacing damaged cells and thereby curing serious illnesses such as diabetes and Parkinson's disease.Currently the use of human embryonic stem cells is highly controversial as they are made from surplus in vitro fertilized (IVF) embryos that are not used for the generation of pregnancies. The embryos are destroyed in the process. Therefore it has been illegal in the USA to to use this method for deriving embryonic stem cell lines. Sweden s legislation has been more permissive. It has been possible to generate embryonic stem cells from excess, early IVF embryos with the permission of the persons donating their eggs and sperm.Read More... Read more »
Sergey Rodin, Liselotte Antonsson, Colin Niaudet, Oscar E. Simonson, Elina Salmela, Emil M. Hansson, Anna Domogatskaya, Zhijie Xiao, Pauliina Damdimopoulou, Mona Sheikhi, José Inzunza, Ann-Sofie Nilsson, Duncan Baker, Raoul Kuiper, Yi Sun, Elisabeth Blen. (2013) Clonal culturing of human embryonic stem cells on laminin-521/E-cadherin matrix in defined and xeno-free environment. Nature Communications. DOI: 10.1038/ncomms4195
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