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  • February 27, 2017
  • 05:29 AM
  • 22 views

Know your brain: Mammillary bodies

by neurosci in Neuroscientifically Challenged

Where are the mammillary bodies?























The mammillary bodies are part of the diencephalon, which is a collection of structures found between the brainstem and cerebrum. The diencephalon includes the hypothalamus, and the mammillary bodies are found on the inferior surface of the hypothalamus (the side of the hypothalamus that is closer to the brainstem). The mammillary bodies are a paired structure, meaning there are two mammillary bodies---one on either side of the midline of the brain. They get their name because they were thought by early anatomists to have a breast-like shape. The mammillary bodies themselves are sometimes each divided into two nuclei, the lateral and medial mammillary nuclei. The medial mammillary nucleus is the much larger of the two, and is often subdivided into several subregions.  What are the mammillary bodies and what do they do?The mammillary bodies are best known for their role in memory, although in the last couple of decades the mammillary bodies have started to be recognized as being involved in other functions like maintaining a sense of direction. The role of the mammillary bodies in memory has been acknowledged since the late 1800s, when mammillary body atrophy was observed in Korsakov's syndrome---a disorder characterized by amnesia and usually linked to a thiamine deficiency. Since then a number of findings---anatomical, clinical, and experimental---have supported and expanded upon a mnemonic role for the mammillary bodies.The mammillary bodies are directly connected to three other brain regions: the hippocampus via the fornix, thalamus (primarily the anterior thalamic nuclei) via the mammillothalamic tract, and the tegmental nuclei of the midbrain via the mammillary peduncle and mammillotegmental tract. Two of the three connections are thought to primarily carry information in one direction: the hippocampal connections carry information from the hippocampus to the mammillary bodies and the thalamic connections carry information from the mammillary bodies to the thalamus (the tegmental connections are reciprocal). These connections earned the mammillary bodies the reputation of being relay nuclei that pass information from the hippocampus on to the anterior thalamic nuclei to aid in memory consolidation. This hypothesis is supported by the fact that damage to pathways that connect the mammillary bodies to the hippocampus or thalamus is associated with deficits in consolidating new memories. Others argue, however, that the mammillary bodies act as more than a simple relay, making independent contributions to memory consolidation. Both perspectives emphasize a role for the mammillary bodies in memory but differ as to the specifics of that role.Further supporting a role for the mammillary bodies in memory, there is evidence from humans that suggests damage to the mammillary bodies is associated with memory deficits. Several cases of brain damage involving the mammillary bodies as well as cases of tumor-related damage to the area of the mammillary bodies suggests that damage to the mammillary bodies is linked to anterograde amnesia. Indeed, mammillary body dysfunction has been identified as a major factor in diencephalic amnesia, a type of amnesia that originates in the diencephalon (Korsakoff's syndrome, an amnesia that is seen primarily in long-term alcoholics, is one type of diencephalic amnesia).Experimental evidence from animal studies also underscores the importance of the mammillary bodies in memory. Studies with rodents and monkeys have found deficits in spatial memory to occur after damage to the mammillary bodies or the mammillothalamic tract. In addition to involvement in memory functions, there are cells in the mammillary bodies that are activated only when an animal's head is facing in a particular direction. These cells are thought to be involved in navigation and may act somewhat like a compass in creating a sense of direction.Vann SD, & Aggleton JP (2004). The mammillary bodies: two memory systems in one? Nature reviews. Neuroscience, 5 (1), 35-44 PMID: 14708002... Read more »

Vann SD, & Aggleton JP. (2004) The mammillary bodies: two memory systems in one?. Nature reviews. Neuroscience, 5(1), 35-44. PMID: 14708002  

  • February 27, 2017
  • 04:39 AM
  • 26 views

The First Family of Chaco

by teofilo in Gambler's House

A fascinating and important article about Chaco was published last week in Nature Communications, an open-access offshoot of the venerable journal Nature (already a good sign). Since it’s open-access, the full text of the article is available free online here. The researchers behind the article, based mainly at Penn State and Harvard but also including […]... Read more »

Kennett, D., Plog, S., George, R., Culleton, B., Watson, A., Skoglund, P., Rohland, N., Mallick, S., Stewardson, K., Kistler, L.... (2017) Archaeogenomic evidence reveals prehistoric matrilineal dynasty. Nature Communications, 14115. DOI: 10.1038/ncomms14115  

  • February 27, 2017
  • 03:16 AM
  • 25 views

Low muscle tone and autistic traits

by Paul Whiteley in Questioning Answers

"This large study showed a prospective association of infant muscle tone with autistic traits in childhood."So said the findings reported by Fadila Serdarevic and colleagues [1] who, looking at nearly 3000 children, were able to assess early motor development and muscle tone "between ages 2 and 5 months" and later parental ratings of autistic traits in children at 6 years of age. Said autistic traits were surveyed using the "the Social Responsiveness Scale (SRS) and the Pervasive Developmental Problems (PDP) subscale of the Child Behavior Checklist." Authors concluded that there was something of a connection between low muscle tone and autistic traits: "Low muscle tone in infancy predicted autistic traits measured by SRS... and PDP" and further: "early detection of low muscle tone might be a gateway to improve early diagnosis of ASD [autism spectrum disorder]."Just before anyone gets ahead of themselves with this data, it is worth pointing out that despite the large participant group included for study and the prospective nature of the study design, this was a study only really looking at two sets of variables across quite a long time-frame. It's not beyond the realms of possibility that other factors might influence the presentation of [parent-reported] autistic traits outside of just early measures of muscle tone or anything related...But let's set this research in some context. Muscle tone in a broader sense had been noted to be potentially 'linked' to autism in some of the earliest texts on the topic (see here). More recent discussions on how motor skill in the context of gait for example, might be something important to at least some autism (see here) add to the relevance. One might also look to the some of the typical reasons why low muscle tone (hypotonia) may present to see whether there are areas that could inform autism research too. I note for example, mention of Ehlers-Danlos syndrome (EDS) in some of the texts and this would perhaps appeal to further investigation on any overlap between EDS (or other connective tissues disorders) and autism (see here). Serious infections such as encephalitis and meningitis have also been mentioned in the context of hypotonia, and again, might be indicated in relation to hypotonia and some autism (see here). There is also a possibility that hypotonia could (in some cases) be tied into mitochondrial disease; something else that could be relevant to at least some 'types' of autism (see here). All of these areas are worthy of further research inspection added to the idea that muscle tone might be rather more core to autism than many people might appreciate.'And the best picture goes to'...----------[1] Serdarevic F. et al. Infant muscle tone and childhood autistic traits: A longitudinal study in the general population. Autism Res. 2017 Feb 9.----------Serdarevic F, Ghassabian A, van Batenburg-Eddes T, White T, Blanken LM, Jaddoe VW, Verhulst FC, & Tiemeier H (2017). Infant muscle tone and childhood autistic traits: A longitudinal study in the general population. Autism research : official journal of the International Society for Autism Research PMID: 28181411... Read more »

Serdarevic F, Ghassabian A, van Batenburg-Eddes T, White T, Blanken LM, Jaddoe VW, Verhulst FC, & Tiemeier H. (2017) Infant muscle tone and childhood autistic traits: A longitudinal study in the general population. Autism research : official journal of the International Society for Autism Research. PMID: 28181411  

  • February 26, 2017
  • 06:53 PM
  • 43 views

Expert Knowledge: Birds and Worms

by Joshua Fisher in Text Savvy

As adults with expert knowledge, we see the logical and mathematical similarities between the “how many more” and “won’t get” situations, and, thus we are easily fooled into believing that applying skills and knowledge in one task is equivalent to doing so in the other.... Read more »

  • February 25, 2017
  • 04:07 AM
  • 73 views

1 in 5 children "met criteria for low language at 7 years"

by Paul Whiteley in Questioning Answers

Although primarily looking at the potential predictors of language outcome, the study results published by Cristina McKean and colleagues [1] revealed the rather important title heading this blog entry: "Almost 19% of children (22/1204;18.9%) met criteria for low language at 7 years."The source of the finding was a cohort of some 1900 infants "recruited at age 8 to 10 months" who were followed until aged 7 years old and subject to quite a bit of research inspection looking at "early life factors", maternal factors and "child language ability" at various points through the childhood years. I believe this was part of the The Early Language in Victoria Study (ELVS) initiative; something that has previously created a bit of stir in speech and language circles. The authors reported that alongside the quite high percentage of children who met 'low language' criteria (based on standardized receptive or expressive language scores "≥1.25 SD below the mean"): "Child language ability at 4 years more accurately predicted low language at 7 than a range of early child, family, and environmental factors." Said low language abilities at 7 years old were also "associated with a higher prevalence of co-occurring difficulties."Aside from pointing out that language ability at 4 years old might be quite important to language ability at 7 years old, the question that should be in most people's minds is 'why?' Why are nearly 1 in 5 children presenting with low language ability at 7 years old (and presumably at 4 years old too)? Yes, there are variables such as adverse early life factors (prematurity, birth weight, coming from a non-English speaking background, etc) that will no doubt influence various aspects of language ability, but the authors note that such factors only account for roughly 15% at most of the variation in language scores seen in their cohort (not including "child language scores at ages 2 and 4"). Ergo, there are other factors involved with regards to these findings.In light of the McKean findings, I'm also going to draw your attention back to another occasion when language ability has been discussed on this blog (see here) and specifically: "At school entry, approximately two children in every class of 30 pupils will experience language disorder severe enough to hinder academic progress." [2] Low language (ability) is not necessarily the same as a diagnosed language disorder, and probably accounts for the variation between the studies (1 in 5 vs. 1 in 15). But in amongst a spectrum of language ability (disorder?) the questions about 'why?' still very much remain (and please, no sweeping generalisations about us 'just being better at diagnosing').----------[1] McKean C. et al. Language Outcomes at 7 Years: Early Predictors and Co-Occurring Difficulties. Pediatrics. 2017 Feb 8. pii: e20161684.[2] Norbury CF. et al. The impact of nonverbal ability on prevalence and clinical presentation of language disorder: evidence from a population study. Journal of Child Psychology and Psychiatry. 2016. May 16.----------McKean C, Reilly S, Bavin EL, Bretherton L, Cini E, Conway L, Cook F, Eadie P, Prior M, Wake M, & Mensah F (2017). Language Outcomes at 7 Years: Early Predictors and Co-Occurring Difficulties. Pediatrics PMID: 28179482... Read more »

McKean C, Reilly S, Bavin EL, Bretherton L, Cini E, Conway L, Cook F, Eadie P, Prior M, Wake M.... (2017) Language Outcomes at 7 Years: Early Predictors and Co-Occurring Difficulties. Pediatrics. PMID: 28179482  

  • February 24, 2017
  • 06:18 PM
  • 78 views

Symbiote Separation: Coral Bleaching and Climate Change

by Melissa Chernick in Science Storiented

It’s been a while since I’ve broken down some studies for you, so I took on a big one.I’m sure you’ve heard of coral bleaching. What is it? Why does it happen? Why does it matter? To start off, you need to know a little bit more about the individuals that make up a head (fan, whip, etc.): the polyp. Coral polyps look like tiny plants but are actually tiny animals (less than ½ an inch in diameter). They produce calcium carbonate to create a protective shell or skeleton that, when thousands are living together, make up what you see as a single coral head. Really, only the outer-most layer of a coral head is actually alive (yes, they build their houses on top of the skeletons of their ancestors). Lots of individual corals make up a reef. Polyps have stinging cells (nematocysts) on their tentacles that capture any prey that swims a little too close. But a polyp does not live alone inside of its skeleton-house; it is actually in a symbiotic relationship with dinoflagellates (a.k.a. marine algae) called zooxanthellae (zo-o-zan-THELL-ee). Zooxanthellae live inside the tissues of the coral and photosynthesize, passing some of the energy they make to the polyp. They get a place to live and the polyp gets some energy, it’s a win-win. And, it is the zooxanthellae that give the corals much of their color.When the coral gets stressed, it expels the zooxanthellae, causing them to turn completely white. Not dead, but very stressed and more likely to die. This is coral bleaching.All sorts of things can stress a coral and cause them to eject their zooxanthellae: temperature, light, tides, salinity, or nutrients. A polyp as cemented itself in its skeleton-house so it isn’t able to relocate when conditions change. Coral reefs are one of the most diverse ecosystmes on the planet, definitely in the oceans. Coral is serves as both food and/or shelter for many other species, up to ¼ of all ocean species. And their location means they protect shorelines too. That is a lot of responsibility.Now let’s look at those stressors. Remember middle school chemistry? Yeah, me neither. Here’s a little refresher: water reacts with carbon dioxide to make carbonic acid (H2O + CO2 = H2CO3). Rising atmospheric carbon dioxide (yes, we’re talking climate change here) both increases surface water temperature and water more acidic. That’s two stressors, y’all. And more than 30 percent of human emitted CO2 gets taken up by the oceans. A paper published by Anthony et al. (2008) in PNAS did a nice experiment looking at what happens to coral when the ocean acidifies and/or warms. They collected three of the most important “framework builders” in Heron Reef in the Indo-Pacific and transferred them to lab aquaria: Porolithon onkodes (common crustose coralline algae [CCA] species), Acropora intermedia (a fast growing, branching species), and Porites lobata (a massive species). Next, they used a custom-built CO2 dosing (bubbling) and temperature control system to test different acidification and temperature regimes that simulate doubling and 3- to 4-fold CO2 level increases as projected by the Intergovernmental Panel on Climate Change (IPCC). Then, they waited, they watched, and they took pictures for 8 weeks. From these digital images, they measured the amount of color and reduction in luminance of the corals. They also measured net rates of photosynthesis, respiration, and rates of calcification. They found that increased CO2 (i.e., acidification) led to 40-50 percent bleaching in the Porolithon and A. intermedia. For both of these species, the effect of increased CO2 on bleaching was stronger than the effect of temperature. Porites was less sensitive to increased CO2 alone, but was most sensitive in both stressors. High temperature amplified the bleaching by 10-20 percent in Porolithon and Acropora and 50 percent in Porites. In Porolithon, increased CO2 lead to a severe decline in productivity and calcification that was exacerbated by warming. Acropora’s productivity actually maximized with intermediate increases in CO2, but dropped at higher levels. Porites's productivity dropped with high CO2 but not like that of the Acropora. These species had similar calcification responses to each other, each much less than Porolithon. Overall, the authors proposed that CO2 induces bleaching through its impact on photoprotective mechanisms. Porolithon was the most sensitive to acidification, which is concerning because it is a primary reef-builder and serves as a settlement cue for invertebrate larvae (including other corals).A very recent study by Perry and Morgan (2017) in Scientific Reports zoomed out to look at corals at a large scale. They looked at magnitude of changes that followed the El Niño/Southern Oscillation (ENSO)-induced Sea Surface Temperature (SST) warming anomaly that affected the central Indian Ocean region in mid-2016, sort of a natural experiment. The ENOS-induced SST warming was above the NOAA “bleaching threshold,” defined as the point where SST is 1°C warmer than the highest monthly mean temperature. To do this they went to reefs in the southern Maldivian atoll of Gaafu Dhaalu, ran transects (basically, a line along which you measure stuff), and collected data on coral mortality, substrate composition, reef rugosity (a measure of complexity), and gross carbonate production and erosion. Then they determined carbonate budgets for the 3-dimensional surface of the reefs (there are equations…I won’t go into it…you’re welcome). They found extensive coral mortality over 70 percent. This was mostly driven by branching and tabular Acropora species (remember them from the last study?), which declined by an average of 91 percent! All of this coral death resulted in a decline in the net carbonate budgets. This decline reflected both reduced coral carbonate production and increased erosion by parrotfish as they graze on the algal film that grows on coral rock. Pre-coral bleaching, carbonate production was dominated by branching, corymbose and tabular species of Acropora; post-bleaching production by non-Acropora increased, with massive and sub-massive taxa (e.g., Porites species) more than doubling. Together, carbonate budgets were reduced by an average of 157 percent! All of this equates to a rapid loss in coral cover, growth potential, and structural complexity. The overall impact of the carbonate budget was profound and has major ecological implications. These habitats have gone from a state of strong growth potential to one of net framework erosion and breakdown; basically, the reefs are eroding faster than they are growing. And it may take 10-15 years for a full recovery, depending on the frequency of similar anomalies.So what’s the take-away from all of this? Corals are sensitive to their environment, but not all species of corals respond equally. Climate change is a huge factor in health and recovery of coral reefs, and steps need to be taken soon if we want to keep these little guys and the phenomenal habitats that they create. Here are the studies:... Read more »

  • February 24, 2017
  • 02:30 PM
  • 78 views

Irresistible: Emotions affect choice of breed despite welfare issues

by CAPB in Companion Animal Psychology Blog

Knowing a breed of dog may have health problems does not stop people from wanting one, because emotions get in the way. A new Danish study by Peter S Sandøe (University of Copenhagen) et al investigates the reasons why people acquire particular small breeds of dog and how attached the owners feel to their pet. The research helps explain why some breeds are popular despite a high incidence of welfare problems. The study looked at people in Denmark with French Bulldogs, Chihuahuas, Cavalier King Charles Spaniels, and Cairn Terriers.The results suggest that even knowing a dog of a particular breed is likely to have health problems may not stop people from getting one, because of their emotional response to the breed. Lead author, Peter Sandøe told me in an email,“In all, this study prompts the conclusion that the apparent paradox of people who love their dogs continuing to acquire dogs from breeds with breed-related welfare problems may not be perceived as a paradox from the point of view of prospective owners of breeds such as Chihuahuas and French Bulldogs.  Thus apparently available information about the problems in these two breeds has not served to prevent their growing popularity because fundamental emotional responses to the phenotypic attributes of these breeds are highly effective positive motivators.”Some owners did not prioritize health when getting their dog. As well, for owners of CKCS and Chihuahuas, those whose dog had more health/behaviour problems had a stronger attachment to the dog.French Bulldogs and Chihuahuas were chosen for the study because of their tendency to have problems related to their conformation (or appearance). Cavalier King Charles Spaniels were chosen because they also tend to have health problems, but not related to what they look like. Finally, Cairn Terriers were picked because they are relatively healthy, so they make a good contrast.There were differences in how people acquired the breeds. People with Chihuahuas were most likely to say there “wasn’t really any planning”, and they were also less likely than CKCS owners and French Bulldog owners to have put time into learning about dogs from books or dog professionals before getting it. Cairn Terrier owners were also less likely to have learned in this way, and more likely to rely on prior experience with the breed.People were most likely to get Cairn Terriers and CKCS as puppies from breeders. (In Denmark most dogs come from small breeders with between 2 and 4 breeding bitches). Although breeders were still the most common source of Chihuahuas and French Bulldogs, these breeds had a greater tendency to be acquired from a previous owner (22% of Chihuahuas and 15% of French Bulldogs) or other sources. The researchers found that the dog’s distinctive appearance, breed attributes and convenience were all motivations in getting a dog. Personality was also important.These motivations varied by breed. Distinctive appearance and personality were particularly important for owners of Cavalier King Charles Spaniels and French Bulldogs. For Chihuahua owners, these were less important, but convenience played a bigger role. Owners of Cairn Terriers were less motivated by appearance and more by breed attributes. Interestingly, these motivations were also linked to attachment. People who were motivated by distinctive appearance and breed attributes were very attached to their dog. The scientists say it’s possible that appearance is directly linked to levels of attachment, because facial features that are baby-like may induce parenting behaviours in the owner. This has also been suggested by previous research (see e.g. children’s preferences for baby-like features in dogs and the role of eyebrow movements in adopting shelter dogs).The scientists say the motivations to acquire a dog can be seen as intrinsic (as for Cairn Terriers) or extrinsic (for the three other breeds, where cuteness, baby-like features and fashion play a role).The researchers also collected data on health and behaviour problems. French Bulldogs had the highest levels of problems and the greatest expenses. Although only 67% had visited a vet in the last year for a health check, 29% had had a sudden illness or injury, and almost 9% had a chronic illness. 12% of French Bulldog owners had spent the equivalent of more than US$760 on vet bills in the previous year. Chihuahuas were the most likely to have a behaviour problem (10%) and to have dental problems (33%). Most Cavalier King Charles Spaniels had been for a health check (81%), 19% had had a sudden illness or injury, and 5.5% had a chronic illness. Cairn Terriers had fewer problems and the lowest expenditure at the vet.Interestingly, owners of Cairn Terriers had the lowest levels of attachment, and Chihuahuas the highest, with French Bulldog and CKCS owners in between. For example, if we take the statement, “I would do almost anything to take care of my dog”, 70% of Chihuahua owners strongly agreed. For French Bulldog owners it was 62%, CKCS owners 56%, and only 43% of Cairn Terrier owners.But perhaps this reflects decisions that owners had already had to make about their dog. The scientists wondered if health or behaviour issues would affect people’s desire to get another dog of the same breed.French Bulldog owners were actually the most likely to say “yes, for sure” they would get the same breed again (29%). Only 10% of French Bulldog owners were keen to get a different breed next time, compared to 25% of Chihuahua owners. (This number is higher than the percentage of Chihuahua owners who "for sure" wanted the same breed again, 17.5%). For three of the breeds (Cairn Terrier, CKCS and Chihuahua), health and behaviour issues did not have an effect on the likelihood of wanting the same breed again. But for French Bulldog owners, health/behaviour issues reduced the number who said they wanted the same again, from 31% for the majority with no issues, to 20% for those with one problem and 12% for those with two problems.Data from Swedish insurance company Agria, obtained by the researchers, provides sobering information about the median age of death, as shown in the table (just 2.5 years for male French Bulldogs and 3.8 for females). ... Read more »

Sandøe P,, Kondrup SV,, Bennett PC,, Forkman B,, Meyer I,, Proschowsky HF,, Serpell, JA,, & Lund, TB. (2017) Why do people buy dogs with potential welfare problems related to extreme conformation and inherited disease? A representative study of Danish owners of four small dog breeds. . PLOSOne. info:/

  • February 24, 2017
  • 11:06 AM
  • 96 views

What if black holes were not... holes? A Los Alamos physicist explains his alternative theory behind these mysterious objects.

by EE Giorgi in CHIMERAS

© Elena E. GiorgiThe concept of a “black hole” — a celestial body so dense and massive that not even light can escape its gravitational field — dates back to the 18th century, with the theoretical work of Pierre-Simon Laplace and John Michell. But it wasn’t until the early 20th century that these mysterious dark objects were first described mathematically by German physicist Karl Schwarzschild. Schwarzschild’s work predicted the existence of a finite distance around the black hole (called the “event horizon”) from which light cannot escape. Emil Mottola, a physicist in the Theoretical Division at Los Alamos National Laboratory, laughs as he explains this bit of history behind black holes. “Would black holes have captured the popular imagination if they were still known as Schwarzschild’s solution?” he quips. Mottola has a point. The name “black hole” was coined by the American physicist John Wheeler in the 1960s, when these objects became the subject of serious study and first entered the popular vocabulary.“And then of course, Stephen Hawking made black holes very popular with his own research and theory of black hole radiation,” Mottola adds. “To this day,” he explains, “black holes are far from being understood, and science fiction may have taken over from science fact. We can’t answer many of the most important questions without knowing what the internal states of a black hole are, but no one has ever been inside a black hole, so no one actually knows what is inside.”One particularly vexing feature of black holes is the so-called “information paradox.” In 1974, Stephen Hawking theorized that black holes emit small amounts of radiation (called Hawking radiation). However, if this is true, black holes should eventually evaporate due to the loss of mass, leaving no way—not even in principle—to recover the information that was originally enclosed in it. This question alone has generated hundreds of research papers with still no completely satisfactory resolution. In 2001, Mottola and his colleague Pawel O. Mazur proposed an alternative to Hawking’s black hole theory that eliminates the paradox. “Think of a black hole as having a physical surface,” Mottola says. He imagines this surface to be much like a soap bubble that bends and fluctuates in space. “Our idea is that quantum effects build up right at the event horizon (the bubble’s surface), leading to a phase transition. This in turn creates a gravitational repulsive force inside the “bubble” that prevents the surface from collapsing. This repulsive force is the same ‘dark energy’ force believed to cause the expansion of the universe. We call these objects Gravitational Condensate Stars or ‘Gravastars’— celestial objects that would be compact, cold and dark, and look to astrophysicists just like ‘black holes,’ although they are not ‘holes’ at all. Our hypothesis does not contradict the conservation of information because there is no infinite crushing of space and time inside a Gravastar, and information is never destroyed.”According to Mottola, the mathematical equations Hawking used to describe the temperature of a black hole are in reality describing the surface tension of a Gravastar. “If we assume that black holes have a temperature, then they need to have an enormous entropy too, but we can’t easily explain that enormous black hole entropy. In our theory, black holes don’t have a temperature, they have surface tension, like soap bubbles. In 2015 we showed that this possibility of a surface and surface tension was already inherent in Schwarzschild’s original formulation of black hole interiors in 1916, and so is consistent with both Einstein’s General Relativity and Quantum Mechanics.”As I look over my notes, I pose Dr. Mottola one final question: “Is there any way to find out who’s right, you or Stephen Hawking?”He smiles because he knows that whatever Hawking says these days carries a lot of weight, including when he proposes that black holes could be mysterious portals to other universes. “I believe we may well find out the answer in the next five to ten years,” Mottola says. “If ‘black holes’ actually are Gravastars with a surface, their surface oscillations would cause them to emit gravitational waves at certain frequencies, which is a substantially different signal than that expected from the black holes that Hawking and colleagues theorize. LIGO directly detected gravitational waves for the first time in 2015, so we have just entered a new era of gravitational wave astronomy. In a few years, we may have enough data from the gravitational waves detected by LIGO and its sister observatories to be able to resolve the conundrum.”Needless to say, the Los Alamos scientist is very excited at that prospect. References[1] Mazur, P., & Mottola, E. (2004). Gravitational vacuum condensate stars Proceedings of the National Academy of Sciences, 101 (26), 9545-9550 DOI: 10.1073/pnas.0402717101[2] Emil Mottola (2010). New Horizons in Gravity: The Trace Anomaly, Dark Energy and CondensateStars Acta Physica Polonica B (2010) Vol.41, iss.9, p.2031-2162 arXiv: 1008.5006v1[3] Mazur, P., & Mottola, E. (2015). Surface tension and negative pressure interior of a non-singular ‘black hole’ Classical and Quantum Gravity, 32 (21) DOI: 10.1088/0264-9381/32/21/215024... Read more »

Mazur, P., & Mottola, E. (2004) Gravitational vacuum condensate stars. Proceedings of the National Academy of Sciences, 101(26), 9545-9550. DOI: 10.1073/pnas.0402717101  

Emil Mottola. (2010) New Horizons in Gravity: The Trace Anomaly, Dark Energy and Condensate Stars. Acta Physica Polonica B (2010) Vol.41, iss.9, p.2031-2162. arXiv: 1008.5006v1

  • February 24, 2017
  • 06:00 AM
  • 78 views

Friday Fellow: B. coli

by Piter Boll in Earthling Nature

by Piter Kehoma Boll It’s time to give more space for parasites, including human parasites! So today our fellow comes right from the stool of many mammals, including humans. Its name is Balantidium coli, or B. coli for short. B. coli is … Continue reading →... Read more »

Schuster, F., & Ramirez-Avila, L. (2008) Current World Status of Balantidium coli. Clinical Microbiology Reviews, 21(4), 626-638. DOI: 10.1128/CMR.00021-08  

  • February 24, 2017
  • 03:07 AM
  • 81 views

Say my name

by Paul Whiteley in Questioning Answers

"At 9 months of age, infants developing ASD [autism spectrum disorder] were more likely to fail to orient to their names, persisting through 24 months."So said the findings reported by Meghan Miller and colleagues [1] investigating an often over-looked but typically informative question relevant to childhood autism screening and assessment: the response to name. Anyone who knows a little about instruments such as the ADOS (Autism Diagnostic Observation Schedule) will already know about the importance of response to name ("a full response is defined as orientating to and making eye contact with the examiner who calls his name") as part of assessment.Based on the inclusion of some 150 infants, siblings of children with or without a diagnosis of autism, a response to name task was carried out at various intervals in infancy in this prospective study ("6, 9, 12, 15, 18, and 24 months of age"). At 3 years of age, child participants were "classified into 1 of 3 outcome groups: group with ASD (n = 20), high-risk group without ASD (n = 76), or low-risk group without ASD (n = 60)." As per the opening sentence, consistently not responding to their name was a feature of quite a few of those children who subsequently went on to develop autism. Some but not all. Alongside other findings reported in relation to receptive language for example, the authors concluded: "Infants who consistently fail to respond to their names in the second year of life may be at risk not only for ASD but also for greater impairment by age 3 years."Such work continues a theme from some of the authors on the Miller paper [2] and how relatively simple observations during play interaction [3], could be valuable variables when it comes to ascertaining potential risk of developing autism. Of course one needs to be careful that a lack of response to name does not automatically mean that an autism diagnosis is imminent or indicated as per the typical requirement to check a child's hearing for example and to consider the possibility of other diagnoses being applicable. I might also remind readers of the potential effects of regression when it comes to autism (see here) and how not every child presents with autistic features in early infancy (something that needs to be taken into account when it comes to other recent research too).To close, say my name...----------[1] Miller M. et al. Response to Name in Infants Developing Autism Spectrum Disorder: A Prospective Study. J Pediatr. 2017 Feb 2. pii: S0022-3476(16)31566-9.[2] Nadig AS. et al. A prospective study of response to name in infants at risk for autism. Arch Pediatr Adolesc Med. 2007 Apr;161(4):378-83.[3] Trillingsgaard A. et al. What distinguishes autism spectrum disorders from other developmental disorders before the age of four years? Eur Child Adolesc Psychiatry. 2005 Mar;14(2):65-72.----------Miller M, Iosif AM, Hill M, Young GS, Schwichtenberg AJ, & Ozonoff S (2017). Response to Name in Infants Developing Autism Spectrum Disorder: A Prospective Study. The Journal of pediatrics PMID: 28162768... Read more »

Miller M, Iosif AM, Hill M, Young GS, Schwichtenberg AJ, & Ozonoff S. (2017) Response to Name in Infants Developing Autism Spectrum Disorder: A Prospective Study. The Journal of pediatrics. PMID: 28162768  

  • February 23, 2017
  • 02:59 AM
  • 97 views

"Autoimmune epilepsy is an underrecognized condition..."

by Paul Whiteley in Questioning Answers

"Among adult patients with epilepsy of unknown etiology, a significant minority had detectable serum Abs [autoantibodies] suggesting an autoimmune etiology."So said the findings reported by Divyanshu Dubey and colleagues [1] continuing a research theme previously discussed on this blog (see here) on how epilepsy / seizure-type disorder(s) for some might have more to do with immune function than many people might think.OK, a brief bit of background: epilepsy is a blanket term covering a wide variety of different presentations that affect the brain and specifically, 'the electrics' of the brain. Seizures are the most common symptom. Treatment typically comes in the form of anti-epileptic medicines (although other options are being considered for some). It's been known for a while that outside of the 'brain' focus of epilepsy, other biological systems might also play a role in the development/maintenance of the condition(s); specifically the immune system and quite often in cases where traditional anti-epileptic medicines don't seem to be able to control seizures effectively. The details are still a little sketchy but studies like the one from Dubey et al are trying to put some scientific flesh on to the bones of what facets of the immune system are potentially involved, specifically under 'autoimmune' conditions where the body fails to recognise 'self' as self and mounts an immune response against the body's own tissue(s).Dubey and colleagues looked at a group of participants "presenting to neurology services with new-onset epilepsy or established epilepsy of unknown etiology" and tested donated serum samples "for Abs reported to be associated with autoimmune epilepsy (NMDAR-Ab, VGKCc-Ab, leucine-rich glioma-inactivated protein 1 [LGI1] Ab, GAD65-Ab, γ-aminobutyric acid type B receptor [GABAB] Ab, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor [AMPAR] Ab, antineuronal nuclear antibody type 1 [ANNA-1 or anti-Hu] Ab, Purkinje cell cytoplasmic antibody type 2 [PCA-2] Ab, amphiphysin Ab, collapsin-response mediator protein 5 [CRMP-5] Ab, and thyroperoxidase [TPO] Ab)." Quite a lot of those autoantibodies probably sound like gibberish to the lay reader but some of them have been discussed in other contexts on this blog (see here and see here for examples).Results: some (15) of the 127 participants initially enrolled in the study were "subsequently excluded after identification of an alternative diagnosis." This in itself is interesting, as diagnoses such as "hypoxic or anoxic injury following cardiac arrest" and "ischemic stroke" are mentioned, illustrating how several different roads can lead to epilepsy and/or the presentation of seizures.Then: "Serum Abs suggesting a potential autoimmune etiology were detected in 39 (34.8%) cases." Over a third of the cohort showed serological evidence of autoantibodies and some presented with more than one type of autoantibody as being present. Breaking down those serologically positive participants, we are told that: "19 patients (48.7%) had new-onset epilepsy and 20 patients (51.3%) had established epilepsy." The authors did also subsequently limit their findings to those cases excluding TPO-Ab and low-titer GAD65-Ab (autoantibodies where a specific role to epilepsy is unclear or not specific) but even then reported that: "23 patients (20.5%) with unexplained epilepsy had positive serologic findings strongly suggestive of an autoimmune cause of epilepsy." There is also a final part to the Dubey paper which also merits mention: "Among the 23 patients who were seropositive, 15 (65.2%) received some sort of immunotherapy. Better seizure outcome was associated with use of immunomodulatory therapy... especially with use of intravenous methylprednisolone... or plasmapheresis."Alongside other (independent) studies in this area, the peer-reviewed evidence does seem to growing to suggest that within the wide (and heterogeneous) 'spectrum' that is epilepsy, at least some of that epilepsy might have an important immune component to it. To quote again from Dubey: "The data presented here suggest that autoimmune encephalitis may explain at least 20% of adult-onset epilepsies of unknown etiology." Aside from the importance of screening for said autoantibodies when certain cases of epilepsy appear at clinic, there are a few other potentially important points that could be raised about such data. Autism is area that I would be interested to see some further investigations carried out on with the Dubey findings in mind. Epilepsy is an important comorbidity 'over-represented' when it comes to autism (see here) and given the suggestions down the years that immune function (specifically autoimmunity) might be a facet of 'some' autism (see here for example) it's not beyond the realms of possibility that comorbid epilepsy might be a further facet of any autoimmune processes. Birds of an autoimmune feather tend to stick together and all that (see here). Add in the findings specifically talking about 'anti-NMDA-receptor encephalitis "mimicking an autistic regression"' (see here) and how methlyprednisolone might not be an uncommon medicine for some types of (autoimmune-related autistic presentation) and the hypotheses to be tested are laid out in front of you. By saying that, I don't want to take anything away from the more typical forms of epilepsy that can present (either alone or alongside autism) but rather point to the expanding knowledge base suggesting that immune functions may extend much further than just protecting the host from infection et al...To close, slightly related to some of the content included in this post, the trailer for the film Brain on Fire (from the book of the same name) is out and looking like required viewing.----------[1] Dubey D. et al. Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA Neurol. 2017 Feb 6.----------Dubey D, Alqallaf A, Hays R, Freeman M, Chen K, Ding K, Agostini M, & Vernino S (2017). Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA neurology PMID: 28166327... Read more »

Dubey D, Alqallaf A, Hays R, Freeman M, Chen K, Ding K, Agostini M, & Vernino S. (2017) Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA neurology. PMID: 28166327  

  • February 22, 2017
  • 09:42 PM
  • 96 views

Running economy barefoot, in minimalist shoes and traditional running shoes

by Craig Payne in Running Research Junkie

Running economy barefoot, in minimalist shoes and traditional running shoes... Read more »

Cochrum RG, Connors RT, Coons JM, Fuller DK, Morgan DW, & Caputo JL. (2017) Comparison of Running Economy Values While Wearing No Shoes, Minimal Shoes, and Normal Running Shoes. Journal of strength and conditioning research, 31(3), 595-601. PMID: 28222048  

  • February 22, 2017
  • 12:00 PM
  • 69 views

The Function of Play Bows in Dog and Wolf Puppies

by CAPB in Companion Animal Psychology Blog

New research casts doubt on an old explanation for the play bow – and suggests it’s all about more play.The play bow is a glorious signal in dogs. The bum goes up and the elbows go down, leaving the rear end sticking up, usually accompanied by a lovely happy face (as pictured above). Not just reserved for other dogs, our canine friends will play bow to us too.Traditionally, it was believed that the play bow serves as a signal to say something like, “I’m just playing, it’s not real!”, because many of the behaviours dogs perform in play – chasing, growling, biting, nipping, etc – can also be aggressive. But recent research with adult dogs has thrown that into question.In 2016, Sarah-Elizabeth Byosiere (University of Michigan), Julia Espinosa and Barbara Smuts looked at play bows between adult dogs. If the play bow functions to say “I’m only playing!” then you would expect to see more ‘offensive’ behaviour that could potentially be misinterpreted either just before or just after the play bow. They did not find this. Instead, both the bower and the bowee were typically still before the play bow happened. Afterwards play resumed in the form of chase sequences or both dogs rearing up.In other words, the play bow seemed to function as a signal to make play start again after a pause.Byosiere et al concluded,“the fact that both bowers and partners were often stationary before play bows and highly active after them (in the form of synchronous interactions or runaway/chase dynamics) supports the hypothesis that bows most often functioned to reinitiate play after a pause.”But that study only looked at adult dogs. And in fact, dogs are not the only animal that play bows: coyotes, foxes, lions and wolves have all been seen to play bow. A new study by Byosiere et al investigates the role of play bows for dog and wolf puppies.All of the puppies in this study were hand-reared, which means that the dogs and wolves have all grown up in a similar environment. The wolf pups were born in captivity and hand-reared in small groups; and the dog puppies were born in an animal shelter in Hungary and also hand-reared in the same way as the wolves.The study analysed videos of dog-dog and wolf-wolf play in which at least one of the dogs or wolves was a puppy. The researchers coded play bows that were performed by the puppies during a play bout. The dog puppies were 2 – 5 months old, and the wolf puppies were 2.7 to 7.8 months.It has been suggested before that the play bow is a visual communication signal, which means that it would be performed when the bower is in sight of the bowee. The results found this was the case, as previously found by Horowitz (2009).Photo: Cryber; top, xkunclova; below, Warren Metcalf (all Shutterstock.com)In the wolf puppies, every one of the 69 play bows coded was performed while the two were in visual contact. In the dog puppies, all but one of the 136 play bows was performed in sight of the other dog. And in the one case where the other dog was not looking, the bowee barked, suggesting they knew they needed to get their partner’s attention.As described for the adult dog study, if the play bow is a signal to say “I’m just playing”, you would expect to see more ‘offensive’ behaviour immediately before or after it. This was not the case for either wolf or dog puppies prior to the play bow. After the play bow, the dog partners (i.e. the bowees) showed more offensive behaviours, which is contrary to this hypothesis.The scientists also looked specifically at bites, and found there were no bite-shakes immediately before or after the play bows. This is surprising, because earlier work by Bekoff (1995) found that play bows were associated with bite-shakes. The difference might be because Bekoff looked at younger puppies. In fact there were few bites and nips in the videos of dogs and wolves used in this study.Another possible reason for a play bow might be so that the bower is well-placed either to run away from or chase the other dog. In Byosiere’s earlier study with adult dogs, there was no evidence of it being used to attack the other dog in play, but it seemed possible it was used to escape.In fact for the dog puppies, their partner (bowee) was more likely to play-attack them than the other way around. This was not found in wolves.However, both wolf puppies and dog puppies were more likely to run away after the play bow, suggesting it positions them to escape.As mentioned above, Byosiere’s study with adult dogs found that play bows tended to occur after a pause and serve to re-start play. This was the case for dog puppies, as both bower and bowee tended to be stationary before the play bow. In wolf puppies, however, this was not confirmed, although the bowees did tend to be still before the play bow.Finally, it has also been suggested that play bows might serve to synchronize behaviours between the two partners after the bow. However, this was not found to be the case for either wolf or dog puppies.The results of both studies are summarized in the table.Reproduced from PLOSOne under Creative Commons LicenceThe scientists write,“Taken together, findings from this study and the previous study on adult dogs suggest that play bows do not occur at random and do not, therefore, simply enhance the play atmosphere in a general way. Instead, their association with particular behaviors before and after the play bow suggests strategic use of this play signal to accomplish immediate goals, including continuation of play by enticing the partner into a runaway/chase interaction.”This study finds that the play bow is a visual signal for both dog and wolf puppies, but it does not serve to stop ‘offensive’ behaviours from being misinterpreted, as previously thought. In dogs, it seems to re-start play after a pause, however in wolf puppies the function is less clear. The authors suggest it may be that the intent is still to re-start play, but that it is less likely to be successful in wolves.This is a fascinating study that will no doubt have many of us paying more attention to what happens before and after our dogs play bow.The study of wolf and dog puppies is open access and can be read via the link below, while you can find the adult dog study via Sarah-Elizabeth Byosiere’s Researchgate profile.What do you like about watching dogs play?You might also like: ... Read more »

  • February 22, 2017
  • 07:18 AM
  • 107 views

Hydrolagus erithacus: New Species of Ghost Shark Discovered

by beredim in Strange Animals



Kristin Walovich holds the newly described species of ghost shark
Photo Credit: Kristin Walovich




Researchers recently announced the discovery of a new species of ghost shark, Hydrolagus erithacus. Ghost sharks - which aren’t actually sharks but instead their closest living relatives - are an extraordinarily rare sighting. Actually, it was just a few months ago, when a ghost shark was filmed... Read more »

  • February 22, 2017
  • 07:03 AM
  • 111 views

SciELO Preprints on the way

by SciELO in SciELO in Perspective

The main objective of SciELO Preprints is to speeding up the availability of research results and will contribute to an organized flow of potentially acceptable preprints by SciELO journals, in line with the advances and growing importance of preprints publication internationally. The cooperative construction of the SciELO Preprints modus operandi will encompass the promotion and debate of the preprints concept, the definition of governance and operations structures and the operational implementation. It is expected to be fully operational by mid-2018. … Read More →... Read more »

Berg, J., Bhalla, N., Bourne, P., Chalfie, M., Drubin, D., Fraser, J., Greider, C., Hendricks, M., Jones, C., Kiley, R.... (2016) Preprints for the life sciences. Science, 352(6288), 899-901. DOI: 10.1126/science.aaf9133  

Ginsparg, P. (2016) Preprint Déjà Vu. The EMBO Journal, 35(24), 2620-2625. DOI: 10.15252/embj.201695531  

Pulverer, B. (2016) Preparing for Preprints. The EMBO Journal, 35(24), 2617-2619. DOI: 10.15252/embj.201670030  

Vale, R. (2015) Accelerating scientific publication in biology. Proceedings of the National Academy of Sciences, 112(44), 13439-13446. DOI: 10.1073/pnas.1511912112  

  • February 22, 2017
  • 04:20 AM
  • 120 views

History of bipolar disorder = elevated risk of dementia: is vitamin D important?

by Paul Whiteley in Questioning Answers

"History of BD [bipolar disorder] is associated with significantly higher risk of dementia in older adults."So said the systematic review and meta-analysis published by Breno Diniz and colleagues [1] taking in the accumulated peer-reviewed literature on this topic. Including data for some 3000 individuals diagnosed with bipolar disorder and nearly 200,000 controls (without bipolar disorder), authors calculated something of a significantly higher risk of dementia in those with a documented history of bipolar disorder. They note that there is more research to do in this area, specifically on mechanisms and "to evaluate interventions that may reduce the risk of dementia in this population."Outside of the literature included in the Diniz study, similar findings have been reported in the science literature. The paper by Almeida and colleagues [2] noted that: "Bipolar disorder in later life is associated with increased risk of dementia" based on their analysis of ~38,000 older men (65-85 years old) and their "13-year risk of dementia." Perhaps more worryingly were their findings that: "Bipolar disorder was also associated with increased mortality" in relation to "death by suicide, accidents, pneumonia or influenza, and diseases of the liver and digestive system." Other data looking more generally at clinical depression paints a similar picture [3] suggesting something of a connection between various types of depression and risk of various types of dementia: "depressive symptomatology is associated with pathological mechanisms associated with neurodegeneration."I've tackled the topic of dementia a couple of times on this blog; most recently in relation to how incidental vitamin D deficiency *could be* something important when it comes to at least some cases of dementia (see here). Minus any sweeping generalisations and accepting that there may be many different roads leading to dementia and/or bipolar disorder, I am intrigued at the possibility that the sunshine vitamin might be something to consider as a 'connector' between elements of the depression and dementia spectrums as per other findings (see here for example). At the very least, it invites lots more targeted investigation, including whether vitamin D might indeed be a nootropic of choice for some (see here)...----------[1] Diniz BS. et al. History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American Journal of Geriatric Psychiatry. 2017. Jan 4.[2] Almeida OP. et al. Risk of dementia and death in community-dwelling older men with bipolar disorder. Br J Psychiatry. 2016 Aug;209(2):121-6.[3] Cherbuin N. et al. Dementia risk estimates associated with measures of depression: a systematic review and meta-analysis. BMJ Open. 2015 Dec 21;5(12):e008853.----------Diniz BS, Teixeira AL, Cao F, Gildengers A, Soares JC, Butters MA, & Reynolds CF 3rd (2017). History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry PMID: 28161155... Read more »

Diniz BS, Teixeira AL, Cao F, Gildengers A, Soares JC, Butters MA, & Reynolds CF 3rd. (2017) History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. PMID: 28161155  

  • February 22, 2017
  • 04:01 AM
  • 108 views

Do twitter or facebook activity influence scientific impact?

by Richard Kunert in Brain's Idea

Are scientists smart when they promote their work on social media? Isn’t this a waste of time, time which could better be spent in the lab running experiments? No. An analysis of all available articles published by PLoS journals suggests otherwise. My own twitter activity might best be thought of as learning about science (in […]... Read more »

Peoples BK, Midway SR, Sackett D, Lynch A, & Cooney PB. (2016) Twitter Predicts Citation Rates of Ecological Research. PloS one, 11(11). PMID: 27835703  

  • February 21, 2017
  • 09:00 PM
  • 94 views

Redrawing Ratite Relationships

by Jente Ottenburghs in Evolutionary Stories

Scientists have sequenced the DNA of two extinct birds: the moa and the elephantbird. Comparison with their living relatives led to some surprising findings.... Read more »

Maderspacher F. (2017) Evolution: Flight of the Ratites. Current biology : CB, 27(3). PMID: 28171755  

Yonezawa T, Segawa T, Mori H, Campos PF, Hongoh Y, Endo H, Akiyoshi A, Kohno N, Nishida S, Wu J.... (2017) Phylogenomics and Morphology of Extinct Paleognaths Reveal the Origin and Evolution of the Ratites. Current biology : CB, 27(1), 68-77. PMID: 27989673  

  • February 21, 2017
  • 09:02 AM
  • 130 views

Who Can Swim Further: A Race to the Depths and Back (A Guest Post)

by Miss Behavior in The Scorpion and the Frog

By Jefferson LeThe blue whale (Balaenoptera musculus) is the largest mammal on the planet. Image byNMFS Northeast Fisheries Science Center (NOAA) available at Wikimedia Commons.Helloooooo! My name is Bailey and I am a 25 meter long blue whale, the largest living mammal on Earth! My friend Finley, a 21 meter long fin whale comes in second for largest in size. We had an interesting adventure recently where we were followed by humans. While Finley and I were foraging for food, I overheard the humans talking about investigating our diving behavior when we hunt and not hunt. With that, I will tell you what these foreigners did to investigate our behavior and also what happens when we dive. A chart of whales of different sizes. Image by Smithsonian Institute.To record our dives, the humans travelled to Mexican waters to attach recorders onto our mid-backs using a crossbow. Now, it didn’t hurt much due to my thick blubber. These devices recorded depth of how far we dived, time of dives, and our location. These recorders eventually came off between 5 to 13 hours later. Finley and I were not the only test subjects. Other members of our species were also tagged. After all the data on the devices were collected, the humans finally left our waters and did statistical analyses on our diving behavior. The fin whale (Balaenoptera physalus) rarely exposes its fluke when it prepares to diveto the abyss. Image by Aqqa Rosing-Asvid at Wikimedia Commons.Now, before we talk about what the humans found, I want to share with you the whale secret to a great dive. In case that you ever find yourself in the ocean or your local pool, you can try it! The nose for Finley and I are called blowholes, which are found on top of our heads. This tract is separated from our digestive tract so we do not have to worry about having food go down our blowhole. When I am about to dive, instead of gulping in lots of oxygen, I exhale out as much as I can. This causes my lungs to collapse and flexible walls in my chest allow even more compression. Also, tiny structures in my lungs called alveoli collapse which halts any gas exchange. All of the decrease in lung space decreases buoyancy so I can descend down to the depths. As I descend, my heart rate lessens to reduce energy used during the dive. The oxygen that I had obtained before the dive is stored in my blood and muscle tissue. Since the deep depths are really cold, blood flow is temporarily halted at the thinner areas of my body, like flippers, and some organs to keep the main body going. When I ascend back up, I gradually increase space in my lungs and my alveoli regain full function to allow gas exchange. If you were to ascend too quickly, you could get shallow water blackout or even worse, the “bends” (where nitrogen bubbles in your blood) and I heard it is painful. After ascending is complete, I can release my blowhole open and take in fresh oxygen again. I was secretly told what the results to the humans’ experiments were. They found out that fin and blue whales dove deeper when hunting on shallow dives when not hunting. It makes sense! Why spend so much energy diving when not hunting? Also, they noted that our lunge feeding frequency was different. Lunge feeding is where we propel ourselves towards our prey with our mouth open and grab as much food as we can into our mouth. Blue whales lunged about 2.5 times more than fin whales! That’s a point for the blue! However, the record dive depth came from a fin whale. Hmm… I wonder if Finley broke that record. Did you find my secret and what the humans found interesting? I surely did. I never thought about how I dive and how I behave as it is practically in my blood! Well, the next time you are at a deep pool, try those secrets I spilled to you. It might be fun! Then again, you might be thinking, how does a whale communicate with a human and understand scientific data? That is a secret you may never know… Literature Cited:Croll DA, Acevedo-Gutiérrez A, Tershy BR, & Urbán-Ramírez J (2001). The diving behavior of blue and fin whales: is dive duration shorter than expected based on oxygen stores? Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, 129 (4), 797-809 PMID: 11440866Hill, R. W., G. A., Wyse, M. Anderson. (2008). Animal Physiology. 2:641-660 ... Read more »

Croll DA, Acevedo-Gutiérrez A, Tershy BR, & Urbán-Ramírez J. (2001) The diving behavior of blue and fin whales: is dive duration shorter than expected based on oxygen stores?. Comparative biochemistry and physiology. Part A, Molecular , 129(4), 797-809. PMID: 11440866  

  • February 21, 2017
  • 03:39 AM
  • 132 views

Neuropsychiatric disorder onset "temporally related to prior vaccinations"?

by Paul Whiteley in Questioning Answers

"Given the modest magnitude of these findings in contrast to the clear public health benefits of the timely administration of vaccines in preventing mortality and morbidity in childhood infectious diseases, we encourage families to maintain vaccination schedules according to CDC guidelines."The quote opening this post comes from the paper published by Douglas Leslie and colleagues [1] (open-access) and offers not a conclusion from their study looking at the possibility that "the onset of some neuropsychiatric disorders may be temporally related to prior vaccinations in a subset of individuals" but a caution that cause-and-effect were not 'proven' in their study. Anyone with any knowledge about previous occasions where administration of vaccines have been correlated with specific psychiatric or behavioural outcomes (see here and see here for examples) will recognise how important such a caution is, bearing in mind that vaccines are medicines (albeit preventative) and are subject to similar monitoring for safety and the small possibility of adverse effects as other medicines.Based on the examination of "the MarketScan® Commercial Claims and Encounters database", a US drug and medical insurance claims database, researchers looked at various diagnoses of interest including OCD (obsessive compulsive disorder), AN (anorexia nervosa), anxiety disorder, tic disorder, major depression, bipolar disorder and ADHD (attention-deficit hyperactivity disorder) in children/young adults aged 6-15 years old. This alongside several other classes of diagnosis including broken bones and 'open wounds'. Participants were matched one-to-one with controls without said neuropsychiatric diagnoses and exposure(s) to various vaccinations - "influenza, tetanus and diphtheria (TD), hepatitis A, hepatitis B, meningitis, and varicella" - were 'tracked'. Interestingly, this is not the lead authors' first foray into using the MarketScan database [2], where autism was the previous topic of analysis (specifically healthcare service use and costs).Results: bearing in mind that samples sizes varied according to those diagnoses under investigation, the authors report: "Receipt of any vaccine in the previous 6 months was highest for children with AN (21.4%), followed by OCD (15.9%) and tic disorder (15.8%), and was lowest for children with open wounds (10.3%)." This information needs to be treated carefully because - again - it tells us nothing about any cause-and-effect relationship, just correlation and trend; trends that could be there for all-manner of different reasons outside of the variables looked at. Further: "HRs [hazard ratio] associated with receipt of any vaccine were highest for children with AN... followed by OCD."The authors also looked at specific vaccinations in relation to those neuropsychiatric disorders included in their study. They report: "Influenza vaccinations during the prior 3, 6, and 12 months were... associated with incident diagnoses of AN, OCD, and an anxiety disorder." Conversely: "children with major depression were less likely to have received the influenza vaccine in the previous 3 months" and "children with bipolar disorder were also less likely to have received the influenza vaccine in the previous 3 or 6 months."OK, it is worth reiterating - yet again - that this was a study looking at possible associations and not necessarily cause-and-effect. Indeed, judging by that last paragraph and the table of HRs produced by the authors (see here) one might easily claim that flu vaccination might potentially shield someone from developing major depression as much as 'cause' AN, OCD and/or anxiety disorder. Such is the nature of such studies and the findings being reported. And indeed someone has actually looked at depressive symptoms (symptoms that is, not depression as a clinical diagnosis) before and after an influenza vaccination and found very little...I note that with specific regard to the influenza vaccine and the findings that "children with AN, OCD, or a tic disorder were more likely to have received the influenza vaccine in the preceding periods" the authors head into the research talking about narcolepsy and the "AS03-adjuvanted H1N1 vaccine" as a possible template for their findings. This despite not covering the diagnosis of narcolepsy in their study (they could have). I've touched upon this area of research before on this blog (see here) (something that continues to appear in media discussions) and whilst not disputing the findings, do for example, wonder why in the work of Szakács and colleagues [3] ADHD was picked up as a comorbidity present in their "post-H1N1 vaccination (PHV) narcolepsy group" but in the Leslie data the HRs showed little evidence of any relationship. Yes, H1N1 vaccination is not necessarily the same as influenza vaccination reported in the Leslie data (we don't actually know what specific influenza vaccines were administered), but surely if discussions turn to an 'autoimmune' element as a possible mechanistic feature potentially linking vaccination and [some] neuropsychiatric disorder(s), one would expect to see the same/similar pattern of conditions being represented and reported? For balance, I should also point out that other independent study has talked about eating disorders potentially having "immune-mediated mechanisms" connected, particularly those associated with autoimmunity [4] although I don't doubt such a connection is likely complicated and probably not universally applicable.It's not difficult to find issues with the Leslie paper and no doubt these will be emphasised in any further discussions about the data reported even when the authors stress throughout that "findings do not demonstrate a causal role of vaccination in the pathoetiology of any of these conditions." The strengths of the data - e.g. the use of that administrative database for confirming diagnoses and vaccine exposure - are worth mentioning again in light of other debates on data sources from other 'disappearing' manuscripts in this area. I might also add that by focusing in on various diagnoses but not autism (which again, they could have done) and not a certain vaccine, the authors seem well aware of the history in this area - "the association of the measles, mumps, and rubella vaccine with autism spectrum disorder has been convincingly disproven" - and probably either thought nothing more of it or chose to steer well clear of it (or perhaps a combination of both).Is there a 'where next' when it comes to the Leslie data? To quote again from the paper: "findings require replication in a larger population-based sample, possibly including assessments of various potentially important host factors, e.g., the individual’s ... Read more »

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