The power assumption : Do we really want to be the alpha males?

BPS research digest has just published some articles and one of the article that seemed to catch attention was related to pursuit of power. As per this, game theoretical experiments have demonstrated that, if given a choice, we would like to have more power over ourselves and our behaviors, than over others behaviors. This seems to be a groundbreaking study, that posits that in the dimension of power we are more motivated by being masters of ourselves than being an alpha male and dictating terms for others.

In other words, they believe we're driven to increase our 'personal power' over
ourselves, but not necessarily our 'social power' over others.

In another post on BPS related to the brain centers engaged during eyes closed and eyes open situation in a dark room, it is posited that in the dark room condition, eyes open leads to an 'exteroceptive' state characterized by attention and oculomotor activity while eyes closed corresponds to an an 'interoceptive' state characterized by imagination and multi sensory activity. Here it is claimed that in eyes closed scenario, imagination and corresponding sensory activation are utilized. This seems to be counterintuitive, as in a dark room, with eyes open, we should be paying more attention to any threatening stimuli- why this does not lead to greater sensory acuity in visual/auditory senses needs explanation. In the eyes open, one could hopefully relax and indulge in night-dreaming.

What would be the brain activations in the closed eye and open eye conditions in a brightly lit room? Would that mean that different systems kick in, not only during eyes open and closed conditions, but also in night/day conditions?

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Down in the dumps: time to pop the sleeping pill?

A recent article on depression, in the latest issue of open-access medical journal PLoS Medicine, seems to suggest that the current disease-based model of depression should be replaced by a drug-based model and to treat particular symptoms like sleep deprivation it may be better to administer sedatives like benzodiazepine.

Taking a drug-centred approach to the treatment of depression, we would conclude that no presently known effects of any drugs, including antidepressants, are likely to do more good than harm in the long term. In the short term, sedative effects of drugs may help people who are acutely anxious, highly aroused, or have difficulty sleeping. The common practice of prescribing short-term, low-dose sedative TCAs, for which general practitioners have frequently been criticised, may therefore be a rational one. Similarly, short-term benzodiazepine prescribing may occasionally be justified, bearing in mind the problem of dependency.

To me this seems to be an overkill and a case of throwing the baby with the bath-tub.

While the premise that SSRI's are not the panacea-for-depression-and-are-not-god-sent-for-the-specific-purpose-of-treating-depression is attractive, the alternative pitted against this that Depression is not a 'disease' and is not 'biological' in nature is hardly tenable.

There have been studies linking the hereditary aspects of depression (and more so of psychotic diseases like Schizophrenia), both based on twin studies and clustering amongst relatives (or running in families). Genetic studies are on-going to identify the underlying genes or 'diathesis' and just like Diathesis-stress model of Schizophrenia, a similar model is proposed for Depression.

Moreover, research is now focused on identifying endophenotypes of depression like sleep-disturbance and linking it to genes/ environmental stressors.

In the PLoS medicine article, many of the arguments are specious and I will try to address them.

1. Monoamine hypothesis.

Independent evidence has not confirmed that there is a monoamine abnormality in depression. For example, the findings of brain imaging studies of serotonin abnormality are contradictory. Some found reduced serotonin 1A receptor binding in drug-free patients who were depressed, consistent with the hypothesis that selective serotonin reuptake inhibitors (SSRIs) improve depression by correcting a deficiency of serotonin activity [4,5]. Other studies, however, have found no difference between patients who are drug-free and controls [6,7] or increased binding potential in depressed patients [7,8]. Postmortem findings of receptor changes in the brains of people who committed suicide have also been inconsistent [9–11]. In some studies, with patients who had recovered from depression, a tryptophan depletion challenge led to a transient increase in depressive symptoms. However, these results have not been confirmed in volunteer studies [12], and the effect appears to be dependent on previous SSRI use [13].

Granted that studies are still inconclusive about how exactly the SSRIs work and whether other neurotransmitters/neuromodulators apart from sertonin are also involved, but it is instructive to note that neurotransmitters/modulators may work differently in different brain regions and may have paradoxical activation profiles in different regions. While Schizophrenia is generally thought to be due to over-activity of Dopamine and Prakinsonism due to under-activity, more informed experts know that in both there is not global excess / deficiency but it is localized in one region (say increase in the reward circuit, while decreasee in some other region) . Thus, the global deficiency-of-sertoninn hypothesis may be, and in my opinion is, wrong; yet the depressive symptoms and the 'disease' depression is a fairly clustered set of symptoms that have a biological origin and are either due to chemical imbalances or defective processing/ networking of brain channels.

There are many compelling theories of depression including an evolutionary one based on 'social-negotiation-hypothesis' or a cognitive one based on 'learned helplessness' and may include diverse mechanisms like invocation of an evolutionary-no-more-relevant-module-and-corresponding-mechanisms/adaptations-that-were-once-suitable, to changing-cognitive-schema-based-on-some-past-failures-and-now-no-more-exploring-to-find-if-the-schema-is-still-relevant mechanisms.

But all explanations will ultimately rely on biology for manifesting into stable symptom clusters. And this may be mediated by changes in the opponent-process mechanism of some emotions or motivational activities like exploration/hunger or rest and relaxation set-points mediated in turn by gated inputs, where the gates may be in the form of neurotransmitter levels and activities. Refer to my earlier postings on opponent-process mecahnisms in relation to color vision.

2. Depression rating scales

These scales contain items that are not specific to depression, including sleeping difficulties, anxiety, agitation, and somatic complaints. These symptoms are likely to respond to the nonspecific sedative effects that occur with most tricyclic antidepressants (TCAs) and some other antidepressants. Hence, changes in rating scale scores may merely reflect drug-induced effects

Sleep difficulties/ somatic complains may not be specific to depression in the sense that they may manifest in situations that are not necessarily due to clinical depression; but that does not prove that they are not relevant as salient depression symptoms. If a drug reduces scores on these dimensions it is definitely helping to relive the symptoms of depression.

3. Animal models of depression

These models, which usually involve biochemical orbehaviorall processes thought to mimic aspects of depression in humans, do not select antidepressants reliably but produce numerous “false positives” with other drugs, including stimulants, opiates, and neuroleptics. They also produce some “false negatives” with supposed antidepressant drugs [15].

Animal models of any human psychological condition is still an oxymoron as animals cannot exhibit the complex psychological mechanisms and symptoms that humans can. "Depressed" mouse may just be some mouse with Sertonin related genes knocked out. These mya be good to study the particular endophenotype like effect of sertonin-on-sleep-cycle, but not to totality of depressive symptoms.

4. Antidepressants versus other drugs

Many drugs not normally considered to be antidepressants show comparable effects to antidepressants when given to patients who are depressed in some randomised controlled trials (RCTs) [1,16]. These include benzodiazepines [17], opiates [18], buspirone [19], stimulants [20], reserpine, and other antipsychotics [21].

This may question the crowning of SSRIs as depressants but have nothing to say about depression being disease-based or drug based.

5. Healthy volunteer studies

The fact that antidepressants do not appear to elevate mood in healthy volunteers [22–26] might suggest that they have a disease-specific action. However, because of the nature of depression rating scales (as explained above), it is unclear that antidepressants specifically affect mood in patients who are depressed. Any effect they have over and above placebo may also be attributable to an “amplified” placebo response (see below). Although there are some reports of improved sleep in patients with depression who are given SSRIs versus volunteers' reports of decreased sleep when given SSRIs [27], in general, side effects in patient studies are consistent with effects on volunteers. For example, TCAs show sedation and cognitive impairment [28,29], while SSRIs show gastrointestinal upset and drowsiness, both in patients and in healthy volunteers [22].

It is clear from above that SSRI's do have very specific effect on mood when depressed and the drug action on volunteers (lets leave the side-effects aside for a moment) is not the same -viz elevating mood or restoring sleep-cycles - as in the diseased persons. This fits well with opponent process and set-point hypothesis whereby if the underlying chemical is increased beyond normal levels it does not necessarily lead to increase in primary affect.

6. Outcome of depression

There is little evidence outside RCTs that the long- or short-term outcome of depression is changing as a consequence of antidepressant use. Recent sharp increases in antidepressant use have been accompanied by increased prevalence and duration of depressive episodes [30] and rising levels of sickness absence [31]. Naturalistic studies have also shown that depressive episodes are more frequent and last longer among antidepressant users than among nonusers [30] and that sickness absence is more prolonged [32], although severity is likely to explain some of this effect (i.e., it is likely that patients are on antidepressant drugs because they have more severe disease). Follow-up studies of people treated for depression indicate high levels of nonrecovery or relapse [33–35].

The argument is like that if you once recover from viral fever using an antibiotic and on same later day relapse to viral fever again, then the viral fever is not a biological disease. Granted that better methods like CBT/psychotherapy alongwith medication and changes to socio-environments (to reduce stressors) is required to prevent relapse, but relapse is hardly an argument against a 'disease' model.

Overall, the ideological rooting of the author in not treating depression/ mental illness as physical phenomenon has resulted in a research that is highly provocative and ignores many other accumulated literature. I too do not side with the Drug companies and am aware of their wrong tactics, but that should not be a reason to take extreme positions that are not viable.

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The importance of being Earnest

While many may concur with Shakespeare that 'what is called Rose would smell as sweet by any other name', yet some Cornell researchers have just published a finding whereby if Rose's substitute was not a 'typical' noun, then though it may smell the same, but would take longer to pronounce.

As per this study claiming association between the figure of speech and phonological composition of a word, verbs and nouns have different phonological properties and for atypical nouns and verbs, it takes longer to pronounce them or read them.


As this is a seed magazine article, I'm sure that this would be picked up by many other fellow Science bloggers. What the article does not mention is whether the results have been obtained for one language only (English) or are generalized. Also how does this relate to observations that one is able to find word boundaries in a speech which is from a foreign language?

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Eve's Lasting Legacy: The Serpent and The Apple

As per a recent scholarly article it seems that mammalian evolution may have been driven by the predatory presence of snakes. While some mammals adapted by becoming better snake sniffers, others developed immunities to serpent venom; while in the case of humans, the primates developed a good visual system to detect the snakes.

The other factor that drove human evolution (and hastened descent from the garden of eden after falling prey to serpent's designs :-) ) was the fact that anthropoid ate fruits (substitute apples :-) ) and this frugivorus eating habit endowed them with enough-glucose-availability-in-the-brain to act as a pre-adaptation necessary to the evolution of brain matter required for visual acuity needed to detect snakes and take appropriate action.

Fox news has an excellent article on the same which is a needed reading before one can try to appreciate the excellent coverage of the same done by John Hawks.

I'll try to summarize the arguments.

1. It is common knowledge that runaway arms-race between predators and preys lead to selective development of traits in a particular direction. For eg, the great cats and the antelopes, both developed systems for high speed chase and run-away and thus some of the fastest runners are either predators; like leopards or preys like the antelopes. What food (and energy one gets from it) also ensures who outnumbers whom in the arms race (the tiger wins!). The responses may not be symmetric, while Great Cats may develop claws and teethes, the antelope may develop antler ( though antler evolved more as species specific displays to attract opposite sex).

2. Snakes are one of the predatory species for mammals. Earlier snakes relied on Boa constriction method to kill the preys, but evolved venom about 60 mn years ago as their second weapon. Mammals reacted by either detecting them (in close range) by sniffing, or developing venom resistance etc.

3. Primates leading to Humans reacted by detecting motion (via MT and other motion detecting brain areas), color and other relevant visual stimuli to predict and detect the snake's presence at close ranges and take appropriate areas.

4. The increased encephalisation (dependent on processing of more visual stimulus and reacting to it) was dependent on a previous adaptation related to fruit eating and abundant availability of glucose in brain.

5. The features of human vision like orbital convergence (leading to depth perception and 3D vision) are tuned for such snake -detection mechanisms.

6. The koniocellular pathway is crucially involved (among other tasks) in pre-attentional visual detection of fearful stimuli, including snakes and the evolution of this system points to snake-primate arms race pressures and how the primates adapted.

7. The Parvocellular pathway is also implicated in the study (as details and color are important for snake detection). Although the magnocellular is not , but I believe movement is also very crucial as snakes have a typical motion.

Lastly, while the analogy of the snake and the apple is quite relevant in the Christian mythology context, the snake is a revered creature in many mythologies (dragon in Chinese for example) and we in India celebrated Naag Panchami - a day when snakes are fed milk- a couple of days back.

Some parting notes:

1. In experiments with monkeys and humans it has become apparent that we have specialized fear associations for snakes. For example a young monkey, which sees another monkey as reacting in a frightened manner to say a plastic snake, would by even a singular exposure to such a display of fear, clear to have fearful associations with say the plastic snake. This association can be even when the observed behavior is seen on TV (and is recorded and not happening in real-time) Like the disgust reactions and avoidance-of-just-before-taken-food in response to a single vomit, it seems the avoidance learning for snakes is also built-in and can be triggered even by one exposure and by observational learning. Thus, there is strong evidence that we have specialized circuits for responding to snakes. It makes merit to assume that we should have for detecting too.

2. In Indian philosophy, one perennial question, focused on differentiating reality from illusion is differentiating snake for the rope. the rope in dark gives illusion of a snake, but we need to enhance our perceptions and awareness to realize that the fear of the snake is illusory and that the feared object is only a rope. This example, which is in ancient texts, is evidence of the importance of snake detection from prehistoric times.

Endgame: Can one identify from which book this drawing of boa constrictor and elephant is inspired?

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The Cognitive Neuroscience Arena

I recently came across the Cognitive Neuroscience Arena . The Cognitive Neuroscience Arena provides researchers, instructors and students in Cognitive Neuroscience with information on the range of journals and books produced by Psychology Press and Routledge.

I am sure this would prove to be of great service to the CogSci enthusiasts. I, myself, have been avid readers of Routledge classics (Psychology section) like Man for Himself, A sketch for a theory of emotions, Totem and Taboo etc. and in the new titles listed there I could find some to add to my wish list ( like Environment Perception and Cognitive Maps ).

The site also has introductory lectures on Cognitive and Social Neuroscience, so should be a good guide for the newbies to the field.

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Encephalon #3 is online now!

Thinking Meat has just published a brand new edition of Encephalon, the Encephalon #3.

One of the postings, from the neurophilosopher, is a review of Eric Kandel's book-cum-autobiography. In the review , the neurophilosopher draws an analogy with Steven Rose's book Making Memory. I have that book by Rose and had started reading it sometime back, so can appreciate how deftly some people can mix personal memory with the supposedly-dry-academic memory research. If I manage to read Rose's book sometime soon, expect a review here.

Neurotopia has an article on ALS. I was introduced to ALS as part of reading "Tuesdays with Morrie". It is interesting to note that microglia play an important part on prognosis and the study helps differentiate between onset and progression.

Talking of diseases, Neurocritic has a post in which about spindle neurons, which seem to be implicated to greater degree in Alzhiemer's and to a slightly lesser degree in Autism. What is interesting is that they are mostly found in ACC (anterior cingulate cortex) and are exclusive to humans. Thus focus on them, Neurocrtic suggests may be of much better use, then on Mirror Neurons. There are some posts about mirror neurons too as part of the carnival.

There is a post by Developing Intelligence, regarding noise and information theory, which seemed to go over my head in first go. Will have to read the original articles more keenly to make more sense.

Finally, there are other posts like Binaulral beats or how robots can get a Theory of Mind or atleast a 'shared world'.

And of course, there are articles from this blog - mostly on Color vision.

More cool stuff there. Have a nice read.

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IQ variations across time and space : the why and wherefore?

Mind Hacks has two posts on IQ: one focusing on IQ variants across time and discussing Flynn effect and the other focusing on variation across space (different population groups!) and discussing variation in IQ of identical and fraternal twins and taking help of adoption studies with special focus on economic background of biological and adopted parents.

I'll discuss the second posting first which is based on this NYT article.

This article mentions a few observations based on meta analysis of data related to twin studies and also a study of adopted children -raised either in environments (adopted homes) that are of same socio-economic status as that of their biological parents or in different socio-economic environments.

Some of these observations are (first six are from adoption studies and the seventh is from twin studies. :

1. Children of well-off biological parents reared by poor/well -off adopted parents have Average IQ about 16 point higher than children of poor biological parents
2. Children of well-off biological parents reared by well-off adopted parents had average IQ scores of 119.6
3. Children of well-off biological parents reared by poor adopted parents had average IQ scores of 107.5 - 12 points lower
4. Children of poor biological parents reared by well-off adopted parents had average IQ scores of 103.6
5. Children of poor biological parents reared by well-off adopted parents had average IQ scores of 92.4
6. In another study, the average I.Q. scores of youngsters (from an orphanage at ages 4-6)placed in well-to-do homes climbed more than 20 points, to 98 - a jump from borderline retardation to a whisker below average , when measured after 9 years of placement in the well-off home. That is a huge difference - a person with an I.Q. of couldn't explain the rules of baseball, while an individual with a 98 I.Q. could actually manage a baseball team - and it can only be explained by pointing to variations in family circumstances.
7. In a meta-analysis, it was found, that among the poorest families , for those twins raised in the poor families, the I.Q.'s of identical twins vary just as much as the I.Q's of fraternal twins; while in rich families the IQ's of Identical twins are more identical than is the case for the IQ differences in fraternal twins.

First let us discuss the Twin studies (observation 7). If some trait A is found to co-occur say 80% of the times in identical twins (which have identical genotype) that are raised apart and if the same trait A is only found to vary 40 % of the times in fraternal twins (that have only 50 % of genes in common) that are raised apart; then one can conclude that this trait A is highly heritable and genetics dependent, with environmental influence limited to say affecting only say 20 % variation in the trait.

The premise is that if it is conclusively proved that if two organisms (identical twins) which contain more similar genes (double the number in comparison to fraternal twins) than a control pair of organisms (the fraternal twins); and effect of environment is subtracted (by letting the two organisms live in dissimilar environments - one adopted, while the other in biological home atmosphere); and if it is found that some trait A is found to concur more in these organisms (identical twins) compared to the control pair (the fraternal twins), then that trait must have a genetic component and is heavily influenced by genetic factors as opposed to environmental factors. So far so good.

In the normal twin studies, the adopted twin generally belongs to the same socio-economic status as the one reared by the biological parents.

The normal observation that identical twins belonging to well-off/middle class families have IQ rates similar as compared to fraternal twins, thus indicates that for children from well-off background (biological/adopted), the IQ (observed phenotype) is mostly due to genetic factors (underlying genotype) and environmental factors are not a big determinant.

The paradoxical observation that identical twins belonging to poor families have IQ rates as varying as compared to fraternal twins, should indicate that for children from poor background (biological/adopted), the IQ (observed phenotype) is mostly due to environmental factors and genetic factors (the underlying genotype ) are not a big determinant.

How do we conciliate the two observations. The paradox becomes a non-issue when one shifts focus from either-or thinking in terms of gene-environment influences and moves towards an interactionist view point viz. Nature via nurture as outlined by Matt Riddley amongst others and using genotype-phenotype distinctions. As per this viewpoint, any genotype is a potentiality and only if proper environmental factors are available can it lead to the desired (adaptive) phenotype. In absence of the required environmental factors, the genotype may not lead to the phenotype or may lead to sub-optimal phenotype expression. In a typical example, a fish may not show the color that the genotype codes for, if the environment under which it is developing provides little incentive to exhibit that color for reproductive/survival fitness. In less dramatic example, one may have genotype for having a more than average height, but if proper nutrition during a critical phase of development is not provided, then that height may not be exhibited.

Returning back to our discussion, it is apparent that IQ , though highly heritable ( and being genotype based), remains as a potentiality and only if environmental factors ranging from nutrition to socio-economic factors resulting in environmental influences like number of words exposed during childhood, results in appropriate IQ scores and intelligence (observed phenotype) only when such environmental influences as measured by socio-economic atmosphere during childhood are present during critical stages of development. Thus, while children of and raised by well-off parents could have a high correlation between genotype and phenotype ( and thus show high correlation in IQ across identical twins vis-a-vis fraternal twins), the same would not be true for children of poor parents where environmental factors will limit the observed IQ scores ) and thus, though the genotype of identical twins is similar than fraternal in this case too, the variation would be greater as the genetic influence has been subdued by environmental (negative) influence.

Now to explain the first observation, viz. that children of biological parents have average IQ higher than children of poor/working parents can be explained by the fact, that as a group, the well-off parents would have higher IQ than poor/working parents- as intelligence would be one of the major factors predicting who would be well-off and who would be poor in a fair world. Thus, it is no surprise that their children, would also have higher intelligence as compared to poor children- as the rich parent's child would on an average get better IQ genes than a poor children would get from its poor (and less IQ) parent.

The observations 2 and 3 taken together corroborate the fact that IQ flowers only under the right environment. When 2 child start with similar average IQ potentialities (as they are from well-off parents), they nevertheless end with different final exhibition of intelligence (as measured by IQ scores) based on the limiting influence of environment on the genes.

The observations 4 and 5 taken together yield to similar interpretations.

The observation 6 is a stark example of how providing a proper environment can lead to drastic improvements in the exhibited phenotype and lead to the phenotype attaining the maximum potentiality present in its genotype.

It is clear that affirmative action is needed to ensure that environmental influences do not lead to sub-optimal flowering of intelligence. These affirmative actions should be based on reducing poverty and focused on that alone. Other options like Mandal commission reservation of jobs (after the child has already got a sub-optimal IQ due to early socio-economic environment) are clearly counter-productive and unfair. Poverty is the only evil to be tackled.

Returning to the first post on Mind Hacks related to Flynn effect,based on this American Scientist article. To me, it seems apparent, that biological evolution is very slow in comparison to social and environmental evolution that we humans have managed to achieve. I believe that based on our current genotypes for intelligence, we have achieved a plateau in terms of providing the maximal socio-economic environmental conditions necessary for full flowering of intelligence. Thus, we seem to be reaching a plateau in terms of increases in IQ score from one generation to the other. The Flynn Effect, in my opinion, was not a change in genotype, but in exhibited phenotypes, due to availability of proper environmental conditions.

For IQ to change within generations due to underlying change in genotype is assuming heavy and continuous selection pressure on those genes responsible for IQ. I believe that IQ (and intelligence) would keep on improving, as it may be part of runaway selection due to other-sex mate preference (reproductive advantage) - like that of evolution of beauty - or peacock's tail - or it may keep evolving as intelligence does confer survival advantage too, but such increases would not be as dramatically observable as the Flynn effect.

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Mirror, mirror on the wall, who's the most blogged of them all!

Mirror Neurons seems to be the answer as per the Neurotopia's post encouraging all bloggers to come together and raise a toast for the mirror neurons (though Neurotopia's article is more of a critical tone lamenting the fact that mirror neurons get so much attention in the blogosphere) !

Small Grey Matters too has taken the gauntlet and responded to some of the concerns raised by Mixing Memory regarding Mirror neuron research and attention. The defense is mostly on procedural concerns and does not tackle the defense of the more 'speculative' research in the filed for eg. related to language evolution.

Frontal Cortex speculates on the importance of mirror neurons in areas as diverse as sports, autism and movies.

It is interesting to observe that the debate on how much focus mirror neurons are getting has come full circle. My first, and I believe the most authoritative , encounter with the reason for focusing on Mirror Neurons was due to this Edge lecture by V S Ramachandran in which he laments the fact that mirror neurons is one of the most underrated discovery of our times (it was 1995 then). This Edge discussion is a must read for anyone interested in the topic.

I will discuss the mirror neurons in some detail in a later post, but what I encourage is that some edition of an online carnival like Encephalon or Synapse be focused on Mirror Neuron related contributions, so that one can clear the aura surrounding the matter for once and for all.

Before I part a few observations.

Neurotopia has a figure of a Brain Scan that shows that pars opercularis is activated differently in controls and autistic people indulging in imitation behavior. It is instructive to note that pars opercularis (along with ACC) has elsewhere been implicated in executive tasks like set-shifting tasks . This set shifting may be involved in going from concrete to abstract sets for a problem or from human to non-human set shift -this set-shifting would occur in normals and would not occur in autistics as autistics treat humans and non-humans alike.

Also, it is instructive to note, that by their very nature, mirror neurons have a strong role to play in empathy and social evolution as well as the observational learning that Albert Bandura proposed.

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