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Well can you calculate it for even one thing?

Sure, it's not very expensive to capture CO2: $94 to $232 per ton CO2 from the atmosphere The question is what to do with it afterward but I'm sure there are good uses.

So that price is just added to the cost of everything depending on how much CO2 it takes to produce? A carbon tax?

No I mean specifically on this issue?

Why are you asking me what you mean?

You said: "Everything in my power to ensure better environmental policies are put in place."

I'm asking what specifically that entails.

Well can you calculate it for even one thing?

Sure, it's not very expensive to capture CO2: $94 to $232 per ton CO2 from the atmosphere
The question is what to do with it afterward but I'm sure there are good uses.

No I mean specifically on this issue?

Why are you asking me what you mean?

Plastic is toxic. Always has been.

The problem with that statement is that what's considered a plastic is chemical diverse. We do know some plastics do not have the kind of negative heath effects that BPA has because they are far more chemically stable. If you read the actual study, you'll see this is only in relation to "structurally similar bisphenols", not plastics in general.

The real problem we have here is that companies have been allowed to use any old molecular structure in their products they wish without proving anything about the health impacts it may or may not impart.

Speaking of diverse, one of the early plastics was made of casein, from cow milk. https://www.scientificamerican... Milk and vinegar will do it.

Plastic is toxic. Always has been.

The problem with that statement is that what's considered a plastic is chemical diverse. We do know some plastics do not have the kind of negative heath effects that BPA has because they are far more chemically stable. If you read the actual study, you'll see this is only in relation to "structurally similar bisphenols", not plastics in general.

The real problem we have here is that companies have been allowed to use any old molecular structure in their products they wish without proving anything about the health impacts it may or may not impart.

Also note that the study did not use kimchi or anything like that, quoting https://www.cell.com/cell/fulltext/S0092-8674(18)31102-4:

During the probiotics phase participants consumed Supherb Bio-25 bi-daily

I have a lecture I give every now and then to various public audiences on tissue engineering (I'm faculty at the University of Calgary). On one of the first slides I show a picture of Dolly the sheep, and also some mice from Wakayama et al, Cell Stem Cell 12(3): 293-297 (2013) (TLDR: they cloned a mouse, then cloned that mouse, etc - 25 generations at time of publication, of which the first 16 had aged through their normal lifespans by that time with no detectable abnormalities).

Lots of interesting things come out of that work, but the key one for this discussion is that a single cell, from an animal that may be old, or sick, or injured, contains the information necessary to recreate the entire body of that organism when it was young, healthy and whole. There's the proof-of-concept - now we just have to figure out how to implement (which won't be trivial).

Hassabis believes that sensory learning in the cortex is supervised and based on backpropagation. Not even wrong. Is this the man who is going to solve AGI?

From his recent Cell paper, Neuroscience-Inspired Artificial Intelligence:

A different class of local learning rule has been shown to allow hierarchical supervised networks to generate high-level invariances characteristic of biological systems, including mirror-symmetric tuning to physically symmetric stimuli, such as faces (Leibo et al., 2017). Taken together, recent AI research offers the promise of discovering mechanisms by which the brain may implement algorithms with the functionality of backpropagation. Moreover, these developments illustrate the potential for synergistic interactions between AI and neuroscience: research aimed to develop biologically plausible forms of backpropagation have also been motivated by the search for alternative learning algorithms.

What?

Either further tests by researchers will prove that the perceived effect was a mistake or due to something besides the blood itself,

In short :
- Blood tranfusion from blood banks is really only red blood cells. And almost nothing more.
- Hooking two mices together, is way much more than that.

Out of the top of my head:
- Means that the old mouse's blood is processed by the organs of the younger one :
kidneys, liver - organs which are in charge of eliminating/chemically processing toxins.

- There's more that simply red cells that the old mouse is getting from the young one :
platelets, white blood cells and antibodies (ie.: imune system),
hormones and growth factors (the original study mentions quite a few of them),
etc.

Oh, and - mentionned in TFA :
these results haven't been replicated successfully yet.

Disclaimer: I*A*AMD, I just don't dabble into casual vampirism.

2015 - A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan
http://www.cell.com/cell-metab...

2016 - Fasting: Awakening the Rejuvenation from Within | Valter Longo | TEDxEchoPark
https://www.youtube.com/watch?...

2017 - Fasting-Mimicking Diet Promotes Ngn3-Driven -Cell Regeneration to Reverse Diabetes
http://www.cell.com/cell/fullt...

You can replicate the study at home with 4 days of a ketogenic fasting mimic diet every 10 days for six cycles with a %5 carb ( 20 net carbs of nuts/greens/dairy) / %75 fat (nuts/olives/fish/eggs/butter) / %20 protein (nuts/fish/eggs/greens/bacon) macro and 50% then 20% , 20% , 20% calorie restriction (the 3 day 10% restriction of the study on mice was extreme and not for the faint of heart). Throw in multi vitamin and probiotic day 3 and 4 and lots and lots of water with pinch of salt now and then/mineral water/coffee/tea during the fast and... amazing. You lose fat, feel better, and if the studies are right; get some nice anti-cancer, anti-aging, anti-disease, body regeneration benefits.

2015 - A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan
http://www.cell.com/cell-metab...

2016 - Fasting: Awakening the Rejuvenation from Within | Valter Longo | TEDxEchoPark
https://www.youtube.com/watch?...

2017 - Fasting-Mimicking Diet Promotes Ngn3-Driven -Cell Regeneration to Reverse Diabetes
http://www.cell.com/cell/fullt...

You can replicate the study at home with 4 days of a ketogenic fasting mimic diet every 10 days for six cycles with a %5 carb ( 20 net carbs of nuts/greens/dairy) / %75 fat (nuts/olives/fish/eggs/butter) / %20 protein (nuts/fish/eggs/greens/bacon) macro and 50% then 20% , 20% , 20% calorie restriction (the 3 day 10% restriction of the study on mice was extreme and not for the faint of heart). Throw in multi vitamin and probiotic day 3 and 4 and lots and lots of water with pinch of salt now and then/mineral water/coffee/tea during the fast and... amazing. You lose fat, feel better, and if the studies are right; get some nice anti-cancer, anti-aging, anti-disease, body regeneration benefits.

First I want to express my empathy with your difficult situation.
Further beta-cell regeneration is only necessary in type 1 diabetes, which is covered in the article, although I feel also there is a suggestion that the damage to the beta-cells could be caused by the high levels of insuline that have to be produced from the time the insuline resistance kicks in in those mice.
The insulin resistance which type 2 sufferers suffer from, can be reversed by a 'not so very strict diet' for about 6 to 8 weeks only and without a very rigorous training, let alone for years.
I'd say try again, a little longer, and no guarantees promised.
(And yes, you're right, HFCS is pure shit.)

I mean: what does in benefit rather simple organisms to continue to pass along resistance to a spectrum of anti-biotic that their ancestors hadn't been exposed to in decades (and that's how many bacterial generations)? Isn't there a 'carrying capacity' or 'memory limit' to what can be added to their code that has to be slowly deprecated / de-prioritized just for physical space constraints? Asserting they have the Borg-like ability to perfectly add to their defenses without end, sounds a bit too apocalyptic to me.

http://www.cell.com/abstract/S0092-8674(08)01391-3

Basically, when a new resistance mutation first appears, there is an accessory cost to having the trait. This cost is due to some interaction/incompatibility between the resistance trait and other aspects of the cells' biology. Even with these costs, the resistance gene trait still spreads because it results in a net improvement under the selection stress of antibiotic use. If the antibiotic stress goes away in the short term, the accessory costs rise to the forefront and any lineages with the resistance trait will be selected against (resulting in loss of resistance in the population). If the antibiotic stress is maintained over time, additional mutations occur and/or are collected that minimize these accessory costs. These additional mutations eventually negate the accessory costs to having the resistance. Now when antibiotic use is ceased, the bacteria will retain the resistance for the long term because there is no selection force against it. Only genetic drift would result in breakdown of this resistance, but this process takes far longer than selection-driven evolution

The time frame between the start of use of an antibiotic and when it becomes persistent due to the reduction in accessory costs is a complete unknown. Evolution is a bitch. We need to be continuously researching antibiotics if we want to stay ahead of her.

Mitosomes in Giardia, Entamoeba, and Microsporidia represent the most extreme cases of mitochondrial reduction known to date, and yet they still contain recognizable mitochondrial protein translocases and usually an ISC system. The specific absence of all these mitochondrial proteins in the genome of Monocercomonoides sp. indicates that this eukaryote has dispensed with the mitochondrial compartment completely.

Sorry, but the length guide is *not* sufficient.

While it's more specific than sequence homology predicts, it's less specific than the laser focus it's portrayed as having.

I understand the need to portray it as being as close to perfect as possible to preserve funding (and the research *should* be funded!), right now, the best method we have of ensuring that off-target mutations do not occur is via post-sequencing.

See these papers regarding "Dammit, I missed!":

New Sequencing Methods Reveal Off-Target Effects of CRISPR/Cas9
https://www.genomeweb.com/sequ...

Unbiased detection of off-target cleavage by CRISPR-Cas9 and TALENs using integrase-defective lentiviral vectors
http://www.nature.com/nbt/jour...

Analysis of off-target effects of CRISPR/Cas-derived RNA-guided endonucleases and nickases
http://www.ncbi.nlm.nih.gov/pm...

CRISPR-Cas9 Specificity: Taming Off-target Mutagenesis
http://www.genecopoeia.com/res...

Digenome-seq: genome-wide profiling of CRISPR-Cas9 off-target effects in human cells
http://www.nature.com/nmeth/jo...

Quantifying on- and off-target genome editing
http://www.cell.com/trends/bio...

CRISPR/Cas9 Guide
https://www.addgene.org/CRISPR...
Salient quote: "The randomness of NHEJ-mediated DSB repair has important practical implications, because a population of cells expressing Cas9 and a gRNA will result in a diverse array of mutations (for more information, jump to Plan Your Experiment). In most cases, NHEJ gives rise to small InDels in the target DNA which result in in-frame amino acid deletions, insertions, or frameshift mutations leading to premature stop codons within the open reading frame (ORF) of the targeted gene. Ideally, the end result is a loss-of-function mutation within the targeted gene; however, the “strength” of the knock-out phenotype for a given mutant cell is ultimately determined by the amount of residual gene function."

P.S.: And you know as well as I do that the 'P' in "CRISPR" stands for "Palindromic".

Recognizing that a particular genome contains sequences related to heart disease or lung cancer in no way makes it identifiable or linked to a particular person.

It's the other way around. Here you already know the identity of the person and their genome sequence, and are trying to work out if that genome is present in a database of genomes devoted to, say, heart disease, implying that this person (or perhaps a family member) has the condition. Although the 'beacon' databases that the attack targets release only small pieces of anonymous data, the results of multiple queries can be combined to figure out if the database contains the genome of interest.

This is just another scare mongering story, probably clickbait ... nothing to see here, please move along.

Judge for yourself - here's the original paper:

http://www.cell.com/ajhg/fullt...

They are taking naps 7% of days in the winter (i.e. about every 14 days) and 22% in the summer (about every 4-5 days).

Which they have measured by the fact that the wrist bracelet wasn't moving for periods longer than 15 minutes.
On 94 people, across 2 continents and 3 countries, in groups of 5 to 15 people.

But regardless of those sketchy definitions and methodology the point is that they are actually reporting 1.2 - 1.4 longer daily sleep periods than those listed in summary and the npr article.
That's a lot of time being motionless on a kudu or an impala skin on the floor of the hut for someone not sleeping.
They are sleeping much closer to 6.9 - 8.5 hours - NOT just 5.7 - 7.1.

And then there's the crappy measurement tool they are using.

This study that Philips lists as the proof of actigraphy units being "a gold standard" shows moderate correlations at best (but mostly weak to moderate) with more accurate methods of measurement - if you measure sleeping patterns of patients suffering from depression and insomnia.
http://onlinelibrary.wiley.com...

This one on the other hand, cited by the study in question shows a MUCH HIGHER correlation between actigraphy and PSG.
http://www.ncbi.nlm.nih.gov/pu...
A sensitivity (both methods showing sleep at the same time) with a 0.965 correlation and accuracy (total proportion correct) with a 0.863 correlation, while specificity (both methods showing awake at the same time) being rather weak at a mere 0.329.

Still, pretty good results - if you are fine with p values of 0.363, 0.389 and 0.195 for sensitivity, accuracy and specificity, respectfully.
I.e. More than 1 in 3 chance of false positives. About 1 in 5 for being awake.

Which is why sleep time measurements in the hunter-gatherer study, which they average out to 6.4, have deviations as high as +/- 1.39 hours.
On average, that 6.4 hour average of theirs has a 0.87 hour deviation.
So, while that particular 5.9 hour measurement (one with deviation of 1.39 hours) varies from 4.51 - 7.29 hours, many others go as high as 7.5 hours.
Which is pretty damn close to the 6.9 - 8.5 average of 7.7.
Adding their sleep and wake onsets to that - and it's about 8 hours.

I.e. They are interpreting readings from an inaccurate tool, with a known overestimation bias as an overestimation EVEN WHEN IT IS NOT ONE - due to high rate of false positive built-in into the tool.
Those people are lying motionless on the skin of an impala, on the floor of the hut (during the rain season - otherwise in open air), with things buzzing, flying and crawling around...
And the algorithm is telling them "No, no... an insomniac in a bed in North Carolina would not be asleep yet."

Better treatments are possible but all of the funding and hype on finding a cure is holding them back.

This is bullshit.

I think the major reason that the CFF is ignoring treatments is that any treatment which does not result in a cure is, by definition, an ongoing revenue stream for big pharma, and therefore big pharma has that angle covered: if they come up with a treatment that works, they have a customer for the rest of that customers life. And there is no incentive for big pharma to then work on a cure.

In fact, if you were to come up with a cure for something which represented a huge existing revenue stream, you would likely have an "accident" before you were published.

In terms of CF itself, the current state of things is that researchers have demonstrated CRISPR/Cas9-mediated repair of the CFTR locus in human intestinal stem cells -- which means, were they reimplanted in the donor, they would replicate and replace the defective intestinal cells over time.

If the technique can be successfully used in vivo (we have so far been reluctant to use CRISPR/Cas9-mediated modifcation on living humans, since it can impact germ line cells), then it represents a cure. See also:

http://www.cell.com/cell-stem-...

The full paper itself is downloadable, without charge, from that location.

As to the major question of why concentrate on a cure ... so that your children and grandchildren don't inherit the disease, of course.

Ask any police officer or health care provider how people act during the full moon. They will almost always tell you that they are busier and people are crazier around that time of the month - consistently - although they can't quite explain why.

Confirmation bias. I've heard the same thing from nurses, but the fact is, no correlation has been found.

There have been studies showing it messes with a good nights sleep. Your own link even admits that, Lack of sleep does tend to make people a little crazier.

Injection of a solution of the JQ1 molecule to bind to a pocket of BRDT necessary for chromatin remodeling, which gives the proteins that regulate how genes act access to the genetic material.

Citation: Matzuk, Martin M.; McKeown, Michael R.; Filippakopoulos, Panagis; Li, Qinglei; Ma, Lang; Agno, Julio E.; Lemieux, Madeleine E.; Picaud, Sarah; Yu, Richard N.; Qi, Jun; Knapp, Stefan; Bradner, James E. (2012-08-17). "Small-Molecule Inhibition of BRDT for Male Contraception". Cell 150 (4): 673–684.

doi:10.1016/j.cell.2012.06.045

PMC 3420011 PMID 22901802.

Injection of a solution of the JQ1 molecule to bind to a pocket of BRDT necessary for chromatin remodeling, which gives the proteins that regulate how genes act access to the genetic material.

Citation: Matzuk, Martin M.; McKeown, Michael R.; Filippakopoulos, Panagis; Li, Qinglei; Ma, Lang; Agno, Julio E.; Lemieux, Madeleine E.; Picaud, Sarah; Yu, Richard N.; Qi, Jun; Knapp, Stefan; Bradner, James E. (2012-08-17). "Small-Molecule Inhibition of BRDT for Male Contraception". Cell 150 (4): 673–684.

doi:10.1016/j.cell.2012.06.045

PMC 3420011 PMID 22901802.

The referenced UK survey showed that families with engineers in them can have between 2.5 to 8.6 *times* the statistical occurrence of autism in their children.

Just in case anyone reading your message jumps to the wrong conclusion, I'll remind everyone that correlation != causation, even in this case.

There is, however, growing evidence that microexons -- tiny gene fragments that aren't well understood -- that are linked to altered brain development in individuals with autism (paper).

And (IIRC) there is a certain amount of correlation between problems with microexons and older fathers. Due to the cost and length of their education, engineers may not be having children until they are older (and perhaps more established in their careers), increasing the risk factor (it has been well established that older fathers are more likely to sire autistic children).

I'm not accusing you of having much such an assumption. The correlation is interesting and needs further investigation, however it may just stems from age of fathers, rather than any special mental makeup of engineers.

Yaz

Somebody is selling snake oil again. Testosterone may have subjectively beneficial short-term effects (virility, muscle tone, etc), but all current evidence is that it shortens your lifespan.

Studies of eunuchs have shown that they live substantially longer than non-castrated men. That's just one link; anyone with a bit of Google-fu will find others. For example, higher levels of testosterone are thought to be a reason that men have shorter lifespans than women.

Memories are, indeed, tagged with an importance value — the value is represented in the brain as a feeling/emotion. This modulates the strength of the long term encoding of the memory. But unimportant memories don't get "cycled out" as you say. Memories are not stored independently of each other and room for new ones recovered by some mechanism that frees up storage space. Forgetting is caused by a combination of interference from the storage of new memories and decay (two processes proposed independently but with evidence for both). This very much makes sense when considering that memories are stored through synaptic plasticity in the same neural network, which, upon triggering by the right stimulus for recall, recreates an activation pattern in other parts of the brain, including the consciously accessible image-making ones (one proposal for how the latter is accomplished, with some neurological evidence for it, is http://www.cell.com/trends/neu... ).

You might find the information that you seek in their supplemental experimental procedures.

Supplemental experimental procedures

They presented a wide array of disgusting / threatening images, listed as such:

1) Disgusting:

Snakes, Roaches, FliesOnPie, RoachOnPizza, Needle, Garbage, Dirty, Vomit, Dishes, Dog, Mutilation, Mutilation, Mutilation, Burn victim, Mutilation, Mutilation, Baby tumor, OpenChest, Injury, Sliced hand

2) Threatening:

Attack, Attack, Attack, Gang, Police, Plane Crash, Jet, Auto accident, Car accident, Auto accident, Snake, Dog, AngryFace, Tornado, AimedGun, Gang, AimedGun, Attack, Guns, Bomb

Oops http://www.cell.com/current-bi...

For everyone else who has that gene (I don't know if I do, I'm still trying to figure out what SNP KLOTHO references in my genetic results), and can't stand reading the Economist's painfully dumbed-down explanation of the research, here's the actual paper.

http://www.cell.com/current-bi...

Voice-Sensitive Regions in the Dog and Human Brain Are Revealed by Comparative fMRI

        Highlights
        This is the first comparative neuroimaging study of a nonprimate species and humans
        Functional analogies were found between dog and human nonprimary auditory cortex
        Voice areas preferring conspecific vocalizations were evidenced in the dog brain
        Brain sensitivity to vocal cues of emotional valence was found in both species

Summary

During the approximately 18–32 thousand years of domestication [1], dogs and humans have shared a similar social environment [2]. Dog and human vocalizations are thus familiar and relevant to both species [3], although they belong to evolutionarily distant taxa, as their lineages split approximately 90–100 million years ago [4]. In this first comparative neuroimaging study of a nonprimate and a primate species, we made use of this special combination of shared environment and evolutionary distance. We presented dogs and humans with the same set of vocal and nonvocal stimuli to search for functionally analogous voice-sensitive cortical regions. We demonstrate that voice areas exist in dogs and that they show a similar pattern to anterior temporal voice areas in humans. Our findings also reveal that sensitivity to vocal emotional valence cues engages similarly located nonprimary auditory regions in dogs and humans. Although parallel evolution cannot be excluded, our findings suggest that voice areas may have a more ancient evolutionary origin than previously known.

Standard policy. Nature have been doing this for some time. They state: authors are required to make materials, data and associated protocols promptly available to readers without undue qualifications. So have Cell Press and Science. I stopped searching at this point, but I'm sure other major journals do the same thing.

Even there, the open source nature is helpful. The same drug has stirred interest for multiple myeloma, heart failure, contraception, and HIV treatment (it is thought that it can activate latent HIV in the presence of anti-viral therapy to wipe out the reservoir). All 4 could share the phase I safety trial (and it's costs).

"A collaborator of Rienhoff is now engineering a mouse that shares Bea’s gene variant"
That sounds far beyond the capabilities of our current technology. How the heck would they do that?

Genome editing has gotten a lot better; here is a recent example, but I'm sure this isn't the only way to do it. Of course deliberately generating mutant mice is one thing; genetically manipulating live humans to make them healthy is much more difficult. (Hint: there's a lot of attrition in these mouse studies!)

http://www.wired.com/wiredscience/2013/01/dung-beetle-astronomy/

http://www.bbc.co.uk/news/science-environment-21150721

http://www.cell.com/current-biology/retrieve/pii/S0960982212015072

African dung beetles orient to the starry sky to move along straight paths The beetles do not orientate to the individual stars, but to the Milky Way Summary When the moon is absent from the night sky, stars remain as celestial visual cues. Nonetheless, only birds [1,2], seals [3], and humans [4] are known to use stars for orientation. African ball-rolling dung beetles exploit the sun, the moon, and the celestial polarization pattern to move along straight paths, away from the intense competition at the dung pile [5,6,7,8,9]. Even on clear moonless nights, many beetles still manage to orientate along straight paths [5]. This led us to hypothesize that dung beetles exploit the starry sky for orientation, a feat that has, to our knowledge, never been demonstrated in an insect. Here, we show that dung beetles transport their dung balls along straight paths under a starlit sky but lose this ability under overcast conditions. In a planetarium, the beetles orientate equally well when rolling under a full starlit sky as when only the Milky Way is present. The use of this bidirectional celestial cue for orientation has been proposed for vertebrates [10], spiders [11], and insects [5,12], but never proven. This finding represents the first convincing demonstration for the use of the starry sky for orientation in insects and provides the first documented use of the Milky Way for orientation in the animal kingdom.

http://www.cell.com/current-biology/retrieve/pii/S0960982212015072

http://www.wired.com/wiredscience/2013/01/dung-beetle-astronomy/

http://www.bbc.co.uk/news/science-environment-21150721

http://www.cell.com/current-biology/retrieve/pii/S0960982212015072

African dung beetles orient to the starry sky to move along straight paths The beetles do not orientate to the individual stars, but to the Milky Way Summary When the moon is absent from the night sky, stars remain as celestial visual cues. Nonetheless, only birds [1,2], seals [3], and humans [4] are known to use stars for orientation. African ball-rolling dung beetles exploit the sun, the moon, and the celestial polarization pattern to move along straight paths, away from the intense competition at the dung pile [5,6,7,8,9]. Even on clear moonless nights, many beetles still manage to orientate along straight paths [5]. This led us to hypothesize that dung beetles exploit the starry sky for orientation, a feat that has, to our knowledge, never been demonstrated in an insect. Here, we show that dung beetles transport their dung balls along straight paths under a starlit sky but lose this ability under overcast conditions. In a planetarium, the beetles orientate equally well when rolling under a full starlit sky as when only the Milky Way is present. The use of this bidirectional celestial cue for orientation has been proposed for vertebrates [10], spiders [11], and insects [5,12], but never proven. This finding represents the first convincing demonstration for the use of the starry sky for orientation in insects and provides the first documented use of the Milky Way for orientation in the animal kingdom.

http://www.cell.com/current-biology/retrieve/pii/S0960982212015072

They overlooked the part in their model where more acidic seas dissolve existing carbonate faster. Nature recycles. How do you think coral survived 7000ppm CO2?

http://rs79.vrx.net/opinions/ideas/climate/.images/Evo_large.gif

They've overlooked simple biomechanics before: "8th December 2010 13:24 GMT - A group of top NASA and NOAA scientists say that current climate models predicting global warming are far too gloomy, and have failed to properly account for an important cooling factor which will come into play as CO2 levels rise.
http://www.theregister.co.uk/2010/12/08/new_model_doubled_co2_sub_2_degrees_warming/

See also: There are winners and losers among corals under the accumulating impacts of climate change, according to a new scientific study. In the world’s first large-scale investigation of how climate affects the composition of coral reefs, an international team of marine scientists concludes that the picture is far more complicated than previously thought - but that total reef losses due to climate change are unlikely. Ref: http://www.cell.com/current-biology/abstract/S0960-9822(12)00255-2"

One of the big points about viruses that remain in the body long-term, is that they somehow manage to find shelter in which to evade the immune system -- at least for most of the time, and at least from those parts of the immune system that might otherwise eradicate them. (See for example 'virus latency' at http://www.cell.com/cell-host-microbe/abstract/S1931-3128(10)00217-9?script=true/).

Many of the mechanisms of that sheltering are still unknown, or incompletely known. That means, in turn, that it's at least not going to be a surefire winner to have an extra protein -- against which you want a really strong protective immune response -- tagging along with the sheltering virus.

Plus, it would seem that the main article is reporting a theoretical study (from the 'supporting information' for the PNAS paper referred to in the main story -- which is all that I could so far access -- here http://www.pnas.org/content/suppl/2012/11/14/1209683109.DCSupplemental/pnas.201209683SI.pdf -- other than the abstract).

The status of the matter appears to be that this is an 'if only . . . ' -- so far.

-wb-

It was mentioned in an article in Current Biology’s latest issue http://www.cell.com/current-biology/fulltext/S0960-9822(12)01009-3, picked up by the mainstream media and thus went news-viral I suppose.

The Summary links to a (somewhat useful) fluff review by the Medical Daily Web Site (and will hit the visitor with 37 cookies). Fwiw, readers at Slashdot may prefer bypassing it by going the Cell's Current Biology Web Site where they'll be able to find the Authors' Original Summary or perhaps the Full Text instead.

The Summary links to a (somewhat useful) fluff review by the Medical Daily Web Site (and will hit the visitor with 37 cookies). Fwiw, readers at Slashdot may prefer bypassing it by going the Cell's Current Biology Web Site where they'll be able to find the Authors' Original Summary or perhaps the Full Text instead.

The full text of the research online here.

The page 5 of the original article PDF has a size comparison of disected specimens. The treated mice testes weight is roughly halved but the size is 2^(1/3) ~ >0.70 of the untreated ones.

There is a meassurement device called Prader orchidometer that works by comparison with standarized orbs. It's very difficult to get an accurate size/volume in vivo without using ultrasounds and if even the orchidometer method is not precise much less expect that anybody could notice a significant difference just looking at them.

Certainly after some time not even yourself will notice at all. Definitely noticeable if meassured or compared side by side, but most probably irrelevant for a partner. The major issue may be the own psychological selfesteem burden that some insecure people could have of knowing that their testes shrank a bit, but far worse and by large would be that you got instead a vasectomy and later couldn't reverse it.

Always could do nothing and let all the responsability to your girlfriend/wife behaving like a macho(TM) or just ask for her opinion about it and decide together since also are "her nuts".

While I know this isn't what you were answering, but it turns out that lung damage is a major factor in bat deaths near turbines.

http://www.cell.com/current-biology/retrieve/pii/S0960982208007513

http://www.cell.com/molecular-cell/abstract/S1097-2765(12)00341-3

For the smug fatties.

"We have shown that if you live against your body clock, you're more likely to smoke, to drink alcohol, and drink far more coffee," says Roenneberg.

So more likely to indulge, I would wager that includes food.

"Eating at the wrong time hits your entire digestive system at the wrong time, so it cannot efficiently do its job,"

Our results demonstrate that living “against the clock” may be a factor contributing to the epidemic of obesity.

http://www.cell.com/current-biology/abstract/S0960-9822(12)00325-9

"epidemic of obesity" notice the responsibility free title? Again eating before you sleep leads to gaining weight, is that in your control? Yes.
Is what you eat under your control? Yes. Is how much you eat under your control? Yes.
It never ceases to amaze me that the one thing that people have become extremely good at doing is absolving themselves of personal responsibility and adapting this pussified society excuse to their life style.

The OP is correct it's all excuses because what and when you eat is entirely under your control, as is getting exercise but the "fatties" choose not to take responsibility for their "food addiction".

http://www.cell.com/current-biology/abstract/S0960-9822(12)00329-6 in which the authors thank Lynn Margulis and say that she would 'savoured" fart jokes. "We thank the late Lynn Margulis for infecting us with her microbial enthusiasm — she would have savoured the notion of sauropods as walking methanogen vats.

There are multiple genetic factors that are strongly linked to Autism. That's not really a huge debate in the field. None of the factors are absolute: they don't guarantee the occurrence of autism, instead, they are associated with increased risk.

This isn't a novelty in the psychiatric genetics world. The same holds true for schizophrenia, depression and other mood disorders, and most other brain disorders for that matter. It is likely that this has to do with an interaction between disease genes and environmental factors, other genetic factors, or with stochastic (random) processes.

It's not that different than most other complex diseases. For example, you may carry a risk allele for heart disease. If you follow the right diet, and have a blissful, stress-free life, you might be in luck. But, if you're carrying a second risk allele (whoops!), or down a few too many Big Macs... that risk allele will bite you in the ass. For that matter, even if you do take care of yourself, that risk allele may still bite you in the ass. It's an odds game, and each risk factor makes the odds that much worse.

As for your "experiment that everyone conveniently chooses to forget"-- there's an extensive literature of twins with Autism. It also shows that there is a strong genetic component, but it's not absolute. The concordance of Autism in twins is extremely high -- but not absolute. However, even identical twins have significant differences -- yes, even genetically. And, even though they may share the same womb, they may have siginficant differences in fetal nutrition (depending on how the placenta is located), and they may be subject to different gestational stresses or birth trauma.

In other words -- nobody's conveniently forgetting anything.

While the effort put into the analysis in this paper is admirable, it sort of fades into the background of the glut of "we took existing data sets and made a network -- here's the picture" sort of systems biology papers that are being cranked out right now. I'm just wondering, of all the rigorous and higher-impactautism genetics research being done right now, why did this one in particular warrant a slashdot blurb? This certainly isn't the first (or even most compelling) research to uncover convergent biological processes in the autistic brain.

Careful. Though you may have the permission from the authors to redistribute their works, they may not legally be able to give you such permission. See the rules for journal Cell, one of these Elsevier publications, under "Copyright" section:

Yes, you are correct. Intellectual property rights are often transferred from authors/investigators to the publisher with submission. And that's what I'm choosing to ignore. The medical literature is written purposely to share and spread information so that physicians everywhere can improve the care of patients. --JSt

always ask permission from authors and researchers, but no longer from publishers, as they just want to monetize and gouge.

Careful. Though you may have the permission from the authors to redistribute their works, they may not legally be able to give you such permission. See the rules for journal Cell, one of these Elsevier publications, under "Copyright" section:

Upon acceptance of an article, authors will be asked to transfer copyright. . .

They spell out further rules under Authors' Rights: the author does not retain the right to grant arbitrary redistribution rights to other individuals/corporations (i.e. to you). And these rules are actually some of the more lenient ones I've seen...

Scientists do that research too. Bears (and other hibernating animals) are of particular interest here. But humans are (hopefully) approaching a point where famine is not a significant threat to life, so other solutions like this one could also work even though it may increase the metabolic load (in addition to muscle mass) by causing a larger number of mitochondria and higher cellular respiration. (This article's reference paper).

Indeed, even rats have been shown to practice metacognition. Presented with a choice with consequences -- full reward for the right answer, no reward for the wrong answer, and a tiny reward for an "opt-out" choice -- lab rats will choose the right answer when the test is easy, but as it becomes increasingly difficult they begin to hesitate more and more, and eventually start to choose the "opt-out" choice. That is, they know what they do not know and will make choices that are not impulsive, but are well thought out.

The gp could also be referring to delayed gratification, but higher nonhuman animals have also been shown to practice that. For example, if you have chimps in a setup where there's a device that slowly loads up a food dispenser with one desired food item after another, but stops as soon as the chimp takes the food, after prior experience with the test, most chimps will wait until all possible food items have been loaded before taking them. Delayed gratification has also been shown in dolphins and a number of other animals.

Sorry about that. I meant to add the link to the article in Current Biology, but somehow forgot about it before clicking "Submit".

Alas, in my defense, the story was submitted and posted less than a week after the "embargo" was lifter by the publisher -- IIRC, it appeared online on Current Biology's website last Thursday at noon (maybe EST?). At least I didn't wait a year to submit :)