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What does "genetic correlations" mean as opposed to just correlations?
I'm reading the paper "Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior". In Fig. 4 shows "Genetic correlations of same-sex sexual behavior with various preselected traits". This sentence confuses me. I understand that you could do a standard statistical analysis to find correlations between same-sex sexual behavior and various traits. What makes the way they are doing the correlations "genetic"?
(Note: This may be more of a statistics question than a bio question. Feel free to move it to a more relevant SE site.)

They cite reference 16: https://www.nature.com/articles/ng.3406 might be useful to you. I think the question is relevant here, we have some regular users who are well-versed in heritability studies.

I believe this may be more of an English language question than a stats or a bio question. I shall check the article once to verify.

Looks off-topic? to me, this is an english language question, not a biology one, correlations are correlations are correlations, the addition of the word genetic is merely there to highlight the data set / type under current reference in the sentence & nothing more.

I disagree that it's about English language. The question is really "I understand the meaning of a correlation between phenotypes A and B; what is the meaning of a genetic correlation between A and B." That is, how do you have a "genetic correlation" between Same-Sex Sexual Behavior and Depression?

@BryanKrause : You've convinced me, where b4 I only thought it likely I'm now sure that this is definitely a language comprehension issue & not a legitimate biology question :) off topic then.

@Pelinore Then please do explain it: I'm not new to statistical analysis and even I'm somewhat confused what exactly they are presenting. Remi.b's answer helps but is still not quite convincing me. How do you define, mathematically, a genetic correlation between two phenotypes?

@BryanKrause : "How do you define" : I don't, they do, & I've already explained why this is a language comprehension issue, there's no arcane meaning intended they simply say that any genetic correlations found with same sex behaviour may (or may not) also correlate in some degree with other traits, it seems to me that any misunderstanding is simply what we might call a minor senior moment.

@BryanKrause : 'genetic correlations' in this instance simply means any correlations between genes (or genetic markers) & same sex behaviour it doesn't have any special or specific meaning as compared to ordinary correlations of any other data sets. So it's an English language question not a biology question.

@Pelinore No, that isn't true. Please read the paper. Depression is not a gene. Same sex behavior is not a gene. If you want a genetic correlation between depression and same sex behavior you have to define what that means. A correlation between genes and same sex behavior is understood and is not what the OP is asking.

@BryanKrause it actually is about the language. The correlation that is being studied may be between two different conditions but the measured RVs, in this case are the genetic markers. That doesn't make "genetic correlation" a special kind of analysis. One can as well study the neurophysiology in these conditions and use the term "neurophysiological correlations". In both cases, the right phrase would be correlation of (genetic) markers between conditions X and Y.

It is simply a correlation where one of the two variables considered is the genetic state at a given locus. In a GWAS, one loops through all loci and systematically performs a correlation analysis between the genetic states at this locus and the phenotypic trait of interest.
In the example of sentence you cite

Genetic correlations of same-sex sexual behavior with various preselected traits

They looped through each polymorphic locus in their data set and at each locus they performed a correlation analysis between the two variables "genetic states at a this locus" and "same-sex sexual behavior" (whichever way this second variable is recorded).
A study might also be interested in more than one phenotypes. In such case, different phenotypic variables can either be considered separately or can be included in the same analysis through linear models. It is for example not so unusual to include one of the variable as a covariatiate in an ANCOVA type of design.

I think this answer is not quite complete (in the context of the paper OP is referring to)...I'd have to look closer but it seems there is an additional step, because they are talking about two traits and a genetic state, not one trait. I still think you are much better positioned to write the complete answer here, though. :)

I am too lazy to read the paper :D I added a little paragraph about cases where more than one phenotype is considered.

I quote from this paper:

Genetic correlation analysis can separate between shared additive genetic and environmental factors by using the genetic similarity between individuals (monozygotic twins have ∼100% and dizygotic twins and siblings ∼50% genetic similarity). To compute the genetic correlation between two traits the phenotypic correlation is decomposed in genetic and environmental sources of covariance using a maximum likelihood approach in combination with the genetic proximity matrix of the sample 34, 35. Additionally, the heritability of both traits is established to compute the relative contribution of genetic and environmental factors to the phenotypic correlation.

In the same paper you will also find some hints on how it is computed. However, if you want to go into further detail, I suggest you investigate the work of Laura Almasy and John Blangero. They did a lot of work on variance component analysis of QTLs. I remember using their software (SOLAR, which is now SOLAR-Eclipse) for computing genetic correlation in a work, but right now I am not able to find the paper in which they describe computation of genetic correlation.


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Can foraging worker ants become queens?
The TL;DR is in the subject line.
The back story is as follows:
I am combating ants in my high-rise apartment unit.  One piece of online advice was to vacuum regularly, and pay attention to edges of the floor.  I'm considering taping up the vacuum bag opening so that I'm not tossing out a nearly empty bag every day (almost $10 each, and terrible for the environment).
I had initial concern that an ant might get out, so I also double bagged the vacuum bag.  This is making it inconvenient to use, meaning that I'll vacuum less.  Exactly the opposite of the online advice.
I think that the chances of an ant getting out is low, and even if escape was possible, it probably wouldn't be more than one or two.  I can accept that, if they don't go start generating more ants.
I haven't found anything online about workers being able to transform into queens once they are foraging.  What I have read is that it has to do with genetics and extra nutrition during the formative stages.
Is it safe to assume that foraging workers will not be able to turn into queens?
After note: It just occurred to me, if ants can chew through wood, then there's nothing to prevent them from chewing through a vacuum bag over the course of a day or more.  They can even chew through the plastic bag in which the vacuum bag is sealed.  Is this a valid concern, or is their ability to chew limited to wood?

It depends on the species. Apparently there are species where workers can mate and lay fertilized eggs. However, it's unlikely to be a relevant issue for you because without the colony the few escapees won't be able to care for the eggs and larvae. Your issue is the colony and that your apartment attracts foraging ants.

Thanks, Roland.  Did you want to post that as the answer?

Workers cannot become "queens" because the development of a larvae into a worker or a queen happens during the larval stage, depending mainly on the food that the larvae is given. That being said, once the queen is removed from a colony, in many ant and other social hymenopteran species, workers are no longer inhibited by the pheromones produced by the queens that prevent the growth of the worker's ovaries. So in some species, removing the queen can lead to workers laying eggs but these will most often be parthenogenetic and lead to the production of males only. In a very few species, workers can produce female eggs by parthenogenesis or mate with males after the removal of the queen. Such traits are usually associated with large body size and small colony size, so they are unlikely to be the ones you have in buildings.

Bourke, A. F. (1988). Worker reproduction in the higher eusocial
  Hymenoptera. The Quarterly Review of Biology, 63(3), 291-311.
Page, R. E., & Erickson, E. H. (1988). Reproduction by worker honey
  bees (Apis mellifera L.). Behavioral Ecology and Sociobiology, 23(2),
  117-126.
Wenseleers, T., Helanterä, H., Hart, A., & Ratnieks, F. L. (2004).
  Worker reproduction and policing in insect societies: an ESS analysis.
  Journal of evolutionary biology, 17(5), 1035-1047.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


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Person-years and relevance to incidence of condition
If the annual incidence (age and sex-adjusted) of a particular condition x is 21.8 cases per 100,000 person-years and this data was determined in one geographic location, then is it correct to say in a city of 1 million people that we may see that same condition, in one year, in approximately 21.8 x 10 = 218 people? I'm just trying to provide some relevance to a group of students on how common some conditions may be. I understand that the exact incidence would vary along with demographic, geographic and environmental features.

I'm voting to close this question as off-topic because it appears to be about statistics rather than biology.

David is there any way to easily get this question into statsexchange?

I'm not a moderator so I can't transfer it for you. You could just  copy and paste it there and then delete it from here as it's your question and nobody has answered yet. (They don't like the same question posted on two SE lists.)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Does intelligence depend more on environment than on genetic factors?
Many have argued that the test of IQ is simply a test of language. The application of the test consists of asking a number of questions. The person should understand the question presented to them and should be able to answer the questions properly. If a person does not understand the question or do not know to answer or give a wrong answer it results in a negative point.
is there a genetic component in this equation?

Which "equation" are you asking about? ‘When data across all studies are collapsed, genetic influences [on intelligence differences] account for around 50% of the variance’ (Petrill et al. 2004, taken from the Review Genetics of intelligence by Deary et al. 2006).


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Strength of Female Chimpanzees vs. Male Chimpanzees?
Where can I find studies done on the strength dimorphism between male chimps and female chimps?
For example, "one-arm pull strength is 300 pounds for male chimps and 200 pounds for female chimps"

try google scholar or pub med.  Nothing obvious here: https://scholar.google.ca/scholar?hl=en&as_sdt=0%2C5&q=chimpanzee++sexual+dimorphism+%22strength+differences%22&btnG= ... maybe useful references here? https://www.pnas.org/content/114/28/7343.long

Note this is likely do to the difference in size between male and female chimps more than anything else.

not necessarily entirely; the (very small!) sample I show in my answer does show 2 males that both have higher weight-specific strength than 3 females ... (p-value=0.1 ...)

I searched for "chimpanzee strength" on PubMed and followed links from

O'Neill et al. PNAS 2017 "Chimpanzee Super Strength and Human Skeletal Muscle Evolution"

to

Bozek et al. PloS Biology 2014 "Exceptional evolutionary divergence of human muscle and brain metabolomes parallels human cognitive and physical uniqueness" where I found this figure:

which shows pulling strength normalized by individual body weight, with circles for females and diamonds for males.  In fact, the Excel spreadsheet given in supplementary materials shows there were two males and three females, tested in three sessions; in each session weight and pull strength were listed. The ratios of max pull to weight for males were 3.44 and 3.49, for females were 2.9, 3.14, and 3.25 (one of the males was quite small ...)
O'Neill et al. give a few other references, you could follow those as well and see what you come up with.  (I found that "chimpanzee strength" gave better results as a search term than terms including "sexual dimorphism", which tended to be swamped by more general discussions of the evolution of dimorphism in apes.)
@jackaidley notes in a comment that

extreme caution is needed in interpreting these results for Chimp sexual dimorphism, quite apart from the very low number of individuals, there is a significant problem with these measurements - as the paper itself notes "The inability to control nonhuman primates' motivation hinders the exact quantification of the muscular strength difference between humans and nonhuman primates, even in a highly controlled experimental setup." This problem equally applies to male/female differences.

In other words, male chimpanzees might pull harder at least in part because they are more motivated than females in this particular setting, rather than because of intrinsic differences in strength. (That may or may not matter for what you are trying to do with this information.)

Good find, and I suspect this is about as good as it gets. But I think extreme caution is needed in interpreting these results for Chimp sexual dimorphism, quite apart from the very low number of individuals, there is a significant problem with these measurements - as the paper itself notes "The inability to control nonhuman primates' motivation hinders the exact quantification of the muscular strength difference between humans and nonhuman primates, even in a highly controlled experimental setup." This problem equally applies to male/female differences.

Is the x-axis individuals? It seems to not be equally-spaced for some reason.

What is the x-axis even? Some human-chimp-macaque function?

I believe the x-axis just represents individuals (individuals are measured in 1-4 sessions). Don't know about uneven spacing.  The data are there if you want to draw your own version ...


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Do there exist enzymes that can take up multiple cofactors to do different reactions?
I was thinking about enzyme catalysis, and it seems like enzymes can only catalyse one kind of forward/reverse reaction (please correct me if I am wrong). Does there exist an enzyme that can catalyse multiple reactions with different cofactors? For example, an oxidoreductase that has $Fe(III)$ as a cofactor for one reaction and $H_2O_2$ as a cofactor for another reaction.

Can you name an enzyme for which hydrogen peroxide is a cofactor, rather than a a substrate? How much do you know about enzyme catalysis?

@user1136, thank you!

@David, I am not very familiar with enzyme catalysis-just the basics. I was just curious if there existed such an enzyme.

But what you mean by “such” an enzyme is unclear if you are confusing substrate, cofactor and catalytic mechanism. Until you clarify your question it is valueless in relation to the objectives of this site.

It sounds like you are asking about what are commonly referred to as "multifunctional enzymes".
For a reasonably recent article covering this subject — see:
Cheng, X. Y., Huang, W. J., Hu, S. C., Zhang, H. L., Wang, H., Zhang, J. X., ... & Ji, Z. L. (2012). A global characterization and identification of multifunctional enzymes. PloS one, 7(6), e38979.

A specific example of such an enzyme is the fatty-acyl-CoA synthase from yeast — this enzyme catalyzes multiple reaction steps that use both NADP and Coenzyme A and also uses a third cofactor, FMN.

The enzyme from yeasts (Ascomycota and Basidiomycota) is a multi-functional protein complex composed of two subunits. One subunit catalyses the reactions EC 1.1.1.100, 3-oxoacyl-[acyl-carrier-protein] reductase and EC 2.3.1.41, 3-oxoacyl-[acyl-carrier-protein] synthase, while the other subunit catalyses the reactions of EC 2.3.1.38, [acyl-carrier-protein] S-acetyltransferase, EC 2.3.1.39, [acyl-carrier-protein] S-malonyltransferase, EC 4.2.1.59, 3-hydroxypalmitoyl-[acyl-carrier-protein] dehydratase, EC 1.3.1.10, enoyl-[acyl-carrier-protein] reductase (NADPH, Si-specific) and EC 1.1.1.279, (R)-3-hydroxyacid ester dehydrogenase. The enzyme differs from the animal enzyme (EC 2.3.1.85) in that the enoyl reductase domain requires FMN as a cofactor, and the ultimate product is an acyl-CoA (usually palmitoyl-CoA) instead of a free fatty acid.

Source: https://www.ebi.ac.uk/intenz/query?cmd=SearchEC&ec=2.3.1.86

But my reading of the question is that the poster is not thinking of what are in effect multi-enzyme complexes. I suspect from the mention of cofactors in the question that the poster is quite naive. I seem to have heard of enzymes that can change the reaction catalysed in certain circumstances, but two cofactors — unlikely, given their need for specific binding sites.

@tyersome, that is interesting! I understand that multiple functions would need multiple domains. Thank you for your help!


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What does "radiographic progression" mean in cancer?
I tried looking up the definition of the term "radiographic progression" using Google and medical dictionary, etc., but I couldn't find its meaning anywhere. All research articles that I found just use it, so I assume it is something common.
Please explain to me what "radiographic progression" means. I really appreciate it.

"Radiographic" refers to imaging modalities like x-rays, CT scans, MRI, etc.
"Progression" in medical terms is referring to progression of disease, where progression means advancing to the next stage, getting worse, etc.
Radiographic progression in the context of cancer would mean that based on X-rays, CT, MRI, etc, the cancer has gotten worse in some way. The exact meaning of progression has to be defined on some rating scale and will differ from study to study. Radiographic progression is not the only way to measure disease progression, other measures can also be used like symptoms experienced.

Thank you very much! I thought that was the case but I couldn't find the definition of the term anywhere so I was very confused.

@Paichu Yeah, I was pretty certain but to verify what I did was to find some journal articles using the term and saw how they defined it operationally, especially in contrast with other methods. I also never found a place where someone said "the definition of radiographic progression is _________" but from context it was easy to infer.


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A question about how the brain determines the source of a sound
If a person's eardrum vibrates, let's say, 440 times per second for 1 second, how does the brain know its because 1 sound source vibrated 440 times, as opposed to 440 sources vibrating once, one after the other, or 2 objects vibrating 220 times per second, but out of sync with each other, or any other combination? Thanks.

If the sources have different locations then they won't reach the 2 ears at the same time, won't have the same loudness and spectral content (although here you describe a pure tone), so your brain will be able to tell them apart. There is a whole field of neuroscience interested in "causal inference", which describes how your brain makes this type of guesses. For example have a click and a flash been produced by the same source of different sources?
But I think this is not exactly what you were asking. If the signals are identical when reaching the ears then it becomes more of a philosophical question. If you place a microphone in the observer's ear and receive a perfect sine, does it matter that it has, in facts, been produced by multiple sources? That's the classical philosophical question of whether a tree falling in a forest produces a sound or not, if no one is around to hear it. Is a sound a physical signal or is it the percept it elicits in an observer? Take the example of color. If you compare 2 lights, one monochromatic red and one complex spectrum that looks exactly the same red. Do they have the same color or not? Due to the physiological limitations of your sensory organs they elicit the exact same response. Yet they are physically different. There is of course no clear or easy answer to this question as on one extreme you will end up arguing that there is no objective reality and on the other extreme you deny the obvious fact that we experience the world differently.
Shams, L., & Beierholm, U. R. (2010). Causal inference in perception. Trends in cognitive sciences, 14(9), 425-432.
https://en.wikipedia.org/wiki/If_a_tree_falls_in_a_forest

the mammalian ear is a complex mechanism developed to take advantage of how sound is altered by reflection off surfaces, the shape of the outer ear alone gives us directional information,. Mammalian ears are weird and amazing. Mammalian ears developed some odd tricks because by their nature they alter incoming tones in return for amplification, so the neurological mechanisms that correct for this can also be used to extract all kinds of extra data.

Yes, this is the Head-Related Transfer Function (HRTF). But it works only for complex sounds which is why I pointed out the question is about a pure tone, with a single frequency.

do you have a source for that because I was to believe it still worked as long as both ears were picking up a pure tone.

That's a good question, I do not. It's a transfer function so it is by definition a function of frequency. So if it is a perfectly pure tone it is obviously not localizable. However, it is not impossible that the ear itself broadens the spectrum of a pure tone, in a way that is location dependent. I do not know. The problem with sound localization is that it is impossible to dissociate different cues. As far as I know it is not possible to tell whether a sound comes from the front of the back if its source is on the sagittal plane.


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Speed of reaction vs equilibrium
Does increasing the speed of a reaction (say by introducing a catalyst) shift the equilibrium of the reaction? I assume it does not, as Gibbs free energy is not changed, but I am not sure.

You are right in both the conclusion and the rationale. However, you pose the question in the wrong forum. You should pose it in phyics.stackexchange.com.

Welcome Ben. This is a chemistry question rather than a biology (or physics) question - I've flagged it for moving to chemistry.sx.

This is a physical-chemistry question but it is already answered in [chemistry.se].

The equilibrium constant $K$ is the quotient of the rate constants of forward ($k_1$) and backward reactions ($k_{-1}$) (for elementary reactions).
E.g., for an  equilibrium
$$\ce{A + B <=> C + D}$$
we get
$$\frac{[C][D]}{[A][B]} = K = \frac{k_1}{k_{-1}}$$
So,

If both rate constants are affected in the same way (multiplied by the same speed-up factor) so that the quotient doesn't change, then also the equilibrium constant does not change, no shifting, no change in Gibbs free energy.
That would be the case with your catalyst as that facilitates both forward and reverse reaction by lowering the energy of the transition state in the elementary reaction leading to just such a multiplicative increase in reaction rate - but no effect on the energy of educts or products (thus, no change in $\Delta G$).
This has an interesting link to the impossibility of constructing a "chemical" perpetuum mobile by use of a catalyst.
If the rate constant of either forward or reverse reaction (or both, but not by the same factor) change, the equilibrium shifts.
But, yes, that also means that Gibbs free energy has changed.
Thus, there must be a change in free energy of educts and/or products as the energy of the transition state does not affect $\Delta G$, it only affects the reaction rates.
Whether this is possible hinges on the question whether we consider it still the same reaction $\ce{A + B <=> C + D}$ or whether we say that now we have another equilibrium, say, $\ce{A' + B <=> C + D}$ or $\ce{A' + B' <=> C' + D'}$ which of course can have different equilibrium constants. An example where I think one may argue either way would be the dependency of equilibrium constants on solvent.
(And, btw, we still cannot build a perpetuum mobile: solvation energy makes the difference)


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Example of a virus becoming symbiotic with an organism
The human gut has an indispensably beneficial ecosystem of bacteria. What are the examples of a virus that becomes symbiotic with an organism, or even incorporates beneficially into the genome of the organism?

@Jan Symbiotic?

very relevant article https://www.nature.com/articles/nrmicro2491

In humans, endogenous retroviruses (HERVs) comprise a substantial fraction of the genome, as much as 8%.1  While many historical viral incorporation events into the primate genome were likely neutral or detrimental (and therefore selected against), some were co-opted and are now functional elements in humans.  An example: human syncytin is the envelope gene of a defective HERV, and the protein has been co-opted for fusion during human placentation.2  A good primer on the genetics and functions of HERVs can be found in The Pharmaceutical Journal.3  The Feschotte Lab at Cornell studies the evolution of HERVs and other mobile elements in mammalian genomes, and their lab site provides more resources.
In bacteria, prophage (integrated bacteriophage) can be co-opted by their hosts for niche-specific transcriptional control.  A cool example is the pathogen Listeria monocytogenes, which utilizes prophage excision during intracellular growth to activate its Com system and escape from phagosomes.4

References

Lander ES et al. Initial sequencing and analysis of the human genome. Nature. 2001 Feb 15;409(6822):860-921.
Mi S, Lee X, Li X, Veldman GM, Finnerty H, Racie L, LaVallie E, Tang XY, Edouard P, Howes S, Keith JC Jr, McCoy JM. Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis. Nature. 2000 Feb 17;403(6771):785-9.
Dodou K, Whiteley P. We are all part virus — the role of human endogenous retroviruses. The Pharmaceutical Journal, PJ, 1 March 2014, Vol 292, No 7799;292(7799).
Rabinovich L, Sigal N, Borovok I, Nir-Paz R, Herskovits AA. Prophage excision activates Listeria competence genes that promote phagosomal escape and virulence. Cell. 2012 Aug 17;150(4):792-802.

In certain species of parasitic wasp, contained within the wasp genome is the genome for a so-called "polydnavirus". The female wasp somehow creates instances of these polydnaviruses inside its ovaries.
When the wasp injects an egg into a member of the host species (likely a caterpillar), several instances of the polydnavirus are also injected along with it. Although the viruses do not harm the wasp in any way, they do have an immunosuppressant effect on the caterpillar, protecting the wasp egg against the caterpillar's immune system.
I've seen an article in "The Atlantic" which claims the viruses can also manipulate the caterpillar's metabolism in a way beneficial to the parasitic larva, but the article did not provide a source for this.
The polydnaviruses, counterintuitively, cannot actually replicate themselves, and are only "reproduced" when the wasp's cells manufacture them! They do not reproduce inside the caterpillar, serving only to protect the wasp egg/larva and copies of the virus genome encoded in the larva's DNA.
(Actually, for some wasp-species/virus pairings, the viruses may exist and reproduce inside the wasp ovaries instead of being "manufactured" by the wasp.)
If you found this interesting, you may also want to look up "virus-like particles", which are created and used by the wasp in the same way, but do not contain any nucleic acid. Regrettably, I don't know enough about these to elaborate further.
So there you have it! A virus which is very beneficial to its wasp host - or at least to that host's offspring - although certainly not to its later caterpillar host.
Sources:

Hunter P. (2010). The missing link. Viruses revise evolutionary theory. EMBO reports, 11(1), 28–31. doi:10.1038/embor.2009.267
Drezen JM et al. (2017). Endogenous viruses of parasitic wasps: variations on a common theme. Curr Opin Virol. 2017 Aug;25:41-48. doi: 10.1016/j.coviro.2017.07.002. Epub 2017 Jul 17.
Ryan, FP. (2016). Viral symbiosis and the holobiontic nature of the human genome. APMIS 2016; 124: 11– 19.
Drezen JM et al. (2009). Polydnavirus hidden face: the genes producing virus particles of parasitic wasps. J Invertebr Pathol. 2009 Jul;101(3):194-203. doi: 10.1016/j.jip.2009.04.006. Epub 2009 May 19.

See also:
https://www.theatlantic.com/science/archive/2015/09/parasitic-wasps-genetically-engineer-caterpillars-domesticated-viruses/405874/


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Are there any benefits/disadvantages/traits from having a permanent lower core temperature?
My body temperature as far as I remember has always been around 35.6 degrees Celsius, that's a degree less than what is the usually quoted as the average temperature for humans.
Are there any known correlations such as a shorter/longer average lifespan or pronounced traits such as being more sensitive to warmer temperatures or later/earlier onset of hypothermia symptoms?
Or is it not low at all or low enough to have any noticeable effects.

There are many questions you ask, I would suggest revising to narrow it down. Temperature and 'its effects' is quite broad of a curiosity. What would you like answers to focus on? Have you tried searching online for some answers? Have you reached any conclusions? It appears that this information is readily available, and the data points in many interesting and sometimes conflicting directions, e.g. with respect to temperature-lifespan association: colder body temperature is associated with longer life, but women, who live longer on average, have higher core temperatures than men. It goes on!

I gave google scholar a quick search, and although longer temperature seems like an obvious one I coudln't find any paper easily that would point to that for either humans or animals. I was hoping someone might know some of top of the head, I understand my question my seem rather broad.

Are you asking about effect in general or for humans specifically.

Yes absolutely. Body temperature is associated with basal metabolic rate which is linked to life-span/body mass. Keeping your body at temperature is responsible for the majority of your caloric burden majority of your caloric burden, and having a lower resting temperature would mean you require fewer calories to survive. Higher body temps are thought to have been a defense against parasite infection, so reductions in body temperature might leave you more susceptible to disease, however a paper came out recently discussing falling body temperature in the US and its implications, and I think it addresses many of your questions in detail in the discussion.
Edit: To elaborate on that elife paper, they've identified a small reduction in average body temperature overtime using military medical records going back to the civil war. They postulate that the reductions they observe are due to improvements in healthcare and a potential decrease in chronic inflammation in the population which increases your body temperature.

Can you elaborate on the major findings of that linked paper? Link-only answers are discouraged.

Whilst it is possible that your actual core temperature is actually lower than the normally quoted average of 37.5 Celcius by a degree, it may also be the case that where you are measuring is below the average rather than your actual core temperature. For example, you might be measuring under your armpit, and perhaps due to low circulation in that area, it does not fully reflect your actual core temperature. Just a thought.
Mammalian enzymes have an optimum temperature range. Too low, and the rate of reaction is too slow to effectively support the organism. Too high, and the enzymes will denature (loose their tertiary and quaternary structure.)
So if your core temperature really is a degree lower, we might expect your metabolism to be slowed due to the effect on enzyme catalysed reactions. The rule for this is expressed as Q10, Q10 temperature sensitivity units in stack biochem.
Another possible effect is that a lower body temperature could mean being more prone to infection, as discussed in stack geneticsenter link description here. Temperature rise during infection (having a fever) is thought to be an attempt to thwart an infectious organism, so it follows that a lower temperature may aid teh infecting organism.

"Temperature rise during infection (having a fever) is thought to be an attempt to thwart an infectious organism, so it follows that a lower temperature may aid teh infecting organism." That doesn't follow at all. Successful pathogens are successful because they are adapted to the host organism. Their temperature optimum should be in agreement with the host organism's typical temperature.

So why do mammals have a fever? It is an attempt to get rid of the pathogen. It might not always be successful, but so far when I've had a fever, I have got rid of the pathogen each time.

Yes, of course. But decreasing the temperature below normal does not benefit the pathogen. On average, optimum temperature for a pathogen is aligned with normal body temperature.

Not so with fungi. Lower body temperature can benefit fungal infections.

Some pathogens will usually infect the peripheral tissue because the core temperature may be too high. If I recall, the bacteria that causes leprosy is an example.

Parainfluenzavirus is another pathogen whose growth is diminished at temperatures over 37 C.


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Help me identify this Bug species
I found this insect in Pune/India. Its body size was less than 1 cm. It was near light source. I suspected it to be Juvenile Thread-legged Bug, but i am not sure. Is my suspicion right or is it some other insect?

Yeah the Emesinae family is a good guess. It will be hard to tell what species, but on this page you may find more information about Reduviidae insects in India (pdf available) : https://www.researchgate.net/publication/237676358_A_checklist_of_Indian_Assassin_Bugs_Insecta_Hemiptera_Reduviidae_with_taxonomic_status_distribution_and_diagnostic_morphological_characteristics

This isn't a juvenile; zooming in shows me wings.  It isn't a member of the Reduviid subfamily Emesinae (the front legs aren't modified for grasping prey); I believe it to be a Stilt Bug (family Berytidae), but not knowing the Indian fauna cannot go any further than that,

It is Pneustocerus gravelyi, a species of stilt bug that lives in India.
In both of these images, you can clearly see the the bright red coloration of the joint on each leg. The pronotum is also the exact same shape and color, and the bright red abdomen extends beyond the closed wings.

original unmodified image source

It certainly seems correct identification. Thank you!


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How does the helicase enzyme break the hydrogen bonds between the strands of DNA?
I know helicase breaks the hydrogen bonds between the strands of a DNA, but how is this done?
Does it put an ion between the strands of the nucleic acid so that the bond breaks apart itself or is there some other mechanism?

Welcome to SE Biology. I have edited your question for two reasons. We discourage extraneous material and chat in questions — keep to the facts. If you want to add personal information, the most relevant is what level your knowledge of the subject is already. This is not my field, but I found a 2006 mini-review of the topic which indicates that there are many different helicases and their mechanisms of action are not simple to summarize. Someone may be able to do it for you, however.

This is indeed a broad question. For a detailed mechanism you should read a structural biology paper on this topic. This subject is complicated to explain in a site like this (also requires good knowledge of biochemistry and biophysics). A very short answer would be that helicases use energy of ATP hydrolysis to separate the DNA strands.

Im not sure if there is a decided helicase mechanism but the ‘backbone stepping motor’ model has been proposed for
helicase translocation and unwinding. Helicases contain two domains that are analogous to a set of ‘pincers’ (motor domain), when ATP is present, there is only a distance of two nucleotides between the
pincers and so they are closed, whereas when ATP is absent, there is a distance of three nucleotides between the pincers and so they are open. The motor domains interact with the
nucleic acid through contacts between threonine residues on the pincer terminus and phosphoryl oxygen on the nucleic acid. ATP binding weakens these interactions, allowing a pincer to move one nucleotide closer to the second pincer. A third domain (D3), that is part of the helicase but not involved in the binding of ATP, also interacts with the nucleic acid using a threonine residue. As the motor domains move along, tension builds up between the motor domain and D3 and after the motor domain has moved three base pairs, the protein contracts like a spring, pulling D3 toward the motor domains, disrupting the DNA in between. The structures responsible for prying apart the DNA are called “pins” or wedges”, which act as a physical barrier between the two strands of nucleic acid, prying apart its structure. The single
stranded regions are stabilised by helicases as well as other proteins such as single stranded DNA binding proteins, which prevent the reformation of the double stranded nucleic acid.
For more information and good images see: “Translocation and unwinding mechanisms of RNA and DNA helicase”

It's good to have more people answering questions in this area, but as you are a new member of this list, allow me to point out an important feature of answering questions on SE. This is that answers should be supported by external sources — reputable scientific articles, either in print or online (preferably with links). The reason for this is two-fold. 1. Without it it is difficult for the poster or others with the same question to know whether the answer is correct. 2. It is helpful for anyone wishing to learn more about the topic. Could you add references to your answer, please.

Sorry I put the name of the paper at the end which is in my opinion a really good article but I'll add the doi


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How is C4 pathway more water efficient than C3 pathway in photosynthesis?
In the C3 pathway:

1 H2O molecule is required for the fixation of 1 CO2 molecule.
In the C4 pathway:

The only H2O molecule used is in the calvin cycle, so 1 H2O molecule required for fixation of 1 CO2 again.
So, how is C4 pathway more water efficient? I tried looking up more detailed diagrams, but I couldn't find one which gave any different (H2O consumed) to (CO2 fixed) ratio. Any help is appreciated.

Actually, water is used in the light-dependent portion of photosynthesis, not the Calvin cycle.
The added water efficiency doesn't actually relate to water's involvement in chemical processes of photosynthesis at all. Water is instead lost incidentally through stomata when they're opened to allow CO2 into the leaves (see here for explanation). This CO2 IS required for the light-independent Calvin cycle.
Both C4 and CAM plants preserve water by decoupling (in space or time) C-fixation from the rest of the Calvin cycle (see here). They instead "store" carbon in 4-carbon molecules to use as a C source in the absence of CO2 (i.e., when stomata are closed). In doing so, they can perform the Calvin cycle without receiving more CO2. As a result, C4 and CAM plants can photosynthesize without having their stomata open all the time (or during the heat of days for CAM plants). The final result: less water lost through evaporation out of the stomata


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official authoritative source for bacterial shape classification
I'm a bit disappointed but after several hours of search, I could not find an official authoritative source for bacterial shape classification. I find a lot, I mean a lot of links but no original sources, even on  Microbiology society no source....
I believe a convention, workshop or another authoritative source must at one point have worked on this matter...

Oxford English Dictionary? Or, as Steve Jobs said about pornography, I know it when I see it.

Shape based classification is somewhat obsolete.

I am well aware that phenotypic classification for prokaryote is obsolete, but I would like to find the source that describes the official acknowledged bacterial shapes.


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Identify this unusually-shaped, orange-colored fruit that grows in pairs?
The photos below were taken on the island of Penghu in the Taiwan straight in October. This was in a public place and the small tree (about 3 meters tall, trunk perhaps 8 to 10 cm diameter) had probably been planted, so we can't presume it to be indigenous.
Each fruit was about 6 or 7 cm long, the skin was bright orange and seemed a bit waxy. The shape was a little bit like a banana-shaped American football in that it was divided into four quadrants. They attach to a stem in pairs and extend horizontally (sideways) rather than hang down.
Question: What could this gravity defying fruit-bearing tree be?
The first image is cropped, zoomed and sharpened in order to highlight textures.

The seed pods reminded me of the Apocynaceae, so I searched for "apocynaceae china" and found this University of Hawaii page where it is identified as Stemmadenia litoralis.  However, a little more looking it seems Tabernaemontana litoralis may be the preferred name.  There is some debate here.  This book may hold the final answer regarding the genus.
Your picture of the fruit is one of the best one I could find on the internet. There is another good one here with other pictures of the plant.
You were also correct that as a planted tree it might not be native.  This plant comes from Central America.

Wow that was quick, thank you for the thorough answer! I don't think this will become as popular as chili peppers (from the Americas as well I think) but it certainly is interesting to look at.

Locals call it the "Lanyu Tabernaemontana," (named after Lanyu island to the East) which may be classified as  Tabernaemontana dichotoma (Roxb. ex Wall.), Google images, or Tabernaemontana subglobosa (Merr.). Plants of Taiwan at the National Taiwan University.

@GenTest thanks for all the additional information! One of the images in your link leads to toxbaselanka. While I'd never thought to try to taste it, I was surprised to see it on a website of toxic plants!

@uhoh It's in the same dogbane family Apocynaceae as oleandor. The Tabernaemontana genus contains lots of toxin-producing species, and dichotoma's sap may cause redness and swelling if it comes in to contact with the skin. Though it does also contain medicinal compounds and uses..


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Inheritance percentiles
I am aware that the average DNA contribution from each grandparent is 25%, while the possible range is 0%-50%.  I found a source citing 18%-32% as the "normal" range but this was undefined.  I assume it must be referring to a percentile based on the distribution in a Gaussian curve.
After searching in vain for a chart showing "normal" ranges for each level of consanguinity (sibling, grandparent/aunt, great-grandparent/cousin etc.), I started doing the calculations myself on an Excel spreadsheet... and soon went back to searching.  Surely this information is available somewhere, and there must be generally accepted norms.  The math formulas are well established.
Where should I look to find the results summarized in a compact format?
I want to first know, essentially, the statistical results of flipping 23 identical immutable coins to represent the various generational probabilities.  The facts that the chromosomes are not identical, and that recombination is more likely at certain loci on certain chromosomes, are to be considered later as adjustments to the non-biological math.
I will pursue a statistical answer elsewhere if I can get the "biological" answer as to what percentile is accepted as the "normal" range.  (The 25% average for grandparents has a vanishingly small probability of actually occurring, as it would require enough recombination to equal an inheritance of 11.5 chromosomes from each grandparent.)

Good question +1. The actual probability distribution will depends upon the recombination rate and the number of chromosomes. Are you talking about the human genome only? The distribution in recombination rate might matter too but that would make things too complex for a simple calculations so anyone giving it a shot would probably want to assume constant recombination rate. Sexual chromosomes might also make things more complicated.

For your edit, that part is now a (fairly trivial) statistical question involving the binomial distribution with p=0.5 and n=23.

I have seen a spreadsheet with percentiles with real data. I cannot recall where it was, but that resource exists.

Setting up the binomial distribution:
For generation F1 each parent (F0) has a 50% chance of contribution the chromosome (under your simplified model), i.e. p=0.5, n=46 for the binomial distribution. I assume that when you say the 'normal' range you are looking for the mean +- 1 standard deviation? For p=0.5, n=46: mean=23 with standard deviation=3.39116 which helps define: Pr(20≤X≤26)=0.698. So in about 70% of cases a child will inherit 20-26 of their chromosomes from one parent.
For generation F2 each grandparent has a 25% probability of contributing a chromosome so we use p=0.25, n=46 which gives: mean = 11.5, standard deviation=2.93684 Pr(9≤X≤14)=0.6936. So in about 70% of cases a grandparent will have contributed 9-14 chromosomes.


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Can anyone identify this spider for me?
There is a spider on the window of my office that I've been trying to identify for the past few days but can't quite figure it out. My coworker thinks it's a Furrow Orb Weaver but I'm not sure. My office is located near Raleigh, NC and unfortunately I'm on the third floor and the spider always faces away from me, so these are the best pictures that I could get.
[


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Chickpeas as feed for house sparrows , ringneck parrots?
I've put up a bird feeder outside my house, and so far I have been feeding uncooked
 white rice , and the birds seem to enjoy them.
However, since I read somewhere  that a variety should be maintained in the diet, lest the birds start suffering malnutrition, I want to know whether I can use chickpeas as a substitute for a while. Is it safe for house sparrows, ringneck parrots ? These are the only type of birds that have been visiting my feeders for a while now.
Thanks !

I have read that raw rice can be dangerous for birds to the extent that it should not be thrown at wedding., It absorbs water and swells to a dangerous level. From personal experience I can say that can happen in a dog. Why not use bird seed ?

Sorry, but uncooked rice is not harmful for birds. For the time it takes for rice to expand in presence of water, it already gets digested and broken down in the bird's system. So the question of swelling doesn't arise. I have seen parrots break the seeds into smaller pieces before swallowing, so no question of trouble there too.


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Protein A-antibody SDS-PAGE
I wanted to know whether the boiling of Protein A- antibody complex for SDS-PAGE analysis will disrupt the interaction? and result in dissociation of protein A and antibody?
Thank you

Yes. Samples for SDS-PAGE are mixed with a loading buffer containing SDS (final concentration of SDS is usually 2%). Generally, the SDS will disrupt protein-protein interactions, even before boiling. Reducing agent (usually DTT or b-mercaptoethanol) is added to disrupt disulfide bonds.
See diagram here.
There are, however, exceptions. Some protein complexes/multimers are resistant to SDS until boiling, and some even maintain interactions after boiling. Some examples: Xia et al 2007, Kubista et al 2004, Grigorian et al 2009.


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What is this? I found it in tofino, Vancouver island

I'm wondering what this sea creature is that I found washed up on McKenzie beach in Tofino, Vancouver Island? It wasn't dried up or anything. I've seen hundreds before but I cant find anywhere on the internet what they are!


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Why do some ant workers still wander at night?
As far as I have seen, the vast majority of workers in colonies of diurnal, non-nomadic species return to their nests and remain there at night. The colonies seem to forage largely during the day. However, a few individuals of said colonies would still wander far from the nest at night. I don’t believe they are lost because they still seem to be following pheromone tracks.
Why do they do that? What drives them to still come out at night and not remain in the nest like most other workers do? Are they any different in terms of caste? Are they always the same individuals? Is there a selection process to decide who will wander off at night? Are they somehow invalid and can't tell day from night? Is that somehow evolutionarily advantageous (e.g. having a few workers take some risk at night, maintaining the pheromone tracks throughout the night so that the other workers don't have to start all over the next morning)?
Someone (jokingly) told me those ants must still be hungry, but I don't immediately buy that explanation because my understanding is that most species will store food in the nest in one form or another anyway, or they just share food by trophollaxis.

I wonder if the nocturnal ones might have been affected by the Dicrocoelium dendriticum parasite. Can you take a look at https://biology.stackexchange.com/a/89248/55929 and let me know if the ant behaviour matches that given in Example 3 there?


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Formation of disulfide bonds in protein expressed after transduction
Say I transduce a nucleic acid sequence using a viral vector that encodes a protein having at least one disulfide linkage. For simplicity, let’s assume that there are only two cysteines in the protein and the side chains of these cysteines are close together when the protein is folded with the cysteines unlinked (reduced/thiol). Also assume that the cell being transduced is a eukaryotic cell (mouse or human). What is the chance that this disulfide will be linked (oxidized) when expressed by the cell? Does this happen pretty reliably? What might it depend on?

Could you please clarify. 1. By the use of the word transduce I assume you mean by a viral vector. Is that correct?If so, what vector? 2. By cell I assume you mean a eukaryotic cell rather than a bacterial cell. Perhaps you could edit your answer and also change the title to something more precisely descriptive like "Formation of disulphide bonds in proteins expressed after transduction".

In the protein intracellular or secreted?

@canadianer The sequence includes a secretion signal and meant to be secreted. These comments are giving me some ideas about what the formation of disulfides might depend on.

A lot depends on the nature of the disulfide; it may form in the ER during folding. It could also form in the oxidizing extracellular environment.  I don’t have any experience with expressing exogenous proteins in eukaryotic cells so I can’t be of much help.

I am not an expert on expression of genes from viral vectors, but as I requested the poster to clarify his question I feel an obligation to provide at least a partial answer.
The first question to address is whether the mRNA for the protein of interest is expressed in the same way as normal cell proteins. In the case of the lentovirus vectors which are integrated into the genome there is no reason to think otherwise.
In this case the factors determining the formation of disulphide bonds would be the same as for any similar normal cell protein translated from mRNA.
In summary:

Only secreted proteins have disulphide bonds.
In eukaryotes these protein are synthesised on ribosomes on the endoplasmic reticulum, which obviously must be present in the cell in which one is trying to express the protein (i.e. it must be capable of secreting proteins). One assumes that if one is restoring a function found in normal cells this will be so.
Oxidation of sulphydryl groups occurs in the intercisternal space before secretion. It involves a number of proteins and there are reduction and chaperone systems to deal with inappropriate oxidation, which occurs to a greater or lesser extent. A recent freely-accessible account of this topic can be found in a Cold Spring Harbor perspective by Neil Bulleid in 2012.
The (small?) proportion of incorrectly oxidised proteins that are not recycled are presumably removed by the cellular mechanisms that degrade aberrant proteins.

It would not seem possible to answer in a literal manner the question what the numerical ‘chance’ is of correct oxidation, but this would not seem to be pertinent. The question of interest is whether the protein would be oxidised to the correct native structure with the same efficiency as in normal circumstances. There seems no reason to think it would not.

This answer gives me ideas about how to start understanding my problem and what issues might be involved (the viral vector, the secretory pathway, protein disulfide isomerases).

I know you said you are not an expert on gene expression from viral vectors, but you mention "whether the mRNA for the protein of interest is expressed in the same way as normal cell proteins." This implies that there might be vectors that don't express proteins in the normal way. Did you have a particular example in mind?

@WaterMolecule — The way you phrased your question suggested an assumption that the insertion into the viral vector and it’s incorporation into the host genome were done correctly and that the gene would be transcribed normally. Thus your main concern was disulphide bond formation. I was able to answer the latter. However the former is not necessarily straightforward, and if that is a concern you would need to read specialist reviews of that area.


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Can anyone identify this insect from India?
Found this bug in Chennai. Curious to know what kind it is. Does it pose any danger?

This is definitely a bug - as indicated by the characteristic body form and the segmented (it should be five) antenna. My guess here is that this is Nezara viridula, also known as the "southern green stink bug" or the "southern green shield bug".
See this image (from here):

Besides being a pest for agriculture, they are harmless and not toxic, although they can spread a stinking substance when threatened, hence their name. You can find more about them here and here.

Looks like a common green stink bug - https://en.wikipedia.org/wiki/Green_stink_bug
Give it a test. If you put it into a handkerchief and scare it a little, it should give off a foul smelling odor

Unfortunately the article linked by you limits the distribution of the bug to the US and parts of Australia.

The edges around its body also differ from the OP's images

the exact same bug is present in central Europe. I saw it today. So maybe the wikipedia article needs updating

the edges around it's body might be different because of the age difference. The body shape (hexagonal back) looks identical though


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Linkage terminology in drosophila
Consider two linked loci that are 50+ map units apart. I perform a test cross between a female that is heterozygous at both loci to a male that is homozygous recessive. In this case, the phenotypic ratio of the offspring will be 1:1:1:1 suggesting that the loci are independently assorting. Then, I cross a heterozygous male to a homozygous recessive female. In this case I will have just two phenotypes due to the lack of recombination in male drosophila. Do I describe the loci as linked or unlinked in this scenario? Do we consider the loci to be linked for males and unlinked for females?

Is this a homework question? If so please tag it as such and read the site guidelines on homework questions.

No it is a hypothetical. I've never actually come across such a scenario nor have I found any information on it. I just want to know about the terminology.


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Effect of light intensity on the frequency of stomata
According to this article, the frequency of stomata increases with an increase in the intensity of light. What I inferred from this is, since the rate of photosynthesis increases at higher light intensities, more C02 is is required and hence the frequency of stomatal openings increases.
I know that the Light Harvesting Complexes inside chloroplasts use light to release electrons, which are then subsequently used in photophosphorylation. If we compare the process with the photoelectric effect, we shouldn't see an effect of the intensity of light, but instead we should see changes for different frequencies(which we already do).
So how does the rate of photosynthesis increase with higher light intensities?
Is the mechanism of light absorbtion by LHCs similar to that of a photoelectric cell?

You are misunderstanding photoelecric effect.
Intensity of light does not have effect on maximal kinetic energy of individual ejected electrons. Maximal kinetic energy of ejected electron is determined by energy it can get from single photon which is in turn determined by frequency of light.
However, intensity of light definitely does have effect on number of ejected electrons. More incident photons (higher intensity of light) result in more ejected electrons (and higher measured electric current).
In photosynthesis number of utilized photons is more important than their energy. Photon either does have enough energy for separating the electron (e.g. red or blue light) or it does not (e.g. infrared light). If a photon with energy higher than needed (e.g. blue light) is captured then the excess energy dissipates to heat.


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What bug is this? Manchester, UK
The creature appears to have a green body with 5 legs of the same size, and one longer than the rest. It moved this long leg around, and it looked like it was using it to sense it’s surroundings.
Location: Manchester, United Kingdom

Looks like a harvestman (daddy long legs). What size was it? You can try identifying it with the tool here: https://harvestmen.fscbiodiversity.uk/ The image isn't clear enough for me to try.

That looks like what I would call a "daddy long legs", also known as harvestmen. These are arachnids of the order Opilones. There are some 30 species of harvestmen found in the UK. The webpage https://harvestmen.fscbiodiversity.uk/ has a very useful identification tool and based on it, I believe your photograph shows a Leiobunum sp. A:

Please visit the site itself for more details as it doesn't allow copying.

Great ID resource! Bookmarked it for later use.

It's my understanding that crane flies are called "daddy long-legs" in the UK.  So using that name for a harvestman over there might cause confusion.

@EldritchWarlord yep, but I was raised calling them daddy long legs, and I'm not about to change that because I now live in London :) but that's why I mentioned the BrE version too. They're called harvest men there.


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Why isn't life expectancy normally distributed?
Lots of phenomenon in nature can be plotted onto some sort of normal distribution, and that makes intuitive sense to me (such as human height). Why then, does global human life expectancy drop off so suddenly after ~85 years old? Is there some factor which suddenly increases mortality significantly? How come so few people (statistically speaking) age above 85 years old?

Inspried by this question

There's no particular reason everything in nature needs to fit a normal distribution; normal distributions are just one of many different types of naturally-occurring distributions. In some cases, the other types can be transformed (e.g. by logarithms) into a normal distribution (e.g. a log-normal distribution), in other cases not so much.
As to why it doesn't match a normal distribution? Normal distributions tend to occur when they're the sum of many independent processes. Mortality factors aren't independent. Many factors that affect mortality are age-dependent (cancer, heart disease, etc), so they depend on the same factor (age) and accumulate at the same time, not independently. Therefore longevity doesn't meet the basic expectation for a normal distribution.
If you look at specific mortality factors, you might well find some that are relatively independent of age, and these might be closer to normally distributed. But age is extremely important for most forms of mortality, even those that don't accumulate with age (automobile mortality is higher in younger drivers; infectious diseases disproportionately target the very young and very old; maternal deaths are more common in younger to middle-aged women).
Instead, longevity is a negatively skewed distribution. It may crudely be considered as a log-normal distribution, though not perfectly. There are also more sophisticated approaches to model mortality distribution, such as the Gompertz–Makeham model (simplistically, an exponential increase in death rates with age), or the Weibull distribution.
Various publications compare models, or come up with new and shinier models, for longevity:

Comparison of the Gompertz and Weibull functions as descriptors for human mortality distributions and their intersections
A Novel Generalized Normal Distribution for Human Longevity and other Negatively Skewed Data
Predicting Human Mortality: Quantitative Evaluation of Four Stochastic Models

The histogram you show isn't a distribution of age-at-death for individuals, it's a distribution of life expectancies for different countries.  The post you link takes data from a table on the Wikipedia page List of countries by life expectancy.  Interpreting the histogram you posted, we see average life expectancy seems to hit a wall around 85.  This does not mean that individual human life span is not normally distributed.
Excluding deaths at infancy, the peak of the death rate curve appears to be at about 88 years for women in the United States in 2014, as seen in a blog post by the The Max Planck Institute for Demographic Research:

Lifespans are increasing and becoming more similar: While life expectancy of US women rose by almost 19 years between 1933 and 2014 (from 62.8 to 81.3 years), the variance in the distribution of deaths over age shrank by ten years. Data: Human Mortality Database © MPIDR


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Identify this insect (looks like part of a tree)?
I found this insect and thought it was part of a tree at first, then it moved and so I knew it was an insect. I've never seen it before though so I am posting here hoping someone knows what it is.

The location is North East US, during the day, in a tennis court surrounded by trees. The insect was clinging to the cover seen above (which covers the tennis court fence).
Any idea what this insect is called?

Good pics, clearly some kind of stick insect, someone will know it.  Can you add info about your location etc, as much info as you can as suggested here?

Not posting as an answer since I am not an expert, but apparently Diapheromera femorata is the most common species across much of the US.

Bryan, I think you're right! I just googled "Common walkingstick" based on your link, and under image it shows the same exact one. I will accept an answer once you post it, thanks a million!

Let's try to draw the attention of @KarlKjer he will know for certain, the details to check...

It's really hard to identify species with a photo, and I suspect the user just wanted to know it is a walking stick. Thanks for the vote of confidence, but I' not an expert on walking sticks.

Alight, best guess, based on it being the most common species, a decent match in pictures, and a decent match to the description on Wikipedia is Diapheromera femorata, the common walking stick.


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How does the glycocalyx of cells attach together if they are negatively charged?
Context

Thus, the entire outside surface of the cell has a loose carbohydrate coat called the glycocalyx.
The carbohydrate moieties attached to the outer surface of the cell has several important functions:

Many of them have a negative electrical charge, which gives most cells an overall negative surface charge that repels other negatively charged objects.

The glycocalyx of some cells attaches to the glycocalyx of other cells, thus attaching cells to one another.

[Guyton and Hall, Textbook of Medical Physiology, 2nd South Asia Edition ( w.r.t 13e)]
Here, two contrasting statements are written. They seem to differ in the context. Actually, I tried searching for more about glycocalyx and saw the same written in many places without explanation. I cannot understand that how the cells can be attached, if both of them are negatively charged.


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Glycosidation and glycosylation
I read somewhere that the function of Golgi bodies is glycosylation and glycosidation. What is the difference between the two? I searched google but it gives complex answers.

“I read somewhere” is not adequate for this list. Unless you can tell us where and either cite in full we cannot assess the accuracy or examine the context of your assertion.

Glycosylation is a controlled process that involves a carbohydrate being attached to a hydroxyl or other functional group of another molecule. I think you meant to say glycation instead of glycosylation, and that is a random process that involves free sugars attaching to proteins.
https://www.neb.com/faqs/2015/04/10/what-is-the-difference-between-glycosylation-and-glycation

Welcome to [biology.se]. Can you please add some references to support your answer? References are useful for users to verify the answer and for understanding the topic better.

Sure, my bad. https://www.neb.com/faqs/2015/04/10/what-is-the-difference-between-glycosylation-and-glycation

Thanks for the reference. Please [edit] your answer to include it. Comments are only meant for temporary suggestions/requesting clarifications.


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Do astrocytes connect and chemically communicate with other astrocytes?
I am building a novel model of neural tissue for the purposes of Machine Learning and am currently trying to unpick the functions of the astroglia.
The literature suggests that astrocytes ensheath synapses, providing them with structural support, given that the synapse is an oily droplet between two neuron 'tentacles' this makes sense, performs caretaker functions at synapses it ensheaths with regard to neurotransmitters and, via its perivascular feet, provides resources from nearby blood vessels.
The literature goes on to suggest that the astrocyte may play a role in some neurological disorders if the ionic 'effects' from one set of perivascular feet, namely one set of synapses, 'leaks' across an internal chemical barrier within said astrocyte, to spread the 'effect' to another set of perhaps unrelated synapses. I can see how this could influence and cause unrelated learning, which may be a hallmark of some neurological disorders, one of which the paper suggests is schizophrenia and its patterns of unearned and irregular learning.
I can appreciate how some form of localized learning or whole- or partial-pathway learning, as opposed to pure individual neuron-level learning, would certainly be beneficial to a learning network in speeding up learning.
Do astrocytes connect to astrocytes and if so how and what chemical messaging is present there?
I apologize that I am not a neurochemist only a software developer with a background in electronics and while I can follow some of the chemistry, I am interested in the functional purpose of these biological components. Nature only had chemistry to work with when these mechanisms evolved but, as an aside, if it had had access to electronics and software, one supposes the neural tissue would have been far easier for us to comprehend.

Astrocyte‐to‐astrocyte contact and a positive feedback loop of growth factor signaling regulate astrocyte maturation
(29 April 2019)
by Jiwen Li, Rana R. Khankan, Christine Caneda, Marlesa I. Godoy, Michael S. Haney, Mitchell C. Krawczyk, Michael C. Bassik, Steven A. Sloan, Ye Zhang
Published 'Glia'
This appears to give me the details I required.
Astrocyte maturation appears to be accelerated due to chemical signalling from astrocytes in their vicinity, but astrocytes do not 'signal', as understood as a network learning characteristic, to each other.
Thank you for your assistance.


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What's the difference between the terms "gene map" and "genome"?
It seems some sites arbitrarily restrict "gene map" to only a single chromosome, but others don't. Supposing we don't restrict it to just a single chromosome, is it different from "genome"? Are these two terms just synonyms?

Welcome to SE Biology. Please indicate your sources when posting questions of this type. We need links to example sites and text citations to clear up possible misunderstandings. (You should also read how to ask a good question in the Help — "Search and Research".)

This question can be easily answered by reference to reputable sources on the internet, but as it is important to encourage the general use of the term, Genome, I shall cite examples.
Genome

WHAT IS A GENOME?
A genome is an organism’s complete set of DNA, including all of its genes

US National Library of Medicine, Genetics Home Reference
Genetic Map

the arrangement of genes on a chromosome

Merriam Webster Dictionary
This is actually definition 3 of map in the dictionary — i.e. a variant on topological maps. The scientific usage is made clearer in the following:
Mapping

DNA mapping refers to the variety of different methods that can be used to describe the positions of genes. DNA maps can show different levels of detail, similar to topological maps of a country or city, to indicate how far two genes are located from one another.

Nature Scitable
Distinction in a nutshell
A Genome is an entity — a Genetic Map is a graphical representation of features of that entity.
Hence the following sentence makes sense:

There is no genetic map for the genome of Bacillus obscurus.

The two terms are certainly not identical. The confusion of the poster may relate to the practical limitations of representation such that often the map of only one chromosome is presented at a time.

Gene map is the spatial arrangement of genetic markers and the relative distance between each of them. While the genome includes the entire hereditary information of the organism; this includes both genes and the non-coding sequences of DNA (introns).


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How do I prepare a Basal medium for autotrophic mutant creation
Minimal medium (MM) was prepared by adding 2.0 g sodium nitrate (NaNO3) to 1 L of basal medium (BM) fol- lowing Correll et al. (1987). Chlorate resistant sectors (CRSs) were generated on two media i.e. MM and PDA containing 2.5% chlorate (KClO3), represented as MMC and PDC, respectively. The chlorate served as a toxic ana- logue of nitrite (Corell et al. 1987). Four phenotyping me- dia (Correll et al. 1987) were used i.e., i) sodium nitrate (NaNO3); ii) sodium nitrite (NaNO2), 0.5 g of NaNO2 was added to 1l BM; iii) hypoxanthine (HX-), 0.2 g of HX- was added to 1l BM; iv) ammonium tartrate (NH4+), 1.0 g NH4+ was added to 1l BM. MM was also used in pairing of the complementary nit mutants
I’ve tried using the procedure on above but the minimal media is not solidifying

Welcome to SE Biology. Please do not present text as images. It discriminates against people with visual problems and is not indexable by the site. Type out as much as is necessary and provide a link to the source.

How do you expect the medium to solidify without adding any gelling substance like agar?

I added agar to it but it still did not gel


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Why does X inactivation happen?
Is X inactivation really important? Why don’t the dominant genes on one chromosome mask the recessive on the other chromosome? This happens in other sets of chromosomes so why exactly does this happen in the sex chromosomes of a female?
And during x inactivation in the blastula isn’t there a heightened possibility of getting a disorder since you might be inactivating the normal genes and allowing the x linked recessive disorder to show up?

Welcome to SE Biology. Please read the Tour and consult the Help on asking questions. You will see that you are expected to do some research before posting. Where have you looked for articles about X-inactivation? I imagine any account would explain why it is necessary and perhaps even mention alternative positive compensation mechanisms in other species, eg Drosophila. If this is still unsatisfactory come back and tell us why.

Out of frustration I have to say to all downvoters, that I found this question, particularly the last sentence, helpful. I understand that we are supposed to do the research first but it is not helpful when the first thing you do is downvote us.

If both X's are active gene expression is doubled which causes all sorts of abnormalities. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1686009/
a good and short explanation of X inactivation - https://www.youtube.com/watch?v=Y9vXhmI5FXM
Not all cells have the same X inactivated. It happens randomly so women are mosaics of lineage cells with different Xs. If there is a disorder due to bad mutation in one X, it's not present in all cells. This is the reason why boys with MECP2 gene mutation die shortly after birth while girls can live with Rett syndrome. Because not all cells carry the mutation so it's not as bad compared to when boys inherit it

Hi Retardi Grade, I see your profile says you are an independent researcher. Is there any way I can get in touch with you?


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Why is there a mass limit on biological powered flight?
So, this is a thing I never fully understood. There are a lot of reasons for a flying creature to be limited in mass (though I'm unsure if I'm familiar with all of them), from energy consumption to material strength. However, there seems to be an argument that goes along the lines that over a certain mass, no matter what, they can't generate enough power to counteract gravity.
What limitation could they exactly mean with that?

The design of the “wing” and its materials...

One of the physical limits to biological flight is muscle physiology.
Muscle force output is proportional to muscle physiological cross sectional area (PCSA) multiplied by its specific tension (Gans, 1982):
$$F = \text{PCSA} \times \text{Specific Tension}$$
PCSA is basically just the cross-sectional area of a muscle adjusted for its architecture. Pennate muscles have higher PCSA than parallel fibered muscles, because more fibers are packed into the area (at the cost of shorter functional distances). Specific tension is the force output per unit area. For a single species, specific tension is essentially constant.
So the way to make more force is to make more PCSA. But muscles don't scale only in area, they scale in volume as well. Increased volume increases mass as a cubic power, but muscle area only scales as a square power. So any increase in area that requires a volume increase (which is inevitable), will quickly outstrip any gains in force output.
Note that this doesn't mean that very large flying vertebrates were not possible: the largest pterosaurs (e.g., Quetzalcoatlus) had ~15 m wingspan and perhaps weighed 200 kg and the largest birds (e.g., Argentavis) had ~7 m wingspan with a mass over 50 kg. Both, however, were likely gliders.
Gans C. 1982. Fiber architecture and muscle function. Exerc Sport Sci Rev 10:160–207.

There's also the aerobic/anerobic issue.  If you look at the largest flighted birds, they actually use powered flight for very short periods, usually to get airborne.  Then they will soar (or like the albatross, use lift from ocean waves), which uses only a miniscule amount of muscle power for control.  Just as humans in sailplanes or hang gliders can stay aloft for many hours in favorable conditions, if they're towed up or launch from a high place.

Weird. Doesn't the square-cube law apply only when you scale an object in all three dimensions?

@Mephistopheles yes which is the problem the weight increases by the cube but the strength only increases by the square. so you reach a point were you can't add more strength without adding more weight than that strength can offset. And not just muscle, bone and connective tissue have the came problem.

@John I know, but can't you just... make it thicker without changing the length of the fibers?

@Mephistopheles the issues is if you make the muscle thicker you make it more massive, you also have to make the ligaments thinker and more massive becasue they are taking the load, then you have to do it for the bones., ect, then you have to do it for the digestive system and cardiovascular system supplying those muscles, and the lungs, and the ect. it is like the worlds least favorable rocket equation. If you just make hte muscle thicker without changing anything else it just tears itself apart, (which can happen to bodybuilders that put on muscle too fast).

@John So, in the end, it all boils down to material strength?

@Mephistopheles You also get the same problem with the wing themselves, the lift increase with the surface area (a square) the mass increases by the cube. soon the wings weigh more than the air they can shift. It is not just strength it also also things like oxygen (lungs also work of surface area) Muscle is just the most unalterable limit they hit first.

@Mephistopheles there are a few other problems you run into that are well covered in this fun video. https://www.youtube.com/watch?v=faBguu_6LBI

@John So, they also have to keep the wing loading constant. What's up with aspect ratio?


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How does antagnostic coevolution work in ducks?
I recently learned that in ducks, the penis and vagina have coevolved: the vagina of the female ducks gets dead-end sacs and clockwise coils; the penis of male ducks become longest and its morphology changed to adapt to the female vagina. [1] This antagnostic coevolution happened due to the evolutionary arms race between male and female ducks.
This seems counter-intuitive when we think about natural selection. Indeed, if female ducks are forcibly copulated, they are more susceptible to reproducing themselves and sharing their genetic traits.
From  [2], it appears that only 3% of forced copulations results in fertilization. If this is the case, why has the male phallus evolved this way? Indeed, it does not appear to me to be a good evolutionary strategy.
If [1] and [2] are correct, I would think that the duck vagina and phallus shouldn't have coevolved that way. What am I missing?
[1] Brennan, P. L., Prum, R. O., McCracken, K. G., Sorenson, M. D., Wilson, R. E., & Birkhead, T. R. (2007). Coevolution of male and female genital morphology in waterfowl. PLoS one, 2(5), e418.
[2] Burns, J. T., Cheng, K. M., & McKinney, F. (1980). Forced copulation in captive mallards. I. Fertilization of eggs. The Auk, 97(4), 875-879.

Your question is unclear what don't you understand, preferential mate selection? That male and female genes can have an antagonistic relationship?

@John I don't understand why phallus AND vagina evolved that way. According to me, if females are forcibly copulated, their genes should spread (so no dead-end sacs vagina). But if forced copulations don't result into fertilization, it is a bad reproduction strategy for males and they should evolved in a non-rapist species. However, it is not what we see and that is what I don't understand.

There is a difference between spreading your genes and spreading your genes in the most effective way, it is the same reason animals are picky about mates, A male who mates with a female can go find a different female the next day, an impregnated female now can't mate even if better males are available.


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Lions protecting girl in Ethopia -- how plausible is it that they understood situation?
Several years ago we read of a girl who was apparently threatened by humans being protected by lions who chases off the males and stayed with the girl. Explanations like, "her crying resembled that of a cub" etc. were invoked.
Why is it so hard to believe that adult lions who almost certainly know the difference between a lion cub and a human could not have been acting altruistically as they sometimes apparently do with, for example, prey animals that they sometimes encounter? If a domesticated dog or cat protects a human, we accept that they know what they are doing, do not confuse the human with their own young. Lions are plausibly more intelligent than a dog or cat or at least within the dog/cat range.

It would be great if you link the article which reports this and also the ones that provide the explanations?


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Where is catalase produced?
I am doing a research project on the peroxisomes, and in it I referenced the enzyme catalase, which breaks down hydrogen peroxide into water and oxygen. However, the assignment asks me to specify the production location of all enzymes, and I cannot find any useful information about where the enzyme is created. I think it is created in the peroxisome itself, but am not so sure of that. Where is catalase produced?

According to this source https://www.ncbi.nlm.nih.gov/books/NBK26858/ , peroxisomes don't have ribosomes. Thus the source of catalase isn't the peroxisome.

According to this source all peroxisomal proteins are synthesized on free ribosomes in the cytosol.


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How can cats' claw grow sharper without replacing the claw?
I cut my cat's claws once a month. The claws always have pointed and sharp tip even though I had cut them last month. I assumed cats cannot change the shape of the claw by growing new keratin at the tip. Also it does not looks like the cat grow a new claw and abandon the old one every once a month or so. How is it possible that the claw grow sharper?

The horn has a specific structure which is different from the round edge that we see on our fingers. It splinters and cracks into flakes, so it is more similar to a flint than a chalk.
The outside of the cone dries out and flakes and is scratched off by the cat, while the inside of the cone is the newer horn that grows towards the apex as a new blade edge.

The image is from this research. If you search "sharp" you will find astonishing vetinary descriptions quoted. Also see page 641 for the conclusion of the research. He sais that it seems to have evolved in the aim of keeping the feline claws sharp.
If someone has the technical ability to rewrite the researcher's descriptions into everyday words, you would be a first.
Vetinary research quote:
The horn-generating living blade epidermis that is
located most centrally on the slanted face of the curved
ledge is continuous with the parietal epidermis (Fig. 9b),
so that the blade epidermal cells generated here lie next
to the parietal epidermal cells. Therefore, the cornifying
parietal epidermal cells are deflected and entrained apically
as the blade horn is pushed apically by the proliferating living
blade epidermis. The direction in which the blade horn is
pushed forward can also be inferred from the arrangement
of the ridges visible on the dermo–epidermal interface of
the parietal horn (Fig. 7). The living blade epidermis that
is located at the outer edge of the face of the curved ledge
is continuous with the living epidermis of the proximal
cone horn (Fig. 9b). These lateralmost blade epidermal
cells, therefore, form a layer that lies directly underneath
the deepest layer of proximal cone horn, so that the
boundary between the blade horn and proximal cone horn
is indistinct. Hence, the layers of horn that are generated
in the dorso-proximal bend of the curved ledge underneath the combined horn layer of the external coronary
and proximal cone horn cover the sides of the apical cone
horn and are designated as part of the blade horn. As
the superficial coronary horn on the dorsal side of the
cornified claw sheath is worn off through normal use, the
superficial layers of the blade horn are exposed and are
shown to hug the sides of the apical cone horn (Fig. 13a).
Remnants of these blade horn layers are discernible near
the very tip of the cornified claw sheath, which consists
mostly of apical cone horn, because the rest of the coronary
horn, including most of the blade horn, has been worn off
(Fig. 13b,c).
The remaining soft-cornified horn segments of the
cornified claw sheath are found in places where the
hard-cornified horn divisions need to be supported and
cushioned.
The soft-cornified terminal horn is a segment of the
third major horn division (i.e. the Hyponychium; see Table 2).
It is generated by the living terminal epidermis, which is
continuous caudally with the parietal living epidermis and
is supported by the dermis that covers the medial, lateral
and palmar sides of the tip of the bony unguicular process
(Figs 3a, 4a,c, 7, 9b, 11a, 12a–j). It supports the apical cone
and crest horn on its dorso-distal side (Figs 3a, 4a,c, 7, 9b,
13b) and the blade horn on its lateral and medial sides
(Figs 4b, 8, 9b–d, 13a,b). By filling the space created by
these converging segments of hard-cornified internal
coronary horn, it is shaped into an elongated, pointed
cone and extends proximally between the blade and
sole horn (Figs 12c,d,f,h,j, 13a,b). Because the terminal
horn is soft-cornified, it can adjust its shape to the
changing conformation of the space it fills in the course of
the deformations of the cornified claw sheath during its
normal use.
The friable soft-cornified sole horn is generated by the
living sole epidermis, which is supported by the dermis
that covers the proximo-palmar side of the bony unguicular
process (Figs 3a, 4, 7, 8, 9b–e, 12c,d, 13a,b). Along its medial
and lateral sides, it is embraced by the terminal and parietal
horn (Figs 1b, 4b, 8, 9c,d, 13a,b). The sole horn, therefore, fills
the space between the paired cutting edges of the cornified
claw sheath. It is worn off through natural wear and tear,
as well as through repeated compression and release, as
the cornified claw sheaths are deformed when they are
subjected to tensile forces during climbing and prey capture.

Differential wear like this is a common sharpening method throughout biology, from beaver teeth to limpet teeth, to beaks and claws.

Feathers and claws come from re-arranged versions of the same cell groups. The researcher wanted to devise a general theory for many animals, to see if the mechanism is the same for beaks also, so he used cat's claws because they are readily available. He states that it is different for beaks. The cat's claw is nearly the same as the human nail, and small differences in arrangement of the keratin producing cells produces striking differences in the resulting claw. The cat has the same fingers as us with keratin producing cells arranged in an arc. It's a difficult document to comprehend.

Genetic codes paralleling claws/beaks/feathers: https://static-content.springer.com/esm/art%3A10.1007%2Fs00709-016-1019-2/MediaObjects/709_2016_1019_MOESM2_ESM.jpg from here: ... https://link.springer.com/article/10.1007/s00709-016-1019-2


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Which fishes produce alarm signals to warn other group members about in coming predators
Atlantic Goliath Groupers are fishes which produce unique low frequency sounds to mate and when approached by predatory fish . The sounds produced when approached by a predator (or even a scuba diver) are different from those produced whilst mating.
The problem is this fish is found only in the Atlantic.  I'm specifically looking for fishes in the Indian ocean . Thank you for ur time :)

Here are some fishes produce alarm signals as sounds.
members of family Pamadasyidae-the grunts.
the family scaridae e.g.—Parrot fish.
sea catfish Galeichthyes felis
gafftopsail catfish
Indian loach
Trigger fish
Epinephelus striatus
For mor information see the link. http://www.fishfarmingtechniques.com/fish-structure/specialized-organs/sound-producing-organs/sound-producing-organs-in-fishes-specialized-organs-fisheries/13563


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What happens to the absorbed blue and red light in the chlorophyll molecule?
If the chlorophyll molecule (its chromophore) absorbs red and blue light and reflects green light, shouldn't the absorbed blue and red light be emitted back when its excited electrons relax?

It is glad to say that we can enter to this question due to having of valuable theorem of 1st law of thermodynamics. Energy cannot be destroy but it can convert in to another type of energy.The chlorophyll molecule decide it to, become photo energy to chemical energy.

while happening the electron transport chain electrons are going through the primary receptors. This is not happening as the electrons traveling on a trip, this is really a complicated procedure.While they are passing through the primary receptors some reactions are happening. So from which should be contribute to have energy for this reactions. By the energy of absorbed blue and red lights. So it turns it to chemical energy. It store as ATP, and NADPH. So there is no more way for emit that light away. This scenario  is firm by the following.

Reference
- The Light Reactions of Photosynthesis. In: Biochemistry. 5th ed.


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Flowers sent by the birds
Birds have sown seeds on my ground and this beautiful flower has sprung.  What's the name of this flower?
I live in Sao Paulo, Brazil

It's a type of begonia. With 1800 species in the genus, it's hard to say which it is, but the leaves which seem palmate would place it in the aconitifolia species. Your leaves don't appear to be variegated, and your flower is deeper pink, but it's the same flower species.


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Identify brain junk - What are all the known intracellular and extracellular substances which build up with age and clog the brain?
What are the known junk substances which the body is unable to dispose of and which build up in the brain with age to eventually causes age related problems?
Starting with the most obvious ones:
Amyloid beta - https://en.wikipedia.org/wiki/Amyloid_beta
Lipofuscin - https://en.wikipedia.org/wiki/Lipofuscin

I'm voting to close this question as off-topic because a group effort to draw up a list is not a question in the terms of SE Biology.

@david it would be valuable info to have it all in one place, don't you think? I reworded the question

It may well be, but that place is not here — this is a site for answers to specific biological questions. I could perhaps also have voted to close on the basis that your question was too broad, but I thought your misunderstanding of the way SE works needed addressing.  Imagine there are reviews on this topic by people far more expert than those on this list.

Another example is the paired helical filament of Alzheimer's disease, so-called because neurofibrillary tangles have a ribbon-like structure when viewed under the electron microsocope.
It is now accepted that paired helical filaments consist of a single protein, microtubule-associated protein tau, in a polymerized and hyper-phosphorylated state. (see Lee and co-workers).
This old answer might also be of interest and contains a fuller reference list.
Neurofibrillary tangles are one of the two characteristic lesions of brain first described by Alzheimer, and are intracellular. The other characteristic lesion is the extracellular neuritic plaques caused by the build up of amyloid-beta (as the OP points out), which is itself part of a much larger transmembrane protein (of unknown function), the amyloid precursor protein or APP.

RNA-binding proteins TDP-43 and FUS form aggregates that accumulate in the cytoplasm, whereas these proteins would normally be predominantly soluble within the nucleus and shuttling to and from the cytoplasm. - https://www.ncbi.nlm.nih.gov/pubmed/23463272/


text:
Can someone explain this phenomena?
So many parakeets sitting on a tree with no leaves ?

What is your question? Can you please elaborate?

Why are so many parakeets sitting on a tree with no leaves. ?

Please [edit] your question to add all necessary details. Comments are only for requesting clarification. Anyway, can you add why you think this is unusual? Are all the parakeets in this area just sitting on this one tree?

Generally, birds reside on trees during evening and night but those trees do have leaves and hence birds build nests there. Are these parakeets sleeping, if yes then why on a tree with no leaves. And why is such big number ? Is this a specific kind of behaviour ?

Shubhanshu, as I said, please [edit] your question to address these points. Comments are not indexed and hence not searchable. They can also easily go unnoticed. Therefore comments are used only for temporary purposes. A post should be self-sufficient.

phenomenon —  singular. phenomena is the plural

Parakeets are social animals that live in large groups (flocks). Under ideal environmental conditions, they can form flocks composed of thousands of birds. http://www.softschools.com/facts/animals/parakeet_facts/1274/
The fact that this tree is without leaves is irrelevant to the Parakeets. They may or may not have caused it. They chose the tree as a place to relax. It could have been any other convenient place though. If you search google images for "parakeet flock" you will see them perching on various other surfaces in a similar manner


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What makes learning more difficult as we age?
Why is it harder to adapt yourself to different cultures, places, and languages as you age? What makes breaking up with emotional patterns or ideas after years of habit more difficult?
Is there a natural process in which the neuron's synapses are set, while later in life the plasticity of the brain is nearly lost?

I think you need to first provide some evidence that is actually is more difficult.  (Leaving out degenerative disease &c, of course.)  You're perhaps confusing a lack of desire with a lack of ability.  After all, most of us spend much of our lives arranging our circumstances in ways that we enjoy.  Without some strong motivation, why should we want to change?

I don't think age is the major factor.  There is plenty of evidence that physical and mental exercise are both important.  Most people stop being forced to learn after school, and most people don't take the initiative to continue to do so on their own.  Procedural thinking gives way to repetition and reliance on declarative memory; people fall into patterns in their lives that do not require them to continue learning but simply re-inforce what they already know once it is sufficient to get through life with.  Without regular practice, the skill atrophies.

By contrast, plenty of people are engaged in work that does require them to continue learning - sometimes intensely so - for the duration of their careers.  Among those people, my experience is that learning gets easier and faster with age since it builds upon mental tools, information, and experiences that have already been internalized.  In the same way that it's harder to lift weights when you haven't exercised in 20 years, so too is it difficult to suddenly put demands on the brain after leaving it idle for a similar period.

The answer(s) to this question can fill libraries. But I can give a few pointers here, as the question is relevant and timely, giving the tendency to an ever increasing life expectancy of the general populace in developed countries (notable exception: US).
I think your question can broadly be answered by the fact that degenerative processes in the brain slowly, but steadily, impairs all of its functions. Possible reasons for the specific decreased capability of the brain to adapt itself to new situations are:

The hippocampus plays a critical role in forming memory representations that are important for flexible cognition and social behavior (Rubin et al., 2014). Decreasing hippocampal neurogenesis during aging may impair the functioning of the hippocampus (Couillard-Despres et al., 2011)
Degenerative processes in the striatum impairs implicit learning that is necessary for mastering new tasks (Rieckmann & Bäckman, 2009);
Deficits in serotonin and dopamine neuromodulation in various brain structures due to degenerative processes during aging results in decreased learning and decision making (Eppinger et al., 2013);
Age-related altered neurosteroid levels may impair cognitive abilities (Vallée et al., 2011).

And the list goes on.
References
- Couillard-Despres et al., Gerontol (2011); 57: 559–64
- Eppinger et al., Ann N Y Acad Sci (2011); 1235: 1–17
- Rieckmann & Bäckman, Neuropsychol Rev (2009); 19(4): 490–503
- Rubin et al., Front Hum Neurosci (2014); 8: 742
- Vallée et al., Brain Res Rev (2001); 37(1–3): 301-312

There is growing evidence that loss of learning capacity is not primarily age related
Below are just a few articles on this topic... I know there's more.
The short answer is, there is growing evidence that the loss of memory and learning capabilities is NOT a foregone conclusion of aging by itself, but is, in fact, a byproduct of other health issues, specifically not controlling blood pressure and not being "heart healthy".  From a layman's view, this is because damage to the small blood vessels in the brain will slowly damage the surrounding nerve tissue.  If this occurs, you end up with all the affects that AliceD points out.
The point is:  Do not assume that loss of learning is "just a fact of aging".
References:

Protect your heart, preserve your mind?
Intensive treatment of blood pressure helps prevent memory decline in older adults
Can blood pressure drugs help reduce dementia risk?

I felt the need to downvote because the cited references do not support the title conclusion of the answer.