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What factors cause males to be more common than females in humans, from an evolutionary perspective?
Fisher's principle states that there should be a 1:1 ratio between males and females born on average for a population.  However, if you look at birth statistics your find that boys are slightly more likely to be born then girls.   This article talks a little about how it happens
If it was truly advantageous for an even sex ratio to exist at birth I imagine we would have evolved to make that happen, by slightly favoring more female sperm or by having the processes that decides which embryos to spontaneously abort be stricter for males embryos then females.  For that matter since it's more important for males to be exceptionally healthy then it is for females, since males have to compete for a mate while females don't, you would think more strict filtering for 'bad' embryos in the case of males then females would make sense anyways.
Thus I'm inclined to think that the increased number of males to females is not random evolutionary fluke, but adaptive.  I'm wondering what would cause there to be a benefit for males to be slightly more common then females.
I know males are more likely to die in childhood, due to risk taking activities to impress the females, so could it be that the increase in males is due to the expectation that more males will die before reaching sexual maturity?  I'm not certain I buy this logic, it doesn't seem you should favor a sex any more because it's likely to take higher risks.
I know that strong/healthy mates would prefer males and weak ones prefer females, since strong males would out compete weak males for mates it's good to have strong males that can achieve multiple mates and weak females since their guaranteed to have at least one mate.  Is it possible that our increased nutrition and health of recent generations simply results in more males because our bodies judge each of us as 'healthy' compared to the standard that existed for 99% of our evolution, ie, evolution hasn't caught up with technology when judging health to decide which sex to favor?
Is there some more obvious explanation for why favoring males slightly would be adaptive in humans?
Edit: I want to stress again, I'm not asking how the bias happens.  The article I linked clearly explains what causes males to occur more in terms of pregnancy.  I'm asking why the bias happens.  This could be evolved away in the past if it was disadvantageous,  Whatever mechanisms cause there to be a bias this bias is presumably adaptive for it not to be evolved away.  Both the possible duplicate and the current answer only address what causes the bias to happen today, not why it would be evolutionarily adaptive to have.

Answers to this question are also relevant, and one of them directly addresses Fisher's principle: Are human fetuses more likely to be male?

Nice question! The answer is in your linked article. I quote:

When you put this all together, it turns out more males are born because more female fetuses are lost during pregnancy.


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What is the evolutionary advantage of telescopic generations vs normal pregnancy with more young?
There are a small number of organisms, so far I'm aware only of mites and aphids, which practice telescopic generations, where the a female is pregnant with a daughter that is, itself, already pregnant, meaning the adult is carrying two generations within itself.
I'm trying to better understand the evolutionary advantage of this, specifically when compared to the 'normal' evolutionary strategy of non-telescopic generations but giving birth to more young.
In both cases, telescopic generations vs increased young, the mother invests the same amount of resources towards the pregnancy, be it through multiple daughters or fewer daughters but a head start on granddaughters.  At first glance it would seem this would make both strategies about equal in reproductive success.
In the case of mites which reproduce sexually, by mating in the womb, I can see one potential advantage of increased genetic diversity...presuming there is any noticeable difference between phenotype of grandchildren in a species that practices serial obligatory incest.  Since I'm not certain how large a difference in phenotype children can be expected to have after genes have mostly homogenized I'm not certain how large an advantage this may actually offer, if any.  It also doesn't explain the advantage in the case of aphids which are clonal when practicing telescopic generations
So, there any other reasons I'm missing for why telescopic generations would be preferable to birthing more daughters?

Do you mean telescopic generations? Just as an advice, note that long posts without sections tend to be discouraging for users and few people really read them (I did not read your post for example, I only reacted to the title).

@Remi.b yes you are correct, I have corrected my terminology.  I've also shortened the question at your suggestion, I'll just presume anyone who knows enough to give a useful answer will understand what I mean about increased genetic diversity ;)

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Pump to separate protein/DNA instead of electrophoresis?
I know that DNA molecules or proteins can be separated in electrophoresis because the electrical charge is used to pull the DNA through the gel. So instead of using electrical, can I using physical impact like pumping ?

Do you have a particular reason for wanting to use pressure instead of electricity? Any specific application in mind?

Well ... A lot of reason why i think pressure is better than electricity. Pressure will work with any molecule even they don't have charged, so it give better result without denaturing the protein. It's also safe budget, safe time when protein electrophoresis need to using chemical substrate for denaturing the protein. Pressure also safety for a diy bio like me when i don't want to working with high electricity... And i think with pressure i have more and more application, may be a machine that can purify protein, detect viruses in real time from good protein separate result...

Much of this comment should be included in your question. It gives background and makes the question easier to answer, and also shows what particular problems you have been thinking and that you are looking for DIY solutions.

If you tried to set up a system in which movement of DNA molecules through a gel matrix was driven by pumping buffer, the gel would become compressed. I am old enough to remember running vertical agarose gel electrophoresis overnight, and these gels would collapse under normal pressure to about 2/3rds of their initial height. A gel porous enough to give useful separation of DNA molecules just isn't strong enough to withstand pumping.

not from gels but physical force can be used to separate molecules.. e.g. density centrifugation, filtration. Closest to what you are asking is size exclusion chromatography in HPLC where molecules are separated based on size and high pressure is maintained in order to pump the solution (containing the analytes) through the stationary phase.
As Alan Boyd mentioned, the gels cannot withstand high pressure. In HPLC silica beads are used (sometimes coated with specific resins for e.g. in ion-exchange chromatography).
The principal differences between electrophoresis and HPLC (chromatogrphy) are:

HPLC relies on differential interaction of the molecules with the stationary phase (i.e beads) whereas electrophoresis is purely based on the hydrodynamic size of the molecules.
HPLC uses pressure to keep the entire mobile phase (solution) pumping through the stationary phase, whereas electrophoresis uses electric field to move the molecules.
HPLC can also be used for uncharged molecules

Size exclusion and gel-filtration chromatographies resolve the molecules based on size as in the case of electrophoresis but as I previously mentioned, the molecules need not be charged. The techniques used for analysis of molecules in both techniques can be similar. For e.g UV absorption/fluorescence. An advantage of HPLC is that it can be connected to other analyzers like Mass Spectrometer, Flame Photometer etc.

Hello, thank you so much. What is the gel HPLC using for separate molecules ? What different between HPLC and Electrophoresis (i mean in the result)

edited the answer..

Hello, so if i replace the gel using in electrophoresis with the gel-filtration using in HPLC. That mean i can use pressure to separate molecules instead of electrical ?

yes. you can. but HPLC is a different setup altogether. there are pre-packed columns available, which contain the beads.

Amazing ! As what i think in my dream, there are a method like that. Thank you so much !

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For animals with separate hermaphrodite and non-hermaphrodite populations which is more common, female + herm or male + herm?
I think the question already says it all.  I know there exist animals that have both herm and female populations and other's with herm and male populations, I'm not personally aware of any animal that has herms, males and females but I suspect that also exists somewhere.  I'm just curious which of these sex combinations is most common, ie which is most likely to evolve.
If you could also speak to why one sex combination may be more prone to evolve over another I'd be very interested in that, but I'd settle just for knowing which combination is more common.
I'm asking specifically about simultaneous hermaphrodites here, I know sequential hermaphrodites exist but that would just complicate the question.

Androdioecy (the coexistence of males and hermaphrodites) is very rare in animals, and vanishingly rare in vertebrates (just three species of fish). Coexistence of males and parthenogenetic females is considerably more common, at least in insects (often in different generations).
Gynodioecy (the coexistence of females and hermaphrodites) in animals is thought to be rarer by an order of magnitude. In fact, before 1975 no examples were known. Gynodioecy is, however, much more common and widespread than androdioecy in plants (though still <1% of angiosperms).
You can find details of different sexual systems and the number of species they occur in from the Tree of Sex.
Sources:

Mongue et al, International Journal of Organic Evolution, 2021
Weeks, International Journal of Organic Evolution, 2012
Fautin, Nature, 1975

The resource you list doesn't include nematodes (or many other major groups of invertebrates) — Caenorhabditis elegans is a famous example of an androdioecious animal. Can you provide one or more references that directly address the OPs question — whether androdioecy or gynodioecy is more common in animals? Both seem to regarded as rare, but a cursory search only turned up one example of the latter in animals (Epiactis prolifera), which would suggest that the former is fact relatively more common ...

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How does the eye know whether to focus further out or nearer in order to bring a blurry object into focus?
If the eye sees an object, but the object is out of focus, the eye could be focusing too near or too far. How does the eye (or the brain) distinguish one situation from the other?
How does it know whether to focus closer or further?
I'm interested in the case when:

only one eye is open (There must be another way besides parallax clues).
The object is an unfamiliar size
The object is an unknown distance from the eye.

Ideas so far
Does the eye try focusing either a little nearer or further and then if that doesn't help to make the object clearer then the eye focuses in the opposite direction?
Or is there some light-sensitive apparatus that is always a focused a little nearer or further than the rest of the eye, and so for instance if the cells which are focused further out are giving a clearer picture than the other cells then the eye knows to focus further out?
Or is the blurriness of a object closer than the focal point a distinguishably different sort of blurriness than an object beyond than the focal point?
Or is there some other mechanism altogether?

This may be a nobody knows kind of question! My pure guess would be that without depth perception your brain tries to make out edges. If the edges are sharp, it is focused, if its not sharp, it tries refocussing until it gets a sharp edge.

Interesting question! Determining the focus of a visual image is carried out in the visual association area of the brain. Ultimately, this process results in focusing of the retinal image by adjustment of the shape of the lens in the eye. Lens shaping to focus the image is called accommodation
The neuronal circuitry involved in accommodation includes the following structures:
The input to the accommodation response is provided by the retina, optic nerve, thalamus, and visual cortex. The visual cortex projects to the association cortex.
The (simplified) output scheme is the following: The association cortex projects to the supraoculomotor nuclei, which in turn generates motor control signals that initiate the accommodation response. The signal is then sent bilaterally to the oculomotor complex, and hence input from one eye is enough to focus both eyes.
The motor output regulates the ciliary muscles that control the shape of the crystalline lens. Negative accommodation  adjusts the eye for long distances by relaxation of the ciliary muscles. Positive accommodation  adjustment of the eye for short distances by contraction of the ciliary muscles Medical Dictionary.
As to the second part of your question: how out-of-focus images are functionally recognized:
There are at least three mechanisms responsible for accommodation:
1) Detection of image blur: if an image is blurred / out of focus the edges are not clearly defined. Retinal blur can be detected (edge detection) and assessed in the brain. Correction is then initiated as described above, and is basically done by trial and error. If adjustment results in a change of blur, the accommodation response (lens deformation) is detected as useful and accommodation is initiated. The accommodation itself is also based on trial-and-error: if blur increases the accommodation is reversed, if it decreases accommodation is increased in the same direction. (Philips & Stark, 1977). Image blur operates monocularly and is sufficient for accommodation to occur and is likely the most important mechanism for accommodation. It can occur without prior knowledge of distance, size etc.
Two more specific cases also result in accommodation, with likely similar neural circuitry involved:
2) Vergence / retinal disparity. This stimulus is generated when the eyes move both in opposite directions, i.e. when focus shifts toward objects closer or farther away. The temporary displacement on binocular retinal images is detected and leads to initiation of accommodation Fincham & Walton, 1977.
3). The near response: While 1) and 2) are retinotopic responses, the near-response is initiated by spatiotopic stimuli, including perceived depth and distance of objects, which are derived from cues such as relative size, overlap, perspective, shading and texture gradients as well as small timevarying dynamic depth cues which include motion
parallax, loom and motion in depth. Dynamic cues provide time-varying references for perception of relative depth whereas static cues allow simultaneous comparison
of separate absolute distances from which relative depth is perceived (Schor et al., 1991).

If this is the case, what will happen if the object i am seeing does not have sharp edges? For example a blurred image on a computer screen

The neurology of vision is an extremely complex subject and is difficult to describe with any brevity, because there is so very much going on in so many parts of the brain. It is estimated that about 50% of the pathways of the brain, and about 30% of the cortex are involved in vision (where only 8% of the cortex is devoted to touch, and 3% to hearing). Some research estimates that eighty to eighty five percent of our perception, learning, cognition and activities are mediated through vision.1
The ability to accurately focus on an object, sustain that focus, and to change focusing when looking at different distances is called accommodation. That happens with the pupil size, the lens shape, etc. but it doesn't tell us how the brain chooses on what to focus. The short answer is that it's much more than focusing like a camera lens. We have retinal areas that simultaneously pay attention to further and closer areas, light/dark, edges, and more, all going on at once. That and much more information carried to the brain is processed, and efferently focus is honed. It's even more complex when two eyes are involved.
There are so many aspects to sight that an enormous number of kinds of optical illusions exist. They are involuntary. That's why they're fun. In fact, if you weren't tricked, it would indicate a problem in part of your brain. Here's one that relies on processing contrast:

As you scan looking at the white dots, your peripheral vision seems to be able to see black dots, but it's clear on scanning them one row at a time that there are no black dots.
In the following illusion, the red vertical lines are parallel.

The following are summaries of the neuroanatomy of vision.
Eye, Brain and Vision
Anatomy and physiology of the afferent visual system
1 Vision Is Our Dominant Sense

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Why did humans become bipedal?
Somewhere in evolutionary history homo started walking upright and became bipedal. You hear these hypotheses that, by walking upright, they could see better across the grassy savannas to escape predators, find food, find fellow humans etc. However, the most parsimonious way to accomplish looking farther across the grassy plains is by growing taller - much less adaptations necessary and hence more favorable from an evolutionary perspective. Other hypotheses say homo freed his hands to carry things. Quite fine, but some apes are known to carry around stuff. Moreover, walking on all fours increases running speed (you don't have to see far if you can escape faster) and apes climb trees better (what's a better place to hide from predators?). Hence my question: Why has bipedalism been favored in evolution?

I don't have a good source for this, but my anthro class in undergrad claimed it was an energetic efficiency thing. I've also heard it was for cooling reasons (less sun cross section during the hottest part of the day).

As already pointed it out, there is no scientific consensus on the answer to this question. This is because it is hard to test proposed explanations and it's likely that several factors interacted.
All of these have been claimed to be the explanation for the evolution of bipedalism:

Freed hands for increased tool use. (Encyclopedia Britannica)
Freed hands for the use of weapons in hunting or the use of containers to transport plant foods obtained by gathering.
There are three variants: the “man the hunter” version which sees male hunting as the key stimulus (Washburn 1967 in Haraway 2013); the “woman the gatherer” version which sees women needing their hands free to carry gathered vegetable foods as the stimulus; and the “man the provisioner” version, which stresses males carrying food (either meat or plants) to provision females and offspring.
All of these explanations are probably flawed because they invoke present utility to explain the origins of bipedalism.
Bipedalism was created by female sexual selection of males with large, visible genitals.
Although unlikely, this may be correct, but it is impossible to test. (Encyclopedia Britannica)
Bipedalism evolved to aid in avoiding predators. Higher head allows you to see longer distances over the grass. (Encyclopedia Britannica)
Bipedalism evolves because it allows energy efficient locomotion between forest patches in an increasingly open environment.
“Radiator theory”: Natural selection favored bipedalism in open environments because it decreases exposure to the sun and helps keep the brain cool. (Wheeler, discussed in Haviland 2007 and Encyclopedia Britannica)
Brain is highly sensitive to heat stress.
This allowed hominins to be active in mid-day, when competing predators are less active. (Essentials of Physical Anthropology, p. 165). Since the same carnivorous animals with which hominins were in competition (both would scavenge dead game) could attack hominins, hominins were probably safer from predator attacks during midday as well.
Terrestrial bipedalism may be a continuation of an upright body posture inherent in a tree-climbing/brachiating adaptation.
Gibbons, the most arboreal of the apes and the best brachiators, walk bipedally on the rare occasions they come to the ground. (Encyclopedia Britannica)

The earliest hominin fossils appear to have been bipedal, with no clear evidence of a transition through a knuckle-walking stage, the principal mode of locomotion of modern African ape. (Kivell and Schmitt 2009, here's a secondary source, and here's a primary source that disagrees, Richmond and Strait 2000)
If this is true, then the modern African ape mode of locomotion (knuckle-walking) is a derived trait, and vertical body posture may be the ancestral trait in the African hominoid evolutionary lineages. In other words, if this is true, the ancestor of all great apes including humans was already bipedal, and modern African apes have evolved to knuckle-walk since then.
Also if this is true, the previously mentioned factors would reinforce and refine bipedal locomotion in the hominin lineage.
It is likely that explanations 4, 5, 6 and 7 all interacted to select for bipedalism. They correspond best to the paleontological and ecological data. Numbers 1 and 2 are unlikely, because bipedalism appears long before evidence of tool use.

Bipedalism does NOT predate tool use, All the great apes use tools. It iso also worth noting there is a prevalent theory that chimps( and bonobo) may be secondarily quadrupedal and our common ancestor may have been bipedal.

The thunder chimp's answer summarized the answer very well.  To try to pull things together a bit, if you have seven minutes, check out this video.  It shows a man chasing down a kudu. They both run for 8 hours, until the kudu literally collapses and the man calmly walks up to it and slays it.  The video shows the evolutionary adaptions that the man has - he sweats all over his body, cooling himself. The kudu needs shade to cool, and sweats only a little.  The man can carry water, to replenish himself.  The animal cannot.
Perhaps more importantly, the man walks upright on two feet, thus shifting his center of gravity in a energetically favorable way.  The animal is restricted to galloping, which is faster for a sprint but not energetically favorable for long distance running.
Here are some articles for further reading:
Evolution of Marathon Running
The Energetic Paradox of Human Running and Hominid Evolution
Endurance running and the evolution of Homo
They say similar things as the video: that we evolved for persistence hunting in an arid environment.  This is an activity that the other primates don't engage in. Our ability to hunt effectively allow us to eat more meat, and thus favored efficient long distance running.

The ones that co-evolved with us? Or the wild ones in Africa? Or Both? @nocomprende

I doubt you are going to be satisfied with any answer since the authorities on the matter can't test the many hypothesis and don't all agree. Around the time of homo erectus (1.89 million years ago), hominids began walking upright on a more permanent basis but this wasn't the only evolutionary event. Additionally, hominids began growing taller now as well [1].
Charles Darwin hypothesized that upright walking was linked to tool use in 1871 [2]. In 2009, Lovejoy reformalized Darwin's hypothesis and came to the conclusion that upright walking comes down to food and sex [3].

To be successful providers, males needed their arms and hands free to carry food, and thus bipedalism evolved. This scenario, as with all bipedalism hypotheses, is really hard to test. But earlier this year, researchers offered some support when they found that chimpanzees tend to walk bipedally when carrying rare or valuable foods.
At this point, Lovejoy suggests, a mutually beneficial arrangement evolved: Males gathered food for females and their young and in return females mate exclusively with their providers. To be successful providers, males needed their arms and hands free to carry food, and thus bipedalism evolved. This scenario, as with all bipedalism hypotheses, is really hard to test. [1]

In 1980, Peter Rodman and Henry McHenry claimed that bipedalism carries bioenergetic advantages [4]. Then in 2007, another group of researchers validated the energy advantage of walking upright [5].

Raichlen notes that if the same variation existed in our early ape-like ancestors as does in today's chimps, with some finding it easier to walk than others, this could have helped to drive adaptation. "That's what natural selection would be able to work on," he says [5].

Since there is no agreement and testing many of theses hypothesis are impossible since early hominids no longer exist, no one in their right mind can say, "Chris, this is why we evolved to walk." Even if they were correct, it would take some time to cycle through the academic community before it gained enough support to be the consensus.


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Why are neutral [sterile] female flowers present in inflorescences when they are reproductively incompatible?
In many compound and special inflorescences like spadix and hypanthodium there are sterile female flowers along with male and female fertile flowers and are often present in between male and female flowers, but what is their need in an inflorescence?

As far as I know inflorescences are meant for perpetuation of a plant's race by pollination of female flowers by the male gametes [pollen grains which bears vegetative and reproductive cells].
I know the infertile female flowers of the spadix inflorescence possess some surface area and this area would get some of the pollen grains which are coming in to the inflorescence, and eventually a sum of pollen grains might go in vain.
What is the need of sterile female flowers when fertile ones are present in it?

if not the answer can any one suggest me another site where i could find this answer

Sterile flowers enrich pollination quality by promoting pollen export and import, while limiting the mating costs of geitonogamy associated with large fertile displays.

You are actually looking for this paper: Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523656/
Sterile flowers increase pollinator attraction and promote female success in the Mediterranean herb Leopoldia comosa

Key Results
The presence of sterile flowers almost tripled pollinator attraction,
  supplementing the positive effect of the number of fertile flowers on
  the number of bees approaching inflorescences. Although attracted bees
  visited more flowers on larger inflorescences, the number visited did
  not additionally depend on the presence of sterile flowers. The
  presence of sterile flowers improved all aspects of plant performance,
  the magnitude of plant benefit being context dependent. During weather
  favourable to pollinators, the presence of sterile flowers increased
  pollen deposition on stigmas of young flowers, but this difference was
  not evident in older flowers, probably because of autonomous
  self-pollination in poorly visited flowers. Total pollen receipt per
  stigma decreased with increasing fertile display size. In the
  population with more pollinators, the presence of sterile flowers
  increased fruit number but not seed set or mass, whereas in the other
  population sterile flowers enhanced seeds per fruit, but not fruit
  production. These contrasts are consistent with dissimilar
  cross-pollination and autonomous self-pollination, coupled with the
  strong predispersal inbreeding depression exhibited by L. comosa
  populations.


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What is this pink-flowering plant found in Shanghai, China in March?
This plant appears to have fleshy protrusions resembling flowers growing out of its stem (although I am unable to identify them as such).
Does anyone know the identity of these plants?

I think this is the Chinese Redbud (Cercis chinensis), see this image (from here):


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Behavioral change in dolphins during different hemispheres activity periods?
It is known that dolphins never sleep in the sense that we do, instead they have one hemisphere of the brain sleeping while the other one is awake. I wonder, do they show observable changes in behavior in regard to this, depending on which hemisphere is active? Do their hemispheres even have a specification similar to ours (logic and emotion)?

Sleeping is a biological stage which we presume as a relaxation period but its really a highly functional stage for brain. Most of the memory related processing such as management of working memory and cognitive functions such as decision making, reasoning, and episodic memory are closely related with sleep.
Dolphins never sleep in the sense that we do, CORRECT, because we close our both eyes and enter into a stage of decreased ability to react to a stimuli. But in the case of dolphins they need to breath, so by fully entering into a sleep stage like us is suicidal in their case.
Dolphins have a specialised way of dealing with this problem, they do a "unihemispheric slow-wave sleep". They only sleep with one hemisphere of the brain while the other being active, when the right hemisphere is sleeping the left eye is closed and vice-verse, as the right hemisphere controls the left part of the body. The observable change in their behavior is visible from the closed single eye.
Humans and dolphins had a common ancestor that lived 95 million years ago. During the last 50 million years dolphins have been evolving in water and their brain evolution had taken a different route. The neocortex, the outer most layer of brain which is considered as the recent evolved part of brain. The neocortex is actively developing in both humans and dolphins, one of the most striking features among them is that human neocortex is having large thickness and dolphins are having thin one with more folds than ours. The folding in neocortex is a technique to increase its surface area. This substantial difference is due to the evolutionary divergent way both the species took.
Dolphins have a complex echolocation system and binocular eyes, they need to create the visual and sonar image of their surroundings and studies shown that their increased brain size is due to the tremendous volume of data they need to process for these purposes. Also being a social animal their neocortex consists of connections like us but as we both are evolutionary separated for about 95 million years ago most of the brain areas are diversified and evolved.

Dolphins showed that they can understand a symbolic, human-based
  language, where the words are either whistles or hand gestures. And
  the dolphins could easily understand that we use different word orders
  to mean different things. So they understand syntax. The dolphin brain
  is arranged in a completely different way from ours, and yet they can
  still understand what we are trying to teach them. Lou Herman also
  showed that dolphins are right up there with humans and chimpanzees in
  being able to understand that when we point at something or look at
  something, we’re meaning “Don’t look at me; look at what I’m looking
  at.” He’s done all kinds of really fascinating things, and his work
  has contributed the most to our understanding of what these animals
  can do.Reference

"The observable change in their behavior is visible from the closed single eye." Here you have stated that an answer to the question is possible. But other than that sentence, your response does not even attempt answer the question.

@Qubei: yes, I wish there was a more descriptive answer, like does their behavior become more logic or emotional, with examples, if possible.. but strangely looks like there are no people who can say anything like that about the subject..

@noncom:  What do you mean by "does their behavior become more logic or emotional"


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What is this brown insect with a large wingspan?
I found this dead creature on my window last night and spent hours looking for something that could explain what this is. I was unable to inspect it in person though, because opening the window would make the creature fall down.
It is roughly three inches in length and has a wingspan of five inches. I found it in the UK in August.
Here are some pictures:

It is a moth from the Sphingidae family (hawk moths). They are generally large, robust and often have lobed wings (like the one in your pictures). I'm not closely familiar with this group of insects, and not with species found in the UK, but the individual you observed is very similar to e.g. Laothoe populi (Poplar hawk moth), which is also found in the UK.

(Laothoe populi, picture from Wikipedia)

what a beauty! +1 :)


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What is the biological/evolutionary advantage to baldness?
Male pattern baldness is a common genetic trait. With a distinctive pattern/ density gradent (as apposed to general old age thinning as the body ages)
Hair has an advantage of protection from the sun/weather. So to lose it in a distinctive pattern (and lose that advantage) appears to have a reason*; and as it is a genetic trait, it seems like it would have been something that was selected for (or it would be more likely to be selected out).
So why is it better to develop pattern baldness as someone gets older?
So what might be the biological/evolutionary advantage to developing baldness?
Traits get selected for good and bad reasons(in retrospect), however I am interested in the reason why this particular trait has been selected.
* Lets assume that there is a specific cause (causes) and it is not just a leftover evolutionary artifact.

The related question: Why do some bad traits evolve, and good ones don't? provides some interesting background, but doesn't specifically address the What causes in this question.

You need to show some evidence in support of your premise that a trait "looks" selected.

@swbarnes2 I never said "looks" , but I have taken what you on board said and have rewritten to better layout my premise, with evidence for it.

@david Can you please remove the duplicate. As per the 3rd paragraph in this meta post https://biology.meta.stackexchange.com/questions/3116/questions-asking-for-evolutionary-reasons This question is about "specific hypothesis" In other words this is not a 'Why does evolution...' question; but a 'What caused this evolution...' question.

"Appears to have a reason" is not any different from "appears selected". Not every trait you find distinctive has been specifically evolutionary selected for.

@swbarnes2 The question is: there appears to be a reason What is the reason. If you think that the answer is "There is no reason" then put that as a answer and it can be voted on along with other answers of: "The reason is XYZ",  "The answer is ABC"

If I pour our some M&Ms from a bag, and I assert that there are a disproportionate number of red ones in the bowl what is the reason?

@swbarnes2 Either "Common cause" or "Special cause". Respectively:  Luck (Good or bad depending  on your taste in M&Ms) or something (I don't know what, but there is a reason) which is causing the M&M production line to add more Reds than other wise would be expected. "I wonder what the reason is?" How would you work out which of those two options is the actual cause?

I'd be interested if anyone can come up with a plausible evolutionary advantage to male pattern baldness; reduced susceptibility to head lice and lice bourne diseases was the best I could do, but I don't see how it would be selected for when the trait mostly emerges after most of the natural and sexual selection and reproductive successes have already taken place. Mmm, I would also be interested to see a plausible reason why it has to have an evolutionary advantage and cannot be something tolerated.

You aren't understanding.  You can't give a meaningful answer to a question if the premises are unfounded.  You can't meaningful answer "Why is the sky green and purple stripe" if it isn't actually that color.

@swbarnes2 Would it make a difference if the question was changes to: ... appears to have a reason (assuming that there is one, and it is not just a ransom evolutionary artifact)...

@swbarnes2 What makes you think that the premise is unfounded? (unproven, sure; but unfounded !?!)

@KenFabian I (the OP) have one, but I wanted to give others time to put up other conjectures before mine (so I don't taint their responses)

Baldness would appear to be a trait on display. That being said, hair loss can be selected against the opposite condition (full head of hair), or selected by way of precise pattern deemed attractive. So, male pattern baldness evolution for mate selection purposes is probably a factor in play. But, either way, hair loss appears to have both its advantages and disadvantages as far as both fitness and mate selection is concerned.
Similarly, in terms of fitness, the advantage/disadvantage you state is the immediate positive advantage of hair as a protectant.  The immediate advantages of hair diminish as one grows older, making age apparent. Old age is disadvantageous in itself (older can mean less fit). Hence, the immediate advantage for a protection against the elements decreases and becomes less relevant to survival as one grows older. Please see the references below.
https://en.wikipedia.org/wiki/Mate_choice
https://en.wikipedia.org/wiki/Evolution_of_ageing

"Questions like this are in the domain of mate selection (or choice) in biology" - citation needed. It is not at all clear that the answer to OP's question has anything to do with mate selection, unless you can cite evidence that it is.


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Why there are two rounds of cytosine de-methylation in mammalian development?
I assume that the key biological meaning of cytosine de-methylation during germline development in germline progenitor cells is to reset imprinted genes and then set methylation pattern on these genes according to the gender of the embryo. (this is simply my best guess, so if there is an alternative interpretation, please mention it in the answer)
This de-methylation procedure is dangerous, because DNA-demethylation affects a lot of different regions and some transpons get de-repressed. So there is a risk of novel transposon insertions. However, since it is important to set imprinting in your own gamets properly, the embryo takes this risk.
But I don't understand why does de-methylation in mammalian development happen twice. Well, the first round it is not as deep and, I am guessing, that the transposons are probably not affected very much during the first round, so the risk of novel transposon insertions is not as high. However, since the resetting of imprinting marks is happening in the second round anyway, why does the embryo bother the first time around at all?


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Question about what the liver does NOT do
Which of the following functions is NOT performed by the liver?
a) Storage of vitamins and minerals
b) converts glucose to glycogen
c) converts toxins to harmless chemicals
d) produces bile
I chose b and got it wrong, any help?

I'm pretty sure the liver can do all of those things…

A is actually arguable. The other three are perfectly true for liver but I am not sure about option A.

If you are asking a homework question, you must show what attempt you have made to answer it.

Liver does all those functions as far as I know. The liver hepatocyctes are stimulated to create the enzyme glycogen synthase which promotes the conversion of glucose to glycogen in the presence of insulin. Glycogen is stored in the liver after its production for further use. The whole process is explained in detail in this page. Regarding the storage of vitamins and minerals, I have a paper which details the absorption and storage of Vitamin A in rat liver.  I am also linking another paper that details the presence of Vitamin B12 in the human liver.

Even if the liver does store some vitamins, this would not make statement (a) true - there would have to be storage of minerals as well. The liver can store iron as ferritin (along with lots of other tissues).

@AlanBoyd yeah, support both claims to make the statement true which u have done. Reference for the statement is http://library.med.utah.edu/NetBiochem/hi11b.htm Thanks for pointing that out.

animal liver is very rich in vitamin A and iron.

answer a) is definitely the 'least true' and is the right answer for sure. However, the question is iffy and should probably be made a bonus question :)


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What is phenotyping of blood during transfusion process?
Thallaesemic patients are advised to have only "phenotypically matched blood".I mean the transfusion problems arise mainly due to "grouping problems" like mismatch b/w ABO & Rh+/- so what do this phenotyping mean? Isn't "grouping" of blood enough?
Statutory declaration- the link provided in the q is only to clarify in which context the q is asked & nothing more, like promoting Egyptian Gov. Health Service...(or any other CRAZY INTERPRETATIONS like that)**

This question appears to be off-topic because it is about a special process of the egyptian blood transfusion service, which we will not be able to answer.

excuse me....but I think you need to delve deeper into a q b4 u make such....naive comment.....Indian blood transfusion process also follows this....& if you really want to , then try to get through Wintrobe's Clinical Hematology (which is not possible for me at my stage)....

I do not think this question should be closed since I know a similar advice is dispensed in many middle eastern countries!

In response to the above q. many have commented that the process is only limited to Middle Eastern countries....I think the term 'only' will be better substituted by 'mainly', the reason to which , is explained later ....
Now, the main clarification lies in the fact that,

....there are more than 600 known antigens besides A and B that
  characterize the proteins found on a person's red cells. A combination
  of some of these less familiar but commonly occurring antigens are
  absent from the blood of an extremely small percentage of the
  population. There are also a few antigens that almost all people have
  on their red cells but that some lack. - One In A Million
  American Rare Donor Program

Now patients receiving a 1st time transfusion normally do not show any reactions or cross-matching problems with these blood subgroups but during repeated transfusion process like in case of thallaesemia , the receiver's blood gets sensitized against the donor's blood & the problems ensues...

Dr Therese Callaghan said, “All other antibodies are unexpected and
  are of two distinct types, alloantibodies (which target an antigen
  that is not present on your own red blood cells) and autoantibodies
  (which target an antigen that is present on your own cells).
“Patients receiving a transfusion for the first time do not normally
  have problems with matching blood types and antigens. However it is
  during subsequent transfusions when more care needs to be taken. If,
  during a later transfusion, the blood contains the same antigens as an
  earlier one, the patient’s immune system recognises the transfused
  blood cells as ‘foreign’ and the antibodies (formed after the first
  transfusion) will destroy the blood cells the patient has been given.
  This is called a transfusion reaction and can cause serious illness or
  even death if not treated quickly. That is why matching the blood
  phenotype is so important.”

Now coming to "Why mainly in Middle-East ??"
These rare blood groups are distributed into major 30 discrete system, which mainly  are present in different ethnic groups & communities...mainly living in Middle-Eastern states & Asia...& also in African countries...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3353626/table/T3/
Intersted people may also check the following articles (or simply search Google)
To Provide Phenotype-Matched Red Blood Cells or Not – That is the Question!
13.3: Pre-transfusion testing- Joint United Kingdom (UK) Blood Transfusion and Tissue Transplantation Services Professional Advisory Committee
& for a complete picture plz browse through- Immunohaematology


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Stockholm format to dot-brackets format?
I need to convert all my sequences in a Stockholm format into this:
hg19_11_6_Ala          ----------------.GG--gggaguggugu....gguuacgaaugUGGCCUCUGC-----AA.............................................................GCAGACA.........................G..CCUGGGUUCAAUU...........................
#=GR hg19_11_6_Ala  PP .................22..45677788888....899999999996777899988.....56.............................................................8999999.........................9..*************...........................

Into something like this:
 hg19_11_6_Ala         ................((..(((((((((((...)))))))))))))))))))))))....((................................)))))))))......)))).....................

Obviously, being coherent with the stockholm format. Any hint?

If what you want is to find a consensus structure for a group of alignments in stockholm format then you might try with
RNAalifold
 and for single sequence folding check RNAfold. Both have online servers and can also be run offline.
After you get the consensus structure update the stockholm file by adding  a structure consensus line as: #=GC SS_cons followed by the dot bracket notation.
A nice RNA structure editor that will make your life easier is EMACS when complemented with RALEE. It allows you to view and manipulate RNA structures, predict structure folding and color the alignments based on basepairs relationships. It will be worth it to invest time into mastering RALEE.


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What is the meaning of dots and dashes in clustalw?
I am converting outputs in stockholm format to clustalw using
Bio::AlignIO->new(-file => "$ARGV[0]", -format => "stockholm"); and

Bio::AlignIO ->new (-format =>'clustalw');

I am also using
my $new=$aln->remove_columns(['all_gaps_columns'],'.');

and got an output like
head1  ----------------.GG-.-gggaguggugugguuacgaaugUGGCCUCUGC-----A

head2  GGGGGUGUAGCUCAGU.GGU.A......................GAGCGGAUGCUUUGCA

What is the meaning of dots and dashes? Is this natural in a clustalw output? Am I getting a bug?
I was unable to find the sequences I used in the original message but these two pose a similar pattern. These are RNA sequences, including pseudogenes, so there are lots of palindromic sequences.
# STOCKHOLM 1.0
#=GF AU Infernal 1.1.1

head1          --------UGGAGAAU.G--.-ugggcguc.gaucccacUUCCUCUCGCAUGCUAA..............................................................GCGAGC-gcucuaccacuugagcuaauucccc-..-------------..................................
 #=GR head1 PP ........89999988.4....6789****.********999**************..............................................................******.7999999866665555555554444..................................................

 head2         --------UGGAGAAU.---.-gcgggcaucgaucccgcUUCCUCUCGCAUGCUAA..............................................................GCGAGCG.........................-..-------------cucuaccauu........................
 #=GR head2  PP ........89999887......46789************9999*************..............................................................*****86.........................................4555666666........................

 CLUSTAL W (1.81) multiple sequence alignment

 head1  --------UGGAGAAU.G--.-ugggcguc.gaucccacUUCCUCUCGCAUGCUAA....
 head2  --------UGGAGAAU.---.-gcgggcaucgaucccgcUUCCUCUCGCAUGCUAA....

Dash is used for gaps and dots are used for semi-conserved substitutions (similar residues). But this looks weird. Are you sure this is how you got the output because the dots are present below the alignment (next line)?

Sorry for putting this in the Answer box, but I don't have enough rep to comment yet... Can you please post the contents of your stockholm file as well? Also, just to be 100% clear, you are using BioPerl for your conversion, yes?

This looks like you are running clustalw with bioperl. I have answered assuming the original alignment is wrong. Could you post your original alignment, and what versions of these are you using?

Please show us the sequences you are attempting to align. They look like low complexity regions which are very hard to align but we can't judge without seeing the originals.

Yes, I am using Bioperl. I uploaded a sample of the original.

As WYSIWYG touches on in the comments, usually dashes mean that there are gaps in the alignment as the result of an indel event. Dots are used to show specifically point mutations where the biochemical properties are mostly conserved, but the residue has changed.

From original question, not relevant to question as it stands.
You are right in that this isn't a proper alignment, however I'm not sure it is a bug. What you have appears to be the alignment of a nucleotide sequence that has gone horribly, horribly wrong.
As a first guess without any more details I would say it doesn't look like you have installed clustalw correctly or pointed your bioperl to it. From the documentation here are common problems:

Make sure the clustalw executable is in your path so that
  which clustalw
  returns a clustalw executable on your system.
Define an environmental variable CLUSTALDIR which is a
  directory which contains the 'clustalw' application:
  In bash:
export CLUSTALDIR=/home/username/clustalw1.8
In csh/tcsh:
setenv CLUSTALDIR /home/username/clustalw1.8
Include a definition of an environmental variable CLUSTALDIR in
  every script that will use this Clustalw wrapper module, e.g.:
BEGIN { $ENV{CLUSTALDIR} = '/home/username/clustalw1.8/' }
  use Bio::Tools::Run::Alignment::Clustalw;

Unless you are doing massive amounts of sequence alignment, the clustalW2 webserver is quicker, more sensitive and way easier to use.

Based on the edit you made to your op, the dots are present in your initial stockholm alignment, and are simply being copied into the new clustal output.
What is the source of your alignment to begin with? I'm assuming you're selecting individual rows from a larger alignment, given the odd distribution of gaps. This could give you a clue as to the actual significance of the dots (dashes are pretty much always gaps).
Also, just fyi, if you want a command line tool to do the conversion for you, I have a python3 module called SeqBuddy that will work just fine. You'll need BioPython as a dependency though.
$: python3 SeqBuddy.py input.stockholm -sf clustal > output.clustal


text:
Is Gorlin's sign hereditary?
"Gorlin's Sign" is the ability to touch the tip of the nose with the tongue.  It is present in half of people with Ehlers-Danlos syndrome, but is also present in a minority of people without that disorder: among them, both me and one of my sons.
Is it known whether this trait is hereditary?  If so, is it a simple genetic trait (e.g., is it sex-linked, Mendelian)?

Can you please link to your source when you state It is present in half of people with Ehlers-Danlos syndrome, but is also present in a minority of people without that disorder? This source may be a good starting point to try to answer your question.

@Remi.b - I just added source of that statement (Wikipedia).


text:
Selective pressure for reduced rates of growth and maturity in primates
Humans are somewhat notable for the slow rate at which they grow and reach physical maturity.  Some related primates also take over a decade to reach sexual maturity.
However, many mammals – including ones like horses that grow quite larger than any primates – reach their maximum size in only a few years, so the slow rate of primate growth is not due to simple biologic or metabolic constraints on mammalian growth rates.
Are there any hypothesized selective pressures that might explain the slow physical growth rates of higher primates?


text:
Where does crop biomass come from?
Each year, large volumes of crop are harvested from fields.

Where does this biomass get replenished from?

@user137 - It is easy to write a specific answer when you edit the question to your answer...

That's why my answer seems a bit off now :)

Since this is now the second thread where editing the question is not liked by the original author, I will open a thread on meta on this.

@Chris let me know when you do - I don't see anything yet.

There is already an old question about it. I think this can be used as well, it is here.

There are biogeochemical cycles for the building stones of the biomass (e.g. hydrogen, carbon, nitrogen, oxygen, etc...), so all of these atoms are recycled. To recycle them the organisms need energy, which they get from sunlight, from chemical materials, etc... (check microbial metabolism for further details).
Plants use sunlight as energy source, CO2 from air as carbon source, water and O2 from air as oxygen source, and so on... You can find more info about plant metabolism on wikipedia.

The matter in plants is mostly carbon, hydrogen, oxygen, and nitrogen, with various metal ions and some sulfur and phosphorus. The carbon, hydrogen, and oxygen are taken from carbon dioxide in the air and water from the soil through photosynthesis. Nitrogen is taken up from the soil as ammonia or nitrates, or fixed from nitrogen gas, but this only happens in legumes. Phosphorus is also part of a nutrient cycle. Metal ions such as sodium, potassium, magnesium, and calcium are taken up through the roots with water.
If you're asking about how this material is replenished, fertilizer is an important answer. For centuries, nitrogen was a limiting nutrient in farms because it would get removed faster than it was replaced, especially if crop rotation was not used or legumes weren't grown. Thanks to the Haber Process we can produce humongous amounts of ammonia from nitrogen gas, this has greatly increased the amount of nitrogen available for plants, but has also resulted in nitrate pollution in waterways and algal blooms and eutrophication. Phosphate and potassium are also used in fertilizer and are usually mined, however phosphorus reserves are limited.

The biomass of crops is definitely mostly carbon (from the air in the form of CO2) and water. However, in terms of how it affects the environment: Crops use up trace elements that make up a tiny fraction of the biomass, but it is these trace elements that are not ubiquitously available. Most notably phosphorus and to a lesser extent nitrogen. The impact on the environment is that farming, and especially monocultures, deplete the environment of these essential trace elements. It is often these elements that restrict growth due to competition. Therefore, it may inhibit growth of native species. However, a far more devastating effect is that farmers will re-supply these trace elements in excessive amounts through artificial fertilizers, leading to surplus and run-off phosphates (phosphates are the main form in which phosphorus is applied in fertilizers) (Hart et al, 2004). This in turn dramatically shifts the natural competition for this normally restricting element, in turn promoting growth of non-native plants and promoting the growth of P and N-tolerant plants while suppressing the growth of plants that are intolerant. As most plants are actually intolerant it will eventually lead to species loss and imbalance in the ecosystem (popular link).


text:
Phenotype choice for one of a MZ twin pair in a genetic association study
I was having a discussion with a colleague and this question came up...
It is commonplace in molecular genetics studies to only genotype one of a pair of monozygotic twins (and then implicitly impute the other's genotype by assuming the pair is genetically identical).
My question is this: assuming a quantitative trait study, what should the phenotype be? Should it be the phenotype of the genotyped twin OR should it be an average of the two twins' phenotypes?
Example:

I genotype Twin A
Twin A has a phenotype score of 4
Twin B has a phenotype score of 6
Should Twin A's phenotype for the genotype-phenotype test be 4 (the individual's phenotype) or 5 (the average phenotype of the genome)?

Answers from experience and from theory welcome!
Thanks!

I think it's quite unclear what you are asking

Can you suggest what further information you need? Have added an example, if that helps?

Interesting, perhaps it depends what analysis you plan to do later. If the study aims to estimate the heritability of the trait, wouldn't you want to record a separate datum for both twins, so that you can compare the variation present with different degrees of relatedness or genetic similarity.
Can you explain what sort of quantitative trait study you mean and how it is done? Thanks!

Hi Teige, what I meant by quantitative trait was that the phenotype was continuous rather than dichotomous, and so doing an average would make sense (if the test is YES/NO, then it makes little sense to be half a YES!)
I'm assuming there is no genetic variance between identical twins, so there's no new information gained by having both twins' genotypes. I'm talking about an analysis where you're not using the fact they're twins per se, but rather just using one of them as an individual - do you randomly select one twin, or do you combine their phenotypes into one?


text:
What determines the courses of multi-dose vaccines?
I understand that some proportion of individuals will fail to develop immunity from a single dose of a vaccine.  Rather than test every member of the target population following each vaccination, it is more economical to administer multiple doses to increase the population immunity rate.
But what determines how many doses are indicated for a particular vaccine, and how widely they are spaced?  Are these variables rigorously optimized, or are they just accepted heuristics?
E.g., two doses of MMR are indicated, separated by at least 3 years.  Three doses of HPV are indicated, separated by 2 and then 3 months.  Four doses of IPV are recommended, as are five doses of DTaP!

Have you done any research into this? It would seem to be easy to Google. Please share what you found and why this doesn't answer your question.

@anongoodnurse: Best I could find was this, which describes different immunological mechanisms, but which does not answer this quesiton.  Also, this explaining that it's always cheaper to add another dose than to titrate a sample from an individual to determine their acquired immunity.

You should be editing this information into your question. :)


text:
How does the population fitness change after a change in mutation rate?
The mean population fitness as given by mutation load theory depends only on the genome-wide mutation rate ($U$). My question is: How many generations is needed to reach a new mutation load equilibrium after a change in $U$?

Following is an article were they perform the kind of calculations I am interested in:
Let $U$ be the genome-wide mutation rate, $\delta U$ a change (between two time steps) in the genome-wide mutation rate and $s$ the mutational effect (effect on fitness) of a given mutation. In Agrawal and Whitlock (2012), page 13 (or 127 in the journal), $3^{rd}$ paragraph, the authors say:

[After a change in $U$,] it can take a long time to approach mutation-selection balance. For example, if the mutation rate is increased by $\delta U = 1$ deleterious mutation per genome per generation, then it would take ∼120 generations for fitness to decline 80% of its expected amount if s = 0.01. However, by obtaining a time series of data, one could infer the equilibrium load after tens or hundreds of generations even if equilibrium is not reached

How were these ~120 generations estimated/calculated?

A very old question and I assume you would have found the answer by now. The linked article indeed doesn't explain the calculation. Perhaps this paper may be more useful to answer the general question.


text:
Variance in reproductive success and effective population size
Background
The effective population size $N_e$ is the size of the Wright-Fisher population that experience the same amount of drift than the population under consideration.
The higher the variance in reproductive success among individuals, the lower is the effective population. Consider for example, a case where the variance in reproductive success is so high that only one individual reproduces (selfing for example) and contribute to the next generation. In such a case the variance in reproductive success is so high that the effective population size is reduced to 1.
During a meeting I have encountered the following relationship between the population size $N$, the effective population size $Ne$ and the variance in reproductive success $V$.
$$N_e = \frac{N}{V}$$
It makes intuitive sense to me. In the extreme case where $V≈0$, there is no drift and therefore no loss in diversity, everybody contribute as much to the next generation and therefore $N_e=\infty$. By definition, in a Wright-Fisher population $N=N_e$ and therefore $V=1$ should be correct.
Questions

Where does the equation $N_e = \frac{N}{V}$ comes from? How to derive it? Is it an approximation or an equality?
Is it true that $V=1$ in a Wright-Fisher population?

Here is a related post.

If you have a copy of Ewens' "Mathematical Population Genetics", check out chapter 3.7 -- he discusses this.

Yes, I have one. I'll check this out. THank you


text:
How does the cell regulate different metabolic pathways?
I heard somewhere that cells use different nucleosides bound to triphosphates e.g. ATP, GTP, CTP and other modified compounds: NADH, NADPH to distinguish between different metabolic pathways and so they regulate where they use up the energy. I heard that kinases play an important role in the regulation. Is there a connection (I guess there is if I check NADPH)? Is this regulation mapped? I mean is there a simple map which contains the main processes and the energy carrier and regulatory compounds?
I am looking for something like this map (of receptor responses), but for metabolic regulation:

Figure 1 - signal transduction - wikipedia

So it possibly contains mitochondria, O2, CO2, flows, ATP, NADPH, etc... I understand that different cell types can have different energy producer and consumer organelles and it is not possible to create something that is universally true, so I would be satisfied with a map of your favorite human cell type.

That's going to a large image. Is there some specific metabolic pathway(s) you're looking for?

You can check this out, though it doesn't show regulation: http://www.sigmaaldrich.com/technical-documents/articles/biology/interactive-metabolic-pathways-map.html?cm_sp=Insite--Academic--MetabolomicPathways

There's also this: http://www.genome.jp/kegg/pathway/map/map01100.html     Your best bet is probably a textbook like Lehninger.

@canadianer Nope, I am looking for a simple sketch with the important processes, materials without the details (so no enzymes). Just an example from prokaryotes: the photosystems create NADPH and ATP, which can be used anywhere it is needed, e.g. by carbon fixation. Prokaryotes can use other sources of energy which are transformed to NADH and ATP as well. Thanks for the links.

Metabolic regulation is usually mediated by enzymes.

Also, isn't that first link exactly what you're looking for? The enzymes are included only as EC numbers.

The picture that you attached is not directly related to the question and can be confusing. Either put up a dummy network or a simpler diagram. As it is right now, words are sufficient to explain the question.

I heard somewhere that cells ………………………… so they regulate where they use up the energy.

Yes NADP/H is primarily employed in anabolic pathways such as fatty acid synthesis, while NAD/H is employed in catabolic pathways such as glycolysis.
I don't think there is a general rule for other "energy-currency" molecules (pyrimidine triphosphates are not used except in some rare cases such as glycogenesis).

I mean is there a simple map which contains the main processes and the energy carrier and regulatory compounds?

You can search for the term "metabolic network". It would be too huge so it is better to look at specific sub-networks. KEGG is a good site for finding metabolic networks. There are other representations like hive plots, to visualize very huge graphs.

Our body maintains a very delicate balance between the concentration of metabolites and substrates. If a pathway is not regulated, excess of a particular metabolite can disturb the whole process. Let's take cholesterol metabolism pathway for example. there are various means by which the cells control the production of cholesterol. For example AMP controlled kinase protein detects weather the concentration of ATP is high or not, if its low then the cell does not proceed with the production of it, by inhibiting the enzyme that catalysis the production of mevalonate. Other way is through transcription factor that is present  called SREBP. Sterol Regulatory Element Binding Protein regulate multiple genes that are involved in metabolism of cholesterol. Various protein denaturing components are present that upon receiving signal cleaves the intermediate's in the metabolism of cholesterol.
There are n-number of pathways in our body and all are regulated by a complex network of signals that regulate them.


text:
Why don't vaccines cause bacterial resistance?
Since bacteria can evolve to overcome antibiotic use, why wouldn't they be able to evolve to overcome antibody or cell-mediated immunity?
(One possible explanation: antibiotics have only one target while vaccines elicit antibodies against multiple targets and multiple T-cell epitopes. Even more targets arise when comparing sub-unit vs inactivated vaccines, where the number of targets are extremely higher using inactivated vaccines, containing whole bacterial cell.)

why wouldn't be able to evolve to overcome antibody or cell-mediated immunity?...They can; Vaccines are not 100% effective. In some cases they are quite efficient.

In vaccine development today you try to choose evolutionary conserved targets for the vaccine to prevent this.

Thanks @WYSIWYG, it would be great if someone could give some reasons.

Actually most of the nowadays vaccines activate B-cells and not T-cells. Ofc. there can be resistance to vaccines, e.g. by influenza. Bacterias have more complex surface than viruses, that's why they cannot change their surface as fast as it would be necessary to overcome vaccines.

One major difference is that vaccine acts in human host while antibiotics act on pathogen. Antibiotics target a specific pathway in the pathogen while vaccines sensitize humans to all the antigens present in it.

Unfortunately, we do see examples of bacteria and viruses evolving vaccine resistance. For instance, vaccine resistant strains of polio and pertussis have recently been identified.
Yet these seem like the exception rather than the rule. One thing that makes it harder for pathogens to evolve resistance is that vaccines usually generate antibodies to multiple antigens, all of which the pathogen would have to alter.
Another reason vaccines tend not to drive vaccine resistance is that the diseases for which we vaccinate are typically those that are not antigenically variable. (Haemophilus influenza is a notable exception; there we use a conjugate vaccine). This may have something to do with how we view vaccine efficacy. For example, we don't say that the influenza virus evolves vaccine resistance--yet we need a new vaccination each year due to antigenic shift.
If you are interested in learning more, Angela McLean has a nice article looking into this question.

There is another reason why Hib is a conjugate vaccine: The polysaccherid from the capsule alone only triggers a relatively weak immune response. The antigen which is used for the coupled vaccine (often tetanus toxoid) makes the answer much stronger.

Influenza vaccines are renewed annually because the viruses change continuously and thus become resistant to most antibodies people develop, vaccine-induced or not. HI virus (AIDS) also changes so often that vaccines are extremely ineffective against it.

@Archimedix: Exactly -- yet we don't say that influenza viruses evolve vaccine (or acquired immunity) resistance. We just talk about antigenic shift. So it's not so much that immune resistance doesn't evolve, it's that we call it something else. You make an important point: HIV is good example of a virus where this evolution occurs within a single host during the duration of an infection.

Also it is noteworthy that the general idea behind vaccines is to "train" your own immune system to the pathogens. Since we are all different a little bit we produce a little bit different antibodies therefore the pathogens do not have a general counter-strategy or selective pressure compared to antibiotics.


text:
Essential amino acids
Humans and the majority of animal species cannot synthesize essential amino acids (Info: Campbell biology 9th edition). However, meat, eggs, et cetera provide all required essential amino acids. And meat comes from animals.
Main question: So how do these animals we eat get their essential amino acids if they cannot synthesize them either?
My hypothesis: I know they can get it from their diet, but wouldn't it become a never-ending cycle of passing on essential amino acids?
Subquestion if hypothesis is proven: If that is the case, where did these essential amino acids come from?

Bacteria and plants are able to synthesize all amino acids, as they are capable of nitrogen fixation. If animals eat plants, they get the essential amino acids needed for their proteins. Humans get the essential amino acids by eating these animals or directly by consuming plants. So yes, it is a never-ending cycle of passing.


text:
Why can't we find a broad spectrum antiviral drug to viruses like antibiotics to bacteria?
Antibiotics have a very broad spectrum because they attack the metabolism pathways many bacteria share. For example, penicillin inhibits peptidoglycan synthesis, which is vital for formation of cell wall of gram-positive bacteria, so penicillin can be used to treat gram-positive bacteria infections. Streptomycin inhibits protein synthesis of bacteria. Because all the bacteria need protein synthesis, streptomycin has a very broad spectrum.
Why doesn't such strategy work on viruses? For example, nucleos(t)ide analogues can inhibit the RNA synthesis of RdRp. Most riboviruses (except hepatitis D virus) require a viral RdRp to replicate their genome. But why can't nucleos(t)ide analogues be used as broad spectrum anti-riboviral drugs even we have found very good drugs such as Sovaldi?

One of the main issues with nucleotide analogs is that they can also affect the host replication and transcription (though they have a higher affinity to the viral polymerase), and can therefore have adverse side effects. On the other hand, the broad spectrum anti-bacterial antibiotics specifically affect prokaryotic cellular machinery.
(Note that some antibiotics like streptomycin do affect the host mitochondria and thereby cause toxicity. Ototoxicity and nephrotoxicity are known side effects of streptomycin.)
Nucleotide analogs are actually used as broad spectrum anti-virals: For example, Lamivudine is used for both HBV and HIV, which are different types of viruses.


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Can I tell my antioxidants intake based on nutrition facts labels?
The recommended daily intake of fruits and vegetables is 5-10 portions (url), in order to meet the "required antioxidant levels" (dark-leaf green vegetables, berries, cruciferous vegetables, ...).
Can I measure my antioxidant intake based on nutrition facts label, instead of counting vegetable portions?
Adding up the total intake of vitamins A, C, E and magnesium may not be representing because they are not necessarily the "major players" (additional significant players are CoQ10, alpha-lipoic acid, l-carnitine, acetyl-l-carnitine, n-acetyl cysteine).

What do you mean by "major players" ?  Vitamin C (ascorbate) is certainly considered a quantitatively important antioxidant; it is perhaps the most important soluble radical scavenger in mammalian cells. But in many cases, including the metabolites you mention, I think the quantitative important is unclear.

Also, in your original post your specifically asked about vitamins A, C and E. Now it seems you have revised the question to indicate that you don't care about those vitamins.

@Roland I do, if they are significant "players"; updated question.

See revised answer. I don't think it makes sense to think about this in terms of "major" or "minor" players. The relevant distinction is between vitamin compounds, which are required in the diet, and non-vitamin compounds which are not (by definition).

Well yes, you could get this information from food labels, since the recommended daily intake of vitamins is well established. But there is really no need to worry about dietary "antioxidants" (usually vitamins A, C and E, and carotenoids). If you eat a reasonably balanced diet, you are getting all the vitamins you need. Thankfully, vitamin deficiency is very rare in the western world today.
There is a lot of hype around "antioxidant" dietary supplements, but there is no convincing evidence that high levels of these vitamins in your diet has any beneficial effect at all. Randomized clinical trials have failed to show any effects whatsoever of antioxidant supplements on chronic diseases, and excess intake may even increase overall mortality.
Non-vitamin compounds like carnitine are not necessary in the diet at all, since they can be synthesized by the body in sufficient amounts. In general, the fact that a compound is a "major player" in cellular metabolism (in oxidative defense or other wise) does not mean that you have to consume it. For example, the TCA cycle intermediates are arguably the biggest "players" in human metabolism, but none of them are necessary in the diet.

+1 for showing evidence that dietary antioxidants are a waste of time and money

@Sparkler  I revised your edit and added a reference for overall mortality; there is no evidence for a beneficial effect in this measure either.

What about antioxidants that cannot be synthesized by the body and that are not tracked by the nutrition facts label?

There are no known essential antioxidants outside the 13 vitamins. Some minerals like Selenium are required by enzymes involved in antioxidant defense, but these are already included in the recommended intake scheme.  Of course there are many pharmacological compounds with antioxidant properties that do not occur normally in the body, but that's a different story.


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Santa Fe xeric indigenous tree
The hills around Santa Fe are covered in a particular xeric tree which is quite small and looks like some kind of juniper which I have been unable to identify:

What is this species?

Do you have any close-up photos?

I eventually figured it out. It is the one-seed juniper, Juniperus monosperma.


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Name of this kind of stain on fruits and how do they form
Last year I made some photos with avocados touched by some stains. They were even more delicious than the regular ones.
What's the name of such stains and how do they form? My guess is that they form because the fruit was hurt but maybe that's just me.
Later edit: A farmer told me it's a disease. Then I've found that it looks quite similar with apple scabs. Is it correct to call this "Avocado scab"? Is it made by the "Sphaceloma perseae" fungus?
Here are the photos:

You never visited the avocado blemish identification fanpage? do you use google? it's quite good.
http://ipm.ucanr.edu/PMG/C008/m008fpfrtdmg.html
Causes of avocado Damage
Avocado thrips
Anthracnose
Caterpillars
Branch canker and dieback
Fruit and stem-end rots
Genetic mutations
Greenhouse thrips
Latania scale
Mechanical injury
Nutritional disorders
Off-season fruiting
Persea mite
Phytophthora fruit rot
Sooty mold
Sunblotch
Sunburn
Vertebrates
Weather extremes
Wildland fire
mosty they are insects, funghi, viruses, mechanical forces, and sometimes, like the woody avocado, the cause is unknown:

referenced.

Well, I guess each kind of damage looks different and distinct from the others, that's why I was asking what kind of specific damage is the one in the photos I referenced.


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Is antivenom fatal?
Antivenom is used for curing snake bites. Is it fatal when used without being bitten by a snake?

1. Synopsis
I'd like to preface this by saying don't randomly use medicines without a doctor's advice. It's fairly unlikely antivenom would cause you any harm but in some cases, antivenom could be dangerous and even lethal. You have to consider possible allergic reactions and the route of administration. In any case, it would be a stupid idea to blithely inject yourself with antivenom for no reason, so why run the risk?
2. Introduction and Mechanism
Antivenom is made of a type of protein called an antibody. Antivenom acts by chemically binding to the animal's venom in such a way that the venom is blocked from binding to anything in your body. This prevents the venom from causing any damage. In fact antibodies typically bind very specifically, so they wouldn't usually bind to anything other than the venom itself. Hence, it's unlikely that antivenom would bind to anything in your body or cause any off-target effects if they were injected into your body.
3. Anaphylaxis
But antibodies are all proteins, and your body will be skeptical about any foreign protein since it could signal a pathogen. Hence, an injection of antivenom could cause an immune reaction and possibly lead to anaphylaxis. Anaphylaxis is potentially fatal, and it wouldn't be easy to know whether your body will have a reaction to the antivenom so basically keep random proteins out of your bloodstream.
4. Route of Administration
The way you introduce the antivenom to the body will have an impact on its effect. Consider what happens when you eat something. Your body passes the food from your mouth to your stomach, then liver and so on. At each step, the food is processed and broken down. In fact, chemicals like proteins are broken up during digestion, so they typically lose their effects. Hence, the effect of the antivenom will depend on where in this chain it enters the body, which determines how much it's broken down. An intravenous injection of the antivenom could have strong effects that you might be safe from, if you eat the antivenom. This is similar to the adage that you can potentially eat a snake's venom and not get harmed.
This is the reason antibody-based drugs are typically injected. By avoiding proteolysis of the antibody, it retains its shape and can successfully bind to its epitope.
5. Addendum
Your use of the word "cure" in the title is arguably slightly suspect. Antivenom doesn't stop or reverse the effects of venom that's already bound to chemicals in your body, antivenom just stops more venom binding.

“antibodies typically bind very specifically” — Tell that to biologists trying to optimise antibodies for ChIP, they’ll be delighted to hear that their hard work is unnecessary!

Aside: use multiple #s at the beginning of a line to introduce a heading, rather than bold plus two spaces at the end. This makes the formatting more uniform, and also makes the answer’s structure easier machine-readable. E.g. use ###1. Synopsis: instead of **Synopsis:**␣␣.

Hi, @KonradRudolph. Thanks for the note about formatting (I'd wondered about doing it that way but was slightly put off by the large line-break). Also, that's quite interesting about ChIP, I'd not read much about that before! I'd mostly encountered Ab specificity in regards to biologics and the immune sys (where Abs bind sufficiently specifically). Presumably the issue for ChIP is nonspecific binding, which undermines your data since you don't know whether you're binding to the protein of interest?

Precisely: ChIP assays are highly variable in quality depending on the binding specificity of the antibody. Antibody optimisation aims to improve this but is often costly and time-consuming. I’ve seen researchers come to opposite conclusions on specific research questions because they’ve used different, less specific antibodies (an example from my own research: the behaviour of pol III driven transcription).

Anti-venoms are not fatal. They are also ideally not fatal even if administered without any snake-bite, provided the anti-venom has been approved for clinical use by the pharmaceutical regulatory board for the country in question. World-wide, the Food & Drug Admin. (FDA of the USA) standard of phases of clinical trials is generally used or followed.
Anti-venoms become fatal if the person given the drug develops a hypersensitivity reaction to the drug, that is why a skin test using a small amount of the drug is injected intradermally on the forearm is conducted prior to giving the full dose of the drug. This way, toxicity is minimized, usually by not giving the drug when a positive test is unanimously declared by clinic staff.
Simplistically, a good rule of thumb to consider is that all drugs without exception are potentially toxic. That is why drugs are considered double-edged swords. Having accepted that, first, a drug should not cause someone to be sick if given to a healthy person. The related reasoning goes that if a drug causes a healthy person to be sick, then the more a sick person given the drug will more likely feel sick, i.e. 'sicker' than previously when he had no drug treatment. That is embodied in the Phase I clinical trial, where it is implied but not stated the Hippocratic oath 'First do no harm.' Hence, the subjects for that phase are (classically) generally healthy college students. By phase II, (classically) sick patients are added to the test population. By phase III, usually more hospitalised patients are included. By phase IV, generally out-patients become enrolled in the study, and so on.
For the drug company to recoup its investment in drug development, then a suitable sponsor agreement may be undertaken to administer the drug for free, and also to keep the drug industry afloat to develop more drugs.
Well-known snake venoms are phospholipases. Lipases are enzymes that can specifically target the lipid bi-layer of cell membranes of tissues and cause them to disrupt. Most anti-venoms are also enzymes that destroy these foreign lipases, and their toxicity may lie in their ability to disrupt our own lipases needed for critical bodily functions.

I'm not sure whether "destroy these foreign lipases" is the best description since the enzymes are still intact, albeit not functional. The mechanism of antibody-based inhibitors is to bind to the enzyme, such that the enzyme can no longer catalyze any reactions. It would be more like blocking the barrel of a gun, as opposed to destroying the gun itself.


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Are they bed bugs?
I found these two bugs. I know that my pictures are not fully clear, but could they be bed bugs? One was found on the wall between my bedroom door and the other one trap in a Cochrane trap beside my TV in my living room. So far, I haven't seen any bites on my skin. But, I have to admit that I feel very concerned.

Does this answer your question? Insect identification - Is this a bedbug?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). At a minimum please first search on this site for similar questions before posting. ——— Thank you for taking the [tour], but please also go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I did, but I would need more help.

Hi, and welcome!  Would it be possible to post some clearer pictures?  These pictures are not really detailed enough to allow for a positive identification.  Thanks!

I suspect your "Cochrane trap" is a "cockroach trap".

In the cockroach trap is a cockroach. I agree. However for the other (which the unclear picture) I'm still afraid of having to deal with a bed bug. I used permethrin product and the bug almost didn't move at all. If it would have been a cockroach, it should have been killed instantly and fall on the floor, shouldn't it? But I check my bed with a flash flight this night and I saw nothing. No bite either. I'm living in Ottawa. So, today, I've opened my bedroom window. I hope that the cold could slow down a possible infestation.

If you think they're different types of insects, you'll have to provide a clearer picture I'm afraid. The one on the wall doesn't look to me like a bed bug because it doesn't have a clearly defined neck.

Great thank you very much! I hope not to have the opportunity to provide you another picture. But you're reassuring me, and I'm very grateful to you. I checked my bed sheet and there's still no trace of bed bugs. I'm keeping my eyes widely opened and I will share with you if there's something new. Thanks'once again.

They look to me like cockroach nymphs (newly hatched cockroaches). Note the long antennae (more than body length) and the two short protuberances at the rear. Also note that bed bugs have a head distinct from the body, whereas cockroaches have a head that blends into the body.
3 mm cockroach nymph (from Wikipedia)

A bed bug (from Wikipedia)

See also this Q&A on What's That Bug.


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Tree identification from dried branch
I found a very interesting branch last week, and have been trying to identify it but cannot seem to find the answer. If anyone has any suggestion, I would be grateful.
I found it near the forest, around WA area.
Here's some picture:

I just reviewed an edit which seemed to be updating the original answer, but was not by the original poster. If it is actually the same person, I would recommend you recover your password

This looks like dried cholla cactus, although it will be hard to determine the species. It is sold commonly for fishtanks, so might even be found in places where it does not grow naturally if someone cleaned out their fish tank.

EDIT by Ilan: on this image you can clearly see that the tree identified right:


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What type of mushroom/fungus is this?
I had someone gift me some old firewood along with some other wood I had purchased from them.  I was told the wood in question is popple.  However, it was in pretty bad shape and much of it had a mushroom/fungus growing on it.
Does anyone recognize this fungi?  The trees lived in central Minnesota, and sat close to a lake for a year or so.

These are shelf (or bracket) fungi. They love dead or diseased wood, and are as common in woods as dirt.
Yours are kind of in rough shape (it looks like they're experiencing some problems of their own.) It's hard without examining a specimen to determine exactly which it is.

Some are edible, some are beautifully colored, some are hard, some soft, some plump, etc. But they are all shelf fungi.


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What kind of bug/insect is this? photo attached
This morning (a few hours after sunrise) I saw this insect running over the blanket.
I'm thinking what it is, if it's a bed bug that missed feeding time and is out of schedule (as i thought that they come out just before sunrise). And I thought they were brown, too but upon research found that they could (colorwise) look similar to this one too. Also, I have not found another one of these and my wife and I both don't find any bite marks on our bodies.  Our matress is packed in a plastic hull to not allow bed bugs to start living in it. What might this be?
Thanks!

Doesn't look like a bed bug - they have these distinct small heads and this reddish brown oval-shaped abdomen. What it could be is a silverfish nymph (you could tell by the smooth connection between thorax and abdomen) or otherwise something from the order Zygentoma with its filaments missing.

Do you have any other pictures of the insect?

I googled pictures of silverfish and it does indeed look like one. The legs especially, both their orientation and count.

I have a doubt we can answer this question with a high level of accuracy: the sample image is very blurred, it is unclear if there are posterior/lower body elements like forceps as well as other significant features which could help with the identification.
My best guess it is baby of Earwig (2000 species): If I look at the posterior part of the body I can "see" the preliminary forceps as well as other similar features, but still the accuracy of the ID is limited.
Enhanced image:

Baby Earwig:

It's an old post that got bumped, but  this is almost definitively not an earwig. Also, FYI: many insects have cerci on their posterior ends...


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poor RNA quality from zebrafish embryos
Does anyone routinely do RNA isolation from zebrafish embryos?
I have embryos from different stages but all below 24hpf. This is the protocol I follow:

Take 10-20 embryos
Wash once with milliQ water
Treat with 1mg/ml Proteinase-K (5min with gentle shaking) to dechorionate
Wash again with milliQ water
Remove water and add 250 µl Trizol
Homogenize by pippeting
add 750µl more of trizol
Do the standard trizol extraction step (with chlorofom)
Take the aqueous phase and wash again with 200µl chloroform
Precipitate RNA with isopropanol
Wash thrice with 70% ethanol
dissolve in nuclease free water

Despite all this I get a poor A260/A230 : ~0.4
Moreover, this happens consistently in all samples. The RNA bands look fine on the gel.
I have done RNA isolation many times from cell lines and tissues and never faced this problem. Is this common with zebrafish embryos? Is there a way to fix this other than by using kits?

This addition to the protocol worked out and good RNA quality was obtained:
Homogenization

Homogenized the embryos, suspended (and frozen) in trizol by passing through 2ml insulin syringes. (About 10 times).

Washing

Washed 2 times with 500µl 80% Ethanol
Washed 3 times with 500µl 70% Ethanol

Dechorionation was dispensable and Proteinase-K treatment was too harsh on early stage embryos. So I did not dechorionate this time.
I think the number of washes can be reduced (1×80% and 2×70%) but this is what I stuck to (out of superstition :P)

Ah, good to know the solution to this. My guess would also be that the number of washes can be reduced. I wash like this for my tissue samples.

AS you mentioned before, the problem was I guess homogenization. But insulin syringe is a good tool when you have lots of samples and works better than the hand held homogenizer (in this case) .

I'll keep this in mind.

Usually I had no problems with RNA extractions - from various cultured cells as well as a number of different tissues from mouse. If I look at your protocol this is pretty much the same as the one we used or the one recommended here for zebrafish embryo. This protocol "Purification of RNA Using TRIzol (TRI Reagent)" seems also interesting.
What can happen is a contamination by phenol or carbohydrates, then we usually used the protocol below to clean up the sample. You can also use column based methods, but they are more expensive.

add 1/10 vol of NH4OAc (5M), 2.5 volume 100% cold EtOH (100%) and 10µg
glycogen (for total RNA we usually didn't use any co-precipitation
agents) and mix well
incubate 30 min at -80°C
centrifuge 20 min at 12000g at 4°C and remove the supernatant
wash with 75% ice cold EtOH
centrifuge 5 min at 12000 g at 4°C and remove supernatant
Re-suspend the pellet in RNAse free water (can take some time)

well. I had also tried precipitating with 0.1 vol 5M LiCl + 2.5 vol EtOH.. Still same problem.. If it is a phenolic contamination it should go away in the second chloroform wash. This is persistent.

Are your embryos pigmented?

No.. they are very early embryos.. not pigmented at all..

Ok, this excludes melanin contaminations. This is pretty strange.

i tried without dechorionation.. plus 5 times 70% EtOH wash. Better but still not good enough.. Bands still look quite good on the gel.

What means better in terms of 260/230 ratio?

poor ~0.4, better ~1.2

Thats better. This paper says that the quality is going down when the homogenzation is incomplete and recommends the homogenization of frozen embryos.

Thanks for pointing that out.. now i see where the problem is.. I was homogenizing by pipetting.. most protocols suggest using a homogenizer.. since I have a lot of samples I thought I need to clean the tip every time I run the homogenizer.. Chance of contamination increases.. I do freeze the homogenized embryos in trizol and re-homogenize after thawing, just before RNA isolation. Do you suggest a better technique ?

I stumbled upon it today while I was looking for something else :-) This is the downside of using homogenizers. We usually used a ball mill and frozen tissue samples, there the same problem applies. With a lot of samples this takes much longer, no chance to get around it.


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What mushroom is this?
A lot of these popped up recently in our backyard (St. Louis, Missouri, United States).  They are all grouped into these clusters and there were probably 5 of these big clusters.
Anyone know what type of mushrooms they are?

Where do you live?

@Remi.b I live in St. Louis, Missouri, United States.

http://www.mycokey.com/newMycoKeySite/MycoKeyIdentQuick.html found a page might help.


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Insect identification, Bangalore India
Can anyone identify this insect? It was sitting on my refrigerator.
Size: approximately 1 cm height, 1 inch across
My location: Bangalore, India

Some sort of Plume Moth, but I can't tell what kind specifically.

https://en.wikipedia.org/wiki/List_of_moths_of_India_(Pterophoridae) ... one of those then, pick your favourite

So i did some more research and found some canon photos of two moth species both found in india and super similar to this

both of them have brown spots around them
both of them are found in india
 So it was hard for me to eliminate one of them
here are both the insects
Sphenarches Anisodactylus

Sphenarches caffer

So now its up to you to decide which one it is???

Can you elaborate on your answer a bit - how you determined this, what rules out other genera, etc? Also, please include a photo/image in the actual answer rather than a link.

Those are actually the photos

To me they just appear as hyperlinks. If the photos are showing when you look at the answer, I'm not sure what's happening.

I mean not exactly photos but it was sure a photo when i copied the link and inserted link for the image insertion option

Done I inserted the photos

My pleasure to help people