How does low cysteine conditions affect pheomelanin production? So we were studying this amino acid called cysteine. Specifically we were studying it's effect on melanin genesis.
Our teacher told us how excess of cysteine affects the melanin synthesis  by generating more pheomelanin. Low amount of cysteine promotes formation of eumelanin.
 He told us that if the concentration of cysteine is increased in cells then the above reaction starts producing pheomelanin in brown/black skinned people. I searched it on net and it seems to be true.
The question is that if someone who has fair skin (produces more pheomelanin) is forced to live in low cysteine condition, then what happens? Eumelanin production should increase. His complexion must change. But it doesn't occur anywhere. Fair skinned people affected by malnutrition remain fairskinned. How is this possible? The pheomelanin production must stop since they aren't getting enough cysteine. Then how...?

He also told us that onions contain large amount of cysteine yet it can't be used since it is destroyed by stomach acids.

First: Your teacher is right with the statement that a low cysteine concentration affects the synthesis of pheomelanin. To understand this, you need to take a look at the biosynthesis pathway of melanin (from here):

The first steps for both melanin forms are the oxidation of the amino acid Tyrosine to DOPA (L-3,4-Dihydroxyphenylalanine) and the to DOPA quinone by the enzyme Tyrosinase (abbreviated Tyr). In the following step the branches divert, if there is enough cysteine present in the cells, then Cysteinyl-DOPA and subsequently Pheomelanin are synthesized.

If the cysteine concentration in the cell falls below the threshold of 0,13µM (this is taken from this paper), then the switch to eumelanin production occurs.

In the case of you second question, there is a different setting. The overall rate of the melanin production (no matter which flavor) depends on the amount of active Tyrosinase (for the production of the first steps in the synthesis cascade). The production of this enzyme is regulated by receptors in the cellular membrane (and different other factors).

In fair skinned people (classically red-haired and with freckles) these receptors are not fully functional, resulting much less Tyrosinase enzyme in the cells. This results in fewer available precursors for the melanin production and in turn in less need for cysteine. The reason is that the cysteine pool of the cell is not getting exhausted.

"Pheomelanogenesis may have evolved as an excretory mechanism to remove excess cysteine, and in humans this might potentially confer a greater ability to avoid disease such as Parkinson's and Alzheimer's disease, in which excess cysteine is a contributory cause." Source:https://onlinelibrary.wiley.com/doi/full/10.1002/bies.201200017

In this instance your teacher has his information incorrect. L-Cysteine has nothing to do with the production of Eumelanin. "Melanocortin 1 receptor (MC1R) is a key signaling molecule on melanocytes that responds to α-MSH by inducing expression of enzymes responsible for eumelanin synthesis. Some forms of Pheomelanin production lack the MC1R receptor to form eumelanin entirely; others have a weak signal if they have mixed Pheo/Eumelanin. Eumelanin has a strong MC1R receptor connected to the (Melanin Stimulating Hormone) α-MSH. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299862/

Pheomelanin and Eumelanin have completely different pathways of formation. "Pheomelanin, consists mainly of sulfur-containing benzothiazine and benzothiazole derivatives (Figure 1a). L-cysteine is the chief source of sulfur and is, therefore, essential for the pheomelanin synthesis (12). Eumelanin, on the other hand is an extremely heterogeneous polymer comprising of 5,6-dihydroxyindole (DHI) and or 5,6-dihydroxyindole-2-carboxylic acid (DHICA) units (Figure 1b)."https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299862/

Individuals with Eumelanin maybe less able to synthesis Sulfur based Amino Acids like: Methionine, Cysteine, Homocysteine, Taurine, and Glutathion. :)


Do experiences shape actions of insects? Animals? Would an insect behave differently to stimuli depending on what stimuli occurred to them earlier (that only affects them cognitively or their conscience)?

"Simple" insects like fruit flies can learn to associate odors with food, e.g. see here for a pretty classic example. Drosophila even show some kind of depression which is acquired. Their sexual experiences even shape their alcohol intake.

You will find similar examples for other model organisms as well.
So, yes, simple animals behave differently in response to previous experiences.

You say depending on what happened to them. The expression "what happened to them" is so broad that the answer is necessarily yes. I am giving a few very obvious examples.

If you give royal jelly to a bee larvea, it will drastically affect its morphology and behaviour. So yes, presence of royal jelly will affect their future behaviour.
If you cut all the legs of an ant than it will not run toward a smell of food! So yes, depending on what happened to an ant, the response to a food smell stimuli will vary.
If you kill a beetle, it won't react the same way to future simuli either than if you don't kill it!

So yes, even in insects the past affects the present. The same is true for any other living organisms. You might even go on an argue the same for a stone although it might take some consideration of semantic in order to apply the concept of reaction to a stimulus for a stone.


Do any animals other than humans undergo menopause? Do any animals other than humans undergo menopause?

Also, is there any difference between animals in captivity and animals in the wild as regards menopause? For example, even if menopause has been observed in a captive member of a particular ape species, do individuals of that species typically live long enough in the wild to also undergo menopause?

I guess here's what I'm really getting at: is menopause a common thing in the animal kingdom, or is it only a common thing in humans?

Yes. Menopause is common for long-lived mammals. For instance, in the wild, killer whales go in a sort of menopause as reported in 2009 by Ward et al. Front Zool. 2009 Feb 3;6:4. So it is not due to captivity. According to a Nature review, reproductive cessation has also been documented in non-human primates, rodents, whales, dogs, rabbits, elephants and domestic livestock (Packer et al. Nature. 1998; 392(6678):807-11)

Only three — humans, killer whales, and pilot whales.  (Reference)

  Among long-lived animals, scientists have found only three species that undergo menopause: humans, short-finned pilot whales, and resident killer whales. What makes these species so special? A new study finds that it all comes down to their unique social structures.


How did the nucleus of eukaryotic cells evolve? What is/are the most popular theory/theories on how the nucleus evolved?
I know mitochondria came from alpha-proteobacteria, chloroplasts from cyanobacteria and that eukaryotes evolved directly from archaea, but what about the nucleus?

I hope these papers by Wilson and Dawson (2011) and Devos et al. (2014) will help you.

In summary these two review provide evidence for the following statements:

The nuclear pore complex is well conserved with some regions of divergence.
The nuclear lamina appears quite variable between major supergroups.
Centrosomes are ancient structures but exhibit a complex evolutionary history.
There is evidence for prokaryotic ancestors of some nuclear components.
Analysis of divergent organisms is essential to fully understand nuclear biology and its origins.


Bug Identification: Tiny Bugs I have seen these on my hands recently and I am wondering what they are. Urban Setting. South Central Pennsylvania.

This appears to be a bird mite (or possibly rat mite) in the genus Ornithonyssus of the parasitic family Macronyssidae.

 Credit: user Aewills on bugguide.com

Identification:

From Central Exterminating Co.:

  The mites are distinguished from most other common, structural species by the very long legs and very long mouthparts. These long, pointed chelicerae and palps stick well out in front of the head region. The 8 legs are very long and well separated, allowing for good mobility by these mites. The body is oval, with the thorax and abdomen combined to a single segment without separation. The color is light grayish in unfed mites to reddish orange in mites recently having had a blood meal. The fowl mites often seem to have a patchy, mottled appearance of dark areas.

Distinguishing between species is difficult.

Blaine Mathison mentions the following features useful for identifying these mites to lower taxonomic levels under magnification [source: bugguide.com]:

chelicerae shape
dorsal plate breadth and degree of dorsal coverage
spiracle present between legs
genitoventral plate width
sternal plate shape and presence of setae

(see the linked post for pictures and more detail).

You can see videos of these mites crawling on people here and here.

Regarding their affects on humans:

From Penn State Extension:

  Bird mites have piercing mouthparts that enable them to take blood meals from their
  bird hosts. Although the mites will inadvertently bite people, they cannot reproduce without their bird hosts...

  As the mites search for an alternative host, they will crawl onto the skin and conduct an exploratory bite to test the appropriateness of the host. The mite will move on, possibly trying the host again, but will not feed. These bites are felt as a “prick” and a resultant rash and itching, sometimes intense, will occur. Some individuals are apparently capable of sensing the crawling of the mites on the skin. The irritation produced by the bite is enhanced by the injection of the mite’s saliva that can cause a localized histamine
  response.

Management:

Remove birds (and especially nests) from on or near the building. Check for any holes in your building that could be large enough to allow birds inside. Again, these mites need birds to reproduce, so if you eliminate the birds eventually these will disappear. See PSU Extension and Central Extirminating Co. for more suggestions.

Congratulations, you have baby cockroaches!  I have lived with many.  Their shape and coloring changes with age.  Your organism walks too fast and is too big to be a parasitic mite.  So this is good news.


Reference to hypothesis about breast sexual attractiveness? Some time ago there was a hypothesis published,suggesting evolution made breasts mimic buttocks for either primitive men being attracted to women when they started to walk on two legs, or to discourage sexual intercourse from behind for other reasons I can’t remember. I can find many posts about this online, but I can’t find any reference to the original idea. Can anyone provide information about this?

Eventually, I found it, here it is:

  In considering the human animal, zoologists proposed that the human
  female is the only primate that possesses permanent, full-form breasts
  when not pregnant. Other mammal females develop full breasts only when
  pregnant. The zoologist Desmond Morris proposed that the rounded shape
  of a woman's breasts evolved as frontal, secondary sex characteristic
  that is a sexual-attraction counterpart to the buttocks, and so
  encouraged frontal copulation, the reason being that while other
  primates mate by means of the rear-entry position, the upright,
  bipedal human being was likelier to successfully copulate face to face
  in the missionary position.

https://www.reddit.com/r/askscience/comments/uflgy/why_are_breasts_so_attractive_after_all_theyre/


What makes something food? From my (limited) understanding, animals get energy from food by breaking chemical bonds between molecules.

There's a lot of water here [citation needed], so it seems like natural selection would favor any organism that could live off it. Why, in the history of life on earth, hasn't an organism appeared that eats water?

Same applies to dirt, rocks -- (although maybe lichen eat rocks? I'm fuzzy on lichen.)

Or air?

Why are humans and other animals like us only equipped to eat certain types of molecules, when others are so much more plentiful?

You don't get energy from breaking chemical bonds, you only get energy from making chemical bonds, while breaking chemical bonds requires the input of energy.  However, in practice chemical bonds are always broken as others are formed, and the net number of bonds is generally constant.  Otherwise you would end up with free radicals, which are highly reactive and looking to form a chemical bond with the next thing it touches.

For example, the burning of glucose in respiration involves the breaking of C-C, C-H, C-O and O-H bonds in glucose and O=O bonds in oxygen, with the simultaneous formation of C=O bonds in CO2 and O-H bonds in water.  But the C=O bonds in CO2 and O-H bonds in water contain much less energy than the bonds we break within in glucose.  So the key is that the bonds formed contain less energy than the bonds broken, and energy is released overall.

And actually it's a bit more complicated than that, because you also have to consider entropy, which is how disordered the system is.  Generally the more molecules in a system, the more entropy, so breaking a few big molecules down into lots of small molecules tends to release energy by increasing entropy.

So to answer your question, "food" is what we can draw useful energy from in the process of turning it into something else as we make and break chemical bonds.  We can't do this with water, or indeed with rocks, because their chemical bonds would require more energy to break than the energy we'd get back out by forming alternative bonds with anything else.

Plants use both water and air as food using photosynthesis where water is split and recombined with carbon dioxide from air to make glucose.

  Overall, the chemical reaction of photosynthesis is as follows:

Light energy + plant enzymes
6CO2 + 12H2O ------------------------------------------------> C6H12O6 + 6O2 + 6H2O

...which means that it takes

six molecules of carbon dioxide plus
12 molecules of water

in the presence of light and the proper enzymes in the cell, to make

one molecule of glucose
6 molecules of oxygen
6 molecules of water

Energy is released when glucose is burnt

  about 16 enzymatic rxns
  C6H12O6 + 6O2 + 6H2O ------------------------------------> 6CO2 + 12H2O + ENERGY

...which means that

one molecule of glucose in the presence of
six molecules of oxygen and
six molecules of water

can be "burned" to release stored energy as well as the "waste" products of

6 molecules of carbon dioxide and
12 molecules of water

http://www.bio.miami.edu/dana/dox/photosynthesis.html


Has the concept of allostasis been adopted in biology, in place of homeostasis? Peter Sterling, among others, has been a prominent critic of the concept of homeostasis.  He instead proposes a process called allostasis.

Homeostasis involves having fixed set points for physiological parameters, and when we deviate from those set points, there are mechanisms that restore them.

However, Sterling argues that this process of homeostasis is inefficient and inflexible.  Instead, he posits that the brain is constantly predicting physiological needs based on environmental and bodily demands, such that the "set point" changes depending on the context.  So your mean blood pressure might be X in one context, but Y in another.  And rather than responding after a deviation from the mean, the brain predicts those deviations and adjusts the body accordingly.  This is allostasis.

Allostasis is much more in line with what we know about the brain (e.g., Clark, 2013), but has this idea been adopted much in biology?  Based on my memory from biology class not long ago, it seems like homeostasis is still considered a central feature of living things.

Thanks!

Allostasis is more than changing set points. The theory of allostasis attempts to unify the theories of stress and homeostasis. And, although Peter Sterling and Joseph Eyer were the first to coin the term "allostasis", the concept is today proposed by a plethora of researchers.

Allostatic responses ensure „stability through change“ in situations of strain and stress. If in allostatic mode a feedback control system is able to change both its set point and its parameters to approach a state vector that is more suitable for survival. An allostatic response involves the activation of actuator variables that is referred to as allostatic state. Although allostasis is basically beneficial for viability it also exposes the organism to some kind of strain, referred to as allostatic load. If ongoing or being excessive, allostatic load may be life-threatening on its own terms. In this situation, it is referred to as allostatic overload.

Figure taken from Chatzitomaris et al. 2017.

The idea of allostasis might have been omitted in your biology class due to didactical reasons. For an introductory course it may be beneficial to begin with the simpler theory of homeostasis.

Today, the concept of allostasis is of increasing importance for psychology and medicine. As of today, a PubMed search for the term "allostasis" results in 730 papers and a search for "allostatic load" delivers 1123 publications (with growing tendency).

The theory of allostasis helped to improve our understanding of a broad range of diseases and non-pathological bio-psycho-social situations. Typical examples include starvation, obesity, exercise, fever, type 2 diabetes, hypertension, thyroid disorders, post-traumatic stress disorder (PTSD) and psychosomatic diseases. Additionally, the recent development of panels for allostatic load facilitates differential diagnosis near the small ridge between health and disease.

References

Sterling P, Eyer J. Biological basis of stress-related mortality. Soc Sci Med E. 1981 Feb;15(1):3-42. PMID 7020084.
Sterling P. Allostasis: a model of predictive regulation. Physiol Behav. 2012 Apr 12;106(1):5-15. doi: 10.1016/j.physbeh.2011.06.004. Epub 2011 Jun 12. PMID 21684297.
Bizik G, Picard M, Nijjar R, Tourjman V, McEwen BS, Lupien SJ, Juster RP. Allostatic load as a tool for monitoring physiological dysregulations and comorbidities in patients with severe mental illnesses. Harv Rev Psychiatry. 2013 Nov-Dec;21(6):296-313. doi: 10.1097/HRP.0000000000000012. PMID 24201821.
Sagner M, McNeil A, Puska P, Auffray C, Price ND, Hood L, Lavie CJ, Han ZG, Chen Z, Brahmachari SK, McEwen BS, Soares MB, Balling R, Epel E, Arena R. The P4 Health Spectrum - A Predictive, Preventive, Personalized and Participatory Continuum for Promoting Healthspan. Prog Cardiovasc Dis. 2017 Mar - Apr;59(5):506-521. doi: 10.1016/j.pcad.2016.08.002. PMID 27546358.
Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood A, Klein HH, Dietrich JW. Thyroid Allostasis-Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming. Front Endocrinol (Lausanne). 2017 Jul 20;8:163. doi: 10.3389/fendo.2017.00163. PMID 28775711.


Why only female mammals have well developed mammary glands? In course of evolution (possibly), mammary glands became vestigial in male mammals, but became fully developed in females. Is there any plausible explanation for this characteristic?

It comes down to investment in offspring. Males invest little in offspring only a little sperm whilst females have to develop the more expensive egg and the energy used through its development. In the mammalian line, this investment has increased in amount, initially through viviparity and then through the secretion of feeding fluids.

In species, such as humans, where there is a lasting pair bond and both male and female invest in rearing the young then I suppose there could be a situation where it makes equal sense for both males and females to nurse - although the cost of mammaries on other functions may favour specialisation anyway - but remember that, in many mammals, it is the mother alone that rears the offspring.

You may also find the answer to this question useful: Do any birds beside the family Columbidae (or any reptile or mammal) feed their young “Crop Milk”. What I hadn't realised is that there actually two species of bats where the male lactates.

The mammary glands in human males is not vestigial but rudimentary.

Human females have XX chromosomes and males have XY chromosome,here the "Y" chromosome is provided by father and "X" by the mother. At the time of fertilization, the father can provide either X or Y chromosome. If he provides Y chromosome the child will be male and if he provides X then child will be female. The mother always provides X chromosome. So the Y chromosome in the male child is responsible for the development of male sex organs and due to the presence of X chromosome the female sex organs are suppressed. Note that the female organs are suppressed but they are not eliminated. At the time of puberty males don't receive hormones which initiate the development of female sex organs. As a result the mammary glands stay in males as nipples but the hormone effects are only present in females and cause the formation of large amounts of fatty tissue near the nipples and develop as breasts.

  A distinguishing characteristic of the class Mammalia is the presence of mammary glands. The mammary glands are modified sweat glands that produce milk, which is used to feed the young for some time after birth. Only mammals produce milk. Mammary glands are most obvious in humans, as the female human body stores large amounts of fatty tissue near the nipples, resulting in prominent breasts.
  http://en.wikipedia.org/wiki/Female

.

  While estrogens are present in both men and women, they are usually present at significantly higher levels in women of reproductive age. They promote the development of female secondary sexual characteristics, such as breasts.
  http://en.wikipedia.org/wiki/Estrogen


Why do we squint when tasting very sour things? Sometimes while tasting a very sour thing (like tamarind, lemon etc.) our eyes squint immediately and involuntarily for a second, but a little later becomes normal again.

Why, and how, does this reflexive movement occur?

Short answer
Adverse stimuli in general are accompanied by contraction of facial muscles. It is part of our repertoire of emotional expressions.

Background
A disgusted expression and the expression of pain are both accompanied by squinting. Disgusting stimuli include your example of a sour taste, but also include other adverse tastes (bitter) or visual stimuli such as a gross-looking objects. In other words, squinting is likely a common way of expressing adverse stimuli. So the "sour look" may not be easily explained on its own. Instead, it is part of a huge emotional expressive repertoire that makes us human beings. To be able to read these expressions allows us to be empathetic towards others. People with autism and Asperger's syndrome may not be able to do so and are disadvantaged in their social behaviors.

To illustrate the commonalities between sour (#1), disgust (#2) and pain (#3) I would like to share the following web finds.

Sour taste. Source: Getty Images

!
Disgust. Source: Berkeley Emotional IQ test

Pain. Source: Berkeley Emotional IQ test

PS: I am not a psychologist - Consider my contribution as an educated guess.

Squinting is the organism's way to warn us that we are eating something that could eventually be dangerous, acidic or toxic. It's a reflex, developed many many years ago when the ancient people did not know much about the safety of plants, roots and other foods. They used to try them and decide if the object is eatable or not according to its taste.

Also, our tongue has very sensitive papilla, which react to sourness and make the muscles contract.


Required energy to metabolize fat Tl;dr: What is the net joule value of fat if used for energy provision, compared to e.g. carbohydrates. So does 1 Joule Fat intake result in 1 - X Joule energy provided to the cell, or does it work in a completely different way?

My understanding is that if I take in one Joule of fat, my body takes in the energy to move ~100g of mass up by one meter (Wikipedia).

Now for my body to use that energy, it needs to convert it to some sort of Glucose, right?

From the Lipid Metabolism Wikipedia Article I get that my fat needs to become a Triglyceride to serve as energy source.

There are some steps involved, roughly the following:

gastric peristalsis (basically muscle contractions to mix it all up)
peristaltic contractions in the gut (again, mixing is key)
lipase, also working in the gut to finally create Triglyceride
then the fat gets "packaged" in Chylomicrons and put into the bloodstream

releasing energy to the cell involves the following

Lipase unpacking the Chylomicrons
Splitting of the Triglyceride in Glycerin (the stuff we want) and fatty acids

Now this seems like a really cumbersome process to me, and I wonder what the net Joule Value is that arrives at the cell.
Is it significant, or is this process so efficient that it doesn't matter anyways?

So, what I was looking for, but was lacking the knowledge of, was the concept of "Thermic Effect of Food"
I really didn't know how to phrase my question well, due to the fact that I tackled the problem from the wrong angle.
Direct quote from the Wikipedia Article as it answers the question best:

The thermic effect of food is the energy required for digestion, absorption, and disposal of ingested nutrients. >Its magnitude depends on the composition of the food consumed:
Carbohydrates: 5 to 15% of the energy consumed [7]
Protein: 20 to 35% [7]
Fats: at most 5 to 15 %[8]


How does the brain immediately know when one's thirst has been quenched? The question struck me the other day when I drank a glass of water. I understand that there are at least two conditions under which the brain signals thirst: extracellular thirst, when there's not enough fluid in the blood, and intracellular thirst, when the cells need more water to lower the concentration of osmolites.

However, it takes time for water to enter the bloodstream after it has been ingested, and it spends at least a little while in the stomach.

Why does the sensation of thirst disappear despite the water having not yet made it into my bloodstream?

There are two different aspects to or drivers of thirst, osmolality and hypovolemia, with plasma osmolality elevation being the more potent stimulus of thirst.
As stated by @arboviral (and supported by his link), not a lot is known about the mechanisms of immediate thirst satiety. Much more is known about the mechanisms causing thirst, and the mechanisms of return to normal serum osmolality over 120-180 minutes after rehydration than those immediately satisfying it.

Most of the research on this is old (pre-2000). In one often-cited very small study 1, swallowing and esophageal reflexes (or as the authors termed it, “oropharyngeal metering”) had a significant effect on relief of thirst, that is,

  the act of swallowing helps to regulate the volume of fluid ingested by providing an integrated signal proportional to the cumulative ingested volume.2

Study participants were all mildly dehydrated. One (control) group was allowed to drink ad lib. Another was allowed to drink ad lib but as they did so, the fluid was simultaneous extracted from the stomach by a nasogastric (ng) tube already in place. Interestingly, the difference in the amount of fluid ingested between these two groups (N.B. ad lib) was only 15% (the latter group drank a bit more.) The third group was given fluid by ng tube only.

The very act of swallowing fluid boluses induced satiety. However, plasma arginine vasopressin levels (involved in the regulation of fluid intake) dropped rapidly during the first 5 minutes of drinking in both ad lib groups, but not in those given fluids via ng tube, so it is not only mechanical receptors that are involved in quenching of thirst.

This confirmed an older study which demonstrated the importance of the rapid drop in plasma vasopressin in hydration before major changes in plasma osmolality occurred.3

Given the lack of extensive research and the relative immediacy of thirst suppression, The most likely explanation is a combination of sensory modalities and reflexes (mucosal wetness, temperature of rehydration fluid, mechanicoreceptors in the oropharynx, esophagus, etc.), and some rapid hormonal changes - e.g. in AVP - are responsible for limiting the amount we drink when thirsty.

1 Regulation of fluid intake in dehydrated humans: Role of oropharyngeal stimulation
2 Influence of age on thirst and fluid intake
3 Acute suppression of plasma vasopressin and thirst after drinking in hypernatremic humans

I'd say the answer is easy.

Since the whole body is one body all you need is the change of of water saturation in a part of you to determine / extrapolate how much water has been ingested.
We all came from the water and are mostly made out of water. So it's not like water is a foreign substance and we needs special receptors in order to determine water content.
We are water. And the system has evolved over time to be built in. I.e. the ones with a broken system have died of dehydration and anybody else survived.
Of course you might be looking for one singular mechanism that says stop, that's enough. But it's a mixture of body temperature, what you have eaten, how much energy you have, etc. (water requires energy in order to be heated to your body temperature)
That reminds me that apparently in hot regions you are supposed to drink tea or warm water because that allows you to drink more / be better hydrated. Based on that I'd guess it's just a temperature gradient? I.e. the water cools you down, and when it becomes too cold in your insides, you stop until you are hot enough again.


Why are two-winged animals much more common than four-winged? In flying vertebrates, almost all have only two wings (with the exception of Microraptor and its close relatives). This makes some sense because you need some way to walk also, and a wing isn't very good as a leg, hence why bats are so bad at walking. Of course, bats do demonstrate that being able to walk well is not necessary to be a successful clade.

As far as insects are concerned this might seem like an odd question, since most insects technically have four wings. But among the four largest insect orders (which together make up a sizeable majority of insects), Coleoptera, Lepidoptera, Diptera, and Hymenoptera, all of them functionally have two wings. In Diptera and Coleoptera, only one pair of wings is used to fly. In Hymenoptera and Lepidoptera the two pairs are attached and don't move indepedently.

So my question is, why is two-winged flight so much more common than four-winged? If two-wingedness is advantageous, why do other insects retain four-winged flight (most notably Odonata)?

Note you are talking about two very distinct conditions

In vertebrates, 4 "wings" only evolves once in vertebrates (in early birds) and only one set function as wings the others "wings" are control surfaces for low speed stability, they generate insignificant amounts of lift. for large animals like vertebrates you can't fit two sets of functional wings on the same animal. Large wings need a lot of space to flap and you would need to make the torso longer to give enough room for a second set of flapping wings, which would add a lot of weight and defeat the benefits.

In Insects four wings is the default, the groups with two wings got them by transforming one set of wings into something else useful. Wing covers in beetles ,which protect wings from damage, and Halteres in flies which act as a sort of sensory organ to determine position. Two wings are more common numerically becasue those two groups are extremely successful. Basically if you have two of something but one will also work and evolution can turn the other set into something useful then you have a chance to lose one set of that thing. Two wings are more common numerically becasue those two groups are extremely successful. By turning four wings into two those groups ended up with more abilities than their four winged relatives, becasue they did not just lose the wings they turned them into something else.

In insects wings actually evolved from gill covers, insects could have had six wings, why the first set never evolved would be an interesting question. It may be due how HOX genes are expressed in insect segments.

Source

This is far from being the complete explanation (which I don't have). But:

From a molecular standpoint, the symmetry between left and right is achieved often by presence / absence of gene expression of certain developmental genes.

In some cases, these genes could be expressed in a gradient, forming gradual transitions of patterns.

A four winged animal would require a dev gene to be expressed on one axis (generating left and right) but also on another, being expressed in two pulses (two sets of wings). This is much more prone to deleterious mutations, since there are more factors weighing in. Hence, it could be evolutionary more disadvantageous.


What is the smallest difference in light wavelength that the human eye can detect? Is there a lower limit to the difference in wavelength (colour) our eyes can detect? If so, is this consistent between individuals? Are there any other traits correlated with precise colour vision?

The eye really on can sense 3 colors, or to be more precise it only has three types color sensitive each of which detects a large range of wavelengths with no way to distinguish between them within the same cone. We only determine color by the different levels of activation between the different cone cells. This means we need a lot of light to see color and our ability to detect differences in color really depend greatly on where on the visible spectrum that color falls.

As for more precise color vision. The greater the number of types of cones cells the more color sensitive the eye ,birds and reptiles can see far more colors than use becasue they have 4 types of color sensitive cells as opposed to the human 3. More widely spaces base colors will give greater sensitivity. This is why even among trichromats human color vision is poor becasue two of our base colors are close together and overlap greatly.  That is because humans (and primates) are secondarily trichromats, gaining a third base color from a recent mutation. wiki on the subject

About 2 nm wavelength difference. The human eye can detect about 150 different hues in a rainbow, which for us consists of a visible light 380-700nm. About 300nm/150hues = 2nm per smallest detectable difference between two hues. I guess that's the answer you were looking for?


Has a new functional structure ever been observed arising spontaneously? Have we ever observed a new functional biological structure arising spontaneously such as a new functional organ (sensory or otherwise. such as tracing some creature in the past few hundred years which had no electroreception organ and now has evolved this organ)

Or has what we observed been limited to changes in existing structures.

(Lenski's E. coli bacteria is not what i am looking for since it is a change in an existing metabolic system (not a new functional structure) and furthermore e-coli already had some ability to use citrate as an energy source )

Looking for a completely new functional organ (such as a new sensory organ) that we have actually observed - not deduced from fossil record.

Also not looking for something trivial such as a new/modified enzyme or protein molecule but rather a new organ in a species at least the size of an insect.

It seems like you are attempting to frame this as a question about current evolutionary theory. However, current evolutionary theory doesn't expect anything as complex as an organ to arise spontaneously without any precursors. You suggest a new claw in an insect would be something "spontaneous" enough for you. This again shows that your question and the answer you are looking for are not related to evolutionary theory. The insect organs you are talking about are all modified appendages. This includes claws, mandibles, antennae, legs, fangs. These appendages all share a common genetic and developmental framework that has been slightly modified over long periods of time to give raise to the variety of insect appendages that we see today.

The idea that evolutionary theory supports the spontaneous creation of organs is a willful ignorance of evolutionary theory. The molecular mechanisms that generate novelty (e.g. genome duplication, gene duplication, de novo genes, mutation, gene regulation) for natural selection to work on are relatively well understood. Since we have an understanding of how novelty is created it is known that spontaneous organ generation has never happened or is expected to happen under evolutionary theory.

Here is link to the University of California, Berkeley's webpage designed to teach the public about evolution.

There are two main issues in your question that make it hard or fundamentally impossible to answer. The two issues are

What you would accept being an 'observation'
What you would accept being significant enough to be an example of interest.

A big issue in your question is based upon what you call an observation!

When you say

  observed - not deduced

, you highlight the whole issue of what you would consider being an observation.

In science, observations often take complex form. It is not only direct visual observation recorded on a standard camera. It is like asking for, recorded-on-camera evidence that quartz exist. Such evidence don't exist (and cannot exist), yet we know of their existence through other means of observation. It would make no sense for someone to only consider camera recording as valid mean of observation.

Of course, We have never recorded on a camera the evolution of an entire new organ because it takes a lot of time. Yet, evidences are numerous.

This technic of limiting arbitrarily the field of methods that one accepts to recognize as bringing evidence and call "observation" is a common technic from science denier (e.g. flat earth society, creationist). I made a similar point as the one I made here on this post if you want.

How to solve this "What is an observation" problem?

There is only one way to go. It will be for you to be able to understand the forms that observation can take. For this, you will have to learn a little bit about evolutionary biology and evolutionary genetics. For a very short introduction to evolutionary biology, you can have a look at Evo101 by UC Berkeley.

You may have hoped for someone to give an entire course on evolutionary biology to fill up this gap of knowledge of yours but I am afraid it would be way too much work for a single post. If this was your position, then it would be like refusing to accept that earth is a sphere without having yourself explain how GPS data work. We just can't give you an entire course here.

So you have two solutions; rely on authority or understand by yourself. If you rely on authority you have two main options; Rely on those that rely on evidence (science) or those that don't rely on evidence and either rely on other forms of justification (justification theory;such as a religious book for example). (either those that work through observations, scientists). You second solution is to understand the field by yourself and therefore start studying for it.

A second issue is that it is unclear to know what you would accept being "not trivial"

When you say

  Also not looking for something trivial such as a new/modified enzyme or protein molecule but rather a new organ in a species at least the size of an insect

It is hard to know what you would call a significant enough evolutionary event to be accepted. The risk is that you may define it large enough so that it fundamentally cannot be observed by a mean that you would accept.

For your curiosity, this post talks about evolution of lactose digestion in humans and this post about the evolution of cardio-vascular system.

Somewhat related post

You might want to have a look at post Is evolution a fact? and the link posts in the top voted answer.

Just another comment

  random evolution

In the scientific literature, "evolution" is never said to be "random". The fact that you're using this expression shows what kind of literature you are used to.

For all reasons explained above, the question cannot be answered, not by lack of evidence, but because the question is unclear. I am therefore voting to close as unclear. Good luck in your investigation of the question.


How do our eyes detect light at different frequencies? Here is my confusion: we can see colored light of different wavelengths: form red to violet. To my understanding, these stimuli cause a confirmational change in the photoreceptors in our eyes and results in a STP that eventually leads to an "all or nothing" action potential that sends another signal, again an all or nothing action potential through the optic chiasm to the occipital lobe and we perceive the colors as we see them.

My question is *how does this signaling work? *; How can a minor stimulus, resulting in an "all or nothing" chain of action potentials be converted into something as specific as the vision of color?

Asked another way, how does variation in a confirmational change at a receptor that results in "all or nothing" signaling lead to specific signals being sent such as colored vision ?

PS: I dont know jack about sensory physiology

Short answer
Action potentials generated to different colors are indeed similar throughout the nervous system and do not encode color as such. Instead, the different color- sensitive cells in the retina are connected to different neurons and these color-specific signals are kept segregated up until the higher visual cortical areas.

Background
Action potentials are indeed pretty similar throughout the nervous system. However, the color-sensitive sensory cells in the retina, called the cones, come in three flavors: red, green and blue. These colors form the RGB system just like in your LED TV and can together make all the available millions of colors. These three cones synapse ultimately onto color-specific secondary sensory neurons (Fig. 1).

Hence, R, G and B cones indeed generate identical action potentials in downstream neurons, the trick is they do so in different retinal ganglion cells, and at different firing rates depending on the intensity of light that particular cone is sensitive to. These different classes of retinal ganglion cells project onto different classes of neurons in the brainstem (lateral geniculate nucleus, or LGN) and ultimately onto different neurons in the higher cortical visual areas in the brain.

Fig. 1. Different classes of cones synapse onto different classes of secondary sensory neurons in the retina. source: Discovery Eye Foundation

The reason why we can differentiate millions of colors can be explained by the Hering model of color vision (Fig. 2). Basically, the different cones converge pairwise onto opponent color-sensitive cells. The red-green opponent system, for example, operates by weighing the amount of red and green in the incoming signal. This weighting results in an analogue system that can code millions of colors along the red-green axis (Fig. 3).

Fig. 2. Hering model of color vision. source: Webvision

Fig. 3. Red-green color axis. source: SO

How can a minor stimulus, resulting in an "all or nothing" chain of action potentials be converted into something as specific as the vision of color?

Visual phototransduction is the one of answers to your question.

It is a process by which light is converted into electrical signals in the rod cells, cone cellsand photosensitive ganglion cells of the retinaof the eye. This cycle was elucidated by George Wald (1906-1997) for which he received the Nobel Prize in 1967. It is so called "Wald's Visual Cycle" after him.

Overview

The visual cycle is the biological conversion of a photon into an electrical signal in the retina. This process occurs via G-protein coupled receptors called opsins which contain the chromophore 11-cis retinal. 11-cis retinal is covalently linked to the opsin.  When struck by a photon, 11-cis retinal undergoes photoisomerization to all-trans retinal which changes the conformation of the opsin leading to signal transduction cascades which causes closure of cyclic GMP-gated cation channel, and hyperpolarization of the photoreceptor cell.

Signal Transduction

In dark
glutamate is continually being secreted at synapse between photoreceptors and bipolar cells.

In light

1)A light photon interacts with the retinal in a photoreceptor cell.
The retinal undergoes isomerisation, changing from the 11-cis to all-trans configuration.

2) Retinal no longer fits into the opsin binding site.

3)Opsin therefore undergoes a conformational change to metarhodopsin II.Metarhodopsin II is unstable and splits, yielding opsin and all-trans retinal.

4)The opsin activates the regulatory protein transducin.

5) This causes transducin to dissociate from its bound GDP, and bind GTP, then the alpha subunit of transducin dissociates from the beta and gamma subunits, with the GTP still bound to the alpha subunit.

6) The alpha subunit-GTP complex activates phosphodiesterase or PDE.PDE breaks down cGMP to 5'-GMP.

7)This lowers the concentration of cGMP and therefore the sodium channels close.

8) Closure of the sodium channels causes hyperpolarization of the cell due to the ongoing efflux of potassium ions.

9)Hyperpolarization of the cell causes voltage-gated calcium channels to close.As the calcium level in the photoreceptor cell drops, the amount of the neurotransmitter glutamate that is released by the cell also drops.

10)A decrease in the amount of glutamate released by the photoreceptors causes depolarization of On center bipolar cells (rod and cone On bipolar cells) and hyperpolarization of cone off-center bipolar cells.

Impulse conduction
As is explained by AliceD above via CN 2 using labelled line principle.


Protein-protein interactions search I used STRING db in order to find all the interactions of the precursor protein APP. What I specifically need is a confirmation (supported by some article and experiments in it). But significant amount of interactors have only "Database" confirmation (mostly relaying on Reactome and KEGG data). Searching in these db's gives me neither article nor even the presence of these proteins in one pathway (what's weird). How can I obtain the data?
Thanks in advance!

You can try to use IntAct Molecular Interaction Database. The data in this database is based on:

data from the literature or from direct data depositions by expert
curators
<300k binary interactions in 2011  developed by the EBI's
Proteomics Services Team
recent reference: Aranda et al. '10

This is also mentioned in the summary of the Aranda et al.'10 article:

  IntAct is an open-source, open data molecular interaction database and
  toolkit. Data is abstracted from the literature or from direct data
  depositions by expert curators following a deep annotation model
  providing a high level of detail. As of September 2009, IntAct
  contains over 200.000 curated binary interaction evidences. In
  response to the growing data volume and user requests, IntAct now
  provides a two-tiered view of the interaction data. The search
  interface allows the user to iteratively develop complex queries,
  exploiting the detailed annotation with hierarchical controlled
  vocabularies. Results are provided at any stage in a simplified,
  tabular view. Specialized views then allows 'zooming in' on the full
  annotation of interactions, interactors and their properties. IntAct
  source code and data are freely available

Further you can use the Evidence tab in String(I assume you have already tried this but in the case you did not):

You can then click on Experiments, then something like this will show up:

You can see how (e.g. Reconstituted Complex assay) and you can see from which article this interaction is coming from if you click on an item in the table:

STRING database shows the protein-protein interaction network and scores according to the presence and absence of experimental verification which can be protease assay, bait coimmunoprecipitation, western assay etc.

if you need further confirmation you should read as much as related articles as possible related to APP.


How does a cell know what function it has within an organism? Given that all cells in a multicellular organism contain the same DNA (ignoring random mutations during mitosis), how does any given cell know what purpose it is supposed to have within an organism.

For example, how does a cell know to become a muscle cell, a neuron or a liver cell?

The answer to this question can be split into two parts: cell differentiation from stem cells and simple mitosis. Also, the answer I am providing mainly only applies to species that sexually reproduce.

During the primary stages of growth, immediately following the fertilisation of the female gamete, the zygote begins to divide. Most of these initial cells will not be specialised, they will be stem cells and these have the potential to asymmeterically divide. When they do this, each of the daughter cells will have a specific specialisation path to follow. Which path they will follow, muscular, neural etc. is determined by transcription proteins.

Once the stem cells have produced the correct daughter cells, the general structure of the organism will begin to take form. Once this happens and the cells have followed their development paths until they hit their final specialisation, mitosis takes over. This means that a muscle cell will divide, causing the organism to grow. A muscle cell, will only ever divide into a muscle cell, the same goes for all specialised cells. This is how an organism grows and maintains itself.

However, some stem cells do remain after the organism has matured. For instance, a mature neuron is unable to undergo mitosis, so stem cells are needed to allow for the production of new neurons to replace those that die, to take one example.

You can find out more here.


Why is Homologous Recombination (HR) more frequent at long sequence repeats? I'm studying plasmids in bacteria (E. coli), and trying to understand the well-cited phenomenon that recombination frequency increases with longer repetitive sequences. I think this also applies to eukaryotes.

In my (potentially misguided) current view, HR can occur between two DNA duplexes either during or after replication (?). As I imagine it, the new DNA duplex will have near identical homology to the template duplex (from which it has just been replicated), meaning that sequence homology is widespread across the entire molecule. This would mean that sufficient homology between sister chromatids can be achieved anywhere (?), negating the trend for 'long sequence repeats'.

So, why is there a focus on long repeats promoting higher recombination frequencies? Is my view on when HR happens misguided?

HR rarely occurs at all in normal somatic cells, because multiple different mechanisms try to prevent this from happening between sister chromosomes during mitosis; the implications of this recombination can be detrimental to the organism. Instead, in eukaryotes, HR normally occurs during Meiosis, in the formation of Gametes, which will recombine anyway. This actually has a beneficial effect because it increases genetic diversity of offspring, thereby promoting evolution.

As for how homologous repeats enhance HR, it is a rather simple mechanism. Basically, you have the two homologous strands side by side, and you have this extensive repeat section in the middle. The thing is, because the repeat section is so long, and because of the fact that it repeats, really any repeated sequence anywhere along that section can cross over with any repeated sequence on the other strand. This increases the availability of HR sites, as well as increases the number of possible outcomes, therefore increasing the probability that HR will occur. Plus, as the number of repeats increases, the number of possible recombinations increases exponentially, making HR on long repeats much more likely than other cases of HR

I hope that satisfactorily answers your question.

I'm not sure what you mean by "repetitive" sequences because homologous regions don't have to be repetitive, but the relation between long homology regions and increased HR efficiency is due to the mechanism. HR in yeast is achieved by strand invasion of single-stranded DNA (perhaps generated by DNA damage or self-induced in the case of meiosis) at another DNA duplex. The longer the homology region, the more complementary base pairing and the stronger the bond. Conversely if the homology region is short then the bonding is not so strong and the single-stranded DNA will probably get displaced by the other strand in the duplex thus reducing HR efficiency. I believe it's similar in E.coli.


If a given DNA oligo is an aptamer, will the corresponding RNA oligo with the same sequence be an aptamer aswell? Functionality of aptamers depends upon the oligo's sequence and secondary structure. So, if I take a DNA aptamer and make an RNA oligo of the same sequence (T replaced with U obviously), will this RNA oligo also act as an aptamer?

There is at least one known case where both the DNA and RNA versions of the same aptamer sequence bind the same target (Lauhon and Szostak, 1995).

But you can't generalize this, there are two differences in structure between RNA and DNA, the Uracil/Thymine change and the missing 2'-OH in DNA. Those differences can affect the binding and overall structure of the aptamer.

It is possible that the RNA version of a DNA aptamer binds the same ligand, but this won't be always the case.

Aptamers are single-stranded sequences that bind to proteins or other molecular partners. Obviously, ssDNA and ssRNA have very different (in general) binding partners. E.g. DNA is interacting with transcription factors, RNA polymerase, histones etc, while RNA is interacting with ribosomes, reverse transcriptase and others.

So, shortly, it is more likely that protein A that binds DNA aptamer will not bind RNA with corresponding sequence.

Also, DNA and this DNA transcript will probably have very different secondary structure.


How, on a physical level, does ATP confer energy? When ATP is used as the energy currency to make, say, reaction X + Y → Z happen, is what happens on a physical level down at the molecular scale that during the reaction

ATP + H2O → ADP + Pi       ΔG˚ = −30.5 kJ/mol (−7.3 kcal/mol)

that 30.5 kJ/ mol is conferred by ATP molecules physically bumping around the reactants X and Y, the kinetic energy of the above reaction being what does it?

I mean, is the energy coin of ATP conferred to reactions by molecular collisions, or is it an electric field effect in the spatial geometry the way the ATP molecule tends to break apart?

Usually in biology (and being ATP, it most probably is biology), it's one of two things.

The gamma-phosphate (the third one, the one farthest from the adenosine) is very unstable, meaning the phosphoanhydride bond is easy to break.  The cell "allows" it to break, but only at the cost of moving the phosphate to some other molecule, such as a serine or glycerol or fructose or whatever.  This phosphorylation creates a bond with lower energy than the phosphoanhydride, and so is overall favored.  Imagine the personification: the gamma phosphate hates being attached to anything, but hates being attached to an ADP the most.

Alternatively, if ATP hydrolysis is coupled via an enzyme, it is usually done through transient storage of the energy is protein conformation.  An enzyme binds ATP, which makes the protein structure "bend" or conform around the ATP.  This puts loads of strain (energy = A) on the protein which is offset by the stabilization of binding the ATP (energy = B).  This strain can make an enzymatic surface open up on the protein which itself takes a lot of energy to make (energy = C).  The surface can catalyze some reaction (X+Y->Z in your example) that costs some energy (energy = D).  The completion of that reaction alters the enzyme's catalytic site to something new and higher energy (energy = E), which can be alleviated by cleavage of the ATP (-7.3 kcal/mol).  Alas, ADP and P do not fit well into that site of the enzyme, so they float out, restoring that original ATP-binding surface to it's original state.  Provided A>B>C>D>E>-7.3, the cycle will continue until the ATP is exhausted or you have no more Z to make.

Typing "enzyme catalysis cycle ATP" gives a few examples. Here's a few:
DNA gyrase
Actin-myosin cycle

Researching quantum constituents in ADP energy transfer gives this page which describes the ATP reaction with some geometry, aside from electrical/proton transfer of the many energy-expensive reactions like of cells like F-actin filament molecule treadmill lengthening process:

https://pubs.rsc.org/-/content/articlelanding/2016/cp/c6cp01364c/unauth#!divAbstract

This page describes F-actin length and reconstitution using ADP: https://m.phys.org/news/2014-09-scientists-uncover-clues-atp-mystery.html

Video actin treadmilling simulation:
https://m.youtube.com/watch?v=VVgXDW_8O4U

Two parallel F-actin strands must rotate 166 degrees join correctly together. This creates the double helix structure of the microfilaments found in the cytoskeleton.  ATP  is well described on wiki in at that level.

It seems to imply that there is a "static/magnetic" electrical charge differential surrounding the actin molecules and transferred in the minuscule H2O medium which attracts rotates and bonds them.

The electrical differential of Actin is described as heterogenous with surrounding salt bridges and protonationdeprotonation, by this general research:
https://www.google.com/amp/s/www.researchgate.net/figure/The-charge-distribution-on-the-surface-of-F-actin-is-highly-heterogeneous-leading-to_fig5_7090136/amp

I'll try to synthesise some quantim articles of that kind for a coherant sequence of events, ill have to pause because im writing on a phone.

Some info on the H2O alignment involving a different view of ATP is here :
https://www.google.com/amp/s/phys.org/news/2017-03-atp-hydrolysis-energy-large-scale-hybrid.amp


Are peanut proteins similar to chicken meat proteins? I'm studying amino acids content in vegetable food. I was looking at peanut protein and noticed its similarity with chicken meat, as you can see in the table below (quantities are measured in grams). Third column is first column minus second column. Green amino acids are the essential ones.

The biggest difference (-1.11) happens for Lysine, but Lysine quantity (0.901) is still bigger than the lowest one, which is Tryptophan (0.2445). So in this case, is Tryptophan the limiting factor in protein synthesis? (Tryptophan amount is < than any other amount).

The table below lists the optimal profile of the essential amino acids (first column). Second column is obtained by dividing the values in table 1, first column, by 25.3055 and multiplying by 1000.

Notice that Lysine is the only one amino acid less than the reference (36<51).

So the questions are:

1) Have peanut proteins a limiting factor (if yes what is and why?) or can be considered a complete protein?

2) If the answer to 1) is "yes it has a limiting factor" what vegetable foods rich in lysine can be eaten with peanut in order to obtain all the amino acids? And how to calculate the ratio of peanut and the complementary foods to eat in order to get the proper profile of the essential amino acids?

Source for first table (first and second columns) https://ndb.nal.usda.gov

Source for second table (first column) http://nutritiondata.self.com/help/analysis-help

I'm not sure if biology is the correct site to post this question, so if you know a better one let me know, thanks.

I posted an answer to a similar question here: https://health.stackexchange.com/questions/9124/is-all-protein-the-same/9130#9130

  You're not using protein as it is to maintain your body. It's first
  broken down to the individual amino acids, which your body can then
  use to build new stuff.

  If you're lacking one of the essential amino acids, you can only build
  as much new protein until that runs out, and all the other amino acids
  are just excess. A protein that contains all the necessary amino acids
  is called a complete protein, and you could calculate the differences
  in the so-called quality of the protein.

  A perfect protein (i.e. from egg/milk/soy) will contain amino acids in
  exactly the ratio you need, some protein contains so little of a
  certain amino acid that you'd need to eat twice as much of that
  protein (for example rice or peanuts).

  In your case, if beef is making you recover fastest, you'd need to eat
  30*0.92/0.70 = 39g of peas for the same effect.

  You could get around this by combining different sources of protein.
  For example grains are limited in lysine, while beans are limited in
  cysteine/methionine.

Firstly, here are many types of proteins in both peanuts and chicken, so it is a little ambiguous to say "peanut proteins" or "chicken proteins". Secondly, proteins are proteins. "Complete" and "incomplete" are simply nonsensical terms for describing these macromolecules. Each protein performs a certain task, be it structural, like keratin, or functional, like enzymes. The purposes, as well as the abundances and characteristics of the proteins in say, a piece of chicken define its traits. The amino acid content, though related to these things about proteins, do not imply them. Proteins in different food items are simply made up differently.

To answer the question, no, there is no inert limiting factor on the synthesis of proteins in peanuts, and yes, these proteins are "complete".

I hope this helps!


Why does the cold make us sick? From the moment we learn to communicate, we always get told, whether by our parents, or our teachers, or by anyone else, to avoid the cold, or to put a jacket on to avoid catching a cold, to dry our hair before we go outside, because we'll get sick otherwise, so on and so forth. I also was diagnosed with a pneumonia last year, while in Switzerland under chilly conditions ($-20^◦\text{C}$). This made me wonder, why does the cold make us sick? It doesn't seem logical to me that a viral infection like the common cold, or a viral/bacterial infection such as a pneumonia is more prevalent when it's colder outside. I always figured it was because our bodies are less 'effective' under cold temperatures, but this seems lacking to me. Can anyone explain?

it does not, really. unless we're talking about things like frostbite or severe hypothermia.
it's a myth that it does.
the virus is more stable in colder air, however.
see more here:
Study Shows Why the Flu Likes Winter
Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature

Innate responses proved to be comparable between animals housed at 5 °C and 20 °C, suggesting that cold temperature (5 °C) does not impair the innate immune response in this system.

Most likely the energy to stay warm is not being used to fight infection. Also the virus is likely designed to operate with your respiratory system at a colder temperature more effective that the immune system is at that cooler temperature.


How exactly are game theoretical evolutionary models described during implementation for computer simulations? When a biologist or a layman tries to reason the evolutionary explanation for something, they would simply use English with some math thrown in (for a random example, pick any explanation out of "The Selfish Gene" -- for example, the reasoning why "discriminate in favor of one's own eggs" strategy is employed by Guillemots, in "Genesmanship" chapter, page 103. I won't quote it in full since it's a page worth of text).

Another example of such a wall of English is (Dawkins-inspired) Bio.SE question: " Why is 'Grudger' an evolutionary stable strategy? "

When a biologist tries to actually model evolutionary development to see which traits would win, they would need to somehow teach the computer to implement that model: what the environmental factors are, what the genotype involved is, how exactly it's expressed in different phenotypal and extended phenotypal traits, and how environment would affect an individual with that phenotype.

My question is: is there some sort of standard way to build such a model? A domain specific language (in computer science terminology) that is used by many different biologists or some standard modeling packages/software? E.g. some sort of special XML format, etc...

Or is it always just hand-built custom implementation by individual researchers for their current model?

Just to clarify:

I'm NOT asking what the models look like theoretically. I'm asking what language/format (if any standard one exists) is used to encode them to run simulations.
If there are discrepancies between the type/purposes of models, the ones I'm most interested in are game theoretical ones.

The field most closely associated with game theoretic models in biology is evolutionary game theory. If modeling is required, then the typical paradigm is agent-based modeling, and a good introductory book is:

  Yoav Shoham and Kevin Leyton-Brown
  [2009], "Multiagent systems:
  algorithmic, game-theoretic, and
  logical foundations", Cambridge
  University press.

As for actually building the model, and what to describe/how, I will take you through my usual procedure since this is a field I specialize in:

Define what type of strategies you think are relevant to the interactions you are modeling. Select what you expect the payoff of those strategies to be. For instance, if you are studying the evolution of cooperation, you might select 'Cooperate' and 'Defect' as your strategies and the Prisoner's dilemma as your pay-off matrix, but maybe you will pick something more general. Unfortunately, in most of EGT a clear distinction between genotype and phenotype is not drawn, and they are usually equated. At the end of this step you have a game matrix G. Sometimes when mutation or innovation are explicitly necessary even in the inviscid model, further analytic approaches are taken at this stage. I recommend Hofbauer & Sigmund (2003) for a broad treatment of step 1.
Now you need a basic intuition of what the 'default' behavior in this interaction is, so solve the replicator dynamics of G.
The main interest in EGT right now is structured populations. This is where computational modeling is typically used. However, before I turn to simulation, I first try the best analytic approach I know. I use the Ohtsuki-Nowak transform on G to analytically solve the interaction for random graphs (Ohtsuki & Nowak, 2006).
If I am still interested in the question, and steps 2 and 3 didn't capture all the subtlety of the system I want to study, then I start building a multi-agent computational model. I make sure that my model has some way to scale to the completely inviscid case of replicatory dynamics, and the simply-structured case of ON-transform. If my computational model disagrees with the analytic approach in these regimes, then I become worried. Otherwise, I continue with standard agent-based modeling techniques. Personally, I code in Matlab. I have never seen a modern EGT simulation that required the performance of C/Fortran. As suggested in another answer, if you don't have a programming background then you can use NetLogo. However, my experience is that the models are typically simple enough to implement from scratch, and NetLogo models typically hide from you some very important subtleties (like which reproduction rule to use: death-birth, birth-death, immitation?) and usually lead to weaker papers.

Note the broad theme. These models are typically described as differential equations, and this approach is preferred to agent-based models. However, if a clean differential equations approach does not capture all the subtleties of what you are studying, then an ABM paradigm is adopted.

There is no single way to build such a model.  They can vary from a simple mathematical statement like Hamilton's rule (rB>C) to the chemical diffusion models used to describe the patterns in animal skin coloring (like zebra stripes, leopard spots and the like).

There are efforts to build molecular models of entire cells like this model of mycobacterium genitalium dividing, which integrates nearly 30 different mathematical models to describe different aspects of the organism.  There are efforts to build such a model of an entire brain as well.

Another common sort of model for evolutionary biology is the use of game theory, where different strategies can be posed one against another as in the prisoner's dilemma competition Dawkins describes in the Selfish Gene.

It goes on and on.  Basically biological modeling is driven by the sorts of mathematical models that we know.   New models will reveal new paradigms of how biology works.  They can be highly mathematical, but their relative importance and when they apply and what they mean are more analogy than proof.

For instance in the prisoner's dilemma, the first contests showed that Tit for Tat was the strongest model - generally assisting others, but betraying when there is a history of betrayal.  The ideas at the time moved towards general cooperation in populations.  More recent replays have shown that if there is a team of entrants that make extraordinary gifts to each other (allow betrayal without retribution), then they can compete against other models quite well.

One can never prove that a selfish model for the prisoner's dilemma will not show up, though biological systems to seem to be highly cooperative.  That is a model, not a proof.


Difference between inbreeding and interbreeding Is inbreeding the same as interbreeding?

On this site interbreeding is defined as (http://www.thefreedictionary.com/interbreeding):

  To breed with another kind or species; hybridize.
  To breed within a narrow range or with closely related types or individuals; inbreed.

But I am sure that interbreeding is not the same as inbreeding. Inbreeding would be between genetically related members of a species and interbreeding would be between genetically un-related members of the same or different species.

after looking at wikepedia pages for both terms as well as searching the english oxford dictionar I am certain they are different

You are basically correct. Most common usage in my experience:

Inbreeding refers to sexual reproduction between genetically closely related individuals, within a species. Inbreeding will increase the relatedness between individuals in a population.

Interbreeding refers to reproduction with another species (or race), and is often used as a synonym to crossbreeding or hybridization (when referring to hybrid offspring from two different species/races/breeds, not DNA hybridization). This is also how 'Interbreeding' is defined in the Oxford English Dictionary. However, 'Interbreeding' is sometimes used just to signify that two individuals can breed and have viable offspring ("...these two individuals can interbreed..."), and under this usage this can also include/overlap with inbreeding.

The latter usage can be seen in the Species article in Encyclopædia Britannica, online:

  Species, in biology, classification comprising related organisms that share common characteristics and are capable of interbreeding.
  ...
  Interbreeding only within the species is of great importance for evolution in that individuals of one species share a common gene pool that members of other species do not.

interbreeding is a process in which same kind of species are breed together such as(male and female)but outer breeding is a process in which different kind of species are breed together such as(means horse is a specie it will breed with bitch those are different species


Human Demography - Where can I find this statistic? In "An Introduction to Genetics" by David J. Merrell, copyright 1975 by W.W. Norton + Co., p. 742, in the Chapter "Genetic Counseling and Eugenics," the author states: "... 50% of the women produce 85% of all children born in the United States."

The author provides an Additional Reading list, but I'm not a geneticist, nor do I have access to much of the listed material.  With that in mind, 1) where can one find the statistic mentioned above? and  2) has this number changed over time?

OP EDIT: In response to comment (a few examples from Reading List of 30 items):

Davis, 1970, Prospects for Genetic Intervention in Man, Science, 170 279-1283

Dubos,1965,  Man Adapting, Yale Univ. Press

Dunn, 1962, Cross Currents in the History of Human Genetics, Amer. J. Human Genet, 14: 1-13

Ehrlich, 1968, The Population Bomb, Ballantine NY

...

Lynch, 1969, Dynamic Genetic Counseling for Clinicians, C. C. Thomas, Springfield, Mass.

...

Petersen, 1969, Population, 2nd Ed. Macmillan

...

1969, WHO Expert Comm. on Human Genetics, "Genetic Counselling(sic), Tech Rept 416, pp. 1-23

I know I can find stats like average ages, etc from the Statistical Abstract of the United States, but where do geneticists find items like the one cited in the Merrell book?

The CDC has some good stuff. http://www.cdc.gov/nchs/data/nhsr/nhsr051.pdf

But keep in mind that number from your book is likely based on yearly findings in which more than half the women would not be able to have children due to age, voluntary contraception, or other conditions. So it is not reflecting how many children they have over their lifetime. Even in the CDC study more than half the women had no children but few had no plans to have children, couples are moving their first pregnancy to later and later in life, which is going to make it look like few are having children at all on first glance.
 And it's probably not accounting for death rates, the poorest people tend to have the most children but they also have the fewest number live to maturity, which is why they tend to have more (not necessarily consciously mind you) .

You can try to use some standart data sources, for example:

NASA's Gridded Population of the World - LINK
Geonames - LINK


Why are the human knees and elbows bent in an opposite direction I can assume that the hands used to be the same as legs. And they got weaken, and changed direction when human started to walk on two?
Also why do the hand palms facing the body and not facing down like the feet?

I am no expert on comparative anatomy, but I will give this a shot. Please edit if you know more about this subject!

The configuration of opposing elbow and knee joints is a feature we humans share with large group of mammals. For example, below is an image of a shrew skeleton.

Opposing joints are course a major feature of mammalian anatomy, and there are many studies on its functions and advantages. Among other things, this configuration allows for characteristic gaits of mammals such as the gallop of a horse, and it allows mammals to rest with legs protected under their body. See this page for some basic information.

Neil Shubin's book Your Inner Fish on human evolution also discusses the opposing joints arrangement, noting that this is a "key feature that gives us the capacity to walk, one we share with other mammals". A preview of the book is here.

A quick literature search turns up many technical articles on this subject, such as this review series. I'm afraid the details are beyond me (again, experts please edit), but I think it's fair to say that there is plenty of evidence for advantages of this joint arrangement in mammals.

It's an amazing question, really. And you might be right about your assumption. In the womb, our legs and arms bent in the same direction. But as the foetus continued to develop, the legs and arms rotated to bend in opposite direction (to each other). As of now, there is no rational explanation as to why this happens.

So I guess all we can do is be grateful to the way our bodies have come into being. If, for instance, our knees bent backward (just like our elbows), our legs would bend forward like our arms and we wouldn't be able to walk the way we do. Apply the same to the arms and we'd be lifting things in an entirely different way, and backwards too! Also, we won't be possessing the ability to write.

You can check out this page for more info:https://answersingenesis.org/human-body/your-legs-are-on-backwards/


How conscious are mammals that mating leads to pregnancy and offspring? Does a pregnant female mammal know that its pregnancy is the consequence of a previous mating? Or are humans the only mammals which are conscious of it?

I have trouble citing the exact source now as it's in one of my books at home, has 'sex' in the title (Sex in History), and I'm at work and can't Google that. But needless to say, the book made mention of studies of isolated, modern human tribes where it was evident that the people of the tribe had not made the connection between pro-creation and child-birth. Rather, intercourse was often tied to specific rituals that had a side effect of birth.

So there are a few things that one can extrapolate from this:

Pre-historic humans may have often not been aware that sex led to procreation
From that one can extrapolate further that no animals have this awareness either, as we are the most intellectual species on the planet

Further, the evolutionary development of sex points to this too. The ultimate cause of child-bearing is propagation, but the proximate cause of child-bearing is pleasure. Before life could be aware of the connection, there needed to be a reason to have sex, and so we would have developed in a way that encouraged pro-creation for no other reason than we liked doing it. Eventually we were bound to connect the dots, but we're oriented for this behavior regardless.

For that an animal would have to know the concept of mating and pregnancy. It’s not called the sex “drive” because it requires consciousness in order to mate or become pregnant. It’s pretty automatic and subconscious. As any couple that actually tries to become pregnant but can’t can probably attest to.

So unless you need to communicate a concept to somebody else you may as well not have a concept. Like those human cultures that only have three numbers. One two and many.


Are there any animals that celebrate communally? Are there any animals that are known to celebrate events? For example, we humans might celebrate a birthday or passing an important test. An event causes us to perform some sort of celebration that is motivated simply by joy and not any sort of survival instinct.

To clarify, I am more interested in positive celebrations. I know a number of animals having mourning behaviors (which absolutely count as a response to external events, no denying); I'm just more interested in celebrations in a positive sense.

I'd like to take this one step further.

Are there any cases proven or postulated of animals celebrating. I don't necessarily need something firm and proven, could be a theory.

An event causes us to perform some sort of celebration that is motivated simply by joy and not any sort of survival instinct.

Celebrations usually mean large group activity but a play can be considered an event which is simply by joy and not any sort of survival instinct, and hence would fit your question. One can easily spot their pet playing around with objects when they are sitting around, busy in something 'boring' for the pets, like - reading a newspaper. But here it can be argued that pets have learned to do this to get the attention of the owner, and hence associated benefits.

Well, plays of pure enjoyment have been documented in wild animals too.

  I once observed a young elk in Rocky Mountain National Park, Colorado, running across a snow field, jumping in the air and twisting his body while in flight, stopping, catching his breath and doing it again and again. There was plenty of grassy terrain around but he chose the snow field. Buffaloes will also follow one another and playfully run onto and slide across ice, excitedly bellowing “Gwaaa” as they do so (Canfield et al. 1998).

Certainly, there was no motive here apart from having fun.

I would encourage you to go through this article - Bekoff, M. (2000). Animal Emotions: Exploring Passionate NaturesCurrent interdisciplinary research provides compelling evidence that many animals experience such emotions as joy, fear, love, despair, and grief—we are not alone. BioScience, 50(10), 861-870.

Speaking of the celebration, such as - birthday, or the largest homo sapiens gathering Kumbh Mela, I would also be interested to know of some group of animals doing it periodically.

Reference:

Canﬁeld, J., Hansen, M. V., Becker, M., & Kline, C. (1998). Chicken Soup for the Pet Lover’s Soul. Deerﬁeld Beach, FL: Health.

You want scientists to measure animal emotions and social behaviours, and they rarely agree about animal psychology unless it's measured chemically and physically.

Celebration (behaviour for events) is not a word defined zoological science research. You can imagine that thirsty elephants that walk for 3 days to find a riverbank have a celebration when they arrive there.

Scientists don't use the word alien planet to mean exoplanet, and they don't use the word cyberspace to mean internet. For that reason, the word celebration is mostly a dramatic and reporting term that a scientist would be uncomfortable to use with proof as the basis of a document.


PCR Mastermix Preparation I am currently preparing a PCR mastermix for the first time, and have a few questions regarding the distribution. I am trying to amplify a specific gene cluster in a sample of DNA so I can use it in a cloning vector; however, I am not sure how many separate PCR reaction mixtures I should prepare in my mastermix for this purpose? Also, what is the purpose of a negative PCR reaction mixture (withouth the template DNA), as I saw a procedure recomend making one. Should I prepare the same number of negative reactions as positive, or should I prepare only 1?

A PCR Master Mix is just a way to speed up your pipetting. Instead of preparing 10 different reactions of 20ul each (for example) you prepare one reaction of 200ul and then you split it into 10 tubes. This also reduces distraction errors (it is less likely to forget to pipet once 100ul that 20 times 5ul). Also, less plastic (pipet tips) is used.

Some tips:

Given the error of some pipettes, it's generally good to count for an extra reaction every 10. For example, if you need to run 10 PCR, make a Master Mix for 11.

If you are planning to run the same PCR on different templates (which is often the case) then you don't need to add the template in your Mix.

Negative and positive controls should always be included.

The negative control of a PCR reaction is often done by substituting the template DNA with water. The negative control should not show any amplification band. This guarantees that you don't have DNA contaminants in your mix and that you primers do not amplify each other.

A positive control is a reaction that is expected to work. In this case, if your positive control shows amplification but your sample don't, you know it is not because of some component in the reaction behaving unexpectedly (Polymerase, buffer, etc..).

Let's make a practical example.

Let's say I want to amplify the same target sequence from 10 different DNA samples.

The 1X reaction looks like something like:

**PCR 1X**

Template     1ul
Primer F     1ul
Primer R     1ul
H2O         10ul
MgCl2        2ul
dNTPs        2ul
Buffer 10X   2ul
Polymerase   1ul

Now, considering the positive and negative controls, and 10% extra volume, I would prepare a Master Mix for 13 reactions. Of course, the template must be excluded.

**Master Mix 13X:**

Primer F     13ul
Primer R     13ul
H2O         130ul
MgCl2        26ul
dNTPs        26ul
Buffer 10X   26ul
Polymerase   13ul

Now aliquot 19ul in the 12 tubes, add 1ul of the right template to each of them (in the C- just add 1ul H2O) and run it!

There are cases in which you may want amplify different targets sequences from the same DNA. In this scenario, you want to include the template in the Master Mix, since it is the same for all the reactions, but you want to add the primers separately since each reaction will contain a specific set of primer to amplify a specific sequence.

The number of reactions you set up depends on a lot of parameters. To answer this question you'd need particulars about the source of template DNA, melting point of primers, the taq you are using and the size of the product you want to amplify. All of these will dictate how you optimize your PCR. Have a look at the below reference
http://cshprotocols.cshlp.org/content/2009/4/pdb.ip66.abstract


Is it better to take a half dose of paracetamol and a half dose of ibuprofen together rather than a full dose of either? Recently, I heard on this health-related radio programme that it was better to take a half dose of paracetamol and a half dose of ibuprofen together, rather than the full dose of either one, for acute pain. Could anyone explain the reasons for this ? Could it be something along the lines of there being diminishing returns to higher doses, so you get more bang for the buck, as it were, for the first half of a dose than the second, but due to possible toxicity or drug interactions, two full doses are not recommended ?

In the same radio programme it was stated that caffeine also helps. Can anyone explain that ?

There are many different reasons for an acute pain and inflammation (both directly via pain receptors, and indirectly via swelling etc.) plays not the least role in this phenomenon. Therefore the combination of a classic analgesic without anti-inflammatory activity (as paracetamol) with a strong anti-inflammatory agent (as ibuprofen) is a reasonable one and potentially alleviates the pain manifestations in more cases than a single administration of every agent.

You are right with you suggestion that the doubled dose could be dangerous: even though the complications of Paracetamol administrations are not often, they are very dramatic (acute liver failure) with rather pessimistic prognosis. This is why one generally tries to half the doses if combined with other similar-acting agents (historically paracetamol was for the long time a member of the non-steroid anti-inflammatory agents).

Caffeine is generally believed to be a pain reliever, especially as concerns the pains with migraine background (source). One review, however, points out that there are still not enough data to support this belief (source).

The only reason why caffeine helps with migraine pain is because the pain is caused by expanded blood vessels and caffeine's effect is to narrow the blood vessels.
But how it helps with other types of pain I really  can't imagine.

And it depends what you state as "full dose". The dose that can harm your liver for adults is 4g per day, so if you have Paracetamol 500mg you would have to take 8 pills  to reach it. Would you possibly do it? If seeing pain doesn't go away after first pill .. ok, second one?


Is there an Exit site (E-site) on the eukaryotic ribosome? One of my professors mentioned something about the e-site (the exit site for the t-RNA) on a eukaryotic ribosome.  There was a student in the class who objected, saying that there is no e-site on eukaryotic ribosomes; it only exists on prokaryotic ribosomes.  I've tried to find some reliable source to figure out who's right, but to date the only thing I've found is an obscure sentence in a wikipedia article, which doesn't look all that official.

Is there indeed an e-site on the eukaryotic ribosome?

Prelude: Thinking about protein synthesis

I remember the time when there were only two sites on the ribosome, and when it became clear there were more, I resented the need to make my lecture notes and my contribution to a venerable text book more complicated. So I am neither a devotee nor an expert on the exit site, but if asked to guess who was right (even if, or especially if, the student was supported by Campbell’s Biology as @CSharp informs us) I would put my money on the ‘professor’. Why? Because protein synthesis and the ribosome are so ancient that although there have been changes in eukaryotic proteins synthesis, something so fundamental as the sites for the fundamental process would not change.

Answer

Yes, Virginia, the eukaryotic ribosome does have an exit site.

The evidence

Although editions of the venerable text book no longer appear and my research no longer impinges on protein biosynthesis, I still collect papers on the subject with my bibliographic software. The latest relevant publication I have is by Khatter et al. from Nature in 2015, entitled Structure of the Human 80S Ribosome.

As not all list members have access to Nature, as a subscriber I have taken the liberty to reproduce a a section from the abstract (my emphasis) and a pertinent illustration:

  Here we report the near-atomic structure of the human ribosome derived
  from high-resolution single-particle cryo-electron microscopy and
  atomic model building. The structure has an average resolution of 3.6A
  ̊, reaching 2.9A ̊ resolution in the most stable regions. It provides
  unprecedented insights into ribosomal RNA entities and amino acid side
  chains, notably of the transfer RNA binding sites and specific
  molecular interactions with the exit site tRNA.

The cryo-EM map and atomic coordinates have been deposited in the EMDB and Protein Data Bank under accession codes EMD-2938 and 4ug0, respectively.

I admit I haven’t researched and rehearsed the evidence, but I think that would be another question.

No. According to page 369 of the 9th edition of Biochemistry by Campbell:

"The structure of the eukaryotic ribosome is different in that there is no E site, only the A and P sites."


How many cyclic and non-cyclic photo-phosphorylation is required to produce one molecule of glucose? In non-cyclic photophosphorylation 1 ATP and 2 $NADPH_2$ molecules are produced.

In cyclic photophosphorylation 2 ATP molecules are produced.

For production of one molecule of Glucose 18 ATP and 12 $NADPH_2$ molecules are reqiured.

According to my understanding,6 turns of cyclic and non-cyclic photophosphorylation is required to produce one molecule of glucose.

Because 6 turns of non cyclic photophosphorylation will produce 12  $NADPH_2$ and 6 ATP molecules.

And cyclic photophosphorylation will produce 12 ATP molecules.

Total=12 $NADPH_2$ and 18 ATP.

I think Iam missing something , Please answer me if I am correct or not.

In non-cyclic photophosphorylation the stoichiometry of ATP:NADPH is predicted as 3:2, i.e, for every two NADPH formed, a total of three ATP are produced.
Source: Cyclic, pseudocyclic and noncyclic photophosphorylation: New links in
the chain. John F. Allen. TRENDS in Plant Science Vol.8 No.1 January 2003.
Cyclic photophosporylation, does not occur under normal conditions in higher plants. It is believed to occur only when either light intensity is low (lower frequency so as only PS1 can function) or when carbon fixation is not at par with light irradiance (i.e, too much light).
And hence it is not advisable to come to this generalization "Six Turns of non cyclic photophosphorylation will produce 12 NADPH2 and six ATP molecule"

Yes.

One cycle produces 1 ATP and 2 NADPH2.

Cyclic photophosphorylation produces 2ATP in each cycle.

The C3 cycle uses 3ATP and 2NADPH2 in each cycle.

So if if C3 cycle runs one time then both non-cyclic photophosphorylation and cyclic photophosphorylation run 1 time.
For synthesis of one glucose molecule in the C3 cycle, non cyclic photophosphorylation and cyclic photophosphorylation each runs 6 times.


Help identify this mite? I saw a decimal-sized dot walking on my hand. I wanted to know what this is, so I got it onto some paper and sandwiched below a piece of clear tape so I could keep it in place and photograph it. However it's so small that even with my camera lens almost touching the specimen, I can't get a great photo. It's small, about 0.8mm long, beige or gray or brown with a pattern on the back. It's a little smooshed from the tape so it's hard to tell if it has 6 or 8 legs and is an insect or an arachnid. But hopefully based on the shape, size, and pattern it can be identified.

Location is southern California.

Update: I now believe this to be a rat mite or bird mite. I'll include some additional photos that were better quality (photos were taken with a close-focus camera, mites were on printer paper underneath Scotch tape, back-lit by an LED light):

This appears to be a bird mite (or possibly rat mite) in the genus Ornithonyssus of the parasitic family Macronyssidae.

 Credit: user Aewills on bugguide.com
Distinguishing between species is difficult.
In fact, according to idtools.org, identification of Mesostigmata to family or lower can usually only be accomplished only if the specimen is an adult female.
Blaine Mathison mentions the following features useful for identifying these mites to lower taxonomic levels under magnification [source: bugguide.com]:

chelicerae shape
dorsal plate breadth and degree of dorsal coverage
spiracle present between legs
genitoventral plate width
sternal plate shape and presence of setae

You can find existing answers to posts about bird mites on Bio.Stackexchange below:

Bug Identification: Tiny Bugs
Tiny white very hard cell bug! Please help to identify!

It could be a tick nymph. Difficult to tell as you can't see the beak and the front legs very well. Check out this tick identification site:

http://www.tickencounter.org/tick_identification/tick_species

Looks most like the dog tick maybe?


What allows grass eaters to digest cellulose? Scientists are saying that it was a small step for the Panda to move from a meat diet to a grass diet. The article only refers to differences in the Panda's skull, presumably for better chewing.

I've also heard that the Japanese are able to digest Nori because they have the right gut biome because Nori has been part of their diet and the appropriate bacteria has developed over time.

Does that suggest that if the cellulose of bamboo and other grasses were pre-chewed by mechanical means and the right bacteria were introduced into the human gut that we would likewise be able to digest grasses?

Related story

No there is something else missing besides bacteria

humans often already have the right bacteria but they don't digest most of the cellulose they ingest because digesting cellulose with bacteria is SLOW. Too slow to keep up with normal mammalian digestion. You need a specialized gut that  either has a large complex stomach to keep recycling the cellulose in the system (foregut fermenters) or has large storage chambers to keep the cellulose a long time and allow it to be digested slowly (hindgut fermentation).

humans have neither. To make matters worse Humans have huge caloric needs compared to other animals of the same size. Brains are calorie hogs and our brains are so large they consume 1/4 of all our calories. That is 3 pounds of our mass consumes a quarter of all the calories we eat. honestly without the advent of cooking (which drastically improves the caloric availability of food) human brains could never have reached the size they did.

Further reading

More further reading

You might find the answers to a similar previous question interesting:

Human Digestion of Cellulose?

Summary of those answers: It seems that some humans do host cellulose-digesting symbiotic bacteria, and do digest some of their cellulose.  According to Cellulose and the Human Gut, finely ground cellulose with low lignin content is most readily digested by humans who host the right bacteria.


Which plant is this? I'm curious what plant this is! I found it at 37°52'23.2"N 122°16'55.3"W (north of Oakland, California, USA).

It looks a lot like Queen Anne's Lace, but yellow and with more slender leaves. I believe it's Sweet Fennel (Foeniculum vulgare). It's in the Apiaceae family, which has a lot of edibles: carrots, parsley, fennel, anise, caraway, celery, chervil, cicely, cilantro, cumin, dill, parsnips and more. Black swallowtail butterflies lay their eggs on this, so often you can find a really fine caterpillar on them; bees like the flowers as well.

Apiaceae has 3,700 species spread across 434 genera; it is the 16th-largest family of flowering plants. It has a few poisonous plants, like water hemlock (white flower) and poison hemlock (also white). Wild parsnip has a very similar yellow flower but it's sap is wildly irritating in the medical sense (it will cause pain and blisters); its leaves are very different.

If you crush some of the slender leaves between your fingers, it should smell like fennel (a common spice, e.g. in Italian sausage), or if you aren't familiar with that, a bit licorice-like.

Sweet fennel (left, up to 6 feet tall)        Wild Parsnip (right, 3-5 feet tall)

That's East Indian Fennel. It's a member of the celery family. Every part is edible, including the root and the seeds. It's packed with vitamins, calcium and is used to stop restless leg syndrome, among other ailments. The feathers (leafs) can be used to wrap meat and fish before baking or eaten fresh on a green salad. Once par boiled they lose their licorice taste and can be eaten like steamed spinach. The Italians brought it over in the early 1800s and it flourished. It grows along the freeways of California and other states. I pick large batches of it for my juice extractor and other things. Look up the many medicinal uses of fennel. The flowers look similar to dill.