text:
Rampant low Vitamin D
Why have people inadequate vitamin D status? Is it just (the lack of) sun exposure, or is it related to hormone and thyroid function?

@MarchHo - how about this edit?

As far as I know by  inadequate vitamin D the thyroid must produce more thyroid hormone to compensate. I don't think the vitamin D status depends on the thyroid function. I'll look for references.

Here in Australia there are more cases of vitamin D shortage than in England. Given the double amount of sun hours per annum here in Down Under, that's quite counter intuitive. In fact, an estimated 31% of adults in Australia have inadequate vitamin D status, increasing to more than 50% in women during winter–spring and in people residing in southern states (Nowsen et al., 2012).
It turns out that in Australia people are, rightfully, careful of sun exposure due to the thin ozone layer and the resulting high incidence of skin cancer. As a result, people here wear long-sleeves on the beach, use high-factor sunscreens, wear sun hats, use umbrellas to evade the sun etcetera. The Australian  Cancer Council supports the famous "slip, slop, slap" slogan:

Slip on a shirt, slop on sunscreen and slap on a hat, Slip, Slop, Slap! You can stop skin cancer [..]!

Hence, folks here in fact often take vitamin D supplements, despite the large amounts of sun hours.
Reference
- Nowsen et al., MJA (2012); 196(11): 686-7

Vitamin D deficiency is most probably the cause of the thyroid disfunction and not the result. So the cause of vitamin D deficiency is the lack of UV exposure.

To  conclude,  the  results  of  the  present  study  suggest  that
  moderate  to  severe  vitamin  D  deficiency  is  a  risk  factor  for
  hypothyroidism. As vitamin D deficiency is highly prevalent in north
  Indian  population,  these  findings  may  ha ve  some  public health
  implications. Further, large  scale  clinical  trials  and prospective
  studies  will  be  required  to  establish  a  cause  and effect
  relation  of  vitamin  D  deficiency  in  pathogenesis  of
  hypothyroidism.     Supplementation     of     vitamin     D     in
  hypothyroi dism  may  ameliorate  its  symptoms  and  prevent further
  deterioration of thyroid function, so, for the ease, safety and   low
  cost   of   treating   this   modifiable   risk   factor   we
  recommend its screening in all hypothyroid patients.

2014 - VITAMIN D LEVELS CORRELATED WITH HYPOTHYROIDISM IN INDIAN POPULATION: A PILOT STUDY

In the present study, we demonstrated that serum vitamin D levels were
  significantly lower in female GD patients without remission than in
  those with remission.

2013 - Serum vitamin D levels are decreased in patients without remission of Graves’ disease


text:
Difference between the P4 and P5 subtypes of P-type ATPases in plants
In plants there are various kinds of P-type ATPases. What is difference between P4-ATPase and P5-ATPase?

There are numerous differences between the various subtypes of P-type ATPases, simply because they have different amino acid sequences. Three important differences between P4 and P5 subtypes of P-type ATPases are the following:

Structurally, P4 ATPases have their supporting structural domain (S) in the C-terminus, while P5 ATPases have the S domain divided over the N and C termini. Figure 1 shows the basic structure of P-type ATPases.
Structurally, P4-ATPAses require a beta-subunit for proper function (Poulsen et al., 2008). As the substrate for P5-ATPases is unknown, it could not yet be tested if they also require a beta-subunit.
Functionally, P4-ATPases are putative lipid flippases, while P5-ATPase pumps have so far (per the 2011 report cited) no assigned substrate specificity.

Schematic outline of P-type ATPases. Source: Palmgren & Poul Nissen (2011)
References
- Palmgren & Poul Nissen, Annu Rev Biophys (2011); 40: 243–66
- Poulsen et al., Plant Cell (2008); 20: 658–76

source: Stack Exchange

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sort: votes


text:
My eyes were accidentally exposed to high infrared radiation and they hurt, why?
My eyes were exposed to high amounts of infrared radiation. They hurt - why?

I think you should contact doctor rather than asking question here.

@Dexter You should talk to a doctor, yes. However, I think we still need to be willing to answer the question! The person asking isn't asking about how to take care of their eyes, but rather WHY their eyes hurt!

Every kind of electromagnetic radiation can burn if the intensity is strong enough. If you didn't feel burning heat or something like that, then most probably something else causes your eye problems.

Be aware that most of the light sources are not coherent, like lasers, so they emit on different frequencies. Usually we filter the unwanted frequencies, e.g. by solarium we filter the higher frequencies than UVA.

@L.B. I said contact doctor because sometimes people try to self medicate. It is better not to give any medical advice on open online forum.

@Dexter Haha, true, I do it all the time :)

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text:
What is the minimal focal length of the human eye?
What is the minimum length to which the focal length of our eye can go, even when  considering the blurred images too.

Short answer
The focal length of the average, healthy, adult human eye at near-point is about 18.5 mm. Young individuals can accommodate their lenses further to a focal length of around 15.4 mm.
Background
The focal length of the human eye is the distance between the lens and the retina when an object is in focus (Fig. 1). Therefore, the ...even when considering blurred images too part in the question doesn't make much sense. So, I will focus my answer on sharp images only (pun intended).
The lenses of the eye are thicker in the center than at the edges, and hence positive and converging lenses. They form an inverted image on the photosensitive layer in the back of the eye - the retina (Fig. 1) The retinal image is shaped by two lenses: 1) the cornea with a fixed focal length and 2) the eye-lens, which is a lens with variable focal length through shape changes (Fig. 1) called accommodation and is mediated by the ciliary muscles (Kolb, 2012).
When the ciliary muscles are relaxed, the focal length of the eye-lens is maximal and the distant objects are in focus (infinity). When the ciliary muscles contract they shorten the focal length of the eye-lens to bring nearer objects into focus. The two limits of this range are called the far-point, (ciliary muscles relaxed), and the near-point (maximal accommodation) (source: University of Colorado, Boulder).
The distance between the eye-lens and the retina is about 20 mm. When an object is far away from the eye (infinity), the image is located essentially at the focal point. Therefore the focal length of the cornea and the eye-lens should be about 20 mm when the muscles of the eye are relaxed. The lens strength is the reciprocal of its focal length in meters. Hence, the strength of the cornea and the eye-lens at the far-point is about 1/0.020 = 50 diopters (source: University of Colorado, Boulder)..
When an object is located at the near-point (the closest point at which an object can be brought into clear focus on the retina), the focal length of the cornea and the eye-lens must be changed so that the image is formed on the retina, which is still 20 mm away. The typical near-point in an adult is 25 cm, corresponding to a focal length of the cornea and the eye-lens of 18.52 mm using the standard ray-tracing rules of lenses. Hence the strength of the cornea and the eye-lens must now be about 1/0.01852 = 54 diopters. In other words, the muscles of the eye can provide an accommodation range of 4 diopters (source: University of Colorado, Boulder).
Kids can, however focus to points as close as 6.5 cm away, i.e., 15 diopters worth of optical power, i.e., a minimal focal length of 15.39 mm.

Fig. 1. Human eye. Upper panel: non-accomodated relaxed eye. Lower panel: accomodated eye. source: Khan Academy
Reference
- Kolb, Gross Anatomy of the Eye. In: Webvision. The Organization of the Retina and Visual System, Moran Eye Center (2012)


text:
Do adult mosquitoes have color preferences?
Do adult mosquitoes get particularly attracted or repelled by any colour, or darkness or light? If so, what are they?

Night-time mosquitoes sense IR, UV and CO2 and aromatics as well as colors.  Mosquitos can smell blood through the skin too. https://www.asianscientist.com/2015/10/in-the-lab/mosquitoes-detect-veins/
Black converts the most sunlight to infra red, and white does the least.
2009 Significantly more Anopheles quadrimaculatus females were aspirated from resting boxes fitted with red and IR LEDs than from those with blue or green LEDs, or from the unlit control https://www.ncbi.nlm.nih.gov/pubmed/19852218
Here's a earler conflicting study which is less rigorous, it suggests that different mosquitos prefer different night-light colors. https://www.biodiversitylibrary.org/content/part/JAMCA/JAMCA_V14_N2_P186-195.pdf
Section analysis of the mosquito eye conducted by Kay et al. revealed its sensitivity to ultraviolet (UV) rays. Shimoda et al. used LED light sources with low energy consumption and specific wavelengths to pest control7. Field and laboratory investigations into mosquito response to artificial light have shown, that blue and green light is often more attractive than that in the yellow-orange and red regions of the visible spectrum. https://www.nature.com/articles/srep40074 strobe/fast on and off of the lights caused 2.5 times more mosquitos to be trapped.
http://www.cell.com/current-biology/abstract/S0960-9822(15)00740-X

Short answer
Mozzie preference to colors depends heavily on the species under investigation, as well as the specific preference test used.
Background
Mosquito color preference has been investigated mostly by investigating their preference of oviposition (the process of laying eggs).
When given the choice between black and white containers, Toxorhynchites r. rutilus oviposit preferably in black containers, but about
21% of the females laid at least some eggs in white containers, even in the presence of a black one. 26% used a white container only if a black one was not available (Hilburn et al., 1993)
Aedes Triseriatus females also showed a preference for dark sites for oviposition (Wilton, 1968).
Light-trapping has also been used by putting LEDS in traps and see how many mozzies are caught. Here, shorter wavelengths are associated with higher preference (red < green < blue) in Coquillettidia perturbans, but Culex nigripalpus,  Culex tarsalis, Culex quinquefosciatus and Anopheles sierrenis show no preference whatsoever. Anopheles stephensi however, is highly attracted to UV, but blues, greens, and yellows were less attractive as a clear light bulb (Burkett, 1998.
References
- Burkett et al., JAMCA, l4(2): 195-9
- Hilburn et al, Mosquito News (1983); 43(3): 302-6
- Wilton, J Med Entomol (1968); 5(2): 189–94


text:
Why can I raise my left eyebrow independently from the other but not the right?
I've seen the same question on other forums, but have not come across any definitive explanation.  The non-cited answers seem to fit into three categories:

It is due to greater muscle dexterity on one side of the face.
It is a result of being either left/right brained.
It is genetic.

Perhaps it has to do with a combination of these three, or none of them at all.  Some have even said that with practice they have been able to raise both independently from the other.  Why is this so?

The muscle responsible for being able to raise both eyebrows is one and the same (m. occipitofrontalis). You can not raise one eyebrow because the whole muscle is connected to both eyes. It is possible that one side is not connected or less connected but that's usually not the case and such a person would not be able to raise both eyebrows at will.
What happens in almost all people is that they are not raising one eyebrow, but instead keeping one eyebrow down and raising both at the same time thus giving the impression of only raising one. There are various muscles that are able to lower the eyebrows.
So if one person is "not able" to raise one eyebrow, it actually means that they are not able to keep the other side down.

This doesn't answer the question.

Then the original question thus boils down to why some people can keep the other eye brow down and others can't? If you could expand on this and answer OP's question, that would really help. And adding sources to your statements will help improve this post further.

I googled this because: I have a very expressive face and started noticing (perhaps with age, I'm 36), that one side of my face appears more droopy, or sulky, than the other. This lead me to wonder if it's because I raise my eyebrow on the left side of my face quite often and generally have more expression on that side of my face. More expression, more flexion, this more muscle-work. I tried raising just my right eyebrow and realized I cannot, or at least not without raising both. This bothered me and I wanted to know why, hence my Google search. I chose not to believe the answer to this query and started training myself to make little independent movement of my right eyebrow, watching myself on my phone. Within a few minutes I realized I can close my left eye and raise my right eyebrow, seemingly independently. That become a vision that I could see. I opened my left eye and repeated the vision, but in reality. I can now move my right and left up and down eyebrows independently.

Welcome Osiris. Please take our [tour] and refer to the [help] for guidance. You seem to be suggesting that practice helps. You'd need to support any claims with references from credible sources. The rest of your post seems to be more suited to being a comment. You'll be able to leave those once you've gained sufficient reputation.

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text:
What is the medical definition of death?
What is the medical definition of death? And how do medical examiners determine whether a person has really deceased, as opposed to for example a condition like brain death?

I think is mainly opinion based. Even medically there are different definitions  or versions of death (cardiopulmonary death and brain death).

Your question has been asked in a similar form before. Check out this thread: https://biology.stackexchange.com/questions/43554/metabolic-activity-postmortem/43556#43556 - you might find a useful answer there. Full disclosure: top answer is mine.

You might be better asking how we define and determine death.

To rephrase @John's comment, you might be better asking "What are the most common ways we define death?"

From the deleted answer of Kawin M came this link to Quora

Ok. So when a doctor declares a person dead, it is when their heart or brain is totally not working, and won't start working no matter what they do.
This is legal death.
If your heart stops cold, you are clinically dead. This is reversible, if you are lucky. This definition basically only exists so people can say they "died". It has no real biological significance, except for the fact that your heart is not pumping blood and providing you with oxygen. This will cause...
Biological death:
Within 5-10 minutes at room temp you have reached the event horizon of biological death. Biological death is real death.
Once this time threshold is crossed, there is almost always no going back.
This is because Cells in the brain are destroyed by oncosis, and other mechanisms and forces far beyond me.

Can you add your sources?

@AliceD I mean, it's kind of common knowledge.


text:
What is the difference between the otolith membrane and the endolymph?
The human vestibular system contains otoliths to sense acceleration in the vertical and horizontal plane. I cannot find what the difference is between the otolith membrane and the endolymph?
Can anyone show them where they are located in a picture?
It seems they are different as wikipedia has two different entries for them. See for example the two pictures here and here - I cannot pick the difference.

Instead of downvote, please explain what is wrong with the question. My background is math not biology.

I suspect it is because it's not clear why you think they are the same thing, so the question is whether you have adequately tried to understand them before asking.

@kmm, I understand nothing from biology and anatomy and I will not understand them later too. It is like asking you to try understanding optimal control theory or Algebraic Riccati Equations. I just would like to make sure I am not writing a wrong annotation in a report which contains a human anatomy. This is totally irrelevant to my topic.

@kmm, These photos A and B cause I feel they are the same things.

Don't blame me. I was just speculating as to the downvote. You say you will never understand biology, but you are trying to do just that right now. So I think it is incumbent on you to do what you say you won't do. I actually do understand optimal control theory, because I needed to for a project I was working on. I didn't know anything about it, so I did my "homework" to learn what I needed to learn. I suspect the downvoter expected the same of you.

The two pictures you provide in the question (Fig. 2 and 3 below) actually show it all. You just didn't got the scale right. The question shows prior research effort and the inner ear is a complex organ indeed.
Fig. 1 shows a macro-scale overview image of the inner ear, or the labyrinth. The two otoliths are called the sacculus & utriculus, who sense accelerations in the horizontal and vertical planes.
Now if we zoom in on the sacculus you get Fig. 2, which you provided in the question (comment). Here you can see that the hair cells (the sensory cells) are bathed in endolymph, which is the fluid contained in the membranous labyrinth of the inner ear.
Now if we zoom in further to the cellular level we can see the sensory parts of the sacculus (Fig. 3). In the figure you will recognize the other structure you are referring to, namely the otolithic membrane. The otoliths contain small grainy crystalline structures called otoconia. Otoconia move in response to acceleration, because of their inertia. When they move with respect of their surroundings they activate the hair cells. The otoconia are embedded in a jelly like matrix, called otolithic membrane. the endolymph surrounds the region above the otoconia in Fig. 3.

Fig. 1. Overview of the inner ear. source: Dizziness & Balance

Fig. 2. Sacculus. source: Wikimedia

Fig. 3. Sacculus - close up sensory structures. source: Wikimedia

Many thanks. Just another question. Is otoconia the same bone people take out of fish and call it otolith?


text:
Are some animals, like dogs and cats, color-blind and how do we know that?
I have heard that some animals, including dogs, cats and donkeys, are color-blind. They cannot recognize any color. Is that true? And how can humans verify that animals are color-blind, or not? During evolution, has color-blindness not bothered them at all?

We can look at the composition of Cone and Rod cells in their retinas and compare them to our own. We can also look at the pigments that they are capable of producing, like Rhodopsin, and get an idea of the wavelengths of light that these animals are sensitive to. These days you could probably do fMRI or EEG studies to see what wavelengths of light generate activity in their visual cortexes.... http://www.cals.ncsu.edu/course/ent425/tutorial/colorvision.html

TL;DR: We have a good physiological understanding of how eyes work, so by examination of other species' eyes, we can tell a lot about what colours they are capable of seeing.
First, a little bit about the physics of colour
Light is made of photons, and each photon has a wavelength. The distribution of wavelengths coming from sunlight looks like this (wavelengths on the x axis):

Any perceived 'colour' is some sort of summary of the wavelengths of the photons which get into an animal's eyes.
Now, a little about colour perception
There are cells in the eyes which respond to being hit by photons: these are called rods and cones. Colour vision is principally achieved using the cone cells, which have a peak sensitivity at one particular wavelength, and are less sensitive at other wavelengths.
We (non-colourblind humans) have three different types of cone cell, sensitive to photons with wavelengths of 560, 530, or 420 nm, corresponding to the peak sensitivities of three different types of light-sensitive opsins which are present in cone cells. Other types of opsin exist in rod cells (Rhodopsin) and our circadian-rhythm entrainment (melanopsin), but the three different opsins in our cone cells are responsible for our colour vision. Because we have three different types of cone cell, we are referred to as 'cone trichromats'. The sensitivities of the three cone types overlap a bit, looking like this when plotted over the visible spectrum:

When cone trichromats perceive colour, what we're doing is taking the information on how active each of our different types of cone cell are, and using that to infer how many photons there are of each wavelength in the light that hits our eyes.
Of course, cone trichromats can't possibly summarise the whole diversity of wavelengths that are coming into their eyes using just three different measures of intensity - the line is way too complicated to summarise from three points. Also note that for humans, there is no cone cell that is sensitive above about 700 nm, or below about 400 nm. This means that we simply can't see differences in the infra-red or UV parts of the colour spectrum.
How does this all relate to colour-blindness in animals?
It is fairly simple to test the peak sensitivity of a cone cell: you take an eye from a freshly-dead animal, hook up an electrode to a cone cell, and then provide light of different wavelengths, and measure what wavelength causes the cell to 'fire' the most. If you repeat this with a large number of different cells, you can confidently determine how many different types of cone cell the animal has, and what wavelengths those cone cells are most sensitive to. This experiment (or similar ones) has been done for many different species, so we have a good background knowledge of what colours different species are capable of seeing.
Many species, including most non-primate mammals, have only two types of cone cell (i.e., they are cone di-chromats, as against non-colourblind humans, which are cone tri-chromats). This doesn't mean they see no colour, but it does limit the types of colour they are able to see. Many tools exist to simulate the visual ability of cone dichromats, for instance here, or here for browsers without flash support. These tools simulate human vision with different numbers of cone cell types. When comparing across species, it is important to remember that both the number of types of cone cell, and the peak sensitivity of each type, may be different, so the tools do not capture the full range of possible colour-perception abilities across species.
There are also cone tetrachromatic (four types of cone cell) and pentachromatic (five types) species. The record appears to be held by mantis shrimps, which have sixteen different types of cone cell. These species can in principle see a greater diversity of colours than cone trichromats.
Does colourblindness present an evolutionary problem?
Not necessarily. Compared to cone tetrachromatic species, humans are 'colourblind', and it seems to have very little impact on our day-to-day survival. Similarly, most colourblind humans (i.e., with one or more types of cone cell disabled compared to non-colourblind humans) get along perfectly fine - a special test is needed to detect colourblindness in humans. If trichromatic vision gives no particular survival advantage, there is no reason to think that it will be favoured by evolution.

If you could add a paragraph on the pigment molecules (opsins) expressed by the cone cells, that are sensitive to light at the three wavelengths you reference and how they enable color vision, it would complete the answer, from a biochemical perspective. Otherwise this answer would be just as valid in answering a question as to how a CMOS or CCD sensor uses a Bayer filter to record color information. Definitely a well researched and informative answer, I just think that tying it to the proteins that cause the cones to respond to color would help.

@AMR: Good point. I've added some detail on the diversity of opsins in our visual and circadian systems.

Awesome answer. Too bad the best answers typically raise the smallest amount of rep.

@AliceD... I think one of us should ask the question, "I live near a nuclear power plant and was bitten by a glow-in-the-dark spider. When should I expect my Spidie senses and web-slinging abilities to kick in?..."

@AMR - Now that would be a cracker :)

@AliceD I would do it too if I didn't think some of our more humorless compatriots wouldn't vote me down into oblivion. I could even photoshop a photo of a spider bite to have a slightly neon green glow too it, and say I have this sudden craving for stew of Calliphora vomitoria (Blue-bottle Flies).

The colorblind simulation tool linked in the answer requires Flash; nowadays Flash is pretty much dead, so do you know of one that doesn't?

Cheers for pointing that out. Have added an example that doesn't rely on Flash.

Might also note that most mammals other than primates are dichromats, while most birds (and I think reptiles) are tetrachromats, being able to see ultraviolet.

Good point. The OP's examples were all mammalian, so I have added some more background and another citation to this effect. The source gives some background on the evolutionary origins of the opsins in different mammalian lineages.

Short answer

Dichromats can discriminate colors;
Color vision in animals can be tested behaviorally;
Trichromatic vision is not essential for most animals, but is believed to be beneficial to species relying on fruits (frugivores).

Background
I would like to complement bshane's excellent physiological perspective with a more behaviorally oriented answer.
Firstly, it is quite incorrect to say that dichromats can't see color. "Color blindness" is a deceptive term, since dichromats are not blind to colors, they are "blind" to some. For example, the most common type of color blindness, namely red-green color blindness (deuteranopia), is caused by the lack of green cones. Because of the red-green opponency in color vision, they have difficulties discerning greens and reds. However, they can see yellow and blues perfectly fine. Hence, 2 cone classes are sufficient to recognize colors, but missing a green cone simply results in reduced resolution in the long wavelengths.
Evolutionary, the added cone in trichromats is the medium-wavelength green cone. Trichromatic vision has evolved relatively late in evolution in New World Monkeys and is thought to have been beneficial to them to distinguish between ripe (red/yellow) and unripe (green) fruits, as their diet consists for an important part of fruits (Osorio & Vorobyev, 1996). Noteworthy is that trichromatism is more of an exception than a rule. Nocturnal animals are often monochromats, as rod-mediated vision is beneficial under scotopic conditions. Nocturnal species not only are not negatively impacted by a lack of color vision, they in fact benefit from it, because all of their retinal space is occupied by light-sensitive rods. The photon-hungry color-receptive cones need photopic conditions. Dichromats are the rule, while trichromatic vision is considered exceptional.
We can show trichromatic color vision in animals using behavioral experiments. Animals can be trained to perform color recognition tasks, like Munsell papers, that test the ability of the subject to recognize  red, yellow–red, green–yellow, green, blue–green, blue, purple–blue, purple and red–purple colors. When the subject is able to succesfully recognize these colors, it is safe to say they are trichromats. For example, Munsell papers have been used to show that capuchin monkeys (Cebus apella) are trichromatic (Gomes et al., 2002).
References
- Gomes et al., Behav Brain Res (2002); 129: 153–7
- Osorio & Vorobyev, Proc R Soc Lond B (1996); 263: 593-9

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text:
How does valerian make you calmer?
Why do Valerian pills make us calmer? What is the mechanism behind it?
I understand how artificial tranquilizers work. Do valerian pill have similar chemical components?

Short answer
Valerian preparations contain many compounds, but it is not known which may be responsible for its sedative effects. It is likely that there is no single active compound and that valerian's effects result from multiple constituents acting independently or synergistically (source: NIH). Overall, I think it is safe to say that valerian's sedative properties are related to its GABAergic properties (Yuan, 2004).
Background
The constituents of the volatile oil obtained from the rhizomes (underground stems), and stolons (horizontal stems) of Valeriana spec are variable due to  the variability in genetic make-up and environmental factors impinging on the batch of plants used (source: NIH).
The major constituents include the monoterpene bornyl acetate and a variety of sesquiterpenes including valerenic acid.
Some of the sesquiterpenes have been shown to have a direct action on the amygdala, which is a brain structure in the limbic system. The amygdala is responsible for feelings of fear and anxiety. Valerenic acid has been shown to inhibit the breakdown of GABA in the brain, resulting in sedation. GABA is the principal inhibitory neurotransmitter in the nervous system.
The non-volatile monoterpenes known as valepotriates possess sedative activity, but their mode of action is not clearly known. The valepotriates themselves act as prodrugs, and are transformed into homobaldrinal which has sedative properties.
Extracts of valerian roots contain substantial amounts of GABA which could directly cause sedation. However, whether GABA reaches the central nervous system is debated.
Another compound present in extracts is a lignan, hydroxypinoresinol, and it binds to benzodiazepine receptors, which are GABAA receptors and the target of benzodiazepines, i.e. tranquilizers and sedatives (Houghton, 1999).
References
- Houghton, J Pharm Pharmacol (1999); 51: 505-12
- Yuan et al., Anesth Analg (2004); 98(2): 353-8

Valeriana is an extract from the flower of Valerian.

We don't know the mechanism by which it affect our physiology but we have a number of hypotheses.
Quoting the USA National Institue of Health:

Many chemical constituents of valerian have been identified, but it is not known which may be responsible for its sleep-promoting effects in animals and in in vitro studies. It is likely that there is no single active compound and that valerian's effects result from multiple constituents acting independently or synergistically [18, reviewed in 19].
Two categories of constituents have been proposed as the major source of valerian's sedative effects. The first category comprises the major constituents of its volatile oil including valerenic acid and its derivatives, which have demonstrated sedative properties in animal studies [6,20]. However, valerian extracts with very little of these components also have sedative properties, making it probable that other components are responsible for these effects or that multiple constituents contribute to them [21]. The second category comprises the iridoids, which include the valepotriates. Valepotriates and their derivatives are active as sedatives in vivo but are unstable and break down during storage or in an aqueous environment, making their activity difficult to assess [6,20,22].
A possible mechanism by which a valerian extract may cause sedation is by increasing the amount of gamma aminobutyric acid (GABA, an inhibitory neurotransmitter) available in the synaptic cleft. Results from an in vitro study using synaptosomes suggest that a valerian extract may cause GABA to be released from brain nerve endings and then block GABA from being taken back into nerve cells [23]. In addition, valerenic acid inhibits an enzyme that destroys GABA [reviewed in 24]. Valerian extracts contain GABA in quantities sufficient to cause a sedative effect, but whether GABA can cross the blood-brain barrier to contribute to valerian's sedative effects is not known. Glutamine is present in aqueous but not in alcohol extracts and may cross the blood-brain barrier and be converted to GABA [25]. Levels of these constituents vary significantly among plants depending on when the plants are harvested, resulting in marked variability in the amounts found in valerian preparations [26].

Quoting wikipedia

Because of valerian's historical use as a sedative, antiseptic, anticonvulsant, migraine treatment, and pain reliever, most basic science research has been directed at the interaction of valerian constituents with the GABA receptor.[16] Many studies remain inconclusive and all require clinical validation. The mechanism of action of valerian in general, and as a mild sedative in particular, has not been fully elucidated. However, some of the GABA-analogs, particularly valerenic acids as components of the essential oil along with other semivolatile sesquiterpenoids, generally are believed to have some affinity for the GABAA receptor, a class of receptors on which benzodiazepines are known to act.[17][18] Valeric acid, which is responsible for the typical odor of mostly older valerian roots, does not have any sedative properties. Valeric acid is related to valproic acid, a widely prescribed anticonvulsant; valproic acid is a derivative of valeric acid.[citation needed]
Valerian also contains isovaltrate, which has been shown to be an inverse agonist for adenosine A1 receptor sites. This action likely does not contribute to the herb's possible sedative effects, which would be expected from an agonist, rather than an inverse agonist, at this particular binding site. Hydrophilic extractions of the herb commonly sold over the counter, however, probably do not contain significant amounts of isovaltrate.[19] Valerenic acid in valerian stimulates serotonin receptors as a partial agonist.[20]

@christiaan wouldn't like this very much!

@Polisetty - and how do you know that :-) you just unveiled my downvote :-)

Come on, Remi. An answer consisting entirely of two long block quotes, and you didn't even maintain the wikilinks? I expect more out of you... :(

Looks like users with more reputation are more harshly noted. Sometimes, I am willing to help but don't have time to work on the format.

Remi.b - it is one big copy-paste answer, the quotes are stacked with irrelevant info, and include many references not even mentioned in your answer. As @MattDMo says, I just expect better of hi-rep users like you. That's not harsh, it's high expectations not being met. I count on users like you to be critical on my answers too.

Well that's what I meant. Hi-rep users are not judged the same way as low-rep users. But it's fine, no big attack here. I agree that your answers is much better than mine (+1 btw). I though leaving my answer as it links to webpage that offer tons of references.

@Remi.b - a new user would've either gotten a comment, or a comment and -1 when pasting wiki sections, depending on the answer. I basically systematically downvote wiki paste's. In your case I was indeed quicker with the -1 given your rep, true. And thanks for the +1, you deserve the sportsmanship badge!


text:
Why does the refractory period of neurons only allow signals to pass in one direction?
My textbook states that the advantages of the refractory period is that it means that action potentials are discrete and also that it results in signals only being able to pass one way,  but provides no explanation. Could anyone explain why this is?

The axon is an uniformly excitable structure; if you would stimulate an axon electrically somewhere in the middle, an action potential would be generated in both directions. Hence, an axon in itself does not have directionality.
Nonetheless, under normal physiological conditions, an axon  conveys action potentials from the dendritic region to the axon terminal, called anterograde signaling. The reverse direction, retrograde action potentials,  normally do not occur because signals arising in the dendritic region travel unidirectionally to the terminal. The reason why an action potential travels unidirectionally is because of the refractory period. Because the refractory period will cause the part of the axon that just generated an action potential to become unresponsive, the traveling action potential cannot generate another action potential in the retrograde  direction, because the only excitable region available is in the anterograde direction to the terminal (Fig. 1).

Fig. 1. Refractoriness. source: University of British Columbia
As an analogy, it's like a car driving across a road and throwing a temporary road block behind it that first has to be taken away before the road can be used again. This means that when a car leaves the parking lot and enters the road, it can never go back,  because it throws up road blocks that prevent it to return the way it came.


text:
Why do plants not have fat cells, and store their reserves in vacuoles instead?
Why don't plants have fat cells, but instead store reserves in vacuoles. And vice versa, why do humans feature fat cells instead of depositing storage molecules in vacuoles?

Short answer
Parallel evolution can generate similar traits in unrelated organisms based on unrelated structures.
Background
First off, the question is based on a few misconceptions:

First, you are making an apple-and-pear comparison; Fat cells are cells - vacuoles are organelles. Fat cells store fats in liquid droplets, called adiposomes, which are lipid-rich cellular organelles that regulate the storage and hydrolysis of neutral lipids and are found largely in the adipose tissue. Vacuoles have a variety of functions, namely 1) contribute to the rigidity of the plant through hydrostatic pressure; 2) store nutrient and non-nutrient chemicals and 3) break down complex molecules. The latter two functions are quite reminiscent of the function of lipid droplets in animalia.
Plants do not store energy reserves in fats like animalia do. Instead, plants store starch, which is not a hydrophobic lipid, but a hydrophilic glucoside polymer.

Apart from these specifics, the question can be tackled more generally - unrelated organisms can solve the same 'problems' (like storage of energy rich compounds) through parallel evolution (wings in bats and birds for example). Why does a bat wing contain fingers and a bird's wing doesn't? Because they developed the ability of flight through different, parallel adaptations.


text:
What do animal cells store pigment in?
So I know plants store pigment in chloroplasts, chromoplasts, etc., but what do animal cells store pigment in? For example, is there like a chromoplast for melanin in the human body?
I tried Googling my question and didn't find anything, but maybe I was looking at the wrong sources.

I read through the article you linked and it didn't seem to have an organelle or something that contained melanin. I've never heard of melanine, but maybe it's a variation of melanin.

You want to read the Wikipedia page on Melanosomes.

Cool, I did. That was really helpful, thanks!

Melanine is produced and stored in melanocytes. They contain melanosomes that are organelles that store melanine.


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What is the largest animal that has no hard parts?
Some examples of "hard" animal parts are bones, cartilage, and exoskeletons. What animal has the most mass while being completely "soft". I don't think it's the colossal squid, since it has a hard beak and cartilage in their mantle. My guess is the heaviest jellyfish.

What do you consider hard and what as soft? My [now deleted] answer received a downvote and below answer also struggles to find a definition of what 'hard parts' are.

@AliceD Why don't you post a new answer as per his definition?

@TalhaIrfan because the question is ambiguous and below answer is not too bad.

Please forgive me for plagiarizing the open source wikipedia, here are some species of large soft bodied animals. I honestly don't think I could re-write this more clearly for any logical reason:
Citation:
The lion's mane jellyfish (Cyanea capillata) is the largest cnidaria species, of the class Scyphozoa. The largest known specimen of this giant, found washed up on the shore of Massachusetts Bay in 1870, had a bell diameter of 2.5 m (8.2 ft), a weight of 150 kg (330 lb). The tentacles of this specimens were as long as 37 m (121 ft) and were projected to have a tentacular spread of about 75 m (246 ft) making it one of the longest extant animals

The largest roundworm, Placentonema gigantissima,[174] is a parasite found in the placentas of sperm whales which can reach up to 9 m (30 ft) in length
The largest nemertean is the bootlace worm, Lineus longissimus. A specimen found washed ashore on a beach in St. Andrews, Scotland in 1864 was recorded at a length of 55 m (180 ft).[183]
There are a couple of animals that are of interest but they are not technically soft bodied:
The colossal squid (Mesonychoteuthis hamiltoni) is projected to be the largest invertebrate. Current estimates put its maximum size at 12 to 14 m (39 to 46 ft) long and 750 kg (1,650 lb),[185] based on analysis of smaller specimens. In 2007, authorities in New Zealand announced the capture of the largest known colossal squid specimen. It was initially thought to be 10 m (33 ft) and 450 kg (990 lb). It was later measured at 4.2 m (14 ft) long and 495 kg (1,091 lb) in weight
The largest known species of sea sponge is the giant barrel sponge, Xestospongia muta. These massively built sponges can reach 2.4 m (8 ft) in height, 80 kg and can be of about the same number of feet across at the thickest part of the "body". Some of these creatures have been estimated to be over 2,400 years of age.
https://en.wikipedia.org/wiki/Largest_organisms#Invertebrates

I received critiques from another user and deleted my answer. Issue is the species should be devoid of any 'hard' parts - a sponge has a rigid calcareous skeleton and the squid was dismissed in the question too.


text:
Advantage of opponent color?
Opponent process is a color theory that states that the human visual system interprets information about color by processing signals from cones and rods in an antagonistic manner (source).
What is the advantage of opponent color against RGB color? For example, in object recognition or edge detection?
Can we say that it provides some level of invariance to changes in brightness?

RGB color is a more direct representation of the "raw input" received by the (human) eye, since the three types of cone cell have responsivity spectra that roughly correspond to red, green, and blue light:

Opponent color decomposes color into three "dimensions" of opposing properties: dark or light, yellow or blue, and red or green.  This provides some brightness invariance, since changing the intensity of light will change the brightness but not the yellow/blue or red/green balance of the color, even though the stimulation level of all three types of cone cell will change.
One could speculate that opponent color perception is more "meaningful" in real-world environments.  The dark/light axis represents the overall amount of light, the yellow/blue axis indicates which end of the visible spectrum is predominant, and the red/green axis provides a finer distinction for low-frequency light.

"...even though the stimulation level of all three types of cone cell will change": The stimulation levels change, but the ratios of r/g/b/ cone activation remain the same under varying luminance, regardless of the opponent channels. Hence opponency is not necessary for color constancy.

and why would 'end-of-spectrum' information of the yb axis be helpful?

@ChrisStronks Of course color opponency is not the only way to achieve color constancy, I'm not sure what your point is.

@ChrisStronks  The "end of spectrum" information is helpful in finding fruits or young leaves among other foliage.  This is thought to be why trichromacy evolved in primates (most other mammals have only two cones).

Trichromacy helps in fruit recognition  for sure, but the added color is either red or green, the dynamic frequency range wasn't changed much when trichromats appeared. See the benefit of trichromats and fruit in this answer: http://biology.stackexchange.com/questions/24481/is-our-color-vision-calibrated-to-sky-vegetation-and-blood/24544#24544

@ChrisStronks Sorry, I misunderstood what you were asking.  The blue/yellow axis represents whether the light is predominantly high-frequency (more blue) or low-frequency (more yellow).  This is the most basic type of color vision and is helpful because color provides useful information about the world.

I know... My points are (1) opponency is not involved in color constancy (rgb regulated) and (2) yb / dichromatic vision / end-of-spectrum / dynamic range have not much to do with the advantages of color opponency. The fruit hypothesis can be explained at the cone / rgb level.

Let us continue this discussion in chat.

The first question, namely what is the advantage of color opponency 'against' RGB, is technically incorrect. The opponent system (Red/Green; Blue/Yellow and brightness channels) is physiologically situated in the neuronal retinal layer and higher visual structures such as the lateral geniculate nucleus and receives input from the RGB system (photoreceptors in the retina: Red, Green, Blue cones).

Then the question becomes "what is the advantage of adding the opponent channels on top of the RGB system? The advantage of opponency may in fact not be the negative opponent effect so often stressed in the Hering model (and shown in the figure: e.g., blue suppressing yellow etc). The advantage lies in the finding that activity of one opponent pair increases activity of the opponent color in adjacent areas in the retina. This effect results in a sharpening of color contrasts between the opponent colors (Hurvich and Jameson, 1957). Indeed, the poor spatial color-contrast, as provided by the sparsely placed cones in the retina, is enhanced by this mechanism. Especially the blue cones are present in isolated patches in the retina. Because one color in an opponent pair increases the other's activity directly adjacent to it in the retina, the resolution of the blurry retinal image is greatly increased. Hence, as you rightfully say, edge detection and in particular color contrast perception is enhanced.
Object recognition, as you mention in your question, is a process that is facilitated by the visual system through many stages including the higher visual cortices. Enhanced color contrast will likely facilitate object perception, but indirectly since color contrasting makes up just a small portion of a much bigger and complicated neural system devoted to object recognition, namely the visual 'ventral' stream (Ishai et al., 1999).
Lastly you ask whether opponent colors may facilitate invariance to brightness. Assuming you mean color invariance under varying luminance (referred to as color constancy) the answer is no. The RGB cone system can deal with this easily, as the ratio of cone activation yields enough information to code the hue under various luminances. If a certain object reflection activates twice as many red cones than green cones, it will also activate the same ratio when the luminance is increased (Mather, 2006 - Chapter 12).

@AliceD, could you expand on the last point please - why do you think the opponent process does not facilitate color constancy? You're saying that 'RGB cone system can deal with it easily by calculating the ratio of cone activation', - but the opponent process is exactly that, the calculation of the ratio between cone activations. It just so happens that our particular visual system does this via the R-G, B-Y, Brightness variables.

The opponent process is indeed useful for color constancy.
Opponent process maps RGB (or LMS) coordinates to YB-RG-WhiteBlack coordinates:

RG axis, for example, is calculated by the simple algebraic R - G (or L - M).
If the brightness is reduced, there will be fewer photons falling on both the R cones and the G cones.
The WhiteBlack value will change:
R + G + B = ?
8 + 3 + 0 = 11 →
7 + 2 + 0 = 9 →
6 + 1 + 0 = 7 --- notice WhiteBlack value changes

The difference between R and G will remain the same:
R - G = ?
8 - 3 = 5 →
7 - 2 = 5 →
6 - 1 = 5 --- notice RG value stays the same

This ensures color constancy - the visual system has a way to determine that the color of the object didn't change, only the illumination did.

Here is a related quote from Vision Science: Photons to Phenomenology by Stephen Palmer:

The opponent representation is more useful because it helps determine which
differences between adjacent retinal regions result from changes in
the level of illumination (such as when a shadow falls across a
surface) and which result from changes in spectral reflectance (such
as when a surface is painted two different colors). Changes in the
amount of illumination will generally just raise or lower the overall
amount of light (that is, change the output of the B1/Wh system) while
the chromatic balance remains constant (that is, the outputs of the
R/G and B/Y systems are invariant).


text:
How much energy does a small spider expend per day just waiting for its web to vibrate?
Roughly speaking, a small, complex electronic circuit or IC might sit in "sleep mode" using a current of roughly 1 µA (e.g. 1, 2), thereby using roughly $3\times 10^{-6}$ Watts, and that converts to roundly $2.5\times 10^{-6}$ kcal/hour or $62\times 10^{-6}$ kcal/day.
I suppose you could call that 62 micro-kcal/day or 62 milliCalories/day.
One day I noticed a small spider in my home, sitting in its small web, and kept an eye on it. After several weeks of watching I hadn't seen it catch anything. I slightly perturbed the web and it reacted. It was still alive.
Question: I'm curious to know roughly how much energy a small spider needs to sit and wait. Might this be termed roughly the spiders Basal metabolic rate? It could be for any small spider that spends much of its time waiting for prey. As long as an approximate size or mass is available then it could be expressed as kcal/day/kg or some similar unit.
I have read about Kleiber's law in this answer, but I don't think it is meant to extend down to small spiders.
note: I'm just asking for the energy expended during resting periods. Of course during a day the spider may do web maintenance, catch or eat prey, but it's the resting rate of energy consumption, on a daily basis, that I'm asking about.

Short answer
Approximately 240 J on a daily basis.
Background
Ballesteros et al. (2018) modeled basal metabolic rates of insects. They reckoned that endotherms, like insects, basically use energy directly correlated to the number of cells, which is linearly correlated to their body mass. They checked their model with experimental data from Chown et al. (2007) (Fig. 1).
Acknowledging that arachnids aren't insects, but that both are arthropods, let's take an average-sized web making spider, like the black widow, weighing in at 1 g. This yields a basal metabolic rate of 10 J/h, or 240 J/day. However, and given the linear correlation between energy expenditure and mass, a dwarf spider weighing in at 1 mg expends 1000 times less, and a Goliath bird eater approaching 200 g will expend 200 times more.
To convert the unit for the Black widow to a Watt scale, we get 1 J/s that corresponds to 1 W, so 1 J/h corresponds to about 0.3 mW.

Fig. 1. Base metabolic rate for insects. Data from more than 300 species were extracted from Chown et al. (2007). source: Ballesteros et al (2007)
References
- Ballesteros et al., Sci Rep (2018)
- Chown et al., BES (2007); 21(2): 282-90

Wow, all kinds of goodies here; thank you for the well-sourced answer!

@uhoh - thanks! You may wish to check the math, however, where needed - I'm just a Biologist and your post seems to radiate quite some proficiency in math :) I added my sources, so that should work out. Cheers.

A bee perhaps consumes 100 times more than a spider on a busy day, so some added graphs would be helpful. Also consider that a spider at 12'C consumes way less than at 25'C... Essentially you can weigh their energy demands from the mass of their diet, by counting their midden. they can stay alive on about 5-10 times their body mass every year, depending on the species, and they generally get a catch ever few days, so they can go into low wattage mode or high wattage mode, where high wattage mode produces lots of web reserves and broods.

@com.prehensible - the answer pertains to basal metabolic rates only, per the question, and as mentioned in the answer's body text.

basal metabolic rates depend on temperature and food input, i.e. a pregnant woman will spend a lot more energy when pregnant and spiders have dozens of babies... So basal metabolic rate of an idle spider can be equivalent to 5 times it's body mass in lymph per year.

@com.prehensible, yes the paper models energy expenditure for a certain temperature range. And of course there are more exceptions to the rule. Obviously it is the basal rate, no extreme temperatures, no babies, no running, no weaving, no nothing.

@AliceD so, using your numbers, the basal energy consumption of the small IC would be about equal to that of the dwarf spider?

@mpprogram6771, well, yeah, perhaps in the same ball park, but yet a few orders of magnitude larger than uhoh's calculation.

For the black widow, you said it would be 10 J/h, and that 1 J/h = 0.3 mW, so black widow would be 3 mW, which is 1000 times larger than the microprocessor from uhoh's calculation. you also said that the dwarf spider would be about 1000 times less based on mass, which brings it to 3 micro watts, or 3*10^-6 W, which was the measurement that uhoh got for his IC. Is my math right?

@mpprogram6771 - ah yeah, my bad.

This all works out very nicely and indeed at 1 mg spider would seem to be of the order of 3 uW just like a low power IC in idle mode. Cool result, thanks!

@uhoh - thanks a lot for confirming the math here :) My pleasure!

A 400 pound human can survive a year without food, and an arachnid can manage the same, 3000-7000 hours if it consumes it's body mass equivalent.
A spider consumes about 110  to  1933 μW per gram of body mass, standard metabolic rate at 20'C.
By measuring spider oxygen consumption, scientists have found a range of 21–356 μl O2/g per hr.
Its good efficiency compared to other poikilotherms of same size.
A human an adult at rest consumes about 16 liters of oxygen per hour. This gives a nominal basal metabolic rate of 75 kcal/hr which translates to 87 watts(=1.2 milliwats per gram).
1 liter of oxygen gives 5.43 watts per liter... 1 microliter = 5.43 microwatts.
21-456 *5.43 = 110 to 1933 microwatts per gram.
Big garden spiders from temperate regions are about 1g, so a big spider from the garden can use 0.1 - 2 milliwatts at 20'C.
1 gram of fat is about 7kcal, that's 8 Watts. So, if a 1gram spider has a 0.5 gram meal, they can keep going for about 10,000 hours, perhaps 3000-7000 hours at 30/70% efficiency.
https://jeb.biologists.org/content/214/13/2175

Interesting answer. But... How can a 1-gram spider eat half of its body weight? And, probably related, if it can survive 10,000 hours, i.e., more than a year, with a single meal, why would it even bother catching pray at all? And, related, a 'meal' is hardly pure fat, instead, it will mostly be chitin and other proteins. Importantly, why is exotherm data included in this answer? If that human hourly O2 data is used for the later calculus, it is likely inaccurate, as exotherms use a lot more base-energy than endotherms.

Lastly, it's best practice to write the references out in full (J. Doe, Journal of something (2020) etc), as web links may grow cold over time. In fact, they quite frequently do.

Are you saying that respiration and the use of ATP in arthropods and humans generates a different amount of energy? It's the same respiration conversion of oxygen to carbon dioxide, at 20 vs 37 degrees, correct me if I am wrong, it's basic biochemistry with 02 in and C02 out, so the energy maths are the same. Also correct the maths if you see a specific error. If you scale up the black widow to 65 kg and 37 degrees, it consumes almost exactly 1W/gram. Silicon wafers are 50 micrometers, though, so the  IC silicon using a 1x1x0.01mm wafer weighs about 0.00023 grams.

It wasn't clear to me why the human data was in there. Your train of thought slipped me, as it's just respiration Biochemistry you were needing the human data for, it was quite confusing. Thanks for clearing that issue up.


text:
Onset of Autophagy
Fasting and Intermittent Fasting (IF) have been proven to start autophagy (cellular self-digestion). How long does the average man and woman have to wait for autophagy to begin? Does diet prior to fasting effect the onset of autophagy? And lastly, does longer fasting produce more efficient autophagy than IF?

Would you happen to have a reference for your first statement?

http://www.ncbi.nlm.nih.gov/pubmed/21471734; http://www.ncbi.nlm.nih.gov/pubmed/20534972; http://www.ncbi.nlm.nih.gov/pubmed/19200897;

Thanks for the links.  This appears to be a related question that might help: http://skeptics.stackexchange.com/questions/1696/does-intermittent-fasting-improve-immune-function-through-autophagy

Does not quite answer my questions. I am more interested in how long after a fast starts does the mechanism of cellular self-digestion begin.

Yes, but the references might point you in the right direction.  The main issue I see is that a lot of work has been done in non-human animals -- you (or someone else who is familiar with this area, which is not me) might have better luck looking up the signaling pathways involved involved and seeing when and how they turn on in response to fasting.  Another keyword to consider is "starvation".


text:
Mathematical models of lineage selection
I'm interested in the concept of lineage selection (Aboitiz, 1991) as an explanation for why traits would be selected for that enhance the rate at which evolution can occur, rather than directly enhancing an individual's fitness. (Such traits could include gene duplication; body plans that can easily be adapted to new niches; learning (which enhances evolution due to the Baldwin effect) and so on. Questions about the evolution of such traits are collectively termed "evolution of evolvability.") The term "lineage selection" does not refer to group selection or kin selection, but simply to selection between distinct genetic lineages in a mixed population.
What I would like to know is whether a mathematical theory has been developed along the lines of the Price equation that can capture the concept of lineage selection and make predictions about it. Lineage selection does not appear to be modelled by the Price equation itself, at least not in a straightforward and obvious way, because on the face of it the Price equation only directly accounts for the relation between a trait and the number of offspring in the next generation, rather than the number of surviving descendants several generations later, which is what is required for lineage selection.
The reason I'm looking for a mathematical model is that there are a number of intuitions that many people seem to share about lineage selection and I'd like to understand what assumptions are needed in order for them to be true. In particular, it seems clear that large populations are needed for lineage selection to be effective, and I'd like to understand precisely the relationship between population size and the effectiveness of lineage selection. (My intuition is that with a population size of around a million, lineage selection can select for traits that have a beneficial effect around 20 generations later, since $1,000,000\approx 2^{20}$, but this intuition lacks a formal basis.)
A literature search did not turn up anything along the lines of what I'm looking for, but this is not my main field and I may simply not know the most appropriate search terms to use.

Question that is a bit related: Empirical evidence for species selection

I think that there is quite a good agreement among the kin selectionist community that kin selection and group selection is exactly the same thing (see here for example).

You may want to have a look to this post that talks about kin selection and this post that aims at providing an intuitive explanation for why kin selection and group selection are the same thing

@Remi.b I'm pretty aware of that argument (not sure which side I fall on), but lineage selection in the sense I intend it is not the same as either of them - it's not about adaptations that benefit relatives, it's purely about adaptations that benefit your descendants, several (or many) generations later.

@Nathaniel have you  had any luck finding this here or elsewhere?

@sterid I didn't find it in the literature, so I decided to do the research myself. An initial conference paper version of the work should be published soon - I'm revising the manuscript now. I will try to remember to post here once it's available online.

Hi, @Nathaniel, wondering whether the manuscript is complete.  Also, could you explain your 2^20 intuition?

@sterid this ended up being part of a conference paper here, but that didn't include the Price equation aspect. I actually have made some progress on that, and plan to publish it this year hopefully. (But I've not started writing it up yet.)

@sterid the 10^20 intuition turned out to be about right for a well mixed population. The reason is that a neutral mutation will be fixed or become extinct after a time that's approximately the logarithm of the population size on average (multiplied by some constant). You can only have competition between lineages during that the time they both coexist, so fixation time limits the time scale that lineage selection can act upon.

@sterid however, in populations where dispersal is limited, fixation time scales only polynomially with population size, and for that reason the time scales for lineage selection can be much, much longer. This is the main result of the paper I linked above.

I've asked a somewhat similar but narrower question on TCS:  https://cstheory.stackexchange.com/questions/42513/are-there-experiments-in-artificial-life-on-the-emergence-of-sexual-reproduction Crickets to that as well, insofar. Section III of https://www.biorxiv.org/content/10.1101/107847v1.full basically goes over why this is hard to model.

The writings by Samir Okasha (philosopher of biology/science) could be a good starting point. In his book Evolution and the Levels of Selection, he explicitly uses the Price equation to discuss selection at multiple levels (e.g. chapter 2.3: Price's equation in a hierarchical setting), and also derives a multi-level version of the Price equation:
$$\bar{w}\Delta\bar{z} = Cov(W,Z) + E(Cov_k(w,z))$$
where the first part on the right hand side represents collective-level selection and the second part particle-level selection. This is mostly aimed at aspects of group-level selection though. There is also a chapter on "Species Selection, Clade Selection, and Macroecolution" (ch. 7), but this is not directly tied to the Price equation. A note though; I own the book and have read parts of it casually, but I haven't worked with the Price equation myself, and I haven't checked exactly how the extended version of the Price equation is developed and used in the book.
A couple of references that might be useful are Frank (1998) (and other papers by him) and papers by Vrba. The work presented in this recent conference abstract by Rankin, Fox et al (2014), "Using the Extended Price Equation to Analyze Species Selection in Mammalian Body Size Evolution Across the Paleocene/eocene Thermal Maximum", seems to describe exactly the type of theoretical developments that you are looking for (I didn't attend the conference, and haven't heard the talk though).

It's fairly straightforward to expand the Price equation if you fix the genetic operators. This was done in one CS-oriented paper. Bassett et al. (2004) (preprint):

where k iterates over the genetic operators.
But it's not at all straightforward (and I suspect not possible) to do that for an all-encompassing abstract notion of evolvability (of every rule/mechanism that might be evolvable). I mean if the rules/operators are countable, you could write an infinite sum on the right hand side of that equation, but it's not clear how that helps with anything in practice.
If you use the multi-level (= group selection) version of the Price equation (as suggested in the other answer), you still have to decide (a priori) on grouping so basically enumerate over the (potentially evolvable) operators, albeit do that in terms of groups. For example, an operator can be recombination, which is the same as deciding to have groups for sexual and asexual organisms. I think the operator approach may be preferable in some cases because it can be real-valued (i.e. a continuous quantity). Although not using the (above) Price equation explicitly, such research on evolvability of specific (continuous) operators has been carried out, e.g. on the optimal recombination rate (Lobkovsky et al., 2016) etc.

On a different tack, and possibly closer to biology as a general idea, in another CS-oriented paper,  Touissant (2003) proposed a (non-trivial) notion of embedding the evolvability of the parameters of interest into the "normal" genotype space.

In simple cases where the genotype space decomposes (strategy
  parameters) an embedding space of neutral sets is obvious. To generalize to arbitrary neutral sets and arbitrary genotype-phenotype mappings we introduced the σ-embedding, i.e.,
  we embedded neutral sets in the space of probability distributions over the genotype space
  (exploration distributions). [...]
the question of how variational properties evolve has also been raised in numerous
  variations (pleiotropy, canalization, epistatis, etc.) in the biology literature. These discussions aim at understanding how evolution can handle to introduce correlations or mutational
  robustness or functional modularity in phenotypic exploration. Our answer is that variational properties evolve as to approximate the selection distribution. If, for example, certain
  phenotypic traits are correlated in the selection distribution F, then the Kullback-Leibler
  divergence decreases if these correlations are also present in the exploration distribution σ.

Alas he doesn't derive anything resembling a Price equation using his approach. (He does have a twin notion of evolution and σ-evolution, but there's no hierarchy/grouping.) Whether this notion is actually biologically useful, probably depends crucially on the embedding.
There are some papers in actual biology research that are closer to this idea of "embedded" evolvability. For example one paper (Lehman and Stanley, 2013) which looks at (actually defined evolvability in terms of) phenotypic variability.

one widely-held conception of evolvability as the capacity of an organism to “generate heritable phenotypic variation” [...], which is also the definition adopted in this paper. While evolvability is also sometimes discussed in relation to adaptation [...], the chosen definition reflects a growing consensus in biology that phenotypic variability in its own right deserves study in the context of evolvability

So this is one kind of concrete embedding. But no Price equation based on this idea that I could find in there...
On the other hand Rice (2008) does propose a stochastic extension of the Price equation, based on this idea that variability matters (or is all that there is to evolvability according to some):

A number of studies have shown that when fitness is treated as a random variable, meaning that each individual has a distribution of possible fitness values, then both the mean and variance of individual fitness distributions contribute to directional evolution. Unfortunately the most general mathematical description of evolution that we have, the Price equation, is derived under the assumption that both fitness and offspring phenotype are fixed values that are known exactly. The Price equation is thus poorly equipped to study an important class of evolutionary processes. [...]
I present a general equation for directional evolutionary change that incorporates both deterministic and stochastic processes and applies to any evolving system. This is essentially a stochastic version of the Price equation [...]
This [new] equation shows that the effects of selection are actually amplified by random variation in fitness.

Finally, (as acknowledged in this latter paper) all variations on Price equation are over immediate successive generations. If you want to iterate forward (to infinity) you need to use a diffusion equation/model. (See chapter 7 in Durrett's book, for instance.)

Thank you, this is a very helpful answer with some great references, which I will work through in detail.


text:
What happens to neutrophils in whole blood stored for transfusion?
The lifetime of neutrophils is normally quite short, 3-5 days in vivo (link).  On the other hand, whole blood can be stored for a fairly long time, up to 35 days (link).
What happens to neutrophils in whole blood for transfusion that was stored for more than 5 days?

I have not worked in a shop that has whole blood available for transfusion in a while (typically only very large trauma centers use whole blood, everyone else uses individual components), but most packed cells for transfusion are given as leukocyte reduced with those neutrophils being filtered out prior to transfusion.

@RudyB Thanks!  I know whole blood is not common nowadays, it used to be standard in the past.  I'm just curious whether the neutrophils  stay alive longer, or apoptose, or get eaten by macrophages, or something else, in that situation.

There is actually a resurgence of whole blood usage due to trauma studies showing that it is the best resuscitation fluid, but storage, cost, usage, etc. mean that only few places keep it. Outside of trauma, component transfusions predominate (PRBCs/ FFP/ platelets). However, using it is much easier (minutes) relative to thawing FFP (an hour) or trying to get emergent pheresis platelets from Red Cross (multiple hours in the best case).
The neutrophils are the part of blood that clinically nobody wants due to things like graft versus host disease, so I honestly do not know what happens.


text:
Is there a protocol for freezing and thawing Bacillus subtilis cells?
There is a book that says to store Bacillus spores in 50% glycerol at -70 degrees Celsius (doesn't mention if the 50% is final concentration or not). But from what I know, the cells themselves can be stored in any % glycerol as long as the final glycerol concentration is 15% (v/v) at -80 degrees Celsius.
Is there a difference between preserving spores and cells? Because the book said to preserve the cells at a certain glycerol concentration and the spores at a different glycerol concentration.
Also, say I scrape some B. subtilis out from the cryovial for reuse, and they are frozen. Do I wait for the scraped cells to thaw and then plate them, or plate them while they are still frozen?
And if I want to sporulate these cells, should I recover these frozen cells by plating and incubating overnight, or can I just drop them directly into the sporulation medium? I want to get the details down properly.

Welcome to Biology! You wish to store B stubtilis and be able to grow them again later, or to what purpose are you asking this question? Also, why do you think a standard glycerol stocking procedure for E. coli will not work for you? Background info helps folks to answer your question.

I advise you to edit your original question and add these details

Thanks for the edits. I just added a few spaces here and there

This is just anecdotal and I don't know the best method, but I used to store B. subtilis cells in 50% glycerol at -80C. For protein production, I'd thaw the stock completely, plate them to obtain log phase cells and then inoculate the growth medium. Worked every time.

While I have never done bacterial stock cultures from spores, I don't think it is necessary, as the standard procedure for making bacterial stocks should work without problems.
For that you grow your bacteria in liquid culture until you reach the late log phase (so you have a lot of bacteria in your media), take 1 ml of the culture, mix it with 100% glycerol to reach a final glycerol concentration of 50% and then freeze it a -80°C. At this you can store it for long times (probably not indefinitely but for years is possible).
When you want bring your cultures back to life, take the tube and either use an inocculation loop or a pipette tip to scrape a bit of the frozen culture and plate it on an appropriate agar plate. If you want to scale up, pick one colony from the plate into liquid media.
Since glycerol is a pain to pipette (and can also have sterility problems), I have switched over to DMSO as a cryo-protective agent for bacterial cultures as well. Simply add 15% (end concentration) DMSO into the cryo vials (so 150ul DMSO to 850 of culture), mix and then freeze the cells. In my experience this works as good as glycerol.

+1 - just out of philosophical curiosity, you say When you want bring your cultures back to life; do you regard your cells as dead at -80°C?

At least they are not growing and doing metabolism. I would say dead, resting fits probably better.


text:
Do I need to serially dilute E. coli cultures for optical density measures?
I am expected to track cell growth by measuring the incubating culture's cell concentration every 30 minutes or so. So my questions are: Why do I need to do serial dilution (assuming that I do)? Why can't I just fill up a cuvette with the cuvette's volume's worth of incubating culture and measure that against the blank every 30 minutes? And if I do need to dilute, how far should I dilute (1:100, 1:1000, etc)? This is for a culture filled with E. coli.

One is not normally required to serially dilute E. coli cultures for spectrophotometric measurements, at least in the experiments where the OD value is important.
For most protein expression work, the consensus is to start the induction at OD 0.6, and for most chemically competent cells, the optimal OD ranges from 0.3 to 0.8 depending on the competency protocol. At no point in time do you need to perform dilutions, as they are all within the linear range of cell count:OD ratio.
The only time you need to dilute the culture is when you want to find the OD of a very concentrated culture (for example after 24 hours of vigorously shaken incubation).

You should dilute (not necessarily serially dilute) if:

You are exceeding the concentration range detectable by the machine
Scattering starts overwhelming absorption (at high cell densities scattering will overwhelm absorbance). In such cases you can use a turbidimeter.

As such there is no issue of the law not holding true at certain limits of absorbance.
So a general thumb rule for dilution of cells is that the suspension should not look very turbid (You should be able to see your thumb from the other side of the test tube ;-) ).

Reading the optical density of a log phase microbial culture at a fixed wavelength approximates the Beer-Lambert law where A = ecl. This relationship is not linear as the Absorbance approaches 1.0 so at higher cell densities you will eventually underestimate the cell density of the culture. Likewise the law is not accurate below an Absorbance below ~ 0.05, so a 10-fold dilution should be fine.  Eventually the culture's growth will slow down.

It depends on your purpose, but you could seed cells into multiwell plate and let microplate reader monitor the growth. Some microplate readers can incubate cells at a temperature you set, shake the plate, and monitor OD.


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How is color information transmitted from the eye to the brain via the optic nerve?
I would presume that is has something to do with synapses and specific chemicals starting specific charges through the optical nerve's sub-components, and that this is somehow interpreted by the brain to configure an actual image; but in all honesty I have no idea.
The eye is obviously quite complex, and as I am not massively associated with all the terminology yet, I would be grateful for an answer in layman's terms.

Color vision in layman's terms:
The eyes contain a photosensitive layer much like a digital camera called the retina. In the center of this layer is a 3 mm-wide spot called the fovea that contains high densities of photosensitive cells, called the cones. Cones are photon hungry and operate only in bright light (photopic vision). They are called cones because of their conical shape. Rods are abundant in the periphery and mediate gray-scale night vision (scotopic vision).
The cones in the fovea are present in three types: red, green and blue cones - hence they convey color images much like digital pictures, namely as a bunch of pixels with a mixture of red, green and blue.
The cones in the retina are the first nerve cells (called neurons) in a long chain of neurons. The cones are hence called primary neurons. They connect to secondary neurons, namely the retinal ganglion cells (RGCs). These cells have long protrusions called axons. These axons bundle together to form the optic nerve. Each cone in the fovea connects to one RGC. The optic nerve extends from the retina to the brain. Information is sent through the optic nerve in the form of electrical pulses, just like a photosensitive chip operates in a camera. The information from the optic nerve eventually reaches the primary visual cortex in the brain, also referred to as V1 or striate cortex (Fig. 1).
In the visual cortex, there is a retinotopic map, meaning that a topographic representation exists in the brain that matches the retinal image. In other words, images are projected faithfully on the brain's surface as neuronal activity. The brain's job is to process these images further and generate conscious perceptions out of them; we see with the brain, not the eyes (a famous quote from Bach-y-Rita).

Fig. 1. The visual system. source: IEEE
References
- Kolb et al., Webvision. The Organization of the Retina and Visual System. Utah University
- Purves et al., Neuroscience 2nd ed. Sunderland (MA): Sinauer Associates; 2001


text:
Why do fingers swell during cold winters?
When exercising, tissue in the hands may swell. This may be caused by the muscles generating heat, which leads to blood being pushed to the vessels closest to the surface of your body to dissipate the heat. This response triggers perspiration and may contribute to hand swelling (Mayo Clinic).
This all makes sense. But why do fingers swell during the winter in freezing temperatures? It is referred to as chillbains and may affect the toes as well. See the following picture of chillbains affecting the fingers:

I'm voting to close because you asked the same question once and that has been put on hold, Please edit your original question so clarify, so that can be reopened. The original, practically identical question: http://biology.stackexchange.com/questions/31679/why-do-fingers-swell-during-winters

I have edited what else

Well, I've re-read your original post, and as @WYSIWYG said in the comments you already tagged blood circualtion and you also mention this in your post. It is most likely because of that. So you have most likely answered your own question in your post. Also I don't remember experiencin such phenomenon, although I've never watched closely. So this claim stands on personal / anecdotal evidence. If you could provide some reference, that this is indeed a common thing that would help. Also details on how exactly does the swelling happens would be a plus.

The reason for the swelling is the question @poka.nandor so providing that as detail would answer the question...

continue: if you could provide a more clear focus on what you're interested in more than "or what?".  Basically if we simply things enough most things in our body happen because of blood circulation....  your cells respireI'd suggest something like: "I suspect it is because of increased blood ciriculation. Can anyone confrim? If it is the case why is there increased blood flow and how does it cause swelling."

@AliceD well yes, I misphrased that part. i meant the conditions when the swelling occurs, like after how much time, touching anything cold, doing any exercises, or just in general standing in the cold, does it happen when gloves are put on or only when the OP is barehanded etc.

Question edited. @Bhavesh - if this question edit is not to your liking please feel free to roll back.

@NandorPoka it may be personal / anecdotal, but it definitely happens.  Come to Canada during January, and I'll show you.  ;)  I've observed that the degree to which it happens is directly related to the speed at which you heat up the fingers.  For instance, if you stay out in the cold  for a while and get them a bit wet, then come in and run warm water over them to heat them up, they'll almost definitely swell - frequently to the point of being painful.

From the website of Dermatology New Zealand I learned the following:
Chilblains are due to the constriction of blood vessels in cold conditions. Cold causes constriction of the small arteries and veins in the skin to reduce heat dissipation. This is normal and temporary in nature. However, rewarming after cold exposure may result in leakage of blood into the tissues and swelling of the skin. This can occur several hours after exposure to the cold in temperate humid climates. It can be aggravated by sun exposure.
Chilblains are less common in countries where the cold is more extreme because the air is drier and people have specially designed living conditions and clothing.
Chilblains are more likely to develop in people with poor peripheral circulation. Other contributing factors include genetic predisposition, diabetes, smoking and connective tissue disease such as lupus erythematosus.


text:
How can green algae be both multicellular and unicellular?
How can green algae be both multicellular and unicellular? What are the cases in which it can be both uni and multi cellular?

"Green algae "is a broad group. You should add details to your question. And why the "organic-chemistry" tag?

Because Algae are represented across four kingdoms, namely Bacteria (unicellular prokaryotes), Plantae (multicellular eukaryotes), Chromista (multicellular eukaryotes), and Protozoa (single-celled eukaryotes).
For example, I. Chlorophyta is unicellular:

I. Chlorophyta. Source: University of Wisconsin
While kelp can become huge and can form underwater forests:

Kelp. Source: Nature
Reference
Guiry, J Phycol 2012; 48, 1057–63

-1. The taxonomic classification (the four kingdoms mentioned) utilized here and the corresponding habituses are at best inaccurate or incomplete. Moreover the question was about green algae (Chlorophyta), I don't see how this answer addresses it.


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Extracting cell-free DNA
Has anybody had any success in extracting cell free DNA from plasma without using expensive kits? I've already spent a lot of my own blood trying to use standard phenol/chloroform methods with very minimal yield. I know it's possible that since I am not pregnant and don't have cancer (I hope) my blood may not have a large quantity of cell free DNA to begin with but I'm afraid to start using precious experimental samples until I'm confident I have a technique that will work.
For some background, cell free DNA is DNA that is circulating in the plasma (as opposed to the majority of DNA which is cellular). This has become an exciting new way to analyze fetal DNA from a mother's blood without doing a dangerous amniocentesis. There's also strong evidence that tumour DNA can also be found in some abundance this way (most studies seem to be with prostate cancer).
Qiagen has a kit for sale to extract this DNA but it is pretty expensive and I would still think that phenol/chloroform would give me a high (if less pure) yield. There is a paper in Cancer Biomarkers 2013 by Mazurek et al that claims that compares methods and shows a reasonable yield with this method but I haven't reproduced it. Has anybody here had success and if so what modifications did you use? Is it just time to move on to using samples that are more likely to have larger amounts of cell free DNA?

I know that if I inject plasmid DNA into a mouse tail vein with nothing to protect it, it's chopped up within 5 minutes. You sure the DNA is really naked DNA floating freely in the blood? There an awful lot of nucleases in there.

No, it is contained within microparticles or enveloped within a membrane as far as I understand but it is not cellular and can be found in plasma.

How about using a density gradient seperation to enrich your atarting material? Also, instead of precipitation, using silica microbeads to pull the dna after getting rid of the lipid membranes (in presence of appropriate nuclease inhibitor cocktail, of course!) might possibly increase your yield.

purpose of phenol/chlorophorm extraction, as I remember, is to precipitate/separate proteins, lipids and DNA. So if your dna is bound to proteins, you won't clear it

Maybe do a proteinase K digestion before your phenol chloroform extraction. That would destroy the nucleases. If you extract first, you'd probably have some nuclease carry over and damage your freshly unprotected DNA.

Is it worth comparing yields between serum and plasma ?

If you're worried about nucleases, try guanidinium thiocyanate with your extraction. I doubt that's your problem, though.

To note: I have no personal experience with this protocol. I am forwarding this paper, passed on to me by a colleague
There are many kits and methods available that don't rely on Qiagen. Or alternatively, if you ask them nicely, they do heavily discount their first kit you buy off them as a sort of trial (as they dont do samples).
However, to answer your primary question, are you adding a detergent and heat denaturing your samples first before phenol-chloroform (Triton/Heat/
Phenol)?

Blood samples for CFDNA
  analysis are collected into EDTA tubes and held at/or below RT
  (18 °C–22 °C) for no more than 2 h before separation of plasma.
  Plasma should be separated from whole blood samples by double
  centrifugation (800 g and 1600 g for 10 min, separately), avoiding
  leukocyte lysis. We prefer to isolate CFDNA immediately after plasma
  separation to minimize the effect of prolonged storage. Otherwise,
  samples should be aliquoted into small portions and stored at −70 °C
  before extraction because fragmentation of CFDNA might be caused by
  repeated freeze–thaw cycles
For the THP method, 500 μl of plasma/serum was mixed with 5 μl Triton X-100
  (Sigma-Aldrich, UK) and heat denatured at 98 °C for 5 min. Samples were placed on ice
  for 5 min, then extracted with an equal volume of phenol–chloroform–isoamyl alcohol
  (25:24:1, v:v:v) (Sigma-Aldrich, UK) and centrifuged for 10 min at 14,000 g. The
  aqueous phase was precipitated overnight with 1/10 volume of 3 M NaOAc and 2.5
  volume of 100% ethanol at −20 °C. The DNA pellet was washed with ethanol, air-dried
  and resuspended in 50 μl of ddH2O.
In the THP protocol, 98 °C incubation was used to inactivate
  PCR inhibitors and denature proteins in plasma/serum samples.
  Different times and temperatures were tested before choosing this.
  Since we had noticed substantial DNA contamination in SDS, Triton
  X-100 was used in the protein solubilization step. Direct conventional
  PCR was performed successfully on heat-denatured samples
  and able to detect 25 ng/ml DNA, indicating that this simple
  procedure offered sufficient protein digestion and inhibitor elimination
  for PCR analysis. The THP protocol gave a significantly
  higher yield of pure DNA solution for qPCR analysis than the
  QIAamp kit. The THP protocol showed high efficiency even with
  small DNA fragments as low as 100 bp.

You might want to read this:
Xue, Xiaoyan, et al. "Optimizing the yield and utility of circulating cell-free DNA from plasma and serum." Clinica Chimica Acta 404.2 (2009): 100-104.
A quick search of google scholar also revealed a few other papers you might be interested in:
Fleischhacker, Michael, et al. "Methods for isolation of cell-free plasma DNA strongly affect DNA yield." Clinica Chimica Acta 412.23 (2011): 2085-2088.
UPDATE:
After reading this (Fong, Siew Lee, et al. "Comparison of 7 methods for extracting cell-free DNA from serum samples of colorectal cancer patients." Clinical chemistry 55.3 (2009): 587-589.) which gives about 7 protocols (sadly without any references for some reason) I went hunting for  came up with this:

DNA was extracted from 1.0 ml plasma by phenol-chloroform method with slight modifications.
  One ml of plasma was treated with 1x SDS/Proteinase K solution (0.5 mg/ml) (1:1), incubated
  overnight at 56 °C followed by phenol-chloroform (4:1) treatment and centrifuged at 7 000 rpm.
  The upper layer was transferred into fresh 15 ml centrifuge tubes and the same step was repeated
  again; DNA was precipitated by adding glycogen (0.1 µg/µl), ammonium acetate (7.5 M) and
  absolute alcohol. DNA pellet was obtained by centrifuging at 7 000 rpm; was washed with 70%
  alcohol at 10 000 rpm, dried and finally dissolved in TE buffer at 56 °C and stored at -20 °C until
  further use.

You can read about the above method here: Singh, Deepika Misra1 Renu, and Monisha Banerjee. "A simple and reliable method of obtaining fetal DNA from maternal circulation; its accuracy and sensitivity."
Also, if its available to you, it might be worth it:
Gahan, Peter B., ed. Circulating Nucleic Acids in Early Diagnosis, Prognosis and Treatment Monitoring: An Introduction. Vol. 5. Springer, 2014.

Thanks for this! I have used essentially that second method except precipitated DNA with KCl instead of ammonium acetate... can't imagine that makes much of a difference. I also used SDS/Proteinase K but at a lower temperature. Because of my workflow I am unable to extract the DNA right away so I store the plasma at -80. I think the big thing though is that all of these papers use plasma that they expect will have cfDNA in it whereas I'm using control plasma so that may have the biggest impact on my yield I'm starting to suspect.

What temp is your proteinase K reaction? I've only ever seen it at 50 - 60 C.


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Do plants with non-green leaves have chlorophyll and photosynthesis?
Is it even possible that plants with non-green leaves have chlorophyll, and do such non-green leaved plants carry out photosynthesis?

Yes, it is possible, but not necessarily the case.
Non-green leaves with chlorophyl: There are leaves that don't appear green, but do have chlorophyl and therefore can conduct photosynthesis. (See, for instance, refraction effects in white caladiums or the link in the answer by Resonating).
Non-green leaves without chlorophyl: There are leaves that don't appear green because they have no chlorophyl, and so do not conduct photosynthesis. (See, for instance, parasitic plants like the Oronbanche linked by Cactuswoman or this Monotropa)

They do have chlorophyll, at least in general. There are a couple very rare exceptions, but if it can stand up on its own, it contains chlorophyll. The green is just washed out by a very bright red pigment.

All photosynthesis reaction does need chlorophyll,even in cyanobacteria and algae the difference is the type of chlorophyll ( which depends on available wavelength of light and energy efficiency ) fully parasite plants on the other hand doesn't contain chlorophyll and this force them to live as parasites ( keep in mind that we do have half parasitic plants too,which their problem is lack of roots,they do photosynthesis just like other plants ) plants with non-green leafs does contain chlorophyll in some cases even more than green plants ( in my own experience berberis which is a red to alizarin crimson violet shade has more chlorophyll than a greek lettuce) the other pigments are working as helping energy harvesters in photosynthetic reactions, light/shade controllers or simply a survival strategic materials in answer to climate changes,habitat problems and environmental stresses

Parasitic plants such as Orobanche lack chlorophyll and cannot photosynthesize. They obtain all of their energy from paratising another organism.