Is inbreeding really efficient at producing homozygosity?

And the same is repeated , production of F2 offsprings with 50% possibility of heterozygous individuals.

That's not correct.

Let's start with a population with 100% of heterozygotes:

100% Aa

And, just to create a highly exaggerated model, let's suppose that these individuals perform the most drastic case of inbreeding: self-fertilization. Inbreed occurs when an individual perform sexual reproduction with a closely related organism, and no one is more closely related to someone than himself!

After the first "inbreeding" generation, we'll have:

25% AA
50% Aa
25% aa

So, 50% of heterozygotes.

If this population inbreeds again, we'll have at the second generation:

37.5% AA
25% Aa
37.5% aa

So, 75% of homozygotes versus 25% of heterozygotes.

In the third generation:

43.75% AA
12.5% Aa
43.5% aa

And in the fourth generation:

46.875% AA
6.25% Aa
46.875% aa

Thus, in only 4 generations, we have 93.75% of homozygotes versus 6.25% of heterozygotes. Mathematically, the heterozygotes never disappear. Biologically, however, if a population shows self-fertilization, heterozygotes disappear in few generations.

Now, let's get out of this overly exaggerated example with self-fertilization and back to your question, where the organisms perform cross-fertilization:

The problem with your reasoning is that (correct me if I'm wrong) you're starting with a couple (Aa) and supposing that all their descendants will mate randomly. Of course, the allele frequencies will remain the same. But that's not inbreeding. By definition, inbreed is a non-random mating system. For a real inbreed to occur, the mating individuals should be more closely related than
those drawn by chance from the population.

In conclusion, given enough time, inbreeding (and genetic drift as well) has the effect of eradicating heterozygotes from the population.


Is Hydrogen gas present in biogas, and does it spontaneously ignite?

The constitution of the biogas depends greatly on its source and the fermenting microbe. But in general, it does contain hydrogen about 0-1%. Even if it did contain large amounts, the mixture would be inflammable, but it would not burst into flames without any external igniter, which could be any small fluctuation of heat if the mixture is too unstable. But in general, an inflammable gas doesn't start burning on its own.


Is lysergic acid diethylamide (LSD) metabolized in the body?

Short answer
LSD appears to be enzymatically broken down in the liver.

Background
First off, hormones do not break down anything; enzymes are the work horses that mediate metabolism.

According to a review paper (Passie et al., 2008), humans metabolize LSD into structurally similar metabolites (Fig. 1) by NADH-dependent microsomal liver enzymes to the inactive 2-oxy-LSD and 2-oxo-3-hydroxy LSD. LAE is formed through enzymatic N-dealkylation of the diethylamide
radical at side chain position 8. Di-hydroxy-LSD and nor-LSD are also metabolites, as well as 2-oxo-LSD, 13- and 14-hydroxy-LSD as glucoronides, lysergic acid ethyl-2-hydroxyethylamide (LEO), and trioxylated LSD.

Note that the monoamine oxidase (MAO) system is unlikely to break down LSD. MAO are enzymes that catalyze the oxidation of monoamines. Monoamine neurotransmitters contain one amino group that is connected to an aromatic ring by a two-carbon chain (such as -CH2-CH2-). This structure is not present in LSD (fig. 1). A cursory Google Scholar search did not yield any relevant hits ('LSD' + 'monoamine oxidase'), loosely indicating that MAO is unlikely to be involved in LSD metabolism. However, as I suspect some self-help here - I am unsure about MAOI and LSD interactions, and I highly discourage any toying around with MAO inhibitors and any drug in general. For example, 5-HT is a typical example of an MAO substrate and LSD impinges on 5-HT2A receptors. Hence, interactions in pharmacodynamics with combined LSD and MAOI intake are likely to occur.

Fig. 1. LSD metabolites. source: Passie et al. (2008)

Reference
- Passie et al., CNS Neuroscience & Therapeutics (2008); 14: 295–314


How do I identify the different stages of meiosis under microscope?

ID characteristics that can help you recognize diplotene  better:

diplotene :
the only difference between this phase and Diakinesis is that The centrosomes reach the poles.

you can see the photos of diplotene and diakinesis here :

http://www1.biologie.uni-hamburg.de/b-online/e09/meiosea.htm

(a) polyploid nutri-tive cells with many heteropicnotic chromatin bodies; (b) leptotene-zygotene; (c) pachytene; (d) diffuse stage; (e) di-plotene; (f) diakinesis; (g) metaphase I; (h, i) anaphase I; (j) telophase I;. (k) metaphase II; (l) anaphase II; (m) telophase II; (n) round spermatids; (o) elongating spermatids; (p) head of sper-matozoas. Big arrows indicate sex chromosomes, small arrows point to nucleoli and arrowheads indicate m-chromosomes

You can see all the phases clear and perfectly separated here :

http://biology.about.com/od/meiosis/ss/meiosisstep.htm#step1

by the way , try to adjust microscope as best as you can & don't put much  oil immersion .


Evolutionary advantages of wet nose of cats and dogs?

Why did it evolve ?

  Mammals with rhinaria tend to have more acute olfaction, and the loss of the rhinarium in the haplorrhine primates is related to their decreased reliance on olfaction, being associated with other derived characteristics such as a reduced number of turbinates.

  The rhinarium is very useful to animals with good sense of smell because it acts as a wind direction detector. The cold receptors in the skin respond to the place where evaporation is the highest. Thus the detection of a particular smell is associated with the direction it came from.
  The rhinarium is adapted for different purposes in different mammals according to ecological niche.

  In aquatic mammals, development of lobes next to the nostrils allow them to be closed for diving. In mammals that root, the rhinarium often develops into a hard pad, with the nostrils off to the side. In the elephants it has become a tactile organ. In the walrus, it is covered with stiff bristles to protect it during foraging for shellfish. In many animals the form and purpose of the rhinarium remains to be elucidated.

Essentially it is the case of having a better sense of smell provided by the extended surface area, which has evolved to fit whatever the organism in question needs. I'll update this when I find this in a few more papers.

I took this from the wiki:
http://en.wikipedia.org/wiki/Rhinarium

How does it work ?

  A model of the canine nasal airway, developed from a 3-D
  reconstruction of high-resolution magnetic resonance imaging (MRI)
  scans, was used to study the aerodynamics of canine olfaction.
  Simulation results reveal that a unique olfactory airflow pattern
  exists within the canine nasal cavity during sniffing that is critical
  for efficient olfaction.

  Calculations show that this novel olfactory airflow pattern provides a
  crucial residence time for odorant absorption in the sensory region
  and promotes spatiotemporal fractionation of odorant mixtures along
  the olfactory epithelium.

  The canine nose functions similar to a chromatograph that imposes
  odorant-specific deposition patterns upon the thin mucus layer
  covering the nasal cavity....The results show that deposition patterns
  are primarily influenced by the intricate olfactory flowfield and the
  odorant solubility in the mucus layer.

  Highly-soluble odorants are quickly absorbed near the entrance to the
  olfactory region, and thus do not reach the periphery with significant
  concentrations. In contrast, insoluble odorants are deposited more
  evenly and may even exit the olfactory region without being completely
  absorbed. Predicted odorant deposition patterns correspond with the
  anatomical organization of olfactory receptors known to occur in
  keen-scented (macrosmatic) mammals, providing a mechanism that helps
  explain the excellent olfactory acuity of the dog.

In short the mucus on a dog's nose 'pre-sorts' smells by trapping the passage of some odour particles more than others along the nose, with different types of molecules being picked up at different "depths" in the nasal cavity.

You can read about it here:

Craven, Brent, Gary Settles, and Eric Paterson. "The Aerodynamics and Transport Phenomena of Canine Olfaction." APS Division of Fluid Dynamics Meeting Abstracts. Vol. 1. 2008.

Lawson, Michael, et al. "Odorant Transport and Deposition in the Canine Nasal Airways." APS Division of Fluid Dynamics Meeting Abstracts. Vol. 1. 2009.

Craven, Brent A. A fundamental study of the anatomy, aerodynamics, and transport phenomena of canine olfaction. ProQuest, 2008.


What is this 2-3cm insect found in Slovakia?

You have with you a Carpenter bee, which are species of the genus Xylocopa  of the subfamily Xylocopinae

Xylocopa violacea, the violet carpenter bee, is the common European species of carpenter bee, and one of the largest bees in Europe. It is also native to Asia.

Here is a link to a youtube video documentary about the bees.


How Much Longer For The Gene For Blue Eyes?

Never.

Even if the country arrives at the unlikely day when there is no one alive in the United States with the blue eye phenotype, there are still plenty of people with the unexpressed recessive gene, and if two of them get together, those genes can combine to produce another blue-eyed child. If this happens twice, with one boy and one girl, and they happen to meet when they are in college and say "Hey cool, you have the same inexplicably rare kind of eyes as me. I think I want to marry you." then any children they have will also be blue eyed.

So even if the day came when you couldn't find a soul in the world with blue eyes, you will still never know if you've seen the end of them.


Scale up of Bacterial growth from 250mL to 1-5L?

Michaelis-Menten:

$V=V_{max}.\frac{[S]}{Ks+[S]}$

Lineweaver-Burk:

$\frac{1}{V}=\frac{Ks}{V_{max}[S]}+\frac{1}{V_{max}}$

Plot $\frac{1}{V}$ vs $\frac{1}{[S]}$; find the slope and intercept of this plot.

Depending on what you consider as primary substrate (glucose??) measure the concentrations using appropriate assays. Glucose sensors (based on glucose oxidase) are available or you can do conventional biochemical assays (DNSA) for glucose and other reducing sugars. To find the growth rate, measure OD at different time-points and get the differences of OD in a time interval. A better method would be to make a scatter-plot of OD and time and fit a polynomial function. Get rate by taking the tangent of the curve at that time-point.


Are there cases when genus name is equal to the name of a higher taxon?

I answer for botany: no.

The International Code of Nomenclature for algae, fungi, and plants has strict requirements on names:

Article 16.1 has:

  The name of a taxon above the rank of family is treated as a noun in the plural and is written with an initial capital letter. (...)

Article 18.1 has:

  The name of a family is a plural adjective used as a noun; it is formed from the genitive singular of a name of an included genus by replacing the genitive singular inflection (Latin -ae, -i, -us, -is; transcribed Greek -ou, -os, -es, -as, or -ous, and its equivalent -eos) with the termination -aceae (but see Art. 18.5)

And article 20.1 has instead:

  The name of a genus is a noun in the nominative singular, or a word treated as such, and is written with an initial capital letter.

On later article it is explained how to latinize names, with simpler rules (compared to Latin).  So genus are singular and higher rank are plural.

Additionally, for botanical nomenclature, an name for ranks between family and phylum rank is made usually by concatenating a genus name with some suffixes (which are rank specific, see article 16.3, 18.1). So reading a name, one could derive also the rank.  Just few families still have a old name, but still ending with 'ae' (e.g. Compositae, Cruciferae, etc., Art 18.5).  Now (just since 2011-2012 version) there are more exceptions in code, but for historical reasons and for names outside plants in stricter term.

Note: Some old names are automatically corrected with new rules (see e.g. 18.4), so we should have not equal names.


DIY storing family DNAs' samples for future uses (eg medical)

If you have access to a laboratory (or at the very least a centrifuge and pipettes) and some laboratory experience you can extract the DNA from the cells which would be much easier to store. There are a number of commercial DNA extraction kits available that are easy to find on google and order online. I don't want to promote any particular brand but I've mostly used DNEasy made by Qiagen (really just because that's what I'm used to). All the step-by-step instructions are in the kit and all the reagents are also in the kit with the exception of 100% ethanol which should be easy to obtain.

If you have significant molecular biology experience and access to a full lab with a fumehood and appropriate safety installations you can try a manual extraction using trizol or phenol-chloroform. This would be slightly cheaper however given the toxicity of these agents I wouldn't recommend this for you. It really doesn't sound like you have these resources available to you.

Once you have the DNA extracted you can dilute it in Tris-EDTA or the elution buffer that comes in the kit. You can store extracted DNA in a regular fridge (4C) for several years. If you're looking to store for decades you may want to rent space in a -80C freezer but this would be more expensive. A fridge may be just right to suit your needs. You should be careful that this fridge has a backup power supply.

I should be clear that although extracting DNA is the easiest way to do this for somebody with experience, you should not try if you don't know what you're doing. Some of these reagents are dangerous and you are likely to ruin the samples you've taken from your family members and end up with no DNA at all. Good luck!


Basic biology: saliva in digestion is used to digest starches and fats.  It also lubricates food so that it is easier to move down the esophagus.  It is the first response your body has to food entering your digestive system and occurs in advance of food arrival. Pavlov's dog is a demonstration of this.

Rapid salivation occurs most often in two cases.  The easy example is seeing or smelling something like cake or pie, though this applies to any highly desirable food to the individual.  The case we think less of is that of starvation or even deep hunger.  In this case, even "everyday foods" cause rapid salivation as the body needs any calories it can get.


What's the worst that can happen from eating too many spicy peppers? Can you die?

The more "dangerous" properties of spicy peppers are chiefly due to capsaicin.
Sigma-Aldrich sells purified capsaicin, for which they provide safety information, including an MSDS. Most of it is the usual, unsurprising set of warnings about irritation to eyes and the respiratory system. However, there are LD50 numbers:

LD50 Oral - rat - male - 161.2 mg/kg
LD50 Oral - rat - female - 148.1 mg/kg
LD50 Dermal - mouse - >512 mg/kg

From this, we can conclude that one would have to eat quite a bit of capsaicin to die. If lethality in humans is exactly the same as rat (which it probably isn't),  a 70 kg human would need to consume about 11 g of capsaicin to reach similar levels of lethality.
The Carolina Reaper, one of the hottest known peppers, averages about 1.6 million on the Scoville scale. Capsaicin amount is related to Scoville heat units, so we can make an imprecise conversion from one to the other.
Using values given in 2 publications (Nwokem 2010 and Al Othman 2011) we can observe the following trend:

So on average, about $6.25 \cdot 10^{-5}$ mg/g capsaicin per SHU. With this, we get $(1.6 \cdot 10^5) \cdot (6.25 \cdot 10^{-5}) = 10$ mg/g, or 1% capsaicin for dry Carolina Reapers. To eat the equivalent of 11 g of capsaicin in peppers, you would have to eat 1.1 kg of dry peppers - which should be a couple of dozen.
So, I think we can conclude that it is relatively "feasible" to consume a dangerously large amount of capsaicin by eating very spicy peppers. However, there are numerous caveats with my reasoning:

Human LD50 and rat LD50 are not necessarily the same.
Toxicity is not necessarily linearly related to body weight.
Peppers have compounds besides capsaicin that contribute to hotness.
It would be very difficult to eat such a large amount of spicy peppers, and various involuntary reflexes would interfere. Even if one were force fed the peppers, I imagine the body would attempt to vomit it up - which brings up the question of how the toxicologists even managed to feed several milligrams of capsaicin to rats to measure the LD50.


Giving a sign to Pressure Potential, Osmotic Potential And Other Similar Quantities

I think you already know the sign convention in calculating the water potential: the addition of solutes lowers the potential (negative vector), while an increase in pressure increases the potential (positive vector).(Another way of saying the same would be more solute = more negative.) {1} This is the same everywhere.

Pressure potential: The pressure potential in a plant cell is usually positive. In plasmolysed cells, pressure potential is almost zero. Negative pressure potentials occur when water is pulled through an open system such as a plant xylem vessel.{1} This means that it is negative during a "suction" action, otherwise, it is positive.

Osmotic potential (solute potential): The relationship of solute concentration (in molarity) to solute potential is given by the Van't Hoff equation:
Ψπ=−MiRTΨπ=−MiRT

(The formula, note, has a -ve sign.)
For example, when a solute is dissolved in water, water molecules are less likely to diffuse away via osmosis than when there is no solute. A solution will have a lower and hence more negative water potential than that of pure water. Furthermore, the more solute molecules present, the more negative the solute potential is.

Turgor pressure and wall pressure: I recommend reading this for a clearer understanding.

...This actual pressure which develops within such a cell is called turgor
pressure. This term can be applied with equal appropriateness to the actual
pressures developing in purely physical osmotic systems such, for example, as a
sucrose solution enclosed within a collodion or cellophane membrane and immersed
in water. As will become clear in the following discussion, TPs in osmotic systems
can sometimes be negative in value.

When the TP
is negative, that is, when the cell sap is under tension (see later), the WP is
likewise negative, the wall being subjected to a centripetal pull because of its
adhesion to the protoplasmic layer and cell sap mass within the cell.

On the basis of fundamental physical principles it is generally considered
that the WP and TP of a cell are equal in magnitude and oppositely directed.
This situation is not difficult to visualize for a cell in an equilibrium condition.
For dynamic states in which water is being gained or lost by a cell, however,
the validity of this assumption has been questioned.

{1}-https://en.wikipedia.org/wiki/Water_potential


What is the core mechanism behind neuroplasticity?

This is a good first source which suggests further references:

http://www.scholarpedia.org/article/Balance_of_excitation_and_inhibition


The Ecological Data Wiki search for Woody Plants is a good start for some nice datasets. There is also the USDA Plants Database which has information for every plant in the U.S. Woody species are well represented with lots of species specific info. These can be downloaded handily with an R package.

Looking for occurrences? Put the species name into GBIF to get historical records of where and when a species was found. This has an R package as well.

Want distribution maps for all trees in North America? Someone has done that for you here.

Phenology? The National Phenology Network.

Edibility? I've never come across a specific data source for this. But the best reference I've used is the Handbook of Edible and Poisonous Plants of Western North America. It's an amazing book with years of research put into it. It does not have any pictures nor a key to identify plants, but it does have information on pretty much every plant in the Western U.S. at least at the genus level.


How are sequential patterns grouped into meaningful objects in the brain?

The key here is the Gestalt principle formulated in the early 1900's consists of a set of 'laws' describing how perception elements are grouped into recognized objects. The Gestalt laws "prescribe for us what we are to recognize 'as one thing'". Recent data support this view (Pelli et al., 2009).

On a more fundamental level working memory is essential in this process. It is a form of short term memory. An example where short-term memory comes into play is when information is cut up in pieces, like in your example - 'Chunking' is the organization of material into shorter meaningful groups to make them more manageable.

Short-term memory is supported by transient patterns of neuronal communication in the regions of the frontal, prefrontal and parietal lobes of the brain. Long-term memories are maintained by more stable and permanent changes in neural connections widely spread throughout the brain.

The hippocampus temporarily stores information and gates it to the long-term memory. Typically, information is transferred from the short-term working memory to the long-term memory within just a few seconds,

Reference
- Pelli et al., Cogn Neuropsychol (2009); 26(1): 36-49


Were early human beings (about 100 - 200 K years ago) far more promiscuous than we are now?

My hypothesis is "Yes", that is "Early human beings are far more
  promiscuous than we are now". So how i came up this? Cos Human came
  from Chimpanzee right?

No.

  Also, when human evolved, they started to realized that
  promiscuousness wss not healthy & not good for society

I'm sorry, what ancient society are you claiming cracked down on male promiscuity?


Can I compare Shannon indices of metagenome gene data?

I'm not an expert on Shannon-Weaver Index, but according to wikipedia it is the same as exponentially transformed Renyi entropy. If it is the case, you can compare them since they are scale invariant summary statistics. If you want error bars, you can always try resampling methods such as bootstrapping. Hypothesis testing can also be done with bootstrapping, although the power of the statistical test may not be very strong and fail to reject the null.


What does the term 'bioavailability' mean?

Bioavailability is a concept which applies to nutrients and drugs which pass through first-pass metabolism, i.e. orally (and to some extent nasally) consumed substances. Anything absorbed in the gut first passes through the liver before reaching the rest of the circulation, and both the gut and liver may metabolise it to some extent. The liver in specific has the powerful Cytochrome P450 system, a huge variety of enzymes to break down all sorts of substances, although in some cases it can actually produce more active or even toxic forms instead of breaking them down.

This can lead to drastic reductions in the amount available in the systemic circulation after oral administration. E.g. propanolol (a beta blocker) needs to be given in 100mg doses orally while intravenously (avoiding first-pass metabolism) only 5mg are needed.


What is the limit of time resolution in fMRI?

The quick and dirty answer is: fMRI doesn't perform well in the temporal domain, but excels in the spatial domain among non-invasive imaging methods. If you need an answer as to where the action is, use fMRI. If you need answers to temporal questions, I recommend using electrophysiology such as EEG, which excels in the temporal domain, or MEG for a combination of good temporal and spatial resolution.

As to what the limit exactly is, I would say a few seconds. fMRI measures blood oxygentaion responses, (See the answer on the question: "What does fMRI measure exactly"), which are inherently slow. Neural processes in local neural networks occur in milliseconds, in larger networks in the order of hundreds of milliseconds. Blood flow differences, in contrast, occur in the order of seconds.


Did baby bird hair and mammalian hair convergently evolve?

Bird "baby hair" are modified feathers.  (Or perhaps feathers are modified "baby hair".  The ancestral state for feathers was probably closer to the chick's down in appearance, but I don't know whether chick down is unmodified original feather or whether it was feathers and then modified again.)

In any case, mammalian hair and dinosaur feathers (which includes bird feathers) are separately evolved from the same base structure, modified reptilian scales. They are therefore homologous, but evolved independently.

  These results reveal a new evolutionary scenario where hairs, feathers, and scales of extant species are homologous structures inherited, with modification, from their shared reptilian ancestor’s skin appendages already characterized by an anatomical placode and associated signaling molecules.

--The anatomical placode in reptile scale morphogenesis indicates shared ancestry among skin appendages in amniotes


It is the paradise tree snake (Chrysopelea paradisi). It is a colubrid snake and is common in south-east asia. See this site for a better image.


Interestingly it does seem as if this is at least in part the case.

Testosterone levels are tied to sexual impulses, but also risky behavior and aggression.  Its responsible for sexual drive in women as well.  Low testosterone can cause depression and loss of the ability to make decisions.

You'll note that the work cited is done on criminals, patients and rats.  Remember that is not medically or scientifically ethical to change the androgen levels of a functioning human being.  Testosterone supplements might increase the chances of prostate cancer.

While its not scientific, there's a fascinating set of interviews about how testosterone affects human thinking at this transcript of American life, Act 2 :

  After testosterone, there was no narrative. There was no language
  whatsoever. It was just, I would see a woman who was attractive or not
  attractive. She might have an attractive quality, nice ankles or
  something, and the rest of her would be fairly unappealing to me.

  But that was enough to basically just flood my mind with aggressive,
  pornographic images, just one after another. It was like being in a
  pornographic movie house in my mind. And I couldn't turn it off. I
  could not turn it off. Everything I looked at, everything I touched,
  turned to sex.


Plant anatomy, what are these stem like filaments growing under the flower

These are "floral spurs" – they usually contain nectar, and are part of the variety of complex flower shapes that orchids and other flowers, like columbines, have co-evolved with their pollinators.

Essentially, in order for the pollinator to reach the nectar down in the base of the spur, it must move into a position where pollen is deposited onto it; then when it moves to another flower, it can transfer that pollen and the plant is able to reproduce.

Of course, long tongues are good at getting nectar from long-spurred flowers, so there is both species filtering for long-tongued species, and presumably also selective pressure within a species for long-tongued individuals. This, in turn, drives selective pressure on the spurs.

Spurs are a classic example of a "key innovation": they have evolved separately in different types of flowers, and when they evolve, they often lead to rapid speciation (because a small change in spur architecture can constitute a barrier to reproduction). (See, for example, publications of Scott Hodges)


Why pouring salt in the wounds is painful?

De salt particles are alien bodies and can damage the tissue by mechanical means (This would also happen if you pour sand into an open wound). Also, the exposed tissue is vulnerable to dehydration, wich happens faster if the osmotic pressure is higher. Finally, nerve tissue is particulary sensible to changes in the ion composition of its sorroundings, so the added sodium may affect the action potential of the nociceptors.


Why do kefir grains stop growing in soy milk?

Yes, they are behaving differently because of the lack of nutrients, including lactose, and possibly because of the presence of other chemicals in soy milk that aren't in dairy.

Kefir grains are a complex community of different types of lactic acid bacteria and yeasts which metabolize (eat) various nutrients/chemicals in their environment. Because soy milk is a chemically different environment than dairy milk, these communities function in different ways. Over repeated propagations in soy milk, you probably have cultivated a very different community in regards to species diversity and the chemical products.

As Liu and Lin describe here
, the kefir community members in dairy milk are eating mainly lactose, whereas in soymilk they are eating sucrose, raffinose and stachyose. As a result, the reproduction of the bacteria and the yeasts differs, as did the alcohol and lactic-acid contents of the end-product.

Because your question is a practical one, you might be interested to know that in that paper, the authors found that adding 1% sucrose (table sugar) or 1% glucose to the soymilk produced an end-product that more closely mimicked that of dairy milk. You could give that a try and see if it improves your kefir growth.

 Liu JR, Lin CW. 2000. Production of kefir from soymilk with or without added glucose, lactose, or sucrose. Journal of Food Science 65: 716–719.


Why does the face turn pale in dangerous situations?

Red blood cells are not equipped with a motor system to propel them through the blood stream. Instead, they are passively transported through the vasculature by the the pumping action of the heart. The effects of dangerous situations on the skin have to do with hormonal effects on the blood vasculature, and not with direct effects on red blood cells.

Dangerous situations trigger the fight-fright-flight response, and is a direct result of adrenaline being released into the bloodstream. Adrenaline prepares the body to fight for its life.

Adrenaline has a variety of effects including enhancing perspiration (or diaphoresis, which prepares the body for the increase in temperature associated with fleeing/fighting), dilation of the pupils (which increases light sensitivity, but reduces acuity), dry mouth (gastric juices and saliva production decreases because blood flow to the digestive system is decreased), enhanced smell and hearing, and a cool, pale skin.

The cool and pale skin is caused by a reduced blood flow to the surface of the body, while blood flow to the arms, legs, shoulders, brain, eyes, ears and nose can be increased. Besides getting ready to run and fight, the body is preparing to think quickly and be aware of threats by hearing, seeing and smelling things better. Pulling blood away from the skin also helps decrease bleeding from cuts and scrapes (Source: Army, Navy & Air Force Australia).

Adrenaline stimulates alpha-adrenoreceptors in blood vessels, which causes the smooth muscles around the vessels to constrict (Bolli et al., 1984)

Adrenaline (epinephrine) released from the bloodstream dilates vessels in the skeletal muscle via beta-receptors, and constricts them in the digestive system and the skin through alpha-adrenergic receptors. Source: Marian University College, Indiana.

Reference
- Bolli et al., J Hypertens (1984); 2(3): S115-8


If both of the ORFs that the web tool predicted start with an AUG initiation codon, then the textbook answer is that the 5' cap on eukaryotic mRNAs is the first feature that is recognized by the translational apparatus, and the ribosome scans along until it finds the first AUG (it is a simplified description). However, if there are several AUGs near each other then the one that matches the best to the Kozak PWM (position weight matrix) will be preferred. The Kozak sequence can be approximated by: CCATGG which is also recognized by the restriction enzyme NcoI. Highly expressed genes tend to match most closely to the Kozak consensus.


What makes drosophila eyes red? and is it stable?

There's been a fair amount of work on this subject but a lot of it is old - see for example this 1945 paper and this 1948 paper.  That latter one in particular goes into some good stuff: color in the wildtype is due to red and brown pigments, which the authors separated by using acidic ethanol (after grinding up the flies).  Here's a 1961 paper from JSTOR that goes into a bit more detail on some of the red pigments (drosopterin, and isodrosopterin, and neodrosopterin) and looks like a good reference for some other, more basic work on Dmel eye pigmentation.  More to the point, here's a 2013 minireview on the chemical synthesis of drosopterins, which is useful mainly for referencing a lot of other work, in particular this overly detailed chapter from 1970.  That last one has tons of info about some of these pigment-causing proteins in insects.

The only particular reference to stability I could find was from that chapter, on page 144:

  The simple pterines (group 2) are chemically stable under normal physiological conditions, while the substituted (groups I and 3) and conjugated pterines are unstable. Light catalysed oxydation of the polyhydroxy side chain at C-6 is a normal phenomenon. The hydrogenated pterines are extremely unstable, especially at pH 7. Tetrahydrobiopterin, for instance, is oxidized within seconds in the light, but more slowly in the dark. [sic]


According to Wikipedia Electric shock, the Magnitude of electric shock to a body is mainly due to current as well as voltage. Various factor of the environment will also play a major role in damaging the body while under contact. The following quote explains it:

  The minimum current a human can feel depends on the current type (AC or DC) and frequency. A person can feel at least 1 mA (rms) of AC at 60 Hz, while at least 5 mA for DC. At around 10 milliamperes, AC current passing through the arm of a 68 kg (150 lb) human can cause powerful muscle contractions; the victim is unable to voluntarily control muscles and cannot release an electrified object. This is known as the "let go threshold" and is a criterion for shock hazard in electrical regulations. The current may, if it is high enough, cause tissue damage or fibrillation which leads to cardiac arrest; more than 30 mA of AC (rms, 60 Hz) or 300 – 500 mA of DC can cause fibrillation.

To give a clear picture of how various current threshold will affect human body see the image below. (Complete data is available here "Electrical Safety").

Even High Voltage also can be fatal to human body which is enough to cause damage.

  High voltage electrical energy greatly reduces the body's resistance by quickly breaking down human skin. Once the skin is punctured, the lowered resistance results in massive current flow. Ohm's law is used to demonstrate the action.
  At 1,000 volts, Current = Volts/Ohms = 1,000/500 = 2 Amps, which can cause cardiac arrest and serious damage to internal organs.

Now what is the length of time that body is under electrical contact. This length of time exposure is also critical.

  When muscular contraction caused by stimulation does not allow the victim to free himself from the circuit, even relatively low voltages can be extremely dangerous, because the degree of injury increases with the length of time the body is in the circuit. LOW VOLTAGE DOES NOT IMPLY LOW HAZARD!
  100mA for 3 seconds = 900mA for .03 seconds
  in causing fibrillation

(Complete detail is available How Electrical Current Affects the Human Body)


I did a little research and I think it works like that:

Collect a dataset of $n$ observations.
Fit a parametric model to your data. If you want to model the recaptures, I would suggest a Poisson-GLM. You can also estimate the parameter directly from your data and simply parametrize a Poisson distribution. However, this approach would not model the random variation in your data.
Use the fitted model to draw a sample of size $n$
Calculate your desired metric based on the sample. I guess in your case this would be human population size (calculated as ${N} = \frac{nM}{m}$?)
Repeat steps 3 and 4 many times (1000+)
There you go! Now you can easily assess the variability in population size based on the estimates from your bootstrap samples.


How did the nucleus of eukaryotic cells evolve?

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

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

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


How to identify genes required for biofilm formation

You could do different things: First you could, as you say yourself, sequence the complete genomes of the strains from a biofilm and compare these with some, which do not form biofilms. This may give you an idea which genes are involved when they are present in the "biofilm genome" but not in the other. The proof would be to disrupt these genes either by removing or mutating them or by gene silencing techniques and see what the outcome is.

It is also possible that only a mutation in a gene which exists in the sample and the control genome makes the difference. Then site-directed mutagenesis would help to identify the important genes.

The second possibility is that there is no real difference in the sample and the control genome and the difference for developing a biofilm "simply" lies in the difference of gene expression. Then the isolation of RNA (either total or mRNA only) would help to find involved genes. If the environment makes the difference for the development of a biofilm, then the biofilm and the control cells should have show no (or almost no) difference in their gene expression profiles when they are cultivated under identical conditions. You then need to test the gene expression for different environmental conditions (including those that favor the development of biofilms) to find genes which are involved.

This comparison of the different conditions will then deliver genes which are uniquely or more highly expressed in the biofilm group, a lot of genes which are comparable in expression to the control sample, and some genes which have a lower expression than the control. It is now worth looking at the higher (or unique) and lower expressed genes, find out their function and then start mutating them to check their function for the formation of a biofilm.

Additionally there is the chance that the gene(s) which is necessary for the biofilm formation is located on an extra-chromosomal plasmid. I would also check the plasmids present in the biofilm and the control sample, sequence them (if present) and see which genes they express. The function for the biofilm formation can easily be tested with a simple transformation.


While in motion, why do closer objects appear to move faster?

Why do closer things seem to be moving faster?

This is due to parallax. A very simple phenomenon exhaustively explained on wikipedia.

  Why do faster moving things appear unclear?

This is primarily due to retinal persistence also well detailed on wikipedia.

It takes time for the retina to detect a change in light at a given position on the retina. Things that move quickly across your visual field (i.e. retina), or that reflect very low amounts of light tend to blur or simply be invisible. Car headlights moving close to you will blur because it takes time for photoreceptors to 'switch off' and the headlights would appear as a streak or trail of light for you. And similarly, if a car were to move at an incredibly large speed, the car wouldn't reflect enough light to trigger a response in the retina, so it would be unseen by you. Remember that what matters here is how much range of your visual field an object crosses, not the speed of the object itself. For example, a fast car in the distance does not blur since it's crossing a tiny fraction of your visual field, but a slow car right in front of your nose will be crossing your entire visual space very quickly.

These are properties of the retina. It is also possible the encoding of visual information in the brain also plays a role in how your perceive something. However, the illusion you describe is entirely explained by these retinal phenomena due to sensory neuron biology.


How does sunlight affect the longevity of SARS-CoV-2 on surface?

I have no data on SARS-CoV-2 specifically, but for SARS-CoV UV radiation is an effective method of eliminating viral infectivity:

Irradiation of UV for 60 min on the virus in culture medium resulted in the destruction of viral infectivity at an undetectable level.
CONCLUSION: The survival ability of SARS coronavirus in human specimens and in environments seems to be relatively strong. Heating and UV irradiation can efficiently eliminate the viral infectivity.

Stability of SARS coronavirus in human specimens and environment and its sensitivity to heating and UV irradiation., Biomedical and Environmental Sciences (2003)


What is the purpose of requiring two separate binding systems for the antibody response?

Immunity can be a double edge sword. It is aimed to detect and destroy invading pathogens but it can also target the self, as exemplified in autoimmune diseases. To avoid this, many failsafe mechanisms exists.

For example, imagine an innocuous foreign antigen gets into your body and reaches the lymph node. There it may find a naive B cell that has a receptor that recognizes it. Without a double check mechanism this B cell will mature and begin to produce antibodies against this antigen, triggering an immune response that is not beneficial (e.g. in allergy) and is not necessary (the antigen is harmless).

Because of this, activation of the adaptive immune system requires usually two signals. In the context of B cells the other signal usually comes from effector CD4 T cells (of the type T follicular helper Tfh) and is called linked recognition, because both the naive B cell and the Tfh cell have to be specific for the same antigen.

So a possible scenario may look something like this: a pathogen's antigen is taken by DCs. If there is an ongoing inflammatory response this DCs will get fully activated (a process called licensing) and migrate to the lymph nodes. There they present the antigen to naive T cells. Naive T cells specific for the antigen mature and become effector T cells that may include CD8 and several classes of CD4 T cells, including CD4 Tfh cells. The antigen is also transported to the lymph nodes and presented to naive B cells. Naive B cells that recognize the antigen AND also are stimulated by Tfh specific for the same antigen then mature into plasma cells that secrete antibodies.

For harmless antigens, even though DCs may phagocyte them they will not get fully activated in the absence of an inflammatory response. So the activation chain is broken. This system fails somehow in the case of allergy.

Another point is that this mechanism is related to the generation of antibodies against microbial protein antigens. Animals lacking T cells cannot produce them and so they are called thymus-dependent (TD) antigens. Other microbial antigens like bacterial polysaccharides can induce antibody production without the help of T cells. This so called thymus-independent (TI) antigens provide the second signal by direct recognition of the antigen (e.g. through TLRs) or by inducing extensive crosslinking of B cell receptor (BCR). TI antigens include LPS and bacterial DNA. TI antigens appear earlier than TD antigens and although provide some protection they are less efficient than the TD ones because TI-specific B cells do not undergo affinity maturation and isotype class switching as TD antigens do.

Reference: Most of what I describe is found in Janeway's Immunobiology, 8th edition. Chapter 10 (The humoral immune response). In particular the section 10- "B-cell activation by helper T-cells".


Why insects are attracted towards light?

Phototaxis is a common behavior to many species, including insects but not only (e.g. most fishes do phototaxis).

The ethological reason is quite simple: with light you can see, and if you see you can find food, avoid predators and increase your survival chances. Phototaxis is thus a very strong innate reflex: at the neural scale in many species it is "hardwired".

I would say that the initial "purpose" of this reflex was to avoid shade areas during daytime, the light during nightime being pretty rare before man invented artificial light. The fact that insects gather around artificial lights during nightime is, to me, a side effect of this reflex.


The use of the word cognate in molecular biology reflects adjectival definition 2 from Lexico:

2 formal Related; connected.
‘cognate subjects such as physics and chemistry’

The example given shows that this can be used in the most general sense of related, so that there is no requirement for some common antecedent as a surrogate for a human mother or ancestor.

Specifically there is no implication of the involvement of a common DNA sequence, as in the answer from @Dirigible, nor that of a common origin as invoked in an earlier answer on this topic.

This is quite clear if one considers the much earlier usage of cognate in molecular biology in relation to an mRNA codon and the tRNA anticodons that can recognize it, or a tRNA and an aminoacyl tRNA synthetase that can aminoacylate it.

As far as the usage with microRNAs is concerned, a cognate mRNA is one with which the miRNA can interact by base-pairing — no more, no less.


Smoking, cancer, correlation between quitting smoking and increased immediate risk

To summarise your argument, cancer is a disease characterised by uncontrolled cell division of mutant cells. Smoking decreases cell division, thereby smoking decreases risk of cancer. Furthermore, stopping smoking increases growth rates, thus there's an immediate rise in risk following smoking cessation.

Cancer is NOT caused by cell division. Smoking does NOT cause cancer by cell division. That's the flaw in your argument. What's happening is that cell division ISN'T being controlled. Let's propose that smoking does indeed stunt normal cell growth. The carcinogens in tar from smoking are still floating around causing mutations in the DNA. Most of DNA doesn't code for very much, but some parts of it codes for genes which control cell division. If these genes mutate then cell division is no longer controlled by these genes and hence there's uncontrolled cell division a.k.a cancer. Once these cells are dividing in an uncontrolled fashion, smoking isn't going to limit their growth. That's because this cancer has developed in the presence of these toxins that limit it's growth and despite this it's still managed to occur.

And then that cell growth stunting may actually be causing cancer to occur. White blood cell function is impaired by smoking, these cells usually target cancerous cells and destroy them. Without being destroyed, there's a higher chance of cancer.

And then I could go further, usually cells grow older and die. Maybe smoking by stunting growth of these cells leads to cells that last longer than they should. These cells accumulate mutations and become cancerous, where else they otherwise would've been recycled.

Smoking however has been linked to improving the symptoms of some diseases. Just not cancer.


Why the major gene model can be supported by finding de novo mutations in affected cases?

It helps to give context and a source citation in questions like this. With some research I identified the source of the quote as Torre-Ubieta, "Advancing the understanding of autism disease mechanisms through genetics".

The quote comes from a section of the paper discussing the main two different genetic models of ASD: (1) the polygenic (many genes contributing small influences) model, and (2) the major gene model, where a variation of a single gene is responsible. The first two sentences of the paragraph having the quote are:

  The unified major gene model62,63 is supported by the significant increase in damaging de novo mutations found in subjects with ASD as compared to their unaffected siblings44,49. Further support for this model is seen in the phenomenon that there are more inherited SNVs that disrupt protein function in conserved genes transmitted from the mother to individuals with ASD than in unaffected siblings73.

The sentence in question (the first) is simply citing evidence supporting the second kind of model; it is not claiming that the majority of risk is due to de novo mutations.  As to how de novo mutations support the major gene model, it helps to consult the papers cited in the sentence.  Review of citations 44 and 49 show that those with ASD often have rare de novo mutations that look to be gene-disabling, whereas their unaffected siblings do not.  This suggests that disabling of a single gene can bring on ASD, and thus fits with the major gene model, but does nothing for the polygenic model since it supposes one gene difference has only small effect.

Let me add that the two models are not mutually exclusive: a polygenic model might explain the observed familial occurrence of ASD, while a de novo major gene model might explain why only a few in a family are affected.


In Study from Blue Brain they say position of synapses doesn't change even if they modify neurons, only when they change shape of neuron it changes?

It helps to go to the original article for more guidance:

Hill, S. L., Wang, Y., Riachi, I., Schürmann, F., & Markram, H. (2012). Statistical connectivity provides a sufficient foundation for specific functional connectivity in neocortical neural microcircuits. Proceedings of the National Academy of Sciences, 109(42), E2885-E2894.

The point of this paper is that they are looking at the statistics at which neurons make connections with each other in neocortex. Neocortex is a layered structure, and cells of a particular type are identified by the location of their soma as well as the structure of their dendrites and axons. A layer 2/3 pyramidal cell, for example, has basal dendrites that spread a lot in layer 2/3 and creep into layer 4, and an apical dendrite that extends and branches in layer 1. Therefore, it can potentially receive inputs from any cell that has axons in layers 1 -> 4.

One hypothesis is that the primary determinant of which cell types are connected to which is simply the morphology of each cell type. If one cell Type A has a bunch of dendrites in a given layer, let's say layer 3, and another cell Type B has a bunch of axons in layer 3, they will have a lot of opportunities to contact and make synapses.

A second hypothesis is that cells connect with specialized guidance cues. For example, dendrites of Cell Type A release a peptide BALover that is detected by Cell Type B, and causes Cell Type B's axons to grow toward dendrites of Cell Type A. In this system, you could still get lots of dendrites of Cell A in one layer and lots of axons of Cell B in the same layer, but caused by the specific guidance cues from A->B.

In the second situation, however, we would expect the arrangement of axons and dendrites within that layer to be non-random. That is, we would find processes of B in greatest density nearest to processes of A.

If you labeled a bunch of Cell Type A from one animal, and a bunch of Cell Type B from another animal, and overlay them, they should have just as many contacts as if you labeled Cell Type A and B in the same animal if the connections are random due to morphology. If, however, there are specific guidance cues involved, you would find fewer.

Hill et al. 2012 shows evidence in favor of the first hypothesis: they get about as many contacts if they take cells from two individuals and overlay them. This is what they mean by "random placement": not completely random in all dimensions but rather random within a layer in cortex, as if the cells are taken from two different animals. Certainly guidance cues are still used and are still important for setting up the structure of cortex, but it seems like individual cells are mostly just programmed to take up a certain shape, and that shape determines their rough probability of connections. This is a good thing for the Blue Brain project, because it means that they can use composite data from many animals to establish connectivity patterns.


Sorry for the poor quality of the image, but its just as a reference for my answer.

You have made the question too complex. From the figure, we find that 1 H2O gives 2 H+ and 2 e-. 2 e-, through quinone cycle, provide 4 H+ i.e. total 6 H+ which form 6/3 = 2 ATP i.e.

1 H2O => 6 H+ => 2 ATP

Multiply this equation by 8 and you get:

8 H2O => 48 H+ => 16 ATP

So, 16 ATP should be the answer.

Reference:

Pradeep's: A textbook of Biology for Class XI, 2015, Vol. II, page IV/106


Request for an ID of two spider species found in Australia, NT

The bottom one is most certainly a Huntsman. Something akin to a Holconia immanis, aka the Sydney Huntsman. The picture is difficult but a characteristic Huntsman typically has 2 front legs that are longer than the back legs. And of course they tend to be larger spiders.

 Holconia immanis. source: Wikipedia

The top one looks like a type of brushed trapdoor spider (family Barychelidae), typically composed of such species as Idiommata scintillans, which are known as silverbacks or goldbacks depending on the color of the hair on their head (ref).

Idiommata sp., the 'Silverback'. source: Archne.org.au


Could the denaturation of protein during cooking could generate a prion, by any chance?

Just my speculation here. Prions seem to need some sort of template to guide their folding as well as the cooperation of chaperone proteins. https://en.wikipedia.org/wiki/Prion  I would suspect that denaturing, and potential re-folding, of proteins during cooking would be rather random. So even if one, or very few, copies of a potential prion happened to be produced, the high temperatures, rapid pace of denaturation and the lack of chaperone proteins would not allow the formation of meaningful amount of potential prions to cause disease. Add to that the doubtful chance a prion would be produced in the first place, due to the lack of the usual physiological conditions and participants, feel free to eat cooked food!


How can I find the most studied SNP of a gene?

Can you provide the gene of interest?

You can usually search Entrez for the gene symbol in the dbSNP database, which will pull up a NCBI Entrez page for SNPs located in the gene and will also give an indication of their clinical significance (benign or otherwise).

Alternatively, if you have a specific disease in mind, you can check more specific databases for a SNP, such as COSMIC for cancer-related SNPs.

Lastly, merely Googling the gene of interest (for example, "EZH2 SNP") in Google Scholar will bring up articles that present SNPs of interest.

Some combination of those methods should yield what you want, but I might be able to provide a better answer with more info.


Where can I find disease diagnosis datasets?

CDC Wonder, a health database of the US Center of Disease Control and Prevention (CDC), has weekly data for Nationally Notifiable Infectious Diseases and Conditions, United States: Weekly Tables from 1996 to 2020 on the state level for antrax, brucellosis, dengue fever, leptospirosis, malaria, meningococcal disease, Q fever, rabies, etc.

Weekly tables since 2014 are available on Data.CDC.gov.

Weekly tables for 1952-2017 published in the MMWR are available at CDC Stacks MMWR and weekly tables starting in 2018 are available at CDC Stacks NNDSS.

HealthData.gov has two weekly datasets for malaria by US states - here is one.

Open Government Data (OGD) Platform India has data on a district or state level, for example, for malaria.

Keywords that can help in further search:

infectious disease
week or weekly report or data
MMWR (Morbidity and Mortality Weekly Report)
surveillance

Keywords, like diagnosis or outbreak, can limit your search too much.


eye myopia power changes with brightness

NIGHT MYOPIA -  is a tendency for eyes to become near-sighted in dim illumination.  There are multiple theories explaining the phenomenon, most of them are related to accommodation or chromatic shift in scotopic light conditions when to light is focused before the fovea thus worsening the existing myopia.

Citation:

  In dark adaptation the eye becomes more sensitive to shorter wave
  lengths (Purkinje shift- In the light-adapted eye the region of
  maximal brightness is in the yellow; in the dark adapted eye, the
  region of maximal brightness is in the green),and visual acuity
  depends on parafoveal blue cones. Shorter wavelengths come into focus
  in front of the retina, and this chromatic aberration accounts for
  some of the relative myopia that a normal eye experiences at night;
  much of the remainder is due to an increase in accommodative tone in
  the dark.  It is also called dark focus of accommodation, or tonic
  accommodation, or resting state of accommodation. Consequently, a
  measurement of the refraction (i.e. the determination of appropriate
  optical glasses to obtain good vision on these distant objects) gives
  the result that the eye is myopic. Night myopia can reach values of up
  to about - 4.0 D. Night myopia decreases with age31 and therefore it
  can be of special importance for young drivers at night. In one
  experiment with people aged 16 to 25 years, 38% had night myopia of -
  0.75 D or more, and 4% had – 2.50 D or more. Cause of Night Myopia:

  Spherical aberration (The optical effect of the larger pupil decreases
  the depth of focus) Chromatic aberration. Parkinje shift Ciliary spasm
  At low light levels there is a change of the biochemistry of imaging
  on the retina: in bright light the receptors in the retina are cones
  with higher image acuity, and imaging of colors, whereas in low light
  the receptors in the retina are rods with reduced image acuity, and
  imaging of black and white only. The transition between both states,
  i.e. to get maximum sensitivity when moving from the bright to the
  dark, doesn't happen immediately, but takes some minutes33. This is a
  problem e.g. when driving a car in sunlight and entering a tunnel. The
  low light imaging by rods in the retina can be further reduced by a
  lack of vitamin A and zinc Symptoms:
  1. Blur vision only in low luminance.
  2. Feeling discomfort while maintaining fixation in low illumination level.
  3. Difficulty in night driving.
  4. Hallows around light.


Is there any documented evidence for suicide among vertebrates other than humans?

Well, there are certain behaviors that may qualify. The clearest example I know of would be sexual cannibalism, and more specifically (source):

  The redback spider is one of only two animals to date where the male
  has been found to actively assist the female in sexual cannibalism. In
  the process of mating, the much smaller male somersaults to place his
  abdomen over the female's mouthparts. In about two of three cases, the
  female fully consumes the male while mating continues. Males which are
  not eaten die of their injuries soon after mating.

That sounds pretty suicidal to me...

A less flagrant but commoner example is that of mothers dying to nourish their offspring. Again often seen in spiders, the best example I know of is the giant pacific octopus (Enteroctopus dofleini). The female will chose a den and lay her eggs. She will then spend her last weeks tending her young, never leaving the lair to hunt. Eventually she dies of hunger and her body nourishes her young. My source here is the wonderful BBC life documentary series.

Neither of these are vertebrates of course but still, I thought the suicidal little spider was interesting.


Yes 9:7 seems to be the right answer.

F1 progeny should be AaGg... and crossing it will give a ratio of 9:7 as is of any complementary genes


Why are ammonium ions reabsorbed in the thick ascending limb during acid secretion?

Isn't it all to do with the reabsorption of water, i.e. everything gets flushed out in the Bowman's capsule and then some stuff is reabsorbed to lower the water potential of blood, so water is reabsorbed as well.

I guess I figured it was easier to have a leakier sieve at the Bowman's capsule than try to only release the waste products via facilitated diffusion.


How come large herbivores have such thin legs?

Elephant, rhinoceros, &c all have much thicker legs in proportion.  The answer, I think, lies in the fact that the animals you mention all evolved as cursorial animals (that is, they run to escape predators).  Less mass in the lower leg means it swings easier, so the animal can run faster.

There are two things you're apparently not noticing in that picture.  First, the the horse's lower leg is almost entirely bone (and some tendon), and it's bone that does the supporting.  The propulsive power comes from the large muscles of the hip, thighs, and shoulders.

Second, the lower part of the leg (with the white wrappings) is not anatomically equivalent to the human's lower leg, but to the bones of the hand and foot.  You can see this if you look closely at the rear leg in that picture.  The femur, equivalent to the human's thigh, ends at the knee just above the belly line.  Then the tibia extends about halfway down, ending at another joint which you might think is the knee, but which is called the 'hock' in horse-speak.  The white-wrapped part is a metatarsal, equivalent to human foot bones, then there pastern bones equivalent to human toe bones, ending in the hoof/toenail.

So consider that you can, if reasonably fit, walk around on tiptoe without crushing your foot and toe bones, then imagine the end result of your ancestors having done this for the last several tens of millions of years :-)

PS: With horses, there is some effect from human selection, too.  Racing & show breeds tend to have thin lower legs, draft horses & working breeds have proportionately thicker ones.  My first horse, a thorobred/arab mix, had legs about as thick as my wrists (granted, I'm a fairly muscular guy); my current mustang, about the same height & weight, has legs about twice as thick.


How can a plant become resistant to glufosinate?

Phosphinothricin is a metabolite from the bacteria Streptomyces viridochromogenes which has a protein called phosphinothricin N-acetyltransferase (PAT). This Protein inactivates the phosphinothricin which is the reason why S. viridochromogenes is not dying from it. If you want a plant to be resistant to phosphinothricin you can add the gen for the PAT protein to the plant genom.
This is also described in this paper about herbicide-tolerant crobs.

An explanation for the resistant goosegrass could be that somehow it got the gen for PAT, maybe by horizontal gen transfer from S. viridochromogenes.

In your case the publication which is cited in your source contains another possibility. "We hypothesize that reduced herbicide translocation is responsible for resistance to both glyphosate and glufosinate in these populations"


Could mating/recombination be responsible for evolution of entirely novel features?

Could the unison of such divergent sets of alleles theoretically lead
  to unique phenotype and features that bear little resemblance to any
  features belonging to the parents?

Though it is possible that some unique characteristics may emerge but it is very less likely that the offspring will bear no resemblance to the parents. You start with an example of humans. In this case it is, in my opinion, very unlikely because there is not so much of genomic diversity yet that may lead to such an outcome as you ask about.

Some examples exist, such as the liger (offspring of a male lion and female tiger) that is bigger than both the species. This happens because of improper growth regulation because of interspecies differences. This could happen because the divergence between lion and tiger is much more than the intraspecific variations.

Just a speculation : perhaps the offspring of H.sapiens and H.neanderthalis could have had such a feature but it seems unlikely for the current population of H.sapiens


Identification of a beetle found in a basement in Virginia, USA

That is a female Eastern Hercules beetle. Dynastes tityus https://bugguide.net/node/view/4462 Family Scarabaeidae, Subfamily Dynastinae. One of the largest of the beetles in the South-East U.S.


A haplotype is commonly defined as

  ...a group of genes within an organism that was inherited together from a single parent. -- Nature Scitable

This definition of haplotype applies whether it is just a few genes or all of the genes on an entire chromosome$^1$. In the case of the major histocompatibility complex, it is a group of more than 200 genes on chromosome 6 (Janeway et al. 2001). The set of alleles$^1$ inherited together from one parent form the MHC haplotype. Thus, one offspring will inherit two different MHC haplotypes, one from each parent. The different haplotypes with so many genes helps keep genetic variation in the overall complex, which improves the immune response ability of the organism.

The term is derived from haploid, which means half of the normal set of chromosomes. Humans for example are diploid, meaning it has two copies of each chromosome, one inherited from the mother (maternal) and one inherited from the father (paternal). So, when you inherit just one half of the crhomosome pair, you are inheriting a haplotype.

For general reference, it's important to note that haplotype was not always used to reference a group of two or more genes inherited together. It was commonly used to as a term to represent a sequence of nucleotides together on the same chromosome, even if only part of a single gene. For example, Bowen et al. (1995) used mitochondrial haplotypes to study the migration of loggerhead turtles across the Pacific Ocean. They used 350 nucleotides of the mitochondrial control region. The control region is over 1000 nucleotides in size but Bowen and colleagues only used 350 nucleotides from part of the control region.  This use was very common in the 1990s and early 2000s before it became easier and less expensive to sequence entire genomes, or at least many genes.

Citaton

Bowen, B.W. et al. 1995. Trans-Pacific migrations of the loggerhead turtle (*Caretta caretta) demonstrated with mitochondrial DNA markers. Proceedings of the National Academy of Sciences USA 92: 3731-3734.

Janeway, Jr., C.A. et al. 2001. Immunobiology, 5th edition. Garland Science, New York.

Footnote

More accurately, it would be the set of alleles at each gene locus (gene location) inherited together. The same genes are inherited from either parent, but the alleles (variations of the gene) may be different between the two parents.


Is there a DNA test to identify dog mixes?

There are many commercially available mixed breed ID tests, as a quick Google search will tell you.  However, I cannot vouch for their accuracy: this news article may be of interest. Also this.

The genetic markers used to identify breeds in a mixed-breed are microsatellite markers (sometimes SNPs): you can read more here, but from the abstract:

  We used molecular markers to study genetic relationships in a diverse collection of 85 domestic dog breeds. Differences among breeds accounted for ∼30% of genetic variation. Microsatellite genotypes were used to correctly assign 99% of individual dogs to breeds.

If you're interested in dog genetics, I encourage you to check out Elaine Ostrander's work.  She's written at least one book for laypeople, in addition to her numerous journal publications.


Do our belly buttons consist of scar tissue?

The place where the cord was cut do not stay with us - it falls in a week +- after the birth, while the umbilicus is the only visible natural scar formed by natural processes, not by gynecologists:

Multiple sources say the umbilicus has a scar tissue in it.

  After birth the umbilicus is the only naturally formed visible scar on
  the body.

Br J Plast Surg. 1998 Oct;51(7):538-41. Umbilicosculpture: a concept revisited.

  Umbilicus is a scar, which is the place of the previous merger of the
  fetus with the umbilical cord.


I'm not an expert by any means, and anyone with proper training could probably provide a more informed opinion, but here's my thoughts. The patterning looks similar to Oligodon taeniolatus, an small, nonvenomous snake found throughout the region:

I'm not entirely sure about this identification, mostly because the pattern on the head looks a bit different. Sri Lanka has a large diversity of snakes and finding an definitive identification might be difficult without better images. There seems to be only a handful of snakes considered deadly, and this doesn't appear to be one of them. However, as I said, I'm not an expert, and even if it's not one of the 'deadly' ones, that doesn't mean it couldn't be dangerous to small children or pets. If you intend to capture and release the snake away from the house, I'd still recommend caution when handling it or contacting a professional.


How is monoclonality or polyclonality determined?

There are a few ways to determine clonality. Sequencing-based methods are probably the cheapest, given the current costs of either sequencing, or the even cheaper PCR-based clonality assay. Other methods might include histomorphology, looking for known chromosomal aberrations and/or immunophenotyping, among others. Here's a nice review of some of the clonality testing methods.

Sequencing and PCR would be the most definitive ways to determine clonality of a tumor, since they provide information on the exact sequences of sets of cells.

Exome sequencing would be a good way to determine clonality in a large group of cells, where you don't necessarily know what to look for a priori. PCR is a lot cheaper and more focused and might make a better choice when you do have a specific target to sequence, such as highly polymorphic genes like some androgen receptors and the genes involved in VDJ recombination.


There is one main answer to this question: The Zika virus spreads so fast because it never emerged in this part of the world. Hence there is no natural immunity available in the population and a lot of infections occur. Once this "first wave" of infections is over, the level within the population will fall drastically. Some more information on this topic can be found here.

It is of course possible that the Zika virus has acquired a new mutation which adapts it better to humans and allows spreading much easier, but this is not yet known, since the situation in South America is still changing very fast with a lot of cases occurring and analysis going on. It still can be enough that the virus never emerged in Southern America and that there is no natural immunity available.

According to the paper in reference 1 (which is only a brief communication) the sequences of the envelope proteins of the virus are similar to the strains circulating in Asia and do not carry novel mutations:

The Surinam strains are the ones published in the paper mentioned above and are from South America. I haven't (yet) found any other analysis, but this will only be a matter of time. At the moment we cannot make a final statement on this although there is some speculation around.

Edit 23/02/2016: There is still no final conclusion available, but there is an interesting paper available on the Biorxiv-Preprintserver, which analyses the mutation rate in the genomes of the publically available strains. It can be found in reference 2.

Based on the available genomes, the author calculates the mutation rate of the Zika virus to about 10 Mutations/year. The virus is a RNA virus which have generally higher mutation rates than DNA viruses.

In the analysis he finds a number of non-synonymous mutations (mutations which lead to a basepair exchange), as seen in table 2:

Especially named is the M2634V mutation, but since this is in one of the envelope proteins, the author finds it relatively unlikely (although not completely), that this causes a much higher mutation rate.

In the Diskussion of the paper he writes:

  The sudden spread of Zika to South and Central America does not appear
  to have been due any particular change in the mosquito vector or
  anything to make the Zika virus itself more virulent. But rather from
  the fact that infected people are now able to fly rapidly from country
  to country, thereby spreading the disease extremely easily. This means
  there is little to stop the epidemic continuing to spread to further
  areas of population which have little, if any, herd immunity against
  the virus.

Edit (23.10.2016): There is now an interesting website which builds a realtime phylogenetic tree from the data published (it can be found here). The data also shows where in the virus the mutations occur:

References:

Zika virus genome from the Americas
ZIKA - How Fast Does This Virus Mutate ?


By shin splints you probably mean the pain on the inner front side of the lower 2/3 parts of the shins? This is called medial tibial stress syndrome (MTSS).

Causes, mechanism, prevention and treatment of shin splints are still poorly understood.

From what I managed to find, custom-made cushion insoles are the only proven prevention that can help in some cases.

What has not been proven to help (I'm not saying it does not help, only it has not been firmly proven):

various types of shoes (supinator/pronator)
taping
stretching/strengthening exercises
various running techniques (pose-tech, chi-running, barefoot...)

Possible causes:

running downhill or on an uneven terrain with heel striking and forefoot slapping
sudden increase in running intensity, mileage or frequency
a way of running with moving the hips (left , right) forward
(my experience): running in a forced, conflicting way, like you feel you should not run and you still go...

Possible mechanism: vibration stress in the shinbone (tibia) and the pulling force of the muscles and tendons attached to it and possible local inflammation of then periosteum.

Do not try to run through the pain. The pain will go away but on the long-term, shin splints may worsen.

Source: Shin Splints (MTSS) (Ehealthstar)


How exactly does marijuana damage brain cells?

There is no damage of brain cells, as in the context of lesions in neurodegenerative disorders. There are, however, two mechanisms attributed to the memory loss associated with cannabis/marijuana and these are purely physiological responses.

Astrocyte mediated: CB1R (cannabinoid receptor) in astrocyte gets activated and promotes glutamate release. This glutamate induces Long Term Depression in post synaptic neuron.
Synaptic currents can cause both LTP and LTD. The properties of the synaptic current wave dictates the outcome. Please refer to review articles on LTP and LTD for more information.
GABAergic interneuron mediated: CB1R activation in GABAergic interneurons (inhibitory neurons) causes activation of mTOR pathway and promotes protein synthesis. CB1R activates mTOR through PI3K/Akt.


Is Aspergillus clavatus an unicellular organism?

You're right in saying that yeast is single celled.

However, moulds are described to be filamentous fungi that are multicellular. The filaments of the mould give colonies "a woolly, fluffy, or velvety appearance, sometimes punctuated with a granular or powdery aspect that is produced by the formation of asexual reproductive structures"(1).

Aspergillus is such a species. The filaments are called hyphae. In Aspergillus, hyphae have divisions or walls which separate it into multiple cells. This is called septate hyphae.

McPherson, et al. Henry's Clinical Diagnosis and Management by Laboratory Methods. 22nd ed. 2011. Saunders.


Nerve fiber responses to intense stimuli

Short answer
It depends on your definition of 'instantaneous' and on your definition of 'stimulus'. I can safely say that secondary neurons can fire multiple action potentials to a single, short physical stimulus delivered to the associated sensory neuron.

Background
Physiologically, external stimuli are processed by sensory neurons. Sensory neurons generally work with graded potentials, not action potentials. Sensory neurons typically convey their graded response onto a secondary neuron that translates it into a frequency-modulated pulse train.

Hence, I interpret your question as "can a single, short stimulus delivered to a receptor generate multiple action potentials in the associated secondary neuron".

If sensory neurons were restricted to one action potential per stimulus, then a stimulus could only be detected in terms of its onset or offset. We can, however, sense prolonged stimuli. For example, we can perceive a continuous auditory tone and we can look at an image for extended periods without it fading away.

However, it all depends on the sensory system. A great example is the tactile system, where some receptors mediate prolonged sensations, whereas others only mediate onset or offset responses. Their associated secondary neurons are therefore classified as rapidly adapting and slowly adapting fibers.

Figure 1 shows the response profiles of various secondary neurons connected to different mechanoreceptors in the skin.

Fig. 1. Responses of various secondary neurons to tactile stimulation. Source: Mann (1997)

For example, the Pacinian corpuscle is a rapidly adapting mechanoreceptor. If it receives a static pressure difference, its associated neuron fires only a single action potential (or very few action potentials) at the start and end of the stimulus. Slowly adapting receptors causes their associated neurons to continue firing even after prolonged stimulation. Slowly adapting mechanoreceptors are Merkel's disks and Ruffini endings (fig. 2)

Fig. 2. Skin receptors. Source: Purves et al. (2001).

If you, however, mean with an 'instantaneous' stimulus a nearly infinitesimal short stimulus, then this question becomes a search for the shortest possible stimulus still capable of evoking a response in the secondary nerve fiber. In the auditory field, the shortest acoustic stimulus possible is probably the click stimulus, which is akin to a pulse stimulus. An acoustic click is hence about the shortest possible stimulus known to activate a sensory neuron. An acoustic click can be as short as 30 microseconds. A short stimulus like that, however, still evokes multiple action potentials in auditory nerve fibers (Parham et al., 1996). Admittedly, due to the mechanics of the inner ear, most notably the basilar membrane and the travelling wave the click evokes, the factual physiological stimulus may be longer, but in the auditory field at least, tens of microseconds is about as short as it gets.

Hence, I would answer "yes, instantaneous stimuli can evoke multiple action potentials in a given nerve fiber'.

References
- Mann. The nervous sytem in action (1997)
- Parham et al., J Neurophysiol; 76(1): 17-29
- Purves et al., Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates (2001)


Stem cells and if they can correct a lack of apoptosis

The answer is no.  There is no method currently known whereby we could get a stem cell to transfer its genome to a cancerous cell and thus get its apoptosis mechanism functioning again.  It's just not that easy to get a genome transfered - destroying the defective copy of the genome which is stored in the nucleus and getting a new copy of the entire genome into the same.
Remember that to transfer almost anything (except small non-polar molecules) in and out of the cell, you need highly specialized transporters (ie., ion channels, Na+/glucose pumps).  This is particularly true of large molecules like glucose and sucrose (plants). But even those molecules are extremely small compared to an entire chromosome, for which there is nothing even close to a transporter.  It would therefore be impossible to get the chromosome into the cell.
But even if you could, you have yet another hurdle: you have to get the new chromosomes into the nucleus... and that only after having destroyed the original genome in Cell 1, without making the environment in the nucleus toxic for the new genome (ie., CAD activity...)  This represents innumerable challenges, including the fact that you're going to need to alter the nuclear membrane to allow the entry of a massive macromolecule, without impeding the function of the cell...  The problems, unfortunately, go on and on.
TL;DR:  Nice idea, and would be really cool if it worked, but it has way, way, way too may complexities and insurmountable hurdles to be even remotely workable.

Sources:

Lemoine R. 2000. Sucrose transporters in plants: update on function and structure. Biomembranes 1465 (1–2): 246-262.


1: Yes it is possible

2: It's not as easy as lab conditions because of variable conditions, chances of equipment breaking, especially when small children are involved.

3: You can also look at a Foldscope. Its a small, but powerful microscope made with paper. It was developed by a scientist called Manu Prakash, and although it is still in its beta testing stage, I'm sure you would be able to obtain a few for your students. It is incredibly cheap, very customizable and really user friendly.

P.S.: With the amount I endorse the Foldscope, you would have thought they could have shipped one of the damn things to India for me.


How much heat for how long to Kill RHDV?

Often, in studies of viral infection, heat-inactivated viral stocks are used as a non-infectious control.  See Matthaei et al. 2014 1 for an explanation of how such a stock was prepared for RHDV:

Heat-inactivated RHDV stock was generated by incubating the virus preparation in 2 ml screw cap tubes for 180 s at 85°C in a water bath to ensure a drop in infectious virus of more than 99.9%

The methods section for that paper cites a study by Duizer et al. 2 on the inactivation of caliciviruses (which include RHDV).  Therein, the authors tested the heat inactivation of canine calicivirus no. 48 (CaCV) and feline calicivirus F9 (FeCV) at 4, 20, 27, 37, 56, 63, 71.3, and 100°C for time periods varying from weeks (4°C) to seconds (71.3 and 100°C):

Times required at different temperatures to achieve a 3 log10 reduction in viable virus titer (TCID50) in DMEM (3 to 4 μg of protein/ml).

Note that, in both studies, viral heat inactivation is carried out in liquid culture, where it is easy to obtain a uniform temperature by mixing.  For heat inactivation of RHDV on food/hay, rate and uniformity of heating will be different.
Citations

Matthaei M, Kerr PJ, Read AJ, et al. Comparative quantitative monitoring of rabbit haemorrhagic disease viruses in rabbit kittens. Virol J. 2014;11:109.
Duizer E, Bijkerk P, Rockx B, De Groot A, Twisk F, Koopmans M. Inactivation of caliciviruses. Appl Environ Microbiol. 2004;70(8):4538-4543.


How did scientists establish the reactions that occur in metabolism?

In addition to biochemical methods, a lot of this was figured out using radioactive tracers. Cells would be fed a radioactive substrate and as they convert the substrate to other molecules through metabolic reactions, the radioactivity can be detected in the products and intermediates.

Calvin's 1940s-50s experiments to establish carbon flow during photosynthesis (i.e. the Calvin-Benson Cycle) using $^{14}CO_2$ remain some of the most elegant work along these lines. You can actually read some of his reports here, though maybe someone else has a good link to a less technical overview.

Similar methods are still used today, though stable isotopes instead of radioactive ones are more commonly used.


Why does the liver produce ketone bodies instead of exporting acetyl-CoA from beta-oxidation for use elsewhere?

This is simplified version of a complex situation, but in summary:

A key role of liver is to control the distribution of metabolic fuel
for the other tissues (it always has enough for its own
requirements).
The way it behaves differs in the fed and fasted states (because of control by hormones and the concentration of metabolites).
In the fed state (after storing some sugars as glycogen) the liver will synthesize triglycerides and export them as lipoproteins to the adipose tissue, which will take them up and store them. (Other tissues in the fed state will be able to obtain glucose or fatty acids from the blood.)
In fasting and starvation the triglycerides in the adipose tissue will be broken down to fatty acids and glycerol, much of which will be used by tissues such as muscle.
The priority of the liver in starvation is to provide fuel for the
brain and nervous tissues in the form of glucose, by gluconeogenesis. The substrates for net gluconeogenesis under these conditions include glycerol and some amino acids derived from breakdown of protein.
Other amino acids, produced in protein breakdown lead to acetyl CoA,
which cannot serve as a precursor for gluconeogenesis. However it can
be converted to ketone bodies (acetoacetate and β-hydroxybutyrate)
that the brain can use to replace some of its glucose requirement.

With this in mind, it can be seen that the reason for producing ketone bodies is not to generate a molecule that can cross the cell membrane into the blood, but to generate a molecule with special properties, lacking in fatty acids or acetyl CoA, that allows its use by the brain in life-threatening circumstances.

Of less importance, but worth mentioning, is the fact that citrate is used as an export form of acetyl CoA (when there is sufficient oxaloacetate available), a surrogate role it plays in any case in the transfer of acetyl CoA across the mitochondrial membrane for fatty acid synthesis. So it is not necessary to export acetyl CoA, and perhaps preferable to it keep intracellular.

A more detailed account of this is available at NCBI bookshelf online in Berg et al. sections 30.2 and 30.3


How does CpG island methylation lead to gene silencing?

CG methylation has long been associated with gene silencing due to the generally negative correlation between gene promoter methylation and transcription levels.

When CG methylation occurs in the promoter or enhancer region of animals (where these 'CpG islands' tend to be), methylation seems to impede (to some extent) transcription factor (TF) binding.  That is the baseline mechanism for gene repression.  The altered chemical properties of the DNA make it less favorable binding site for its cognate TF.

In some cases, methylation clearly prevents TF binding.  For instance, some TFs bind DNA to block methylation, which facilitates access of another TF or set of TFs to the bound DNA (for instance, this paper by the Schubeler lab about NRF1).  In the case of other TFs, their binding is less reliant on methylation state, possibly due to the strength and breadth of the binding site (for instance this work from the John Stam. lab about CTCF).

Methylation also can affect nucleosome positioning and stability in some contexts; the nucleosome effects are poorly understood currently  because nucleosomes and methylation likely feedback on one another.  See this work from the Zilberman lab for an example.

The role of a higher-order repressive structure forming is arguably not obvious yet; for instance, histone H1 bining does not appear to be heavily influenced by methylation state (although this is somewhat contentious because there is often a positive but weak correlation at repressed elements in the genome between H1 and methylation--for instance just pubmed 'h1 chip' with reviews and read a recent one).  More certain is the relative change in location of methylated promoters within the nucleus to a place of transcriptional 'silence' (inactivity).  These repositioning phenomena are under intense investigation; you can learn more about this by googling for 'nuclear topology and gene repression' or something like that.

hope this helps


Are bacteria incapable of producing cytokines such as interleukins?

It seems especially pertinent to point out from the start that many cytokines are anti-inflammatory/immunosuppressive. The immune system has evolved to remove pathogens from the body, and normally these cytokines act to deactivate the immune response once an infection has been cleared. It should not be surprising that pathogens have co-evolved defences to the immune system, including interference with cytokine networks and even production of anti-inflammatory cytokine homologs, ostensibly to subvert the immune response. Below are but a few examples of this.

Viruses
Kotenko SV, SAccani S, Izotova LS, Mirochnitchenko OV, Pestka S. 2000. Human cytomegalovirus harbors its own unique IL-10 homolog (cmvIL-10). Proc Natl Acad Sci USA 97(4):1695-1700.

Many viruses exploit the strategy of using homologs of cellular cytokines or cytokine receptors to shield virus-infected cells from immune defenses and enhance virus survival in the host. The presence of virus-encoded homologs of cellular proteins may be an indicator of the importance of these cellular components in immune mechanisms for combating this virus in vivo. A number of herpes viruses harbor homologs of IL-10. Epstein–Barr virus (EBV)-encoded IL-10 (ebvIL-10), the first viral homolog of IL-10 identified, shares many but not all of the biological activities of cellular IL-10 and may play an important role in the host-virus interaction. In addition to EBV, another virus, the Orf poxvirus (OV), which can infect humans, has its own IL-10 homolog, ovIL-10.
...
IL-10 has several immunosuppressive activities that would be favorable for CMV, such as down-regulation of MHC class I and II expression, inhibition of production of inflammatory cytokines, and interference with antigen presentation. Murine CMV infection induces transient early expression of IL-10, which plays an essential role in MHC class II down-regulation. EBV infection causes expression not only of ebvIL-10, but also of human IL-10. We demonstrated here that human CMV encodes its own functional IL-10 homolog, which is expressed by CMV-infected cells. Thus, it seems likely that herpes viruses acquire many advantages by using IL-10-specific biological activities either of virus-encoded or host IL-10s.

Parasites
Ouaissi A. 2007. Regulatory Cells and Immunosuppressive Cytokines: Parasite-Derived Factors Induce Immune Polarization. J Biomed Biotechnol 2007(4):94971.

Another intriguing aspect in the parasite relationship is the fact that parasites could release factors that mimic host cytokines. For instance, (1) hydatid ﬂuid fractions mimicked IL-1, IL-2, and IL-6; (2) an IFN-γ homolog that binds to the IFN-γ receptor and induced change in lymphoid cells has been identiﬁed in an intestinal nematode; (3) two homologs of the human macrophage migration inhibitory factor (MIF) have been characterized in the human parasitic nematode Brugia malayi and termed Bm-MIF-1 and Bm-MIF-2, both having functional properties similar to the MIF human counterpart; (4) Toxoplasma gondii releases cyclophilin-18 (C-18) that signals through the chemokine receptor CCR5 leading to the IL-12 synthesis by dendritic cells and a strong protective response; (5) the tapeworm Hymenolepis diminuta has been shown to express an IL-12-like peptide, one of the suggested hypothesis being that the peptide could act as a competitive antagonist for the IL-12 receptor, thus contributing to the general immunosuppression.

Bacteria
I have not found such explicit examples of bacteria producing cytokine homologs. However, their ability to produce immune modulating, paracrine signalling proteins, which is essentially the definition of a cytokine, is well known. The following reviews are quite extensive and provides numerous examples:
Wilson M, Seymour R, Henderson B. 1998. Bacterial Perturbation of Cytokine Networks. Infect Immun 66(6):2401-2409.

In recent years it has become apparent that bacteria produce many molecules which have profound effects on the capacity of leukocytes and tissue cells to produce selected cytokine networks. Thus attention will have to switch from the current view of the host cell as the only controlling factor in cytokine biology, once the bacterium has stimulated this cell, to one in which the bacterium, by modifying its exported or structural molecules or by direct interaction with the cell, can directly modify cytokine networks.

Henderson B, Poole S, Wilson M. 1996. Microbial/host interactions in health and disease: who controls the cytokine network? Immunopharmacology 35(1):1-21.

Recent cytokine transgenic knockouts demonstrate that the normal benign response to commensal gut microflora becomes a lethal inflammatory state in the absence of the cytokines interleukin 2 or interleukin 10... We propose that the ability of the multicellular organism to live harmoniously with its commensal microflora must depend on mutual signalling involving eukaryotic cytokines and prokaryotic cytokine-like molecules. Such interactive signalling sets up non-inflammatory cytokine networks in tissues which form the background on which responses to infectious microorganisms must be built and related... It is now clear that bacteria contain and produce a large number of diverse molecules which can selectively induce the synthesis of both pro-inflammatory and immunomodulatory/anti-inflammatory cytokines.

Finally, the mechanisms by which bacteria can co-evolve such cytokine-like molecules is discussed in this review:
Stebbins CE, Galan JE. 2001. Structural mimicry in bacterial virulence. Nature 412(6848):701-705.

Recent studies have begun to reveal that many bacterial pathogens mimic the function of host proteins to manipulate host physiology and cellular functions for the microbe's benefit. This is in contrast with the strategies used by some pathogens that involve microbial products with activities lacking clear counterparts in eukaryotic cells. Here we consider recent structural work that provides unique insights into the mechanisms of host mimicry by bacterial virulence factors. In some cases, these factors are homologues of host proteins that have been incorporated into the genome of the pathogen and subverted for its benefit. In others, convergent evolution has produced new effectors that have no obvious relationship to host factors. However, although hidden at the sequence level, the determination of the crystal structures of several bacterial factors and bacterial–host protein complexes has revealed the presence of mimicry at the molecular level.


I think you this paper is what you need. The many concepts of trait are discussed in the functional ecology background. But basically, a "trait" can be defined as

  " 'Functional traits’ are defined as morpho-physiophenological
  traits which impact fitness indirectly via their effects on growth, reproduction and survival, the three components of individual performance." (Violle et al. 2007)

Which are not so different from the definition you posted.
Some organisms have an improved methodology to collect and measure traits, like plants. But this is not common to all organisms.
As for the method to correct for phylogenetic correlation, this is a whole different field called Phylogenetic Comparative Methods. To choose the method you need to know the kind of data you have and the question being asked.


Infant mortality was high during the paleolithic, so the fecundity of females had to be quite a bit higher than 2 to sustain viable populations.

A recent paper by White (2014) that explores how the ratio of young and old individuals in a population relates to demographic rates compiles data on hunter-gatherer societies from previous studies that you will probably find useful. Among other statistics, that paper reports a range in total fertility of 2.6–8.0. One of the source papers (Hewlett, 1991, pdf here) has data for individual hunter-gatherer societies (along with data from other types of pre-industrial societies). Many populations lie in the range 4-7 offspring. Note however that most (all?) of these values are from current or recent hunter-gatherer societies and not paleolithic societies. However, to give a ballpark estimate they are probably useful and fairly accurate. Also note that the child mortality rate of these societies are often between 40-50% (infant mortality ~10-30%)


If plants benefit from carbon dioxide, why is car traffic something bad?

There are at least two separate answers to your question.  First, with respect to plants needing CO2, they have evolved to deal with the limited amounts of CO2 normally in the atmosphere.  That's really all they need, or "want": adding more doesn't really benefit them.  Think of it this way: you need water to live, right?  And drink a certain amount of it every day.  But drinking large amounts of water can kill you https://en.wikipedia.org/wiki/Water_intoxication and holding you under water for a few minutes certainly will.  (As in the comment above, and even better example would be oxygen: we need it to live, but too much can cause all sorts of problems: https://en.wikipedia.org/wiki/Oxygen_toxicity )   Likewise, plants need nitrates, but applying too much can kill them.  So extra CO2 in the air is of little or no benefit to plants.

The second answer has nothing to do with plants.  It's that atmospheric CO2 traps solar heat, causing the Earth to be warmer than it otherwise would.  Without the extra CO2 from fossil fuels, Earth maintained a comfortable temperature, one that we'd all (and I mean not just humans, but all life) had gotten used to.  Add more CO2, and more solar heat is trapped, making the Earth uncomfortably warm, to the point that many plants & animals can't live where they are, and generally can't migrate.  So you wind up with a lot of dead plants and animals.

Of course there's more going on than this, things that are feedbacks from and side effects of the increased CO2, such as ocean acidification.  If you really want to know more, here's a good starting place: https://history.aip.org/climate/index.htm


Would a plant need light if the chemicals gained by photosynthesis were given through the roots or as a foliar spray?

Not exactly the same thing, but a species of algae has been genetically altered to allow it to  uptake glucose, bypassing the need for photosynthesis: http://www.unisci.com/stories/20012/0615013.htm