What is the difference between a cytokine, a hormone and a protein hormone?

Parts of the answer are in the text that you provide yourself. But I shall try to add where i can.

What do each of these three terms [hormone, cytokine and protein hormone] mean  and how are they different?

Both cytokines and hormones are a class of signalling molecules that are secreted by cells.

Cytokines are a group of small protein that  have a fundamental role in the immune system. They are typically short lived and typically have local effects and are specific cytokines are often produced by multiple cell types.

For example they cause local cells to generate heat and cause blood vessels to become wider and more permeable to blood cells. parham (2015) Some cytokines can act over longer distances, IL-6 for example cause local inflammation and regulates fever by targeting the  hypothalamus causing it to increase body temperature overall. For more information check this link.

Hormones are secreted into the blood by dedicated endocrine cells so the can regulate other cells across the body.(alberts, 2008)

Do any of the three terms represent a superset of the others?

Protein hormones are a subset of hormones. An other important subset are steroid hormones.

It can be argued that cytokines function as hormones in some situations. For example: in the case of an infection high concentrations of cytokines can regulate body temperature causing fever. IL-1α, IL-1β and IL-6 are good examples here

Are the terms context specific at all?

In some situations it can be argued that cytokines act as hormones. But the feature that groups them is that the are an actor in the immune response. This wiki discusses some differences.

Classical hormones are produced by a gland and excreted in the blood. This is not context depended.

Are cytokines actually fundamentally different from hormones?

All Cytokines are proteins and don't act fundamentally different from protein hormones. Both have to act through membrane bound receptors since proteins can not pass the cell membrane on their own. Steroid Hormones can pass the membrane and typically have intracellular receptors.

Are there any canonical examples of each?

Interferons and Interleukins are a large classes of cytokines. IFN-γ and IL-6 a well known examples.
Androgens are steroid Hormones . Testosterone is one of them.


A reasonable question, but it contains a fallacy. This is because what are referred to as the forward and reverse reactions being catalysed by different enzymes are generally not, in fact, the same overall reaction.

Consider the relationship between DNA and its constituents (or RNA or Protein or fatty acid). You may be thinking of this as:

  DNA ⇌ DNA constituents

But in fact, because hydrolysis (actually a hydrolase reaction) is thermodynamically favoured, synthesis of DNA (a ligase reaction) needs to be coupled to the hydrolysis of ‘high group-transfer’ deoxynucleotide triphosphates in order to shift the equilibrium in its direction. So the two reactions are (somewhat simplistically):

  DNA → n dNMP (catalysed by DNases)

and

  n dNTP → DNA + n pyrophosphate (catalysed by DNA polymerases)

Although in certain circumstances you can force reactions of this sort into reverse, in the cell they tend to be unidirectional, and are classified accordingly.

(In this sort of ligase reaction in the cell there is a further factor affecting the observed direction. That is the presence of pyrophosphatases that catalyse the thermodynamically favourable hydrolysis of pyrophosphate to orthophosphate, removing the former.)

Coda: Is the reaction in the reverse direction from a ligase necessarily catalysed by a lyase?

Although not affecting the principle expressed in my answer, I think that the latter part of the statement quoted from the Wikipedia page that “(synthases)...belong to the group of ligases, with lyases catalysing the reverse reaction” is not generally true. As mentioned above, the enzymes catalysing the reactions in the reverse direction from ligases involved in ‘polymerization’ are generally hydrolases (EC 3.1...), not lyases (EC 4...). I couldn’t immediately find an example of a lyase that fitted this description. You can peruse the links on this authoritative page if you wish to follow this up.


That's an Alligator snapping turtle, Macrochelys temminckii.

Here is another picture of it (from the same Wikipedia page linked above):

It should not be mistaken for the Common snapping turtle, which belongs to a different Genus.

There is a problem, though: in 2014 Thomas et al. divided the Genus Macrochelys (which originally contained only one species, Macrochelys temminckii) in three species: Macrochelys temminckii itself, Macrochelys suwanniensis and Macrochelys apalachicolae.

Therefore, narrowing this down to the exact species (according to the current taxonomy of the Genus) may be way more complicated.

Source:

Thomas, T, Granatosky, M, Bourque, J, Krysko, K, Moler, P, Gamble, T, Suarez, Leone, E, Enge, K, & Roman, J, 2014. Taxonomic assessment of Alligator Snapping Turtles (Chelydridae: Macrochelys), with the description of two new species from the southeastern United States. Zootaxa 3786 (2): 141–165


Are hormone secretion variations the same for a pair of monozygotic twins?

Bartels et al. 2003 is a review that reports an estimate of the heritability of the cortisol level of 0.62. In comparison to most traits, it is a relatively high heritability.

So, in short, the answer is "no". Cortisol level variation is lower among twins than among unrelated individuals. If the definition of heritability is a little bit unclear to you, you should have a look at this post.

The reaction norm of cortisol level (and other stress response) with varying stress level also seems to be heritable (Ilsing and Hoelsboer 2006, Volckaert et al. 2012).


At night several changes occur in the body due to absence of sunlight and other surrounding changes. The biological clock inside the body performs certain function in a healthy body whenever changes are sensed.

There are many receptors in our body located on cell membrane. They are made up of proteins and their function is to receive information from neurotransmitters. This information will be sent to specific part of the brain. If we take sensory information then it is Parietal lobe. This lobe receives the sensory information from all over the body and responds to it when body is active. During sleep, the senses that go through the thalamus, are shut down by gating either in the Nucleus Reticularis Thalami (NRT) or in the Thalamus itself. GABAergic inhibition of the thalamus, most likely deriving from the NRT is probably a part of the reason that sensory stimuli doesn't penetrate during sleep.

This is also influenced by release of hormones in the body whose level when rises in the blood causes certain changes in the concentration at some regions such as receptors which gets blocked temporarily and stops signaling the brain. There is a study on how muscle relaxes when we sleep can be found here Muscle sleep. So it is all the neurotransmitters job at the receptors which stops signals going into brain but internal to the brain it will be active controlling other routine works which it has to do when we are asleep.

The main thing to note here is the 5 different stages of sleep such as non-REM and REM sleep. During those stages several changes take place in the body. The below website gives an excellent insight into different changes happening inside the body when body takes rest at night.

Please refer to "What happens to your body while you are asleep".


Does anyone know the explanation for branches with different flower colors (see picture)?

Many ornamental cherries are grown on a hardier root stock, that is, they are propagated by grafting onto hardy wild cherry saplings. This is because the ornamental variety will not produce offspring that are true to the parents, if they produce offspring at all.

  All are grafted plants and mainly on wild cherry (gean) rootstock.  Such trees should be planted with the graft union above ground level.  Seed, rarely produced, will give rise to new hybrids.

This is a picture of an ornamental cherry of the pompom variety:

My guess is that the tree in your picture sent a shoot off the main trunk under the graft site, resulting in a branch of native cherry, which is mostly white and a much simpler flower than the ornamental variety that was grafter onto it. Another possibility is that two different specimens were grafted onto the same stock (but since the white blossoms are very simple - like a wild cherry - I would guess the former occurred.)

This is a picture of a wild cherry (gean):

So you have the grafted ornamental cherry blooming alongside of the rootstock cherry it was grafted to.

The rootstock (although usually wild cherry) can vary, so... can't identify with certainty the rootstock, but can explain what you're seeing.

It's not rare, but it's not usually desirable. Some newer growers are grafting several varietues of cherries onto the same rootstock to intentionally produce a tree with different kinds and colors of flowers. See, for example, this artist's work.

The Hamada Cherries


How can I text-mine full-text articles from PubMed?

Below is a Python script that might help you to get started  (apologies if it fails the Pythonic test - it works!). It uses the Entrez part of the Biopython library. The script sets up a query, in this case yeast AND Saccharomyces against the pmc database. Also note that this script uses the 2 step process that NCBI likes you to use - the first part of the fetchByQuery function gets a set of results then the second part uses those results to actually obtain the data.

The output is an xml file which you get to parse with your favourite tools. In your case you will need to get out the text sections and do your token analysis. If you use Python for that I recommend the Natural Language Toolkit (NLTK).

In your case you could just set up search terms as a Python list and loop through writing each dataset to a file named from the search term.

from Bio import Entrez

import urllib
import urllib2
import sys

def fetchByQuery(query,days):
    Entrez.email = "xxx" # you must give NCBI an email address
    searchHandle=Entrez.esearch(db="pmc", reldate=days, term=query, usehistory="y")
    searchResults=Entrez.read(searchHandle)
    searchHandle.close()
    webEnv=searchResults["WebEnv"]
    queryKey=searchResults["QueryKey"]
    batchSize=10
    try:
        fetchHandle = Entrez.efetch(db="pmc", retmax=100, retmode="xml", webenv=webEnv, query_key=queryKey)
        data=fetchHandle.read()
        fetchHandle.close()
        return data
    except:
        return None

days=100 #looking for papers in the last 100 days
termList=["yeast","Saccharomyces"]

query=" AND ".join(termList)
xml_data=fetchByQuery(query,days)
if xml_data==None:
    print 80*"*"+"\n"
    print "This search returned no hits"

else:
    f=open("pmcXml.txt" ,"w")
    f.write(xml_data)
    f.close()


I am interested in Sociobiology. Which academic field should I study?

What fields are sociobiology and evolutionary psychology?

Sociobiology (aka. social evolution) is a subfield of evolutionary biology.

Evolutionary psychology is a subfield of both evolutionary biology and psychology. Evolutionary psychology is, for the moment, very theoretical without much (if any) empirical testing. For this reason, not only natural scientists
 and social scientists work on the subject but some philosophers have also contributed (such as Daniel Dennett for example).

How to become a researcher in one of these fields?

Biology.SE is not BiologyCareerAdvice.SE. We have way too few information about you to give reliable career advice anyway. Also, I am not trained in any way to give you carrer advice.

That being said, a priori, start with a Bachelor in Biology and follow up with a master in Evolutionary Biology. Because evolutionary psychology is very inter disciplinary, I would personally advice to go with whatever broad field of study attracts you most. If you are more into psychology than biology, please go with psychology. If you are more into philosophy than biology, then go into philosophy.

Short intro to evolutionary biology

For a very short intro course to evolutionary biology, you can have a look at evo101 by UC Berkeley.


Relation between a compound's toxicity and it's concentration level

The article at linked at the bottom says that the marine organisms keep the concentration of Ammonia under very strict control.

pH of the ECF (Extra Cellular Fluid) is said to play a very important role.
The concentration of ammonia in the environment (ambient ammonia levels) also plays an important role.
Less importantly temperature also plays a role.
Ionic strength of water also is involved.

The NH3:NH4+ ratio seems to be more important than the abosolute value of ammonia.

Ammonia is more toxic than ammonium ion. The lipophilic (ammonia is amphiphilic - soluble in both water and lipid) nature of ammonia allows it to easily cross the cell membrane and the blood brain barrier (in organisms where BBB exist) and affect the physiologic functions. The ammonium ion on the other hand can't enter the cell as easily, as it is not as soluble in lipid as ammonia.

For ammonia and marine organisms see http://www.sciencedirect.com/science/article/pii/S1546509801200053
For more on ammonium toxicity see: http://www.ucl.ac.uk/~ucbcdab/urea/amtox.htm


Strange fast growing mushroom like entity

This is dry rot. It could be one of several species, including Serpula lacrymans, Meruliporia incrassata and Fibroporia vaillantii. It is a fungus that feeds on and decomposes wood. Despite the name, some moisture is required for growth, so
it makes sense that your wall suffered from damp. The fruiting body will darken at the center as the spores appear.

Example images of dry rot fruiting bodies:

Photo by Seabrooke Leckie

Photo by Dave Brown


Vanillin is the chemical that gives vanilla its flavour and smell [1].

  Vanillin is pharmacologically active, causing depressed blood pressure, increased respiratory rate & death due to cardiovascular collapse [3].

  Non-Human Toxicity Values [4]

  LD50 Rat oral 1580 mg/kg
  LD50 Rat ip 1160 mg/kg
  LD50 Rat sc 1500 mg/kg
  LD50 Mouse ip 475 mg/kg
  LD50 Guinea pig oral 1400 mg/kg
  LD50 Guinea pig ip 1190 mg/kg
  LD50 Rat oral 2.8 g/kg
  LD50 Guinea pig oral 1.40 g/kg
  LD50 Mouse ip 0.78 g/kg
  LD50 Rat sc 1.8 g/kg
  LD50 Dog iv 1.32 g/kg slow in fusion.

References:

Wikipedia contributors, "Vanillin," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Vanillin&oldid=613429267 (accessed June 26, 2014).
PATTY F. A. 1963. Industrial Hygiene and Toxicology. Volume II Toxicity, page 1696 (referenced from TOXNET, Vanillin - Human Toxicity Excerpts)
TOXNET. Vanillin


How can highly virulent but uncommon diseases (like ebola) maintain a stable equilibrium?

Viruses and other disease causing organisms are usually in an ecological steady state in different organism, called a vector.  When they start to infect another organism similar enough that they can reproduce, they may turn out to be more virulent or fatal than is optimal for the organism.

The classic example is the case of influenza outbreaks, the flu virus is causing mild infections in other animals such as birds or pigs and then a human being catches it and it may be serious or even fatal.  This is classically because the viruses lytic cycle (where it reproduces and then kills host cells) is not tuned to the equilibrium ideal for viruses in the new human environment, which is not fatal which gives the virus the best chance of reproduction and retransmission.

In the case of Ebola and Marburg viruses the vector is not known but there is speculation and research going on. So in the extremely rare handful of events where these hemorrhagic fevers have been caught by people they fatal.

Its the non-equilibrium case where the virus is not adjusted to human hosts and adjusted for its vector population where it is usually most dangerous.

If these viruses were allowed to persist they would theoretically come to the point where it wasn't fatal.  The problem being that people would die and there is always the risk that the virus would burn through all possible human hosts before it adjusts...

I want to say that this is all driven by evolutionary forces.  If the environment encourages pathogenic characteristics then human pathogens can persist forever.  Flesh eating bacteria and MRSA and other antibiotic resistant bacteria have found a competitive environment where causing disease and death are the only way to go - hospitals with antibiotics. In the case of Ebola/Marburg, there may be a disease reservoir of monkeys acting as a pool for the high fatality strain.  Anything can happen with the right geography and dynamics.

If you've been thinking to yourself, 'what are the odds that a virus or bacterium would be extra virulent versus not infectious at all?', you are right. One should also note that fatal outbreaks are rare and exceptional.  There are clearly plenty of cases where viruses or pathogens from other organisms can't get any traction at all in humans.  We are practically swimming in viruses and bacteria all the time.


The whole point about your question is to define what is an "evolved trait"? The concept of "evolved trait" does not exist in evolutionary biology. Here are various definitions I can think of that could apply to the expression "evolved traits".

Heritable Traits

Does evolved traits mean heritable traits?

A trait may be heritable or not. See for example my answer to this post to understand what heritable mean. You may want to understand the difference between the narrow and broad sense of heritability. Greed is probably heritable as several studies showed that many personality traits are heritable. This post will maybe give you more info.

--> Greed is probably a heritable trait

Traits that evolve

Does evolved traits mean traits that can evolve?

Any (existing) biological trait evolves. Not necessarily because they are selected for or against, neither even for genetic reasons, but traits change through times. Culture changes.

--> Yes, greediness can evolve

Traits that are adaptations

Does evolved traits mean traits that are adaptations?

The concept of adaptation is not always easy to define and its definition may vary from authors to authors. Simply speaking, an adaptation might be defined as a trait that is now fixed in the population (meaning that all individuals in the population carry this trait) but when it was not fixed yet it was beneficial. Such definitions would not fit the concept of greediness if we assume there is some genetic variance for greediness. But while I am not aware of any study on the subject, a level of greediness very probably influence the fitness  (=~ reproductive success) of its carrier. If someone is extremely greedy, he might not find a mate and may fail to reproduce. On the other side, someone that is extremely generous may give everything it has up to its life and would definitely fail to reproduce. Therefore, it seems at first though that there is what we call stabilizing selection on the level of greediness.

--> It depends on the meaning of adaptation. But yes, it seems intuitive that greediness is a trait that undergoes (stabilizing) selection.

Social traits

Greediness is the kind of trait that are particularly interesting because it influences not only the fitness of its carrier but also the fitness of other individuals in the population. We say that it is a social trait and the field that study such traits is called social evolution. You'll need to get in touch with Hamilton's rule (Kin selection) and evolutionary game theory to understand more about the evolution of social traits. This post may eventually help you.


What do you call the non-Wild Type allele?

Usually its major allele and minor allele.  When you hear this language, you feel that the major allele is the 'wild' type, but its more precise to avoid 'wild'.

This language avoids the question of which one is 'wild' since different populations may have different ratios of the two.


Akaryote is not used for a group of organisms in the way that prokaryotes and eukaryotes are used.  The word akaryote is not a common word, but when used it is a synonym for akaryocyte meaning "a cell that does not have a nucleus" and is used in the context of eukaryotes, in which cells normally do have a nucleus.  (It is not used in the context of a prokaryote, which does not have a nucleus but does have a cell, or in the context of a virus, which does not even have a cell.)

The diagrams in your question have confused two different things.  The first illustration is indeed a virus, as stated.  The remaining illustrations are not of a virus, though.  You may have thought they were visually similar, but they are not similar in the details.  The "fibres" may look like like "flagella", but they are different.  The virus is not a cell and has no cell membrane. Viruses are not prokaryotes.


What is the difference between scale vs cataphyll?

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):
Scale:

Any thin, flat, scarious structure

Note: "Scarious" = Thin, dry, and membranous in texture; not green

Cataphyll:

Brown or colorless scale-like structures believed to be modified leaves

So "scale" is going to be used more broadly, while a "cataphyll" (though scale-like) is more specifically always some type of modified leaf.
According to Wikipedia:

Cataphylls include bracts, bracteoles, and bud scales, as well as any small leaves that resemble scales, which are known as scale leaves.

You can find good illustrations of cataphyll examples here.


How to tell if a given gene is a tumor suppressor or oncogene?

I assume these are all carcinogenic mutations. Because some them are clearly recessive loss-of-function mutations (like loss of transcript), you can conclude that the function of the gene consists of "holding back cancer". When these mutations occur, they can generally be complemented by a healthy allele on the sister chromosome.

Oncogenes on the other hand, require gain-of-function mutations, like translocation to a more active promotor or dominant negative mutations (like a loss-of-function mutation in a protein which forms multimers, which get "polluted" by the mutant and thus can not be complemented by the other allele). In most cases this "increases" their stimulation of cell division and thus cancerous growth.

Loss of transcript of an oncogene would not cause cancer.


For the lac operon there are two possibilities for constitutive expression mutations:

The operator is never closed.

Reason: Mutation of the repressor, so its not present, doesn't bind or binds only with very low affinity for the operon.

The repressor can not bind.

Reason: The binding site for the repressor is mutated.

See this Website or this Website for more information.


Solitary flower means one flower at a specific position of a plant. It usually accompanies with another word either terminal or axillary.

Soliary terminal means a flower present at the apex of the main stem or its branches. e.g.  Trillium grandiflorum.

 Image taken from http://ohioplants.org/inflorescences/

Solitary axillary means a flower arising from the axil of a leaf. e.g. China
rose.

Image taken from https://commons.wikimedia.org/wiki/File:China_rose.JPG

 This is Sida rhombifolia. This picture is clearer.

No. It doesn't mean that a plant has a single flower.It speaks all about the position of the flower. Think of roses , they are solitary terminals and are in numbers in each plant, always growing at the apices of branches.

Source: My two years of learning Botany as an additional Undergraduate subject.


Is there variation in which olfactory receptor genes are functional in humans?

Perhaps the most dramatic example of variation in olfactory abilities in humans is anosmia, or the inability to smell. However, this isn't always due to broken olfactory receptors -- some total anosmias are due to cilia (small hairs) that don't function properly. (This paper mentions that.)

Specific anosmias, or insensitivities to particular smells, are probably closer to what you're asking about. The textbook chapter I linked to below talks about how proportions of the population lack the ability to smell certain odorants -- for example, about 1/10 people cannot detect ethyl mercaptan, which is the scent given to natural gas leaks. These specific anosmias are generally restricted to just one odorant (smell), which suggests that it is likely a receptor deficit. (EDIT: The comments below have even more examples of scents that vary from person to person.)

Interestingly, many conditions are associated with a decline in smelling ability and range, like Alzheimers, diabetes, and taking certain medications. These declines can be because of fewer olfactory receptors or because of deficits further along in sensory processing.

I couldn't find any papers assessing smell variation across all humans -- doctors rarely think to assess smell, so there isn't much data on "normal" populations. Also, it doesn't seem like the genes controlling olfactory receptors in humans have been characterized well, so it would be extremely difficult to do a comparison on the genotypic level.

In sum, there are definitely differences in the ability to smell a wide range of scents. To my knowledge, this hasn't been characterized in an especially systematic way. (If it has, I hope somebody on here knows otherwise!)

This chapter of Purves' Neuroscience gives a basic run-down of olfaction and some possible variations in it.
https://www.ncbi.nlm.nih.gov/books/NBK11032/


What is the probability of having a son with blood type O?

7/16 for any child to be blood group O, half of that (21.875%) for a son with blood type O.
P  x  M
HA    HB
HO    HO
hA    hB
hO    hO
HA = 0/4 blood type O
HO = 2/4 blood type O (HO-HO, HO-hO)
hA = 2/4 blood type O (hA-hB, hA-hO)
hO = 3/4 blood type O  (hO-HO, hO-hB,hO-ho)
= 7/16 chance of type O
son = 1/2
Chance of blood group O = 7/16 * 1/2 = 7/32 = ~0.22
Edit: as it's not clear from the question, anyone who has genotype hh is not able to express either A or B antigens, so is always blood group O.


From what I could find the .gen file format for SNPs was developed for the IMPUTE2 program and is generally meant to be a flexible file format for SNP data. The description of the file format is supposed to documented here (multiple pages pointing to that link), sadly that link is broken / the site is removed.
However, I found some other descriptions of the format:

  In the GEN format each SNP is represented as a set of three
  probabilities which correspond to the allele pairs AA,AB,BB.

from here

  The genfile contains predictor values, one row per predictor.
  --gen-skip indicates how many header rows (typically 0 or 1);
  --gen-headers indicates how many header columns (typically 0 to 5).
  --gen-probs should be 0, 1, 2, 3 or 4:
   0 - haplotypes - predictor values should be "0 0", "0 1", "1 0" or "1 1"
   1 - dosages - predictors provide the (expected) number of A alleles
   2 - two probs - providing probability of being AA or AB
   3 - three probs - providing probabilities of being AA, AB or BB
   4 - four probs - providing probabilties of being AA, AB, BB or NA, where A and B are the A1 and A2 alleles

from here

Like finswimmer already wrote in his answer, it is very important to be clear about what is considered an allele in the context of SNPs. For the .gen file format this is the identity of the base at a given (SNP) position and since humans have a diploid genome, the allele of a specific individual can be one of three versions (usually called AA, AB & BB).

Regarding your specific points:

  Since each SNP has associated allele A and allele B, I assume that the file only contains Causative SNPs, and not Linked SNPs, since the former reside in the gene, and the later don't. Since each SNP in the file has an associated gene (actually genotype, some combination of allele A and B). Correct?

The alleles in the .gen file refer to the respective SNPs not genes.
There is no reason to assume that an given .gen file only contains certain SNPs; if it does this is not due to the data format.
The SNPs in a .gen file do not generally have to be linked to a gene.


Is it possible to stop more/extra fat from being stored in the body?

Fat storage comes from conversion of glycogen (a glucose polymer) to triglycerides (fats).  (source: https://en.wikipedia.org/wiki/Glycogen).

Intuitively, the simplest way to prevent fat storage is to block conversion of glycogen to fats. Unfortunately, this will cause a glut of glycogen which can cause an entirely different set of problems (see https://www.hopkinsmedicine.org/health/conditions-and-diseases/glycogen-storage-disease ), so you would want to couple this with a mechanism to eject excess glycogen.

Referencing what user1136 posted: uncoupling oxidation from phosphorylation is a really bad idea. That would basically "burn" fuel while blocking the expected ATP outlet. This will cause a dangerous energy buildup in the mitochondria which has to be unloaded somewhere - provable simply by conservation of energy. Energy can be converted to other forms of energy, but it is never destroyed. Physics is the ultimate anti-cheat tool.

Blocking expected energy outlets is almost always a bad idea in practice. Just to name some practical examples:

In archery class, instructors will warn you never to "dry-fire" a bow (draw the string back and release with no arrow). This can compromise the bow's structural integrity, causing it to splinter, snap, or explode later.
Microwave ovens should never be operated empty with no sink for the electromagnetic radiation they produce - this can damage them. See https://physics.stackexchange.com/questions/309154/what-happens-in-an-empty-microwave-oven for more info.
If you jam the pistons in a standard cylinder-based combustion engine (prevent them from moving), you end up with a lot of energy that needs to go somewhere, which will end up as massive vibration and extra heat - either of which could damage the engine as the design never expected this to happen.


Is there any evolutionary/physiological advantage to multi-lateral symmetry?

Signs of symmetry are determined by the environment. Completely isotropic ecological niche corresponds to the maximum degree of symmetry of organisms (spherical symmetry). Asymmetrization on the axis "up-down" took place under the influence of gravity field and lead to radial symmetry. Bilateral symmetry of the multicellular animals arose with movement.


Since @biogirl has given an answer, I'll add my opinion:

β-galactosidase would be expressed but the permease and transacetylase would not.

The operator lies adjacent to/slightly overlaps the promoter, upstream of the lacZ gene. Binding of the repressor to the operator blocks the promoter, and induction of theoperon involves the repressor leaving the operator unoccupied. If you precisely excised the operator and transplanted it between the lacZ and lacY genes then I think the promoter would be constitutively expressed leading to β-galactosidase synthesis, but the operator would block the polymerase from transcribing the permease gene. In this view the operator would be acting more like a terminator.

Then, if an inducer was added it would relieve the effect of the transplanted operator and the downstream genes would be transcribed. It's even possible that this experiment has been done sometime in the last three decades.

added later:

The OP has now edited the question in such a way as to make my answer, and the answer from @biogirl, nonsensical. The original wording referred to moving "the lac operon" not "the lac promoter", hence my question in a comment asking "operon" or "operator"?

I'll leave my answer here, but this question is now so compromised that I advise everyone to just forget about it.


Proteins can move around the membrane.
Most proteins do move within the membrane. The membrane is a liquid crystal and has fluid behaviour. Specifically, this is due to the membrane being in a gel-state. This gel state allows phase behaviour which means that the protein is able to move around on the surface. This results in an effect that is often referred to as the fluid mosaic model.
Proteins tend not to move out of the membrane.
The protein doesn't leave the membrane as a result of the transmembrane helix being very hydrophobic. This hydrophobicity and the hydrophobicity of the lipid tails means that they self-associate. A better way of describing it is that they fiercely dissociate from the water. A molecular dynamics simulation showed that even in simulations the membrane will readily self-assemble as a result of the hydrophobicity.
This is achieved by a few properties of the TMH sequence. There is a large amount of hydrophobic residues like leucine. At either end of the helix are large aromatic residues called the aromatic belt. Further is the electrostatic satisfaction offered by Gunnar von Heijne's famous positive inside rule and the recently identified negative-outside rule present in helices with evolutionary pressure to optimise anchorage.

(Image source: Baker et al., 2017)
Cymer et al. published a study showing the free energies associated with each part of the transmembrane protein helix (figure below). The overall ΔG for a transmembrane helix in the membrane is ~-12kcal mol−1. This means that the association of the helix in the membrane is typically spontaneous.

(Image source: Cymer et al., 2015)


Mammalian rod cells, the most numerous photoreceptor cells in the retina, reach a max depolarization after a single photon stimulus at 100-120 ms, implying a time constant (1/k) of about 25 ms (see Chen et al., Nature 404:557).  This is on the same order of speed as the fly eye, maybe a tad faster.  Non-photoreceptor GPCRs are probably slower, but few folks have tried to measure these effects. The m1 muscarinic acetylcholine receptor catalyzes Gq activation with a time constant of about 500 ms (Mukhopadhyay and Ross PNAS 96:9539), but there may be faster ones.


Check out the sources of Wikipedia article: the mortality rate is up to 4%.

The main causes of "immediate" death in penetrating trauma are shock (low blood pressure due to external/internal hemorrhage, especially arterial hemorrhage), pneumothorax, penetrating heart injury (with resultant hemopericardium) and other less frequent causes.
The same causes account for "later" lethal case plus some specific causes like infections, emboly etc.

The overall mortality rate of stab wounds is far from 100%, and according to different studies is between 1% to 4%, but rarely more. The morbidity depends on depth of wound, place of injury, overall health status etc, thus multifactorial analysis is required to get an overall image of the penetrating wounds of the body.

Some sources:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627025/ -
 (4.3% mortality in stab wounds to the anterior abdomen, back, and flank).

http://www.ncbi.nlm.nih.gov/pubmed/3798182 - the mortality in back/flank stab wounds was 1.3%.


This is how I understand it: Bioinformatics tools are amazing at answering questions. The more specific the question each individual module of a tool can answer, the better their quality.

However, what they cannot do is ask the right question. You can find motifs with scores attached to the hit, but you cannot predict the relevance of that find. Is it a motif for a transcription factor binding site that inhibits a promoter for a downstream gene thereby suppressing activity, or does it bind a different factor enhancing a gene further downstream?

These questions need knowledge of the domain and of the genomic context, and this knowledge base is constantly evolving. Tools are getting intelligent, but they cannot have this intuition because they are still designed my human beings and we are always ahead thanks to experience.


Why does glomerulus don't allow white blood cells to leave?

Red blood cells, White blood cells, platelets and proteins with large molecular weight cannot pass through the podocyte and fenestrations in glomerular capillary, but small molecules like water, salts and sugars are filtered out as part of urine.

As these cells and proteins are large to cross through this filter, they remain in the capillary and create osmotic pressure within the capillary. Bowman’s space has osmotic pressure approximately zero. So, only hydrostatic pressure works in this state and help in movement of fluid across the capillary wall.

Via:  https://opentextbc.ca/anatomyandphysiology/chapter/25-5-physiology-of-urine-formation/


I'm just about 100% certain that this is a Hobo Spider, which belongs to the species Eratigena agrestis. As stated in my comment, the blemish on the vacuum cleaner's plastic makes it difficult to observe the full pattern on the spider's abdomen, which would have otherwise made for a much quicker identification.

Once realized though, the distinguishing feature for me was in fact the pattern on the abdomen. If you look at the picture I provide and consider at the abdomen, it looks like a face with two eyes, a mouth, some hair, and a beard; i.e., a hobo. Now look at the picture in the OP -- the exact same "face" can be seen, excluding the right "eye" of the hobo (our left), due to the blemish on the vacuum's plastic. The "hair" at the pedicel, the down-turned "mouth", and the "beard", are all visible in both images, and are near perfect matches. The legs, overall body coloration, size & proportionalities, and slight discoloration on the cephalothorax, also match.

I had to maximize the OPs image to 200% zoom to get a detailed enough view of the spider to then make these conclusions.

This species spider is most commonly found in your region, that being north west USA, however, they've also been seen in Asia and Europe. And as for if this is a venomous spider (since you're concerned about your daughter): according to Wiki, this kind of spider doesn't bite unless forced to defend itself, and, the CDC does not consider it to be dangerously venomous.


Does bleach destroy RNAse activity, and if so, how does it do it?

RNAses are enzymes, and there are various ways to inactivate them. Unfortunately, RNAses are rather stable proteins and autoclaving doesn't completely kill their activity. The common methods to inactivate are unspecific methods that will destroy any enzymes, either through covalent modification or degradation.

The most common methods for RNAse inactivation are:

Treatment with DEPC. This covalently modifies histidine and a few other amino acids, which will inactivate RNAses.
Heating to 200-250 °C for at least an hour, this is most commonly used for metal and glass equipment
Incubation with 1M NaOH for an hour at 37 °C, which will hydrolyze proteins

Using bleach is not a method I've used, but it should work in principle as hypochlorite will react with proteins.


Is studying chemical and physical properties of chemical substances that make up organisms really a task of molecular biology?

If you look at the Google ngram for the term ‘Molecular Biology’ you will see that it first appears just before 1960, and it is relevant that the Journal of Molecular Biology was founded in 1959. It is not biochemistry — indeed the name was meant to indicate its difference from biochemistry, and I heard second-hand (so I cannot vouch for its truth) that Hans Krebs (Professor of Biochemistry at Oxford University at the time) referred to it as “biochemistry without a license”. What I can vouch for is that the contempt was mutual.

At the outset the term ‘molecular biology’ was used to combine two rather disparate areas of biological science that today we might refer to as Structural Biology and Molecular Genetics. The link between these was the work on the structure of DNA and proteins at this time,  and the molecular analysis of the genes that controlled the synthesis of proteins.

If you look at the definition in the short Wikipedia article, only Astbury — who worked on protein structure in Leeds — is quoted, but The Journal of Molecular Biology was initially almost the house journal of MRC Cambridge, the love-child of Crick and Perutz, as it were, with an emphasis on nucleic acid as well as protein structure, leading to the other side of the coin which was the genetic code, the lac operon and the study of bacteriophage.

Of course, terms change their meaning as science changes and what was once new and trendy becomes “yesterday’s girl”. It really doesn’t matter that much. Systems Biology anyone?


Relationship between food decay and electric current

Bananas, unless you like mush, become inedible long before any bacterial decay. The brown spots and softening that occur are due to ripening  processes in the banana. Some of the amino acids in the banana are metabolized to produce ethylene. As with other fruits, ethylene acts as a hormone to accelerate the conversion of starches to sugars. The banana gets sweeter while at the same time getting musher. http://www.livestrong.com/article/466183-is-eating-a-banana-with-brown-spots-bad-for-you/

As far as your experimental design, you would need to stick electrodes into the banana to attempt to run a current through it. But I doubt this will work because, to conduct the current inside the banana, there needs to be a certain amount of water, free ions and the structure to allow the ions to move. In my opinion, bananas have too little moisture content for this to occur.

Aiming to affect bacteria on the surface of the banana might be a doable experiment. But the methods that come to my mind involve immersing the banana in an electrolytic solution possibly leading to un-yumminess and not at all guaranteed to work.


What does the phrase 'background level' mean?

The phrase “background level” is generally used in an experimental context where you are measuring the effect on a variable of some agent or stimulus. You might expect that your control condition(s) — without the stimulus — would give you a measurement of zero, but often that is not the case, and one needs to subtract this control value — often referred to as ‘background’ — from the experimental value.

Such background values can be real — e.g. background radiation — or artefacts caused by fundamental limitations in the measuring system used. Generally the implication is that their origin is unknown or is not specific. That is why I think that the use of the term ‘background’ in the context of the lac operon is somewhat unfortunate. I would have used (and encourage you to use) the term ‘basal level’ instead*. As the text states, there is a low — but specific and necessary — expression of β-galactosidase in the non-induced situation, so that when lactose is added some of it can be converted to the inducer, allolactose, which will then result in the synthesis of the greater amount of β-galactosidase needed to deal with the rest of the lactose.

*Footnote

In fact I hate the term ‘level’ except for water in the bath tub, and I would have used ‘amount’ or ‘activity’, but that’s not the point at issue here.


Why don't stem cell therapies use viruses?

Stem cell therapies do in fact utilise viruses. In the examples cited, the stem cells were infected by viruses in vitro, genetically modified, and then reintroduced into the target as autologous transplants. The main issue at hand is that live viruses introduced directly would be targeted and destroyed by the immune system, which greatly reduces their efficacy in causing transformation of cells.

In a recent Nature paper, zinc finger nucleases were used to target and disrupt the CCR5 or CXCR4 gene, which greatly reduces the efficiency of HIV binding to CD4+ T cells. The zinc finger nucleases were introduced into the cells using an adenovirus vector.

  Generation of cxcr4 ZFN adenovirus and CGW-siX4s lentiviral vectors. The CXCR4 targeting locations of siX4s and ZFN are shown in Supplementary Figure S1.

This technique was then used in a number of clinical trials to modify hematopoietic stem cells using zinc finger nucleases, as summarised in this review paper. The recent advent of CRISPR-Cas systems will probably lead to an increase in similar techniques, due to the higher specificity and ease of engineering of Cas9-based nucleases.


The placenta does not turn "hostile" to the mother or fetus. Placentation abnormalities can result in harmful situations, but these are a secondary result.

Structural anomalies of placentation:

placenta accreta/percreta: means that the placenta took hold not only in the uterine mucosa, which is the normal state, but through it up to the myometrium (muscle layer, in placenta accreta), or even up to the serosa (outermost uterine layer, in placenta percreta). These anomalies will convey a much higher chance of massive haemorrage at delivery, and therefore are dangerous to the mother.
placenta praevia: placental insertion covers the entrance to the uterine cervical canal, partially or totally. Therefore, the way of the fetus for natural delivery is blocked, and the placenta will tear during labor, causing massive haemorrage.
marginal implantation of placental vessels: vessels linking the placenta to the fetus (the umbilical cord) are implanted on the periphery of the placenta. This causes structural fragility, and a greater risk of bleeding for both the mother and fetus.
retroplacental hematoma: in such cases, the placenta partially or totally loses its hold on the mucosa, and blood fills the space left behind. This is an immediate threat to both the fetus and mother because of the potential for massive haemorrhage and interruption of oxygen delivery to the fetus.

Deleterious side effects of pregnancy:

preeclampsia/eclampsia: misunderstood biological syndrome that causes the classical signs of arterial hypertension, peripheral edema, hepatic cytolysis, and thrombocytopenia in the mother. Eclampsia is all that plus added seizures (in which case maternal mortality is high). This is not due to placentation abnormalities, even if it is true that delivery is the only cure, and can justify a premature artificially induced delivery in extreme cases.
fetal/maternal rhesus factor incompatibility: During labor and delivery, a small amount of fetal blood will come into contact with the mother's organism. If the mother is Rh neg, and the baby Rh pos, the mother can develop antibodies against the rhesus factor. This can cause haemolysis in the newborn, and in grave cases, kernicterus (toxicity of degraded red blood cell metabolites to the baby). While this may threaten the baby to be born, problems are much more common for subsequent Rh pos pregnancies. We check for antibody presence in the mother with the Kleihauer test and give preventive injections of rhesus antibodies to Rh neg mother with a Rh pos pregnancy to decrease the chance that the mother develops her own antibodies.

Other special cases:

molar pregnancy/choriocarcinoma: A structural genetic accident happening on fecundation that can cause the embryo to behave as a type of cancer.
ingesting placental extracts: this is mentioned is another answer here. This has nothing to do with the placenta, but the deleterious secondary effects are due to direct toxicity of the hormones contained in those extracts ingested in an inadapted situation. This is not to say that one should take them while pregnant, because hormonal deregulation would also be toxic in a normal pregnancy.


Is the resting state of the forearm in the pronated or supinated position?

The main reason why the anatomic position is supinated is because the radius and ulna are crossed when the arm is pronated and parallel when the arm is supinated. It doesn't have anything to do with the resting state of the arm, it's just the easiest way to arrange the bones neatly for description and analysis.


Where does the exudate comes from during inflammation?

exsudates almost exclusively come from the capillary compartment. If you think about the structure of the vessels, this appears logical.

The capillary compartment :

has vessels only several microns thick
has only the endothelial and basal lamina layers
spans an enormous surface, far greater than arterioles or venules

So when the fenestrations and tight junctions of the capillaries are impaired, serum directly passes into the extracellular medium.
A good example of that would be advanced anaphylactic shock. In this situation, the general inflammatory state causes a loss of endothelial integrity. Adrenaline given in such a state will have an inotropic and chronotropic effect on the heart, will cause vasoconstriction, but will also act to restore endothelial integrity. This last element is the main reason why allergic people carry an epinephrine syringe at all times.


Why MHC class I antigen presentation exist in normal cells?

It is of use. They're saying that naive T cells cannot be activated by normal cells because the latter lack the appropriate co-stimulus, namely B7. However, activated CD8+ T cells can recognize antigens presented by normal cells and form a response. This is how cytotoxic T cells are able to eliminate transformed or infected cells.


Yes, Sciurus carolinensis has been invasive in France, Italy and Switzerland for quite a few years already (Bertonlino and Genovesi, 2003).

Note that the "original" distribution of S. carolinensis is over eatern Canada and USA. Not Canada only.


How did interspecies reciprocity involving cleaner wrasses originate?

Cleaner wrasse don't only clean within the mouth; although some species may specialize towards mouth-cleaning, it's likely that this behavior began with cleaning elsewhere on the fish's body.

Some studies (e.g. Bshary, 2003) suggest a large effect of cleaners on fish populations/diversity, so it seems that there are strong selective pressures for evolving behavior permissive to cleaning fish.

The cleaners themselves seem to have evolved cleaning traits on many occasions (see Baliga & Law, 2016). Although there are some obligate cleaner species, it's more common for cleaners to clean as juveniles, and the most common transition between cleaner behaviors is from non-cleaners to juvenile cleaners.

Therefore, it seems like the first cleaners were very small fish outside the typical prey target size of the cleaned fish. If there is strong selection towards individuals who tolerate these small, non-prey cleaners, it's reasonable to expect that this behavior could expand towards larger cleaners, and eventually to the more extreme versions of the behavior like allowing cleaners in the mouth.

Baliga, V. B., & Law, C. J. (2016). Cleaners among wrasses: phylogenetics and evolutionary patterns of cleaning behavior within Labridae. Molecular phylogenetics and evolution, 94, 424-435.

Bshary, R. (2003). The cleaner wrasse, Labroides dimidiatus, is a key organism for reef fish diversity at Ras Mohammed National Park, Egypt. Journal of Animal Ecology, 72(1), 169-176.


Has the age at which menopause occurs changed throughout history?

Quick answer: Yes, but not in the last 150 years.

There seems to be no clear link between age at menarche and age at menopause (taken from [1]):

  While earlier studies were able to establish an association between
  early age of menarche and later menopause (Frisch 1978; 1987), more
  modern studies have not been able to confirm this effect (Whelan et
  al., 1990; van Noord et al., 1997).

  Aristotle's assessment was similar to those of Hippocrates and also
  Roman authors, so it seems that 2000 years ago most women entered the
  menopause in their early 40s. Mediaeval authors, however, gave the 50s
  as the age when menses ceased-much closer to the timing for twentieth
  century women.

Jean Ginsburg in [2] states (emphasis mine):

  In the past 100 years data from schoolchildren have shown a steady
  fall in the age at menarche in industrialised communities. Has
  there been a corresponding change in the age at the menopause?
  Unfortunately, reported surveys of the menopause have suffered from
  methodological defects. [...]

  Nevertheless, those studies least subject to bias show a striking
  agreement that the median age at the menopause is currently around 50
  in Western industrialised societies. In Britain it is 50.78, in the
  United States 49.8 and in white South Africans 48.7 with little
  apparent change over the past century. In non-European women, however,
  the menopause seems to occur earlier-in South Africa and the United
  States black women have an earlier menopause than white women.

So, while early menarche is, apparently, irrelevant, age of onset of menopause has increased since antiquity but has remained relatively stable since the middle ages. Therefore, there have been no significant changes in the age of onset of menopause in the time frame you defined (150 years).

Finally, Bengtsson et al [3] state that:

  Our study has, thus, not supported the view that the menopausal age is
  rapidly changing.

C. Keck, Predictive Factors to Determine Age of Onset of Menopause, PAMJ
, 3, 2005
Ginsberg J. What determines the age at the menopause? BMJ. 1991 Jun
1;302:1288-9.
Calle Bengtsson, Olof Lindquist, Lasse Redvall, Is the menopausal age rapidly changing?, Maturitas, 1(3), February 1979, Pages 159-164


How do stem cells produce 200 billion new blood cells every day? Does 1 stem cell division result in production of just 1 blood cell or many?

The hematopoietic stem cells are quite rare, and each progenitor cell produced by a stem cell gives rise to a large number of red blood cells (and other blood cell types).

I'm not sure if the precise number of offspring for the earliest progenitor cells is known in vivo, but recent cell culture models indicate that early progenitors can give rise to as many as 70,000 mature red cells. We also know that the erythrocyte burst-forming cell, a later stage cell in the erythroid lineage, gives rise to around 5,000 mature erythrocytes.

Red blood cells eject their nucleus in the final stages of maturation, and cannot divide thereafter. The ejected nucleus is consumed by a bone marrow macrophage, so it cannot be "reused" in any way. Hence, loss of the nucleus is probably not an advantage in terms of "production economy" --- a nucleus must be generated for each single red cell anyway.


I saw these patterns on a hill. Which insect makes such a pattern?

It could be an antlion. Antlions are a group of about 2000 species that can be found all around the world (including India). Antlions mainly live in the kind of dry areas you describe and that we see in your picture. I don't think one could be more accurate and tell the genus without a picture of the individual but I might be wrong.

Here is an adult antlion:

and here is a larva antlion

The small pits you see are made by larvae. The larvae make these small trap pits to capture ants (and some other small insects). The larvae is buried in the soil at the center of the pit and simply waits for prey to fall into the pit. Below is a picture of such a pit:


Some parts of viruses are consistently shaped, in particular anything that is made of multiple copies of a protein sticking together. There are methods to determine the structures of these regular components to high precision, like single particle analysis (eg. zika) and X-ray crystallography (bacteriophage HK97). Other parts of the virus are less consistent, either because they are flexible or because they are produced slightly differently each time. The nucleic acid core is often arranged semi-randomly, and the lipid envelope of many viruses can vary greatly, dependent on the process by which parts of the host cell's membrane is pinched off to create new viral particles. Here's an example of pretty extreme variability of influenza particles, based on what cell type they have infected. Virus particles with different shapes can be just as infectious, but if they are too large the number of new viruses produced by an infected cell may be too low.


1% water solution of deoxycholic acid. How is it prepared?

According to the sigma document you referenced (emphasis added by me):

"The free acid is soluble at 0.24 g/L in water at 15ºC, while the sodium salt is soluble at >333 g/L in water at 15ºC. Therefore, pH control is very important to the use of this product. Aqueous solutions precipitate as the pH is lowered to 5."

According to the FDA document (emphasis added by me):

"Each 2 mL vial of KYBELLA® (deoxycholic acid) injection contains 20 mg synthetic deoxycholic acid as the active ingredient and the following inactive ingredients: benzyl alcohol(18 mg), dibasic sodium phosphate (2.84 mg), sodium chloride (8.76 mg), sodium hydroxide(2.86 mg) in water for injection, USP. Hydrochloric acid and additional sodium hydroxide are added as necessary to adjust the formulation to pH 8.3."

The solubility of 0.24 g/L in water at 15ºC is determined by dissolution of the free acid in pure water. As you dissolve an acid in pure water, the pH will get progressively lower, and since this compound is less soluble at lower pH, it limits it's own solubility in pure water.
The sodium hydroxide in the KYBELLA is a strong base, which raises the pH and, when mixed with the deoxycholic acid, forms an aqueous sodium salt and water via an acid-base reaction. The conjugate base of deoxycholic acid in aqueous solution is deoxycholate. This portion of the compound remains unchanged, regardless if it is part of a free acid or a sodium salt. The sodium phosphate is a buffering compound which helps stabilize the pH and allows for finer adjustment to control the final pH to ensure it remains soluble.


It is a vespid wasp (family vespidae). Bees are generally hairy, and this one has the typical wing folding of a vespid. Genus Vespula. There is a New Zealand website that shows the differences among common NZ wasps here:
https://www.landcareresearch.co.nz/science/plants-animals-fungi/animals/invertebrates/invasive-invertebrates/wasps/identification/key-differences


Why does sequence of amino acids presented on the Catalytic Site Atlas from a given protein differs from the sequence on the RSCB Protein Data Bank

Crystallography results (pdb files) almost always contain a truncated sequence.

Both ends of a protein are often flexible (even in a crystal) and don't result in enough data for a good fit. The corresponding residues are removed from the model and the sequence, and you're left with only the residues that show a defined electron density.


Would some dinosaur egg be the most massive cell that ever existed? Are dinosaur egg relatively small compared to eggs of modern birds?

The biggest known egg was laid by Aepyornis, the so-called Madagascan "elephant bird." See this short video. Of course, the eggs of most dinosaurs are unknown, so there could be something more massive waiting to be discovered. But the eggs of species much bigger than Aepyornis have been discovered, and the eggs just don't measure up to Madagascar's champion.

I'm not an expert on dinosaur eggs, but if you're looking for information, try searching for Protoceratops and Maiasaura peeblesorum. Protoceratops is a ceratopsian, ancestral to the more familiar Triceratops, whose remains are abundant in Mongolia. I believe many Protoceratops eggs have been discovered. (See At Last, A True Protoceratops Nest)

Maiasaura is a duck-billed dinosaur (hadrosaur) that left numerous fossils in what is now Montana. The fossils include some fabulous remains of nurseries (e.g. Egg Mountain). (See Maiasaura)

These links may not feature any information about egg size, but they should at least give you some background information. I'm sure Dr. John Horner has commented on the size of Maiasaura eggs somewhere. He's written on a wide variety of topics, including dinosaur growth rates, physiology, etc.

P.S. Here's a cool link. There's a photo of a fossilized Maiasaura embryo emerging from its egg (#4, I think). Another page (8?) claims that no dinosaur egg could be more than two feet in diameter.


Low-tech or low-cost technique for quantitative estimation in enzymology

If there is a way to:

Make the replication of a common culture organism (e.g. E. coli) dependent
upon the inhibitor or substrate of interest, possibly with a restrictive media.
Express the enzyme of interest in a relatively controlled manner in such organism (e.g. well caracterized promoter in plasmid with well characterized copy number),

Then you can get good mileage out of some serial dilutions and a OD600 meter. Even better with a plate reader.
Exact protocol will depend on the quantity under consideration, but mostly will amount to substituting around in the enzyme kinetics equations until the quantity of interest is a function of the concentration, and devise a scheme to cancel out the other unknown quantities (often substrate concentration ramp + starting OD ramp + curve fitting)


Aside from Homo Sapiens, do the males of any other species care for the offspring of those unrelated to them?

Yes most commonly in a reciprocal altruism fashion, when you aid any offspring of your species or any in your herd/pack. Crocodiles are known for this. They respond to any crocodile (of their species) distress call from any baby crocodiles. This tends to be an advantage because proximity usually means relatedness and even when it doesn't crocodiles are high enough on the food chain the risk to the males is low compared to the time and effort that would be needed to identify the offspring first.

likewise in herd animals it can be an advantage because it ends up with everyone protecting everyone else's offspring but usually has to be paired with some ability to punish freeloaders/cheaters (individuals who don't help protect the offspring).

Of course you also have males who are tricked into it, after all a male does not always know what are its offspring.

You also have males that will help with a current brood to court the mother, or even unrelated females. Basically they are showing off how good a parent they can be, some believe this is what humans are doing. This is seen in some social primates. It might happen in some birds too but I am not sure.


Why isn't direct diagnosis of infectious disease through microscopes a common thing?

The problem with this is that A) the infection may be local, and very few if any bacterial cells may be in circulation, and B) even if the infection is systemic, there could be as few as a couple of bacterium per million red and white blood cells, making visual confirmation impossible. More often, if the attending physician feels the need for a direct ID in order to prescribe the correct medication, a culture is taken from the site of infection or blood is drawn, and then subjected to one of any number of different automated ID systems and/or culture conditions to identify the particular type of bacteria present. This can be as simple as Gram staining to identify Gram positive vs. Gram negative bacteria (different types of antibiotics work on the two classes) all the way to a full identification (genus, species, strain) based on molecular sequencing, typically of ribosomal RNA.


How is the beginning of an episodic memory encoded in the brain?

We don't have a full understanding of how episodic recall really happens in the brain, but there are theoretical approaches to understanding memory that are supported (but not shown definitively - it is really difficult to design appropriate experiments that are not beyond current technological capabilities) by experimental evidence. These approaches don't require any sort of hard "start" or "end" signal for episodic memory to work. In these approaches, an episodic memory is thought of as a sequence of brain states that correspond to previously experienced states.

The sequence occurs because connectivity promotes the network to progress from State A to State B to State C, etc. Additionally, all of the states consisting of that one "connected" memory are also associated, so that they prime one another.

To recall, you don't need to start at State A - you can start anywhere in the chain, and just recalling State C will prime you to also recall State A and B, so you can mentally "rewind" the memory a bit (we have no idea how exactly this type of conscious control works), even though it progresses most clearly in the A->B->C sequence.

The point of entry that allows you to initially get in to this chain might not be part of that episodic memory, either. For example, maybe you see a cat, and this leads to to an episodic memory of one event you shared with your own cat 5 years ago.

Brains are very dynamic, they do not behave like a feed-forward computation you might implement in a simple computer program. It is possible that there are "start" or "end" signals for episodic memories that we haven't found yet, but they may not be necessary at all.

For some further reading you could look for references on attractor networks, pattern separation and pattern completion, and theories of memory formation.

The book by Dayan and Abbott on theoretical neuroscience is also a good approach to some of the more basic background and includes an introduction to biologically-inspired models of learning and memory.


What neurons' projections comprise the olfactory nerve (Cranial Nerve 1)?

Olfactory receptor neurons (ORNs) in the olfactory epithelium in the nasal cavity project to the olfactory bulb; this projection is Cranial Nerve 1 and it's more of a collection of fibers rather than a highly organized nerve.

Your surprise or confusion is probably based on this:

  My understanding is that the projections that emanate from the olfactory bulb and terminate in the brain constitute the olfactory nerve

...which is false: the olfactory nerve is the step prior to the olfactory bulb. The olfactory bulb is part of the brain.

I'll add that I have seen poor diagrams of the brain that point to the olfactory bulb and label is as cranial nerve 1, which is false or at least misleading.


How are ions 'pumped' across a membrane during electron transport?

Short answer:
Electrons flow through membranes by floating through kind of channels made out of iron-sulfur clusters.

Long answer:
Let's take a look at the electron transport chain in the inner mitochodrial membrane. There is a proton gradient across the membrane building up a potential difference by pumping protons across the membrane as electeons flow through the respiratory chain. They (electrons) like to flow throught the respiratory chain because they can go from enzyme to enzyme each with a lower standart free energy. These enymes together form one big complex within the inner membrane with Fe-S clusters enabeling electrons to flow through the membrane by giving them a kind of a power stroke (see here).
This as an simplyfied answer on a example.


Which process is right to describe V(D)J recombination? RAG-1 and RSS recurring process

Excerpt from Cellular and Molecular Immunology, 8th ED, p.181-182. Don't up-vote me, i just thought this text offers a good, up-to-date explanation.

  The Mechanism of V(D)J Recombination

  Rearrangement of Ig and TCR genes represents a special kind of non-homologous DNA recombination
  event, mediated by the coordinated activities of several
  enzymes, some of which are found only in developing
  lymphocytes, whereas others are ubiquitous DNA double-stranded break repair (DSBR) enzymes.Although
  the mechanism of V(D)J recombination is fairly well
  understood and will be described here, how exactly
  specific loci are made accessible to the machinery
  involved in recombination remains to be determined.
  It is likely that the accessibility of the Ig and TCR loci to
  the enzymes that mediate recombination is regulated
  in developing B and T cells by several mechanisms,
  including epigenetic alterations in chromatin structure
  and DNA as discussed earlier, and basal transcriptional
  activity in the gene loci.
  The process of V(D)J recombination can be divided
  into four distinct events that flow sequentially from one
  to the next (Fig. 8-10):

  1. Synapsis: Portions of the chromosome on which the
  antigen receptor gene is located are made accessible
  to the recombination machinery. Two selected coding segments and their adjacent RSSs are brought
  together by a chromosomal looping event and held
  in position for subsequent cleavage, processing, and
  joining.

  2. Cleavage: Double-stranded breaks are enzymatically generated at RSS-coding sequence junctions
  by machinery that is lymphoid specific. Two proteins encoded by lymphoid-specific genes, called
  recombination-activating gene 1and recombination-activating gene 2(RAG1and RAG2), form
  a  complex, containing two molecules of each protein,
  that plays an essential role in V(D)J recombination.
  The Rag-1/Rag-2complex is also known as the V(D)J
  recombinase.The Rag-1 protein, in a manner similar to a restriction endonuclease, recognizes the DNA
  sequence at the junction between a heptamer and a
  coding segment and cleaves it, but it is enzymatically
  active only when complexed with the Rag-2 protein.
  The Rag-2 protein may help link the Rag-1/Rag-2 tetramer to other proteins, including accessibility factors that bring these proteins to specific open receptor
  gene loci at specific times and at defined stages of lymphocyte development. Rag-1 and Rag-2 contribute to
  holding together gene segments during the process of
  chromosomal folding or synapsis. Rag-1 then makes
  a nick (on one DNA strand) between the coding end
  and the heptamer. The released 3′OH of the coding
  end then attacks a phosphodiester bond on the other
  DNA strand, forming a covalent hairpin. The signal
  end (including the heptamer and the rest of the RSS)
  does not form a hairpin and is generated as a blunt
  double-stranded DNA terminus that undergoes no
  further processing. This double-stranded break results
  in a closed hairpin of one coding segment being held
  in apposition to the closed hairpin of the other coding end and two blunt recombination signal ends being placed next to each other. Rag-1 and Rag-2, apart
  from generating the double-stranded breaks, also hold
  the hairpin ends and the blunt ends together before
  the modification of the coding ends and the process of
  ligation.

  RAGgenes are lymphoid specific and are expressed
  only in developing B and T cells. Rag proteins are
  expressed mainly in the G0and G1
  stages of the cell
  cycle and are inactivated in proliferating cells. It is
  thought that limiting DNA cleavage and recombination
  to the G
  0 and G1
  stages minimizes the risk of generating inappropriate DNA breaks during DNA replication or during mitosis. Mice without functional Rag1
  or Rag2genes (Ragknockout mice) fail to develop B or
  T lymphocytes, and Rag-1 or Rag-2 deficiency is also
  a rare cause of SCID, in which patients also lack all
  lymphocytes.

  3. Hairpin opening and end-processing: The broken
  coding ends are modified by the addition or removal
  of bases, and thus greater diversity is generated. After the formation of double-stranded breaks, hairpins must be resolved (opened up) at the coding
  junctions, and bases may be added to or removed
  from the coding ends to ensure even greater diversification. Artemisis an endonuclease that opens
  up the hairpins at the coding ends. In the absence
  of Artemis, hairpins cannot be opened, and mature
  T and B cells cannot be generated. Mutations in
  ARTEMIS are a rare cause of SCID, similar to patients with RAG1or RAG2mutations. (see Chapter
  21). A lymphoid-specific enzyme, called terminal
  deoxynucleotidyl transferase (TdT), adds bases to
  broken DNA ends and will be discussed later in the
  chapter in the context of junctional diversity.

  4. Joining: The broken coding ends as well as the signal ends are brought together and ligated by a double-stranded break repair process found in all cells
  that is called nonhomologous end joining. A number
  of ubiquitous factors participate in nonhomologous
  end joining. Ku70 and Ku80 are DNA end-binding
  proteins that bind to the breaks and recruit the catalytic subunit of DNA-dependent protein kinase
  (DNA-PK), a double-stranded DNA repair enzyme.
  This enzyme is defective in mice carrying the severe
  combined immunodeficiency (scid)mutation, and mutations in the gene encoding this enzyme have also
  been discovered in human SCID patients (see Chapter
  21). Like Rag-deficient mice, scidmice fail to produce
  mature lymphocytes. DNA-PK also phosphorylates
  and activates Artemis, which, as mentioned before, is
  involved in end processing. Ligation of the processed
  broken ends is mediated by DNA ligase IV and XRCC4,
  the latter being a non-catalytic but essential subunit of
  the ligase.

Figure 8-10, Cellular and Molecular Immunology, 8e, p182.


Since cells are the origin of every life, any tissue must at least be based on cells. Some tissue matter is outside the cells (plant cell walls), some apparently non-cellular tissue is really a bloated organelle. Both happens. As to your theses,

yes, an example are oil reservoirs in plants
no, these are just big cells. A striking example is spinal cord nerves that can be very long; irreparable if injured, because you can't repair single cells
connective tissue is cartilage, bone, adipose tissue, blood, hematopoietic tissue and lymphatic tissue. These together fit in both the organelle and extracellular substance slots, so you would have to differentiate
bone belongs to connective tissue

So, yes, you can differentiate between functions belonging to whole cells, cell organelles, or extracellular material. And there is no reason to narrow this question to humans.


What voltage damages a neuron or a group of neurons?

It probably mostly depends on how you stimulate them, when we probe the ulnar nerve in practical classes with a stimulator on the skin, then 20V seems about fine. Most students will handle 20V 100 ms pulses, but some will flinch.

If you have a neuron connected directly to an electrode (in a dish), then you will get decent responses from 50-100mV square voltage steps. Individual cells will respond after 10-40 mV (depending on cell type), much more than 150-300 mV will probably be problematic (and not physiological) for single cells.

It sounds like you need to read some early electrophys, start with the squid giant axon, then Neher and Sudhof were the gods for the start of my PhD.


Lead acts as a poison in a variety ways relative to what tissue it is exposed to. For example, lead is able to pass through the blood-brain barrier where it can act act as Calcium homolog to interfere with neurotransmitter release. In the blood, Lead inhibits porphobilogen synthase, an enzyme required for heme synthesis.

Lead's toxicity mechanisms include:

Its ability bind sulfhydryl groups, common to many enzymes
Its ability displace metals in enzyme complexes
Its ability to act as a Calcium homolog

Lead's valence electron configuration is $\require{mhchem} \ce{[Xe] 4f^14 5d^10 6s^2 6p^2}$; which means it has two electrons in its valence shell. This pair of valence electrons contribute's to Lead's ability to act as a Calcium analog and to Lead's tendency to form compounds in which it has an oxidation state of +2. Many such compounds dissolve in lightly acidic solutions. This has created lead exposure hazards when acidic tap water was pumped through lead pipes and when fruit juices have been served from ceramic vessels with lead-containing glazes.

Lead Poisoning

Lead


Why is the DNA codon table "equal" to the RNA codon table

Genetic code and codons are always used with reference to RNA. When talking about DNA, the the sense strand of a gene is considered its sequence. The anti-sense strand though is the template for mRNA synthesis, does not represent the gene.

DNA-codon table has simply U replaced by T. Apart from a wikipedia article, I don't find the term being popularly (not colloquially) used elsewhere.


Does retinal detachment happen more frequently at night?

In case of normal, healthy person, no, I don't think so. In fact, retinal detachment could happen at anytime of the day. Main causes are diseases and illness, such as AIDS, diabetic retinopathy, cancer, or trauma such as post-cataract surgery and being hit/kicked hard on the eyes.


Calibration curve for single radial immunodiffusion

When the radial immunodiffusion method is used to measure antigen concentrations in samples, a plate or slide is set up using agarose containing an antibody or antiserum. Holes are punched out of the agarose to form wells into which antigen is dispensed. The antigen diffuses out into the agarose and when the antigen/antibody ratio is favourable an immunoprecipitate will form as a ring (immunoprecipitin ring). The final diameter of the ring is proportional to the initial concentration of antigen.

Addressing the question: isn't this simply explained because the values on the Y axis are squares of the diameters of the rings, and this includes the well into which the antigen is dispensed?


It appears the author of the question is trying to use "thylakoid electron transport chain" in an overly specific way. The chain from which PS I receives electrons has far more components and is different from the shorter chain to which PS I passes its electrons. But according to my copy of Biology, Campbell & Reece 7th edition, both are called "electron transport chains" and both reside in, or on, the thylakoid membrane. Perhaps the "directly" in the question refers to the fact that PS I's electron is first captured by a "primary receptor" before being passed to ferredixon, the first member of the chain to which PS I passes electrons. But, again according to Campbell, this primary acceptor is considered part of the photosystem.

I used to teach this stuff. I'd toss out the question.


Regarding detection of pregnancy during post mortem

Answer is obviously yes. Here's an article reporting a forensic method used to detect pregnancy using placental markers in a Reverse Transcriptase PCR from a DNA sample. It could be applied in a death body, when it's possible to get a DNA sample from a tissue.


Biological term for close species rivalry

Citing wikipedia

  Character displacement refers to the phenomenon where differences among similar species whose distributions overlap geographically are accentuated in regions where the species co-occur, but are minimized or lost where the species’ distributions do not overlap. This pattern results from evolutionary change driven by competition among species for a limited resource (e.g. food). The rationale for character displacement stems from the competitive exclusion principle, also called Gause's Law, which contends that to coexist in a stable environment two competing species must differ in their respective ecological niche; without differentiation, one species will eliminate or exclude the other through competition.

  In ecology, the competitive exclusion principle, sometimes referred to as Gause's law of competitive exclusion or just Gause's law,[2] is a proposition that states that two species competing for the same resource cannot coexist at constant population values, if other ecological factors remain constant. When one species has even the slightest advantage or edge over another then the one with the advantage will dominate in the long term. One of the two competitors will always overcome the other, leading to either the extinction of this competitor or an evolutionary or behavioral shift toward a different ecological niche. The principle has been paraphrased into the maxim "complete competitors cannot coexist"


Often the phenotype caused by a given allele depends on the alleles present in other genes; this is termed epistasis. In the context of tumors, selective pressure is primarily associated with the ability of cells to grow and divide (without dying). It could be possible for two mutations which each confer some tumorigenic properties to conflict with each other, such that when both mutations are present they interact to either kill the cell or otherwise block the effect of the other mutation. The expected result would be that few tumor cells would exist with that combination of mutations because they would proliferate less than those cells with just one.

However, I suspect they are just addressing an non-significant difference from chance that they felt was too big to ignore entirely in discussion. You left out the rest of the sentence including a key word 'either' which I think is entirely misleading here and I wish you would not have done that (emphasis mine):

  frequency of comutations in FGFR3 and KRAS or PIK3CA and KRAS was lower than predicted by chance, suggesting either a lack of selective pressure for both mutations to occur or a negative interaction between the consequences of each mutation

Essentially they are hedging the statement that there could be a negative interaction (i.e., selective pressure against) having both mutations with the possibility that there is just no meaningful positive interaction and the observation of a less than chance co-occurrence is not a true result. Note that they have a very small population because these are clinical tumors, and KRAS analysis was only in 59 patients (with only 12 mutants), making the statistical power for interactions very low.

I agree that this wording is imprecise and a bit unclear, so your confusion is understandable, but I think there are two reasons why it is worded this way. First, I believe they are trying to emphasize a possible future research direction and are trying to do so without making a criticism of the paper they are reviewing, because I don't think they view it as a criticism. Had they said "This study doesn't have enough statistical power to determine if there is a negative interaction between these mutations," that would sound overly critical given they are discussing something that wasn't really the intent of the original study. Second, I think the simplest prior expectation (which they do not state but is implied) is that two mutations that contribute to tumor production individually will be even more tumorigenic when present together. By stating the other outcomes: no selective pressure for the two mutations to cooccur or a negative interaction, they are implicitly stating that the simpler outcome, a positive interaction, does not seem to be occurring.

There is also a definite issue of selection bias here (statistically, not evolutionarily). That is, they are investigating a certain type of tumor. If those tumors can be caused by either a mutation in one gene or a mutation in another, then the chance association of those mutations would be the chance in the general population/other types of tumors/noncancerous tissue, which would be low (because most have neither), rather than the chance in patients.

The article you refer to is just a commentary on another article; you should really read Hafner et al instead (and note the original paper doesn't talk much if at all about these co-occurrences).


Yes, the embryo would get that DNA mutation.

Both sperm and egg are haploid, meaning they only have 1 copy of each gene. When the sperm fertilizes the egg, the resulting child is a diploid, meaning he/she has two copies of each gene. However, if the sperm was mutated, then child has one mutated copy of some gene(s).

Depending on the gene(s) that are mutated and the sequence of the mutated gene(s), this could result in non existent to severe consequences.


What's the recommended maximum passage number for mammalian cells (NCI-H441)?

This is a very good question and it highlights a very frequent misconception about cell culture and it is using the passage numbers as an indication of how well a cell is behaving. Although this can be a good barometer but it is misleading. Passaging can stress the cells if performed very frequently, although again that depends on how fast the cells are dividing.

You should not think of passage (and cell culture in general) in terms of the procedure itself but in terms of population doubling (PD) which can be calculated using the formula provided here (http://www.sciencellonline.com/site/techsupport.php). I personally use [Log10(harvesting cell No/seeding cell No)/Log10(2)]. This should allow you to characterise your cellular behaviour between every passage and allows you to draw a cumulative PD graph. Once the cumulative PD versus time becomes non-linear, then you would know that the cells have changed behaviour and it might be best to use a fresh stock.

The main advantage of this method is that you are not relying on guess work and deal with solid numbers and allows you to predict when you should expect to start a fresh batch for passage. Although passage numbers can do the same job if you assume per passage, the cells have done a certain PD but this is more of a guess work and you can not track how well your cells are doing at a given time point. For example one of the main problems with using a passage as a measure is that you can passage the cells at 98% confluence to a fresh flask and although that counts as a passage but it is pretty uninformative in terms of cell behaviour and gives you no solid numbers and you can do this many many times and although you would have done high number of passages but your cells would appear ok. Although such an exercise is pointless and will probably stress the cells but it is just to make the point that passage numbers are not necessarily a very informative and quantifiable measure of how well the cells are doing or behaving hence PD and cumulative PD should be used. Another advantage is that since you are dealing with actual cell numbers, if you changed your cell culture flask size from lets say T-75 to T-25, you don't have to be worried about changes to your frequency of passage or having to make further guess work on how that has effected your cell behaviour.

My main advice is that you should keep you frequency of passage the same at least in the beginning (although keep an eye on the cell density as you don't perhaps want to let cells to be too over-confluent or unconfluent when passaging, depending on your specific methodology and what has been established in your lab), but count your seeding and harvesting density (cell No) and calculate the PD and cumulative PD and draw a cumulative PD vs time graph and monitor the behaviour of cells. This should give you a good indication of you cellular behaviour under the conditions you are working with them since guidelines are just that, guides and they can never substitute experimental characterisation of your cells under your conditions and handling method!


Why are humans so variable in appearance

Because we as humans are really really good at picking up small differences in humans and really really bad at detecting them in anything else.

Animals are often quite good at telling each other apart, far better than humans are, birds in particular are known for this. Just because you as a human are bad at it does not mean they are.

There is a pretty strong evolutionary pressure for humans to be able to tell other humans apart and not much of an advantage for being able to tell two lions apart. We need to be able to tell mates, rivals, relatives, and strangers apart easily. We don't need to differentiating one black bird from another.

We also spend a lot of time around other humans, so we are more familiar with their differences, but the same thing happens to animal researchers whale researchers who spend a lot of time around whales can easily tell two whales apart at a glance. this is also part of the reason some people have trouble telling individuals from a different "race" apart, they are to unfamiliar and uninterested to spot differences. Or the way a car guy can spot the difference between two models at a diffrence but someone else might not.

You see the same effect chimps can tell each other apart but can't tell humans apart, unless they spend a lot of time around humans then they can. They can also match voice to face meaning the can recognize both.

Then of course you have the fact you are focusing on vision, try to tell two people apart by smell and you will likely fail but a dog will have no problem with it. likewise many monogamous song birds can identify their mates from song along, just as we recognize others by voice, penguins are another example. Humans are very visual creatures so much of our identification ability relies on vision we see the same thing in other visual species, animals tend to use whichever sense are their dominant ones. Saying organisms are more visually similar because organisms with far worse vision than humans can't tell them apart by vision alone is simply an unreasonable conclusion.


What are the migratory patterns of Orcas in the Pacific Northwest? Do they pass by Vancouver in the Fall?

There are three ecotypes of orcas which are all members of the same species but tend to display different behaviours, communicate differently and have different prey preference. The most common ecotype near Vancouver are the Resident Orcas, specifically the Southern Resident Orca population. This population is comprised of the J-pod, K-pod and L-pod. These populations feed mainly on salmon which as scarce in the Salish Sea during the winter. Therefore, resident orcas tend to disperse in search of food during winter months in the as far north as Alaska and as far south as Califorina.

As salmon travel to the ocean from inland rivers for food during the summer, the Southern Resident Orcas return to the Salish Sea to feed. By October, many salmon return to their natal stream to spawn and therefore, the abundance of prey for the Southern Resident Orcas depletes. During this time, orcas will begin to disperse North and Southward in search of more abundant prey but some will linger to feed on the salmon late for spawning.

If you're interested in more information about this population, check out Orcas of the Salish Sea


Multiple start and stop codons in mRNA and pre-mRNA

Whether or not there are multiple start and stop codons depends on what you mean by "start codon" and "stop codon".

The start codon has the sequence "AUG", and the stop codon has the sequence "UAG", "UAA", or "UGA". Both the pre-mRNA and the mature-mRNA can, and usually do, contain multiple instances of all of these sequences. However, only one "AUG" instance serves as the translational start site, and only one instance of the stop codon sequence serves as the translational stop site.

The translational start site is usually the first (5' most) AUG. However, for reasons that are still not entirely understood, in about 5% of genes the first AUG is skipped, and translation starts at one of the other AUG sequences.

The translational stop site is always the first stop codon to occur in-frame with the translational start site in the mature mRNA.

The stop codon is usually not (I'm tempted to say never) the final sequence before the poly-A-tail. The coding sequence (the RNA region that codes for the protein) occurs in the middle. There is a 5' untranslated region (UTR) before the protein coding region, and a 3' UTR after the protein coding region. The UTR sequences vary among genes and can have different functions depending on the sequence.


How Anopheles crop doesn't digest gametocytes of P. vivax?

Disclaimer: I am trying to answer the question without finding any academic research on the topic. So, appreciate hypotheses and feel free to point out mistakes.

Short Answer : Co- Evolution

Broad Answer: 2 hypotheses

The gamete stage of Malaria parasite simply co-evolved with Anopheles sp. to develop a protective mechanism to survive digestion in crop. Whereas, the other stages of Malaria parasite didn't co-evolve,  so they get digested.
Parasites had already the protective mechanism for surviving digestive enzymes in Anopheles crop. They entered mammals later and evolved a life cycle with a new protective mechanism for new host's immune system.

Why is that?

The answer to this question is not so clear according to known biology, as I haven't found much research in this phenomenon.
But, we have to remember that biology sometimes (or always?) doesn't explain why rather explain how.

The following words are corresponding to what I think about the mechanism of this co-evolution

Hypothesis 1:
It could have simply happened that some point in ancient times, the gamete entered the Anopheles crop from a mammal, but not only that; it tried to continue its life cycle on this new host. But, the environment of crop was unsuitable for the gamete to survive due tto digestive enzymes. So, the first few million or billion tries went into vain. But, the parasite slowly started to evolve to adopt in the Anopheles crop.

After 'some' time, the parasite developed a working protective mechanism from digestive enzymes and continued it's life cycle in Anopheles.

As @Another Home sapien points out, there should be some benefits for this evolution. While it's hard to tell exactly what the benefits could have been; I think it's simply to adopt to new potential host's physiological environment.

But why didn't other stages evolve of Malaria parasite in a same way?

This is another hard question to answer. However, it's not so that only the Anopheles and the parasite co-evolve; the mammal host co-evolved too in this period. And the whole system evolved gradually to get to the present life-cycle of malaria.

Hypothesis 2:

It might have happened that the original host to malaria parasite was indeed Anopheles. So, it had developed a protective mechanism long before entering any mammal host. Then, after entering the mammal host it developed another protective mechanism to survive host's immune system and continued  it's life cycle.

I think hypothesis 2 is more probable as insects pre-existed mammals. Another hypothesis can be drawn the life cycle of parasite is shaped up simultaneously in mammal host and Anopheles host. But, it's hard to hypothesize what could have happened in this scenario.

Reference : 1. Wiki: Co-Evolution

2.Article on this co-evolution


why do chaperones bring protein into mitochondria? why would mitochondria need protein?

As you probably know, mitochondria (together with chloroplasts) are a very interesting organelle: they are a result of an endosymbiotc relationship that took place more than 1 billion years ago.

And, because of that, mitochondria have their own (circular, as a prokaryote) DNA. And here comes the common misconception: a lot of students think that mitochondria (and chloroplasts as well), because they have their own DNA, can synthesise all proteins they have (the most famous ones are the enzymes of Krebs cycle and Respiratory chain). But that's not correct.

What happened is that, generation after generation, along a very big period of time, mitochondrial genes were, little by little, transferred to the host's nucleus. According to Nature (2017):

  During the course of mitochondrial genesis, many genes were transferred from the genome of the mitochondrial endosymbiont to the genome of the host.

Thus, today, a human mitochondria has only 37 genes:

From those 37 genes, only 13 code for respiratory proteins. Therefore, those mitochondrial genes are responsible for only a minor fraction of the proteins present in a human mitochondrion. So, where do the other proteins come from?

They come from the nucleus, encoded in the nuclear DNA. Those proteins are synthesised in the cytosol and, using peptide signals, are transferred to the mitochondria. According to Dudek, Rehling and van der Laan (2013):

  Most mitochondrial proteins are encoded in the nucleus. They are synthesized as precursor forms in the cytosol and must be imported into mitochondria with the help of different protein translocases.

According to the Human Protein Atlas, 1070 proteins have been detected in the human mitochondria. Thus, since 13 of them are from mitochondrial origin, we conclude that at least 98.7% of the mitochondrial proteins are imported from the cytosol.

Sources:

Nature.com. (2017). Origin of Mitochondria | Learn Science at Scitable. [online] Available at: https://www.nature.com/scitable/topicpage/the-origin-of-mitochondria-14232356 [Accessed 5 Aug. 2017].
Dudek, J., Rehling, P. and van der Laan, M. (2013). Mitochondrial protein import: Common principles and physiological networks. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1833(2), pp.274-285.
Proteinatlas.org. (2017). Search: subcell_location:Mitochondria - The Human Protein Atlas. [online] Available at: http://www.proteinatlas.org/search/subcell_location:Mitochondria [Accessed 5 Aug. 2017].


Proteomics data Vs Transcriptomics data?

This is what I found from doing some research. Comments are welcome at any point!

Capture percentage for data gathering:

Transcriptomics Data: There's an amplification step in Transcriptomics data gathering methods. Hence, it's possible to capture almost the totality of the Transcriptome using those methods(scRNA seq methods, Nanopore tech, Spatial transcriptomics, etc)
Proteomics Data: There's no amplification step in Proteomics data gathering methods. Those methods have fragmentation and a rejoining step which leads to a loss of the data.

Scalability of methods:

Transcriptomics Data: Scalable methods available
Proteomics Data: Less scalable methods for protein studies

Reference availability:

Transcriptomics Data: Fully annotated references available on consortiums such as ensembl biomart, etc
Proteomics Data: Universal and Comprehensive Human Proteome reference is still in question and because of the incomplete and inaccurate references, much of the newly generated data is being rendered useless

Uniformity

Transcriptomics Data: Lots of publications on pipelines, and their benchmarking available
Proteomics Data: Lack of uniformity across labs/research groups and lack of related literature lead to differences in protein fragmentation and solubilization and differences in algorithms to run analyses

Technical Bias

Transcriptomics Data: Many methods available to tackle cell-bias, noise in data, and batch effects, so as to capture maximum biological variability
Proteomics Data: Cell-wide Mass spectrometry has a bias towards the identification of peptides with higher concentration or contamination from other experiments