Evolution of hunting behavior of parasitoid wasps

Context is everything. Lets start by working back to front.

  larvae eat the tarantula organs in a specific sequence to keep it
  alive as long as possible.

Most of the time if the larva eat the organs in the wrong order they don't die, they just end up with less food. It is pretty easy to see how this could evolve to be better, larva that eat in the correct sequence end up with more food thus have an advantage, larva that eat in hte absolute wrong sequence don't survive.

  on a [specific] species of tarantula

Again easy many wasps are not as picky they will lay their eggs in/on a wide variety of hosts, but specialization is favored a lot in evolution as it helps your lineage exploit a resource better and better, you only have to deal with the defenses of a single species as opposed to many different ones which might have mutually exclusive solutions.

  lay their eggs in a specific region.

again failing to do this does not necessarily mean their larva die, it just means they are worse off becasue they don't get to eat as much. Again easy to see how this evolves, a wasp that picks its target end up with more well fed offspring. Many don't even lay their eggs inside the host but outside and let them eat the host from the outside in, this is what this species does.

  Upon finding a tarantula, the wasp locks its mandibles onto a foreleg and brings its stinger into position so as to paralyze it.

Again not every parasitic wasp does this many don't paralyse their host, but they jab them with the ovipositor relying in brute force to injure, paralyse, or kill the host. Others just lay their eggs on them and fly away. Others simply kill the host jam it in a hole and lay their eggs on it. But wasps that paralyse the host are less likely to get attacked. but even if they kill the host instead the larva still get a meal. hunting always tends to be risky, but as long as the reward outweighs the risk it can evolve. Additionally many wasps do not target adults but larva and eggs that can't fight back. venomous Stinging is actually fairly rare in wasps occuring only in the ones that attack the most dangerous hosts. Of course once a wasp lineage gets good ant not killing its host then there is little reason for the larva to be able to eat more putrid remains of the host, as such adaptations are costly so you can see how after they stop killing the prey the larva might lose the ability to keep eating dead hosts.

  The wasp then drags the tarantula into a hole that it has already dug.

Again not every species does this, some just lay their eggs on a host, without doing anything else, but this carries more risk of your larva getting dislodged or injured, but insects are not people if there is a parasite on their back there is not a lot they can do about it.

  These wasps are solitary, which means there are no conspecifics to
  teach the new wasp how to do all this. Thus, the entire behavioral
  program described above must be encoded in the wasp's genome.

Even your own source disagrees with this, it shows wasps get better at subduing the host the more often they do it, laying eggs in NOT a once in lifetime thing they may do it many many times, so not being perfect can still work.

Once you see the huge variety in parasitic wasp behavior it is much easier to the step by step sequence that can happen to get to each one. You are not even at the most extreme, there are wasps that go even further, like having viral mutualists, larva that can't poop so as not to contaminate a host they live inside, and even leaving chemical markers to keep other wasps from laying eggs in/on the same host. Parasitic wasps are rather well studied I invite you to look more into them, they are really good models of evolution.


Please help me to identify this red worm

Judging from the photo, it's an earthworm, some species of Lumbricidae. If the accident happened in India, this faunistic paper can be of some help.


Human evolutionary innovation for rapidly restoring glycogen, and link to cardiovascular disease?

Summary

We (Homo genus) used a lot more glycogen as we sweated while we foraged.
Our efficient metabolism allowed us to replete our glycogen stores with seemingly little trade-off.
Those same metabolic genes are associated with obesity risk
Obesity is a risk factor for heart disease

Sweat uses glycogen

...and lots of sweating was beneficial for our species survival

I think what you are indirectly asking about, as unlikely as it seems, is sweat production.

It is known that humans have a large number of eccrine sweat glands compared to other animals, for which glycogen is the primary energy substrate.
The ability to thermally vent via full-body eccrine sweat glands in this way, in conjunction with bipedalism, allowed foraging in the midday heat when predation is low.
This is limited to the genus Homo (Leiberman, 2015), although it is not clear exactly which mutations are responsible as far as I can tell.
Glycogen stores are more supported by their capillaries, and by extension have faster repletion, in primates in hotter drier climates and indeed in humans (Best & Kamilar, 2018).
Now at this point, you are thinking "Aha! More capillaries mean more pressure on the cardiovascular system and more disease".
I cannot find any evidence directly linking those two.

A note on glycogen production differences in our close relatives

The 1,4-alpha-glucan-branching enzyme indeed seems similar across close species.
So either we have relatively larger livers to cope with this, or some complex genetic mechanism produces more of the protein.
A quick BLAST alignment shows the identity of the 1,4-alpha-glucan-branching enzyme of chimpanzee species at >99% and E~0. The top results are shown below:

Entry   Organism    Organism ID Info            Status

Q04446  Homo sapiens (Human)    9606    E-value: 0.0;   Score: 3,814;   Ident.: 100.0%      reviewed
A0A2R9CB94  Pan paniscus (Pygmy chimpanzee) (Bonobo)    9597    E-value: 0.0;   Score: 3,803;   Ident.: 99.6%       unreviewed
H2QMY2  Pan troglodytes (Chimpanzee)    9598    E-value: 0.0;   Score: 3,803;   Ident.: 99.6%       unreviewed
G3SDH8  Gorilla gorilla gorilla (Western lowland gorilla)   9595    E-value: 0.0;   Score: 3,798;   Ident.: 99.4%       unreviewed
A0A096NQ25  Papio anubis (Olive baboon) 9555    E-value: 0.0;   Score: 3,729;   Ident.: 97.6%       unreviewed
A0A2K6ANP2  Macaca nemestrina (Pig-tailed macaque)  9545    E-value: 0.0;   Score: 3,723;   Ident.: 97.3%       unreviewed
A0A0D9R0S5  Chlorocebus sabaeus (Green monkey) (Cercopithecus sabaeus)  60711   E-value: 0.0;   Score: 3,718;   Ident.: 97.4%       unreviewed
A0A2K5W1V0  Macaca fascicularis (Crab-eating macaque) (Cynomolgus monkey)   9541    E-value: 0.0;   Score: 3,716;   Ident.: 97.2%       unreviewed
A0A2I3GDY3  Nomascus leucogenys (Northern white-cheeked gibbon) (Hylobates leucogenys)  61853   E-value: 0.0;   Score: 3,714;   Ident.: 97.2%       unreviewed
A0A2K5I4Z7  Colobus angolensis palliatus (Peters' Angolan colobus)  336983  E-value: 0.0;   Score: 3,713;   Ident.: 96.7%       unreviewed
A0A1D5R8L3  Macaca mulatta (Rhesus macaque) 9544    E-value: 0.0;   Score: 3,712;   Ident.: 97.2%       unreviewed
A0A2K6KT87  Rhinopithecus bieti (Black snub-nosed monkey) (Pygathrix bieti) 61621   E-value: 0.0;   Score: 3,705;   Ident.: 96.9%       unreviewed
A0A2K6PB45  Rhinopithecus roxellana (Golden snub-nosed monkey) (Pygathrix roxellana)    61622   E-value: 0.0;   Score: 3,699;   Ident.: 96.7%       unreviewed
A0A2R9CB98  Pan paniscus (Pygmy chimpanzee) (Bonobo)    9597    E-value: 0.0;   Score: 3,680;   Ident.: 99.0%       unreviewed
A0A2I3T5K0  Pan troglodytes (Chimpanzee)    9598    E-value: 0.0;   Score: 3,680;   Ident.: 99.0%       unreviewed
A0A2I2ZFX5  Gorilla gorilla gorilla (Western lowland gorilla)   9595    E-value: 0.0;   Score: 3,675;   Ident.: 98.8%       unreviewed
A0A2K5QWD9  Cebus capucinus imitator    1737458 E-value: 0.0;   Score: 3,665;   Ident.: 96.0%       unreviewed
A0A2K6SM68  Saimiri boliviensis boliviensis (Bolivian squirrel monkey)  39432   E-value: 0.0;   Score: 3,661;   Ident.: 95.9%       unreviewed
F7FDF1  Callithrix jacchus (White-tufted-ear marmoset)  9483    E-value: 0.0;   Score: 3,627;   Ident.: 96.0%       unreviewed
A0A2K6ANP4  Macaca nemestrina (Pig-tailed macaque)  9545    E-value: 0.0;   Score: 3,610;   Ident.: 95.3%       unreviewed
A0A2I3MXY4  Papio anubis (Olive baboon) 9555    E-value: 0.0;   Score: 3,607;   Ident.: 96.9%       unreviewed

Although this is only one protein of a multi-protein metabolic pathway, I think there must be something much more complex about how our glycogen is repleted to deal with the higher demand than simple differences in proteins.

Increase metabolism and disease

Humans have benefitted from a "thrifty genotype" when it comes to metabolism (Neel, 1999).
This, and the well-cited 1962 paper it is based on linking our faster metabolism to diabetes (Neel, 1962), may indeed be the paper you are looking for, but in my personal opinion, it is not very quantitative by today's standards and comes from the days before we had access to genomic data.

Although glycogen is only part of the story, it is generally accepted in the community that humans have an optimised metabolism. In terms of disease related to our metabolic evolution, GWAS showed that the genes that allow our increased metabolic activity is linked with obesity risk factors (Castillo et al., 2017).

To link that to your original question, obesity is linked with heart disease according to, well, everyone that has ever looked at it. Here is an NHS link to show it is a principal part of modern healthcare.

It may not be the exact answer you were expecting, so it will be fascinating if other papers corroborate this more directly.

Big brains need a faster metabolism

The scipop article you may have read could be from Science Daily, however this does not mention glycogen. This covers the Pontzer et al., 2016 paper which shows that we have a faster metabolism and this is linked with our brain size compared to our close primate relatives (another angle to the Leiberman 2015 paper discussed below).
The scipop article goes on to talk about research linking this to an increased risk of heart disease, not mentioned in the original Nature article.


It seems to be the secondary feather of a Waxwing, a bird from the Genus Bombycilla, like Bombycilla cedrorum:

Cedar waxwing. Source: https://rctfan2.deviantart.com/art/Cedar-Waxwing-285656802

Actually, that red tip gives the bird its name (from the Wikipedia link):

  They have unique red tips to some of the wing feathers where the shafts extend beyond the barbs; in the Bohemian and Cedar waxwings, these tips look like sealing wax, and give the group its common name.

Therefore, the possible species are the Bohemian waxwing (B. garrulus)...

... and the Cedar waxwing (B. cedrorum):

However, since the secondaries of B. garrulus normally have a white area next to the tip...

... I'd guess that your feather belongs to B. cedrorum.

In conclusion

Besides the white patches in the feathers of Bohemian waxwings, OP just confirmed that the range of the Bohemian waxwing doesn't match. Therefore, this feather belongs indeed to a Cedar waxwing.


is it possible to completely reconstruct a family tree by DNA comparison alone?

No, it is not possible to determine ancestry with just two DNA samples, but it is possible with three: http://www.nature.com/nature/journal/v487/n7407/full/nature11251.html.

Essentially, each sequence region in the progeny can be traced to either the mother or the father, but you really need both sequences to have any confidence.  That would get you one node on your tree.  You would need additional samples from higher generations to rebuild an entire ancestry.

However, it might be possible with hundreds of samples from laterally related individuals.  In fact, I think this is the fundamental hypothesis of the 1000 genome project, http://en.wikipedia.org/wiki/1000_Genomes_Project, and it pretty much worked.  Isolated populations can be discriminated by broad DNA sequence analysis.

To reconstruct your tree for a single ancestry, you would just want to use more closely related individuals (many, many of them), and then generate a phylogenetic tree, which should roughly correspond to the family tree you are investigating.


Measuring protein concentration, Bradford vs. Nanodrop?

That depends strongly on your protein and how exact you need this concentration. Both tests (Bradford and the measurement at 280nm) only do an approximation.

The measurement at 280nm relies on the interaction of aromatic aminoacids with the UV light. If you have a protein with few or no aromatic amino acids, your measurement will be wrong.

The same is true for the Bradford assay. Here you form a complex between Coomassie Brilliant Blue and unpolar and cationic side chains of the amino acids. This test is more precise, since it includes more possible side chains, but is still dependend on the composition of the protein.

More precise is the BCA assay, since it utilizes the reduction of copper ions by the peptide bond of the protein.
What you could do is run a BCA assay (or at least a Bradford assay) from your sample and measure the same sample on the Nanodrop at 280nm and compare the results.

You can find an overview over the methods here and here.


Would a spinal injury decrease human height?

As @WYSIWYG pointed, muscular atrophy is the main cause for height decrease.

A spine injury leads to neural impairment and paresis / paralysis. This affects directly muscular trophism. It also limits physical activity, this being another favoring factor for muscular atrophy and overweight issues [1]. Association of bone degenerative processes (osteoporosis, osteopathy, osteolysis) is also a factor and it is dangerous because it promotes spinal cord injuries if vertebral height reduction amount is notable [2].

Focusing on muscular atrophy, here is how it can decrease height: by increasing vertebral column curvatures mostly on the upper region with articulating vertebrae. The vertebral column tends to gain a spring-like, spiral shape, associating accentuated cervical lordosis, accentuated thoracic  kyphosis and thoracic scoliosis.

Image source: Scoliosis Treatment Alternatives. Chiropractic for Scoliosis Treatment Review (2014). Accessed 21.07.2014

While reading the comments to the question I found something interesting:

  we know that the brain tells the body to grow, would a shock or something make the brain tell your body to shrink instead of growing?

Yes, the brain (hypotalamus) initiates a neuroendocrine response that leads to growth hormone secretion. The secretion is about 700 micrograms/day in a young adolescent, while in a healthy adult it is about 400 micrograms/day [3]. The deficiency in an adult person leads to a tendency of fat mass increase and a relative decrease in muscle mass and, in many instances, decreased energy and quality of life [4]. The brain can't "tell your body to shrink", but the lack of "communication" between the brain and organs leads to less to absolutely no use of that organ, thus inducing atrophy. The lack of both external and internal stimuli leads to atrophy (in general) [5].

References:

Gupta N, White KT, Sandford PR. Body mass index in spinal cord injury -- a retrospective study. Spinal Cord. 2006 Feb;44(2):92-4. doi: 10.1038/sj.sc.3101790. PubMed PMID: 16030513.
Ji L, Dang XQ, Lan BS, Wang KZ, Huang YJ, Wen B, Duan HH, Ren F. Study on the safe range of shortening of the spinal cord in canine models. Spinal Cord. 2013 Feb;51(2):134-8. doi: 10.1038/sc.2012.99. PubMed PMID: 22945745.
Wikipedia contributors, "Growth hormone," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Growth_hormone&oldid=616959802 (accessed July 21, 2014).
Molitch ME, Clemmons DR, Malozowski S, Merriam GR, Shalet SM, Vance ML, Stephens PA. Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society Clinical Practice Guideline. J. Clin. Endocrinol. Metab. 2006 May;91(5):1621-34. doi: 10.1210/jc.2005-2227. PubMed PMID: 16636129.
Wikipedia contributors, "Atrophy," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Atrophy&oldid=611770442 (accessed July 21, 2014).


How quantitative is the theory of evolution right now?

Can we tell if a species will develop a specific character, based on the environment they're in?

This is a major part of what quantitative genetics does. Or more detailedly, quantitative genetics can predict, for a population, changes in a trait given a selection pressure. First of all, for evolution to occur there must be variation in the trait you are making predictions about. Secondly the accuracy of the scale of the predictions matter greatly for the evolutionary model to be tested (eg, "Will body size increase?" vs "Will incisors increase 3mm in 300 generations?").

Several things have to be known to predict the evolution of a given trait:

The number of genetic sites controlling this trait (QTL, or quantitative trait loci). If the all the loci for a trait are known, the nucleotide heterogeneity within the population of those sites can be quantified. The number of genetic loci are important for estimating how often they will change from new mutations.
The effect of each genetic locus on contributing to variation to the trait (additive genetic effects).
The heritability of the genetics controlling this trait, (does the environment contribute to variation in the trait (low heritability) or do genetic differences cause more variation in the trait).
The strength and consistency of selection  (how fit are individuals in that environment along to phenotypic distribution compared to previous generations). Is this trait being selected in isolation, or are other traits which share the same QTL also under selection.
The effective population size.
The rate of migration between this and other populations.

So yes, given the our knowledge of quantitative and population genetic theory, predicting evolution of a given trait is possible. Just as predicting the future is possible with the laws of physics if you know the position of every atom in the universe. It's important to remember that organisms are constellations of 'traits', so predicting the evolution of all traits which make up the individuals within a species could be similar to predicting the futures of several multiverses.


Why is hydrogen sulphide being generated on Caribbean beaches?

It would seem from a quick perusal of the literature that this is caused by sulphate-reducing micro-organisms. To quote from the eponymous Wikipedia article:

  Sulfate occurs widely in seawater, sediment, or water rich in decaying organic material. Sulfate-reducing microorganisms are common in anaerobic environments where they aid in the degradation of organic materials.

which is consistent with the situation described.

In biochemical terms, these anaerobic bacteria are using sulphate rather than oxygen as the final electron acceptor (oxidizing agent) in the elctron transport chain which generates ATP through the chemiosmotic mechanism. The reaction for the reduction of the sulphate to hydrogen sulphide (dissimilatory sulphate reduction), according to the Wikipedia article already quoted, is:

A simple way of thinking about this is that in both aerobic and anaerobic respiration the oxidizing agent itself becomes reduced. Whereas oxygen is reduced to H2O, sulphate is reduced to H2S.


Biological origin of shuddering during sleep

These are called hypnic jerks, also known as hypnagogic jerks or sleep starts. They are normal part of the wake-to-sleep transition. Hypic jerks consist of non-periodic myoclonic movements, generally involving an isolated limb.

The exact physiologic origin of hypic jerks is unknown. We can say that they correlate with a particular waveform on the EEG known as a K-complex:

Picture from http://en.wikipedia.org/wiki/K-complex

K-complexes are a normal part of Stage II sleep and can evoked using auditory stimuli, even if sleep is not interrupted. In the case of hypnic jerks, the K-complex is usually followed by alpha (wake) activity. To my knowledge, there is no evidence that hypnic jerks originate in or are routed through the cerebellum. K-complexes themselves are related to cross-talk between the cortex and the thalamus, a circuit that doesn’t involve the cerebellum.

In addition to the EEG findings, it has also been shown that the jerks are accompanied by autonomic activation — transiently increased heart rate and respiratory rate. There is also an (unexplained) subjective aspect. You described it as feeling "as if you are about to fall off,” which seems to be consistent with the published literature on this. As mentioned in the review cited below, some people report a sensation of "falling into the void.”1

The clinical implications, in case you were wondering, are summarized well by Vertugno et al.:

  Sleep starts are common physiological phenomenon affecting up to 70% of the adult population and their course is benign, resolving without any neurological sequel. Therefore, reassurance and counselling are all that is needed to treat the patient. Though an adequate explanation and reassurance may be sufficient, some patients may require a small dose of clonazepam (0.5–1 mg at bedtime) to ameliorate the symptoms on a short-term basis.

1. Vetrugno R, Montagna P. Sleep-to-wake transition movement disorders. Sleep Med. 2011 Dec;12 Suppl 2:S11-6.

You requested in a comment a reference to introductory material on the topic. What we know about the neuro-physiology of sleep is mostly based on the analysis of EEG (brain-wave) tracings. I therefore refer you to this introduction to sleep polysomnography if you would like to get a better handle on how scientists think about sleep.


I think this is an Aphid because it has long, thin legs and two-jointed, two-clawed tarsi and resemble the Russian wheat aphid very much. They are very common in temperate zone and is a major plant pest.

Here's how the Russian wheat aphid looks:

Source:Website of tasmanian government


Are there beneficial genetic mutations identified by consumer DNA genotyping?

First of all, I think it is, to a large extent, the way you perceive it. Instead of cancer-causing allele and hair-loss allele, you can think of them as cancer-protection and great-hair alleles. If you don't have disease alleles, that means that in some sense you have "life-extending" genes! Sounds much better, doesn't it?

Second of all, most funding for research is directed at disease so it is not surprising that most of the scientific knowledge is regarding this type of genetic variation.


How do centrioles auto-locate to opposite sides of cell during mitosis?

During cell-division centrioles move towards opposite 'poles' and finally get attached to cell-membrane. Different factors influence & drives this process, most still not discovered. So this mechanism is largely unknown. From the scientific literatures published on this  matter till recently we can say that this process should include:

A structure along which the centrioles can migrate,
Molecules associated with the movement of centrioles,
Signal molecules triggering this process,
Signal molecules determining the direction of migration.

To answer 1., Microtubules form a intra & inter-cellular network along which subcellular structures can move. Actin & Myosin are also involved in some cells. For reference read Ganong's review of Medical Physiology. (the example you stated in your question about neurons is a substantially different process. But neurotransmitters are carried with the help of Microtubules. Chromosomal structures also are arranged with the help of them.)

For points 2,3 & 4 read this paper, these parts are very clearly described there.

Thank you.


Meaning of “cognate genes encode the basic biological functions of proteins”

The sentence quoted accidentally misuses the word ‘cognate’ because in attempting to appear profound it has become overweight and off-balance. Notice the sentence also contains the meaningless nonsense of “real-time dynamics”, and in the rest of the paper the word ‘cognate’ is (fortunately) nowhere to be found.

What does the author mean? His review is on proteomics, and he wishes to emphasize the importance of post-translation modification of proteins. He needs to refer to the unmodified form of proteins, and so he associates them with the information in their genes, which is limited to the unmodified amino acids. The word ‘cognate’ in plain English has the meaning of ‘related’ or ‘corresponding’, so the author would appear to be using it to imply the relationship between particular genes and the individual proteins that they encode. What he may have meant to say is:

  “Whereas genes encode the basic biological functions of their
  cognate proteins…”

This would have been linguistically correct, although the word ‘cognate’, in my opinion is unnecessary as it adds nothing to the sentence.

You can find a biological definition of cognate on GenScript:

  cognate

  A term borrowed from linguistics, signifying a correspondence;
  e.g. a receptor and its cognate ligand, a tRNA and its cognate amino
  acid.

These two examples are of the most common uses of ‘cognate’ in molecular biology — that for tRNA can be found on the Wikipedia page for aminoacyl tRNA synthetase. A quick search brought up few examples of ‘cognate proteins’ or ‘cognate genes’, and in these cases I found the word was used to refer to similar genes or proteins in different organisms or strains.


What is a gene transcript, how is it different from an allele?

I thought a transcript was the RNA sequence produced from transcription. The RNA copy of an allele that gets spliced and translocated to the cytoplasm for translation. Not sure if Wikipedia references are allowed here, but they seem to agree with my understanding.

An allele is a specific copy of a gene, i.e. you have two copies (alleles) of gene X; allele X1 comes from your mum, allele X2 from your dad.

I haven't heard of the less granular breakdown description of genes, so that might just be a different way of looking at it.


Where do the phosphate units come from when EGF units dimerize?

In protein phosphorylation, the phosphate group transferred from the kinase to the substrate comes almost universally from ATP. However, there is evidence of some protein kinases using GTP as their phosphate source, although they are few and far between.


What properties (if any) do AT rich regions of DNA have?

With regards to DAPI itself, one could tell that the molecule itself has a shape complementary to the shape of A-T rich DNA. So in this case it's "special" because DAPI happens to have the structure to form bonds to A-T rich DNA regions. (There can very well be another organic molecule that binds to C-G rich regions). A quick google search will show how it looks like

With regards to A-T in general, A-T share 2 hydrogen-bonds. However, this is not the reason why it's easier to break A-T rich regions. A-T rich regions destabilize the DNA double-helix. Refer to this http://nar.oxfordjournals.org/content/34/2/564.long. Transcription initiation occurs near T-A rich regions, e.g. TATA box in eukaryotes and Pribnow box in prokaryotes.


It is very common!

Let's have a look at a few examples.

In bacteria, a lot of the genetic expression is regulated at the mRNA level. Certain mRNAs can form complex secondary structure that prevent or allow translation, and can switch from one structure to another based on the presence or absence of a signal molecule. These structures are called riboswitches; a very well-described example is the riboswitch regulating the expression of genes responsible for the biosynthesis of tryptophan.
For more details see this short article or this one.
Some mRNAs include internal ribosome entry sites (IRES), usually just upstream of coding sequences in mRNAs that code for several distinct proteins (polycistronic RNAs). IRES are highly structured RNA structures recognized by ribosomes that allow translation to start at a point in the middle of the mRNA. They are very widespread, especially in viral genomes. You can find a detailed explanation in the case of viral genes here:
In eukaryotes, mRNA molecules undergo a maturation process called RNA splicing that results in the excision of unnecessary internal sequences. During splicing, the mRNA forms a loop and a covalent bond is created at the future junction point; this bond is very transient but absolutely necessary for mRNA maturation and correct gene expression. See here for more explanations.
What about engineered RNA molecules? Self-hybridization of mRNAs is very useful in biological engineering. People reprogram riboswitches and IRES, but also use very useful tools based on mRNA self-binding. For example: based on a similar principle as the riboswitches, the transcription starting site can be masked by articificially introducing a (fairly simple) secondary structure called toehold switch that hides the ribosome binding site; however when a competing RNA sequence (which nature is specified by the sequence of the toehold) is present it opens and binds a part of the toehold, thereby making the ribosome binding site available for gene expression. This website shows an explanation and a real-life application of toehold switches for diagnostics.

These are only a few examples of mRNA self-binding processes; all of these have been extensively studied and are well described in many articles and books. There are many others types of self-hybridization in mRNA, and in pretty much all other types of RNAs too!


Congenital blindness due to retinitis pigmentosa - does it exist?

I have only ever heard of one case where RP caused blindness in a newborn. Unfortunately, I am unable to release the name or any details of the patient because of privacy issues and so forth.

Usually blindness from RP comes after a few years of life (as you said), making blindness from birth (or even early infancy) very rare.

I can tell you, however, that the formerly stated patient suffered from type I Usher Syndrome, if I remember correctly. I apologize for my inability to provide you with more specific details on this.

I don't know how much this will help in your search, but I sincerely hope that it does.

CDB


Does anybody know what kind of snake is this?

This is Orthriophis taeniurus ridleyi, a synonym is Elaphe taeniura. It has a few common names,some are  Ridley's beauty snake,Cave beauty and Cave racer.

https://www.biolib.cz/en/taxon/id310150/

https://www.naturepl.com/search?s=orthriophis+taeniurus+ridleyi2581

https://www.zootierliste.de/en/?klasse=3&ordnung=305&familie=30513&art=21102660

https://www.thainationalparks.com/species/orthriophis-taeniurus

https://en.wikipedia.org/wiki/Beauty_rat_snake

https://www.reptarium.cz/en/taxonomy/Orthriophis-taeniurus/2581


Does drinking coffee have negative effects?

First of all, the fact that a substance is beneficial does not mean that our body will, perforce, produce it naturally. Think of oxygen and water for example1.

As for the negative effects of coffee drinking, yes there are many although coffee has both a positive and a detrimental effect on human health. The main active ingredient in coffee is caffeine which can have the following negative effects:

Caffeine can increase blood pressure in non-habitual consumers.
High blood pressure is associated with an increase in strokes, and cerebral
vascular disease, which in turn increase the risk of multi-infarct dementia.
Caffeine may reduce control of fine motor movements (e.g., producing shaky hands)
Caffeine can stimulate urination.
Caffeine can increase cortisol secretion, some tolerance is developed.
Caffeine can contribute to increased insomnia and sleep latency.
Caffeine withdrawal produces headache, fatigue and decreased alertness.
Caffeine is addictive.
High doses of caffeine (300 mg or higher) can cause anxiety.
High caffeine consumption has been linked to an increase in the likelihood of experiencing auditory hallucinations. A study conducted by the La Trobe University School of Psychological Sciences revealed that as few as five cups of coffee a day could trigger the phenomenon.
High caffeine consumption accelerates bone loss at the spine in elderly postmenopausal women.

The list above comes from the very comprehensive wikipedia page on the health effects of caffeine. In fact, wikipedia is particularly good on this subject, see the following pages:

http://en.wikipedia.org/wiki/Caffeine

http://en.wikipedia.org/wiki/Health_effects_of_caffeine

http://en.wikipedia.org/wiki/Health_effects_of_coffee

1 Our bodies do produce both Oxygen and water as byproducts of various reactions but nowhere near enough to satisfy our need for these substances.


Have any genetically altered organisms actually become abundant in a natural environment?

Many organisms including plants, bacteria, insects, fishes and even mammals have been GMed. Most of them have experimental purposes, but GM crops have been released for commercial purposes. Maybe the most amazing between them is triticale, which is a hybrid of wheat (Triticum) and rye (Secale). Triticale, BT Potato, BT Tomato, BT Maize (I am not sure), BT and Golden Rice and lots of other GM crops have been released in almost all lands in world. Almost all these GM crops suppose to have higher yield and higher resistance to pathogens and physiological problems and as a result they have higher chance of surviving (specially in natural environment).
A study published in Nature in 2001 reported that Bt-containing maize genes were found in maize in its center of origin, Oaxaca, Mexico. In 2002 Nature concluded that the evidence available is not sufficient to justify the publication of the original paper.  A significant controversy happened over the paper and Nature's unprecedented notice. Also there are safety concerns about modified gene transfer during pollination in GM Rice(s). Even some scientists think that that this would not be a problem because rice is a self-pollinating plant. Any way GM crops can become abundant and release their genes by themselves or through gene transfer to other organisms.


You may not realize, but you actually have two questions here.

Question number 1 is this:

  Can birds raise younglings that are not their own?

The answer is yes. We call this Brood parasitism, and it occurs in several species of birds.

There is both intraspecific (between members of the same species) and interspecific (between members of different species) brood parasitism. I believe you want to know about interspecific brood parasitism.

By far the most famous examples are the cuckoos (Family Cuculidae). Some species of cuckoos are obligate parasites, meaning that they only reproduce laying eggs in other birds' nests.

It's very funny (for us, probably not for the host) the fact that sometimes the young parasite is way bigger than the host mum:

A Eurasian reed warbler raising a common cuckoo. Source: Wikipedia

Then, we come to your question number 2, which is different:

  If a scientist were to move a chickadee or pigeon egg from one nest to another, would the new bird (second mother) in the new nest incubate or raise the youngling?

The answer here depends on several factors, mainly the species involved.

For species that suffer broad parasitism, there is egg-rejection if the parasite egg is somehow different. If you look at the adaptations to parasitism in the Wikipedia link I shared, you're gonna see that "among specialist avian brood parasites, mimetic eggs are a nearly universal adaptation".

However, species that don't suffer broad parasitism are more prone to accept egg transfer (see @bshane comment here).


Good thinking. Yes, it is theoretically possible. It is often modelled like this. Have a look at this answer for the maths.

Note however, that to my understanding (and I might be wrong) there is typically either 0 or 1 crossover per pair of chromosomes as cross-over is directly related to the way homologous chromosomes bind together during prophase I of the meiosis by the synapsis. My confusion lies in the fact that, I think, there are sometimes (often?) several synapsis per chromosome pair. Hopefully, someone else will be able to clarify this for us.

As a consequence, the genome-wide recombination rate in humans is almost exactly 23 in humans (Wang et al., 2012). So in practice, such mulitple crossover would very rarely (if ever) happen.


Can scientists name themselves in the scientific name when they discover a new taxon?

The answer is that in general, self-naming is severely frowned upon in the scientific community, but the act itself is not disallowed.

There have been at least two instances of self-naming recorded in literature, as stated in John Wright's book The Naming of the Shrew, page 34, where Jules Bourguignat named a species of snail after himself as Ferussacia bourguignatiana. The naming was apparently very poorly received (being referred to as taxonomic onanism), although I was unable to confirm this by locating the original citation.

Another example was given in the book on Sigismund Hochenwarth who named a species of moth (now Syngrapha hochenwarthi) after himself (original citation here).


Humans do not "need" to cook food, but in general cooking food facilitate digestion and absorption of nutrients.

Heat cause denaturation of proteins. Once denatured, proteins are more susceptible to the enzymatic digestion. Thus, more nutrients are absorbed. There are also macroscopic phenomena in play, for example, a cooked piece of meat is more tender than the raw one, making mastication easier and less energy consuming.

The fact that you may feel your stomach upset because of raw food is probably due to the fact that you were never used to it. Your intestinal flora has been selected during the year to deal with the food you usually eat, any "new" food may cause the same symptoms. Humans that eat regularly raw food will not feel the same way.

Generally speaking, cooking food help killing bacteria, so your body does not need to deal with lots of infections that would occur otherwise. This, on the other side, makes your body weaker compared to the one of a wild animal, for example, that is used to deal with such bacteria. Of course, many animals also die because of food poisoning or food-related infection, only the "stronger" survive so there is a strong selective pressure in wild animals to have "a strong digestive system" (and a strong immune system as well). This selective pressure is less pronounced in modern human society but it is still present in less modernized areas.


Properties of berries that are not shared by strawberries

Botanically a berry is something quite different from what is commonly termed a berry in English.

From that Wikipedia page:

  a berry is a fleshy fruit without a stone produced from a single flower containing one ovary

...

  Berries so defined include grapes, currants, and tomatoes, as well as cucumbers, eggplants (aubergines) and bananas

On the other hand, many things called "berries" (including strawberries) are actually aggregate fruits, which are

  a fruit that develops from the merger of several ovaries that were separate in a single flower

Therefore, the botanical difference is the originating tissue of the fruit: a single flower/one ovary, versus a collection of ovaries grouped together.

These botanical groupings don't have much relevance to practical use (i.e., cooking/nutrition) and there aren't other properties that are definitive for what a berry is and is not. For that reason, there is nothing wrong with referring to strawberries, raspberries, etc, as "berries" in cooking: berry simply has different meaning in botany and culinary fields, just like the many culinary "vegetables" that are botanically "fruits."


Found Skull(?) in Ontario Canada, help identifying please

Yes, this is a synsacrum, a part of a bird's pelvis. I would say it's from a cormorant, as I have found this comparison of different synsacra online (third from left):

No idea about the exact species, though.

Image source:

https://hiveminer.com/Tags/cormorant,skeleton


Neuroscience: zapping an axon connected to thermoreceptor

I and II depend on the type of electrical signal applied to the axon. for III, most receptors can perceive other sense as well, so for example striking a vision receptor may produce the perception of light (even in complete darkness) - my guess is the you would feel pain, even if you could isolate the destructive signal away from nearby pain receptors.

search "action potential" in duckduckgo.com, it will get you going.


In the paper by K. Lily Therese, U. Jayanthi & H.N. Madhavan traditional PCR wasn't sensitive enough to allow for an accurate reading on what they were trying to study. By using nPCR they were able to amplify around the gene they were interested in and then amplify just the gene they were interested in for a more accurate and sensitive study. The successive PCR allowed them to amplify their specific gene even if there was only one copy in the sample.

I recall using this procedure in Molecular Genetics Lab, it was used to make sure that our sample was purer.


Maximum RPM in zero-g before losing consciousness, spinning head-over-heels

I think people can easily endure head-over-heel revolutions in space such as seen in Gravity. I am no mathematician (let alone physicist, both of whom could answer this more accurately) but here is my reasoning (faulty though it may be).

You are assuming that someone would pass out from lack of blood supply to the brain.  Given we have absolutely no problems normally at 1 g (the force of gravity on earth), the average non-couch-potato person can tolerate forces of up to 20 G for less than 10 seconds, to 10 G for 1 minute, and 6 G for 10 minutes before passing out.

But g is very dependent on (as you stated) distance from center. It's also very dependent on revolutions per minute.

$$g=\frac{R\left(\frac{\pi\times rpm}{30}\right)^2}{9.81}$$
or
$$R=\frac{9.81 g}{\left(\pi\times rpm\over30 \right)^2}$$

g = Decimal fraction of Earth gravity
R = Radius from center of rotation in meters
π = 3.14159
rpm = revolutions per minute

The average North American male is 1.75m tall. That means the distance of the top of the head and bottom of the feet (if stretched out at full length) from center is under a meter (.875m). At 60 rpm's (that's pretty fast), solving for the above, g = 3.52.

g = [.875({3.14159x60}/30)^2]/9.81 = 3.521 (so just over 3.5G)

Gravity at the top of the head and the bottom of the feet would be 3.5G, while the gravity at the center would be zero G. The heart can easily compensate for that for a while. An astronaut, trained for increased Gs, can do well for longer.

Much worse than too little blood to the head is too much, which is what I would be worried about. Eventually, slightly less than half the blood volume would end up below the waist with the feet feeling the most pressure, and the rest above, with the brain being engorged with blood, which can cause hemorrhage (not taking into account here precise fluid physics). I'm not sure how this would play out in space over longer periods of time, but survival would be the norm for the scenes we see in Gravity.

An Air Force physician named John Stapp was the first to determine just what humans could take in the way of G forces. On his final run, firing nine solid-fuel rockets, his "sled" accelerated to 632 miles per hour in five seconds, slamming him into two tons of wind pressure, then came to a stop in just over one second. A witness said it was "absolutely inconceivable anybody could go that fast, then just stop, and survive." But Stapp did—in fact, he went on to live another 45 years, dying quietly at home in 1999 at the age of 89—and he experienced a record-breaking 46.2 G's. For an instant, his 168-pound body had weighed over 7,700 pounds.  Stapp's efforts put him on the cover of Time, and he was called "The Fastest Man on Earth." More importantly, his work led to greatly improved safety in both planes and cars, and he gave us a much-improved understanding of human tolerance to G forces.

All About G Forces


Why are market squid attracted to fishing lights but also avoid naturally lit surface waters during daytime/full moons?

Despite many sources stating that the lights attract the squids, the explanation given here is much more logical. Squids feed of small fish, crabs and shrimp, which in turn feed on plankton. Zooplankton is known to migrate vertically during the day (up at night, down during the day), which has also been reported for squids, probably following their prey.

The reason for this migration is that zooplankton feeds on phytoplankton, which can be found at the sea surface, where it gets most of the sunlight. During the day the zooplankton stays in deeper waters, because at the surface its easier to be spotted by predators. It's safer to move up during the night to feed. Other predators feeding on zooplankton follow, including the squids.

The vertical migration might be coordinated by an internal clock rather than light. It would therefore not be inhibited by the bright fishing lights. The squids don't seem to respond to the light, but rather to their prey.

Therefore, rather than attracting the squids directly, the fishing lights will attract phytoplankton, which attracts zooplankton and small fishes, which attract squids.


Can an octopus survive if one of its three hearts stops working?

The Wikipedia entry you linked and the other answer both state that...

  ... the systemic heart is inactive while the animal is swimming and thus it tires quickly and prefers to crawl.

I tried to find an accurate source corroborating this (by accurate I mean a paper in a peer-reviewed journal or a zoology book), but I couldn't. The best source (scientifically speaking) I found was this page from the Smithsonian Institute, which says:

  Octopuses have three hearts. Two of the hearts work exclusively to move blood beyond the animal’s gills, while the third keeps circulation flowing for the organs. The organ heart actually stops beating when the octopus swims, explaining the species’ penchant for crawling rather than swimming, which exhausts them.

A much more reputable source is Octopus: Physiology and Behaviour of an Advanced Invertebrate. It says:

  If an octopus is surprised by a sudden movement on the part of an observer, or a thump on the side of its tank, the systemic hear may miss one or more beats.

Which is, evidently, way less dramatic than having one of the three hearts stopping.

The same author says, talking about Octopus vulgaris:

  Together with changes due to exercise and arrests attributable to sudden tensing of the body musculature, any prolonged recording reveals apparently spontaneous changes in amplitude that are not obviously correlated with anything that the animal can be seen to be doing. From time to time the heart stops for several seconds (as it does, for longer periods, in O. dofleini).

Thus, apparently, the maximum we have here is periods longer than several seconds (which the book, unfortunately, doesn't determine more precisely).

In conclusion, despite their circulatory system being very complex and the systemic heart being able to stop beating for several seconds (or during the whole time of swimming, as the Smithsonian says), it doesn't seem possible that octopuses can survive if one of their hearts stops (forever). Have in mind that the hearts are not redundant, that is, one heart cannot perform the function of the other (if that other one stops).

Source: Wells, M. (2013). Octopus. 1st ed. [Place of publication not identified]: Springer.


Generate mesh surface from protein structure

PyMOL and Chimera can do that, and both can be script-driven. The PyMOL wiki is full of examples, and probably already has some how-to that would get you started. Chimera also has a complete documentation.


I've found a possible workaround to my problem, I filter the vcf input file before loading it into the db by vcfkeepsamples from vcflib.

But I still don't know if the --sample-filter in gemini works, so if you have any ideas, it would be helpful.


Has there even been a clinical study where healthy volunteers consented to be infected with a pathogen?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more.

One can't easily separate ethics from how biology is done, as much as some people have tried. (Though I suppose some have made bioethics into a separate and successful media career, so it can be done in that way.)
In addition to the comment-answer about the Tuskegee Study, Nazi doctors in Germany performed experiments without consent, which included infecting concentration camp prisoners with the bacteria that cause tuberculosis.
Your question is about volunteerism, however, and the victims of the United States and Nazi Germany did not give full — or any — consent to experimentation.
In this week's issue of Nature, there is a news article which interviews bioethicist Nir Eyal about a recent preprint, of which he is a primary author.
In this interview and in the preprint, your very question about coronavirus vaccine research, specifically, is discussed, as it concerns the matters of consent, ethics, and safety of doing accelerated biological research about this virus in a time of emergency.
In answer to your first question about modern clinical studies, Dr. Eyal notes:

Are there any precedents for infecting healthy people with a pathogen?
We do human-challenge studies for less deadly diseases quite frequently. For example, for influenza, typhoid, cholera and malaria. There are some historical precedents for exposure to very deadly viruses. The thing that demarcates the design that we propose from some of these historical instances is that we feel there is a way to make these trials surprisingly safe.

As an example, there was a challenge trial for malaria performed in 2012. Healthy individuals were bitten by mosquitoes carrying the malaria parasite and then treated with antimalarial therapies.
Clinical trials are done under the aegis of government agencies with review and approval processes, some of which are described on the FDA web site. IRBs or Institutional Review Boards provide oversight:

Under FDA regulations, an IRB is an appropriately constituted group that has been formally designated to review and monitor biomedical research involving human subjects. In accordance with FDA regulations, an IRB has the authority to approve, require modifications in (to secure approval), or disapprove research. This group review serves an important role in the protection of the rights and welfare of human research subjects.

History does guide us to worry about the ethical issues surrounding medical trials, especially under exploitative regimes that leave people to fend for themselves during a time of global crisis:

Do you worry that countries with authoritarian governments could conduct such studies on vulnerable groups, such as prisoners or members of persecuted minorities?
We would only recommend conducting the studies in an ethical fashion, with fully informed consent. Vaccine makers want to sell their product to other countries. They want to publish their scientific articles in prestigious journals and there would be many obstacles if their trial doesn’t adhere to widely accepted standards.

But in the modern age, in non-corrupt regimes, science does aim, for the most part, to do the right thing, and there are methods and regulatory mechanisms in place to try to enforce societal standards that move us past the days of Tuskegee and Nazi concentration camps.


Do transcription factors block transcription entirely?

Of course it's never 100%. The protein still has a measurable Kd for the DNA, meaning that there's always some part that's not bound (or some time that it's not bound.

Besides that, you're talking about repressors. There are also activators, and they use many different mechanisms. The same regulator protein can even recognize different sequences of DNA and repress one gene more than another. Some can bind and actually recruit a RNA polymerase, some work only while they're binding small molecules.

https://en.wikipedia.org/wiki/Transcription_factor or your molecular biology textbook might be a good place to learn more.


What plant is this, seen at the Allan Gardens?

This is a Schizanthus "orchid" (actually not a real orchid) called Schizanthus pinnatus ("butterfly orchid" or "poor man's orchid").

  It is native to Chile but the plants are also cultivated as ornamentals. It is commonly known as the "small butterfly" ("mariposita") or "small, white butterfly" ("mariposita blanca").

Description

Annual plant of 20-50 cm in height
Stem: Glandulous-pubescent
Leaves: 2.5-3 cm long; pinnatisect (divided into 6-8 pairs in oblong-linear segments, entire or separated).
Flowers: white, pink or violet, 2-3 cm diameter, arranged in panniculate inflorescences, sometimes dichotomous.


How to check if a fastq file has single or paired end reads

By now I got some interesting answers in this question on Biostars

Basically what I did is the following:

First of all, I checked if Sequence Id contains paired end notation. As described in this wikipedia page, for Illumina reads there are two possible notation for single/paired end reads:

@HWUSI-EAS100R:6:73:941:1973#0/1

If the last number is /2 in some reads then the reads are paired end; otherwise they can be single end.

The second notation is:

@EAS139:136:FC706VJ:2:2104:15343:197393 1:Y:18:ATCACG

If the first number in the second group is 2 in some reads then the reads are paired end; otherwise they can be single end;
Then I checked for multiple files. If a sample has two fastq files it is likely that the reads are paired end. It is to note however that with a single file it is not possible to exclude that paired end reads can be interleaved in one single file, even if it is not common (in my opinion);
The most general method is to cross check each single reads with the whole set of reads. If the first part of the sequence ID (in this case the field starting from @ and ending before the # - in the first notation - or the whitespace - in the second notation) is unique among all the reads (for each read) it is likely that the reads are single reads, otherwise - if can be found a duplicate for each reads - the reads are paired end.
In this case, on *nix systems it can be achieved with the following command (thanks to the biostars answers):

grep --no-filename @HWUSI-EAS100R:6:73:941:1973 *.fastq | cut -d' ' -f1 | sort | uniq -c | sort -rgk 1,1 | head

If the result shows in the first lines a result like this:

1        read1_ID

1        read2_ID

...

It is likely it is single end. Otherwise:

2        read1_ID

2        read2_ID

...

it is paired end.

I skim read BioPython API documentation but I cannot find something useful to do it.

Suggestions and corrections are welcomed.

Thanks


This article hypothesizes that the surviving avians had large and quite complex brains, giving them an advantage in finding food in the aftermath.


How does Humira work when injected into patients with rheumatoid arthritis?

Adalimumab is an antibody that binds to tumor necrosis factor alpha. Antibodies have high-affinity binding sites for their antigen, and for a small antigen such as TNF-alpha, would bind to it and prevent it from binding to its target receptors. Antibodies, like all proteins, degrade after a certain period of time and are removed from circulation, and since the body does not produce more of this antibody, it must be re-administered every few weeks.

The mechanism of this pharmacological is in a sense somewhat ironic in that in nature the chief role of antibodies is binding and neutralization of foreign and potentially dangerous antigens, however, this antibody binds and neutralizes a feature of the immune system itself. This element of the immune system is a cytokine, TNF-alpha, whose function is to promote inflammation, which draws white blood cells to the site of the inflammation and activates them. TNF-alpha also induces fever, and suppresses tumor formation and viral replication by activating programmed cell death pathways.

Aggressive immune responses always cause collateral damage to surrounding tissues, however, in autoimmune diseases such as rheumatoid arthritis the damage is compounded by the fact that the target of the immune response is an element of the body itself. A central function of the immune system is to induce tolerance to self; sometimes tolerance fails and while there are genetic components involved, the process is yet to be well-understood.


Why don't we build up an immunity to sore throat?

Short Answer

It should be noted that there are many non-pathogenic causes of sore throat, and I would suspect that you are not always distinguishing these causes from actual illness.

In most cases, it would not be possible to build a response (immunological or otherwise) to avoid reacting to these stressors.

Bacteria and viruses mutate frequently in ways that make your immune system unable to properly recognize them to ward off initial infection.

Your immune system recognizes specific pathogens based on structural characteristics. If those characteristics change when pathogens mutate (which happens fairly frequently), your immune system will not recognize it as readily (or initially at all).

 Long Answer

Sore throat is most commonly attributed to pharyngitis, or the inflammation of the back of the throat called the pharynx.

Causes

Sore throats can be caused by many things. (e.g., see here, summarized below):

First off, a sore throat can be the result of many things unrelated to illness:

Allergies
Dryness
Irritants
Excessive talking,singing,shouting,etc.
Muscle Strain
Gastroesophageal reflux disease (GERD)

As a result, at least 30+% (higher in adults) of reported sore throat cases (and supposedly many more unreported cases) are not due to any type of illness.

Further, a number of pathogens can cause a sore throat:

Viruses

Rhinovirus, coronavirus, influenza, parainfluenza, adenoviruses, Epstein–Barr, etc.
(see here for one estimate of relative etiologies).

Bacteria

A number of bacterial infections can cause a sore throat. The most common is Streptococcus pyogenes (aka "Strep A").

It turns out that pathogen-caused pharyngitis is fairly common. Supposedly 10% of adults with sore throats have strep, and around 70% of children pharyngitis cases seen by doctors are either virally or bacterially caused.

However, it should be noted that only 20-30% of children and just 5-10% of adults have bacteria to blame for their sore throat, with viral infections being much more common. (source: IDSA).

Sore Throat Frequency

It turns out that sore throats are fairly common; Jones (2004) determined that about 7.5% of people have a sore throat in any three-month period. Further, on average, adults get a sore throat two to three times a year and children about five times a year (Tamparo 2011 and Rutter & Newby 2015), so your personal experience is fairly average.

Because viral causes and non-pathogenic causes make up an overwhelming percentage of overall sore throat cases, it shouldn't be surprising that most sore throats clear up without the use of any antibiotics.

As for those that are caused by pathogens:

Why no Immunity?

Bacteria and viruses both mutate fairly quickly (see Antigenic Variation, Antigenic Drift and Antigenic Shift), so it shouldn't be surprising that you're capable of having an immune response to pathogens throughout life.

If we consider just strep alone, it mutates/reemerges with improved fitness frequently (e.g., see Bao et al 2016 and their citations)
And see Sanjuán et al. (2010) for a reviewof viral mutation rates.

So not only are there a number of pathogens that can cause sore throat, but each of these pathogens can mutate. That leaves you with a fairly sizable number of potential invaders that can illicit a sore throat.

Let's See How Your Immune System Responds:

Your immune system contains cells that can be split into two broad groups: cells that belong to the adaptive immune system, and cells which belong to the innate immune system. [See here for a simple explanation].

Innate Immune system: consists of cells responsible for initial detection of pathogens, recruitment of other immune cells, activation of the complement system, engulfment and (more immediate) destruction of pathogens.
Adaptive immune system: consists of cells which coordinate to develop a memory of the infections they've seen previously in order to mount a faster, more pronounced immune response to repeat pathogens.

Depending on the kind of foreign invasion, two different immune responses can occur in either of these 2 broader "systems": either a humoral response involving antibodies or a cell-mediated repsponse.

A general feature of the immune system is that these mechanisms rely on detecting structural features of the pathogen or toxin that mark it as distinct from host cells (see Chaplin 2010 for a review). The mechanisms permitting recognition of pathogenic/toxic foreign structures can be broken down into two general categories:

hard-wired responses encoded by genes that recognize molecular patterns shared both by many microbes and toxins that are not present in the mammalian host. This is the innate system described above.
responses that are encoded by gene elements that somatically rearrange to assemble antigen-binding molecules with extreme specificity for individual unique foreign structures. This is the adaptive system described above.

Antibodies recognizes a unique/specific molecule of the harmful agent, called an antigen, and binds to it to tag it for immune attack.

  Because the adaptive system is composed of small numbers of cells with specificity for any individual pathogen the responding cells must proliferate after encountering the antigen in order to attain sufficient numbers to mount an effective response against the microbe or the toxin. [Source: Chaplin 2010].

This means that you can still experience some mild symptoms due to the invading pathogen.

The important take-away from all this, though, is that your immune response relies on structural "markers" on pathogens in order to recognize them. This is true for both innate and adaptive immune responses. If the physical/structural properties of a pathogen change (due to antigenic processes and mutations as mentioned above) your immune system will be slower (and possibly ineffective) in responding to an attack.

The result, then, could be another one of those sore throats...

Citations

Bao, Yun-Juan et al. “Phenotypic Differentiation of Streptococcus Pyogenes Populations Is Induced by Recombination-Driven Gene-Specific Sweeps.” Scientific Reports 6 (2016): 36644. PMC. Web. 17 Mar. 2017.
Chaplin, D. D. (2010). Overview of the immune response. Journal of Allergy and Clinical Immunology, 125(2), S3-S23.
Jones, Roger (2004). Oxford Textbook of Primary Medical Care. Oxford University Press. p. 674. ISBN 9780198567820. Retrieved 4 August 2016.
Rutter, Paul Professor; Newby, David (2015). Community Pharmacy ANZ: Symptoms, Diagnosis and Treatment. Elsevier Health Sciences. p. 19. ISBN 9780729583459.
Sanjuan, R., Nebot, M. R., Chirico, N., Mansky, L. M., & Belshaw, R. (2010). Viral mutation rates. Journal of virology, 84(19), 9733-9748.
Tamparo, Carol (2011). Fifth Edition: Diseases of the Human Body. Philadelphia, PA: F.A. Davis Company. p. 356. ISBN 978-0-8036-2505-1.


With R biomaRt you can retrieve them.

  library(biomaRt)

  ensembl = useMart("ensembl",dataset="hsapiens_gene_ensembl")

  filterlist <- list("1:154714693:154754070","protein_coding")

  genes <- getBM(attributes=c('hgnc_symbol', 'chromosome_name',
  'start_position', 'end_position'),
                     filters = c("chromosomal_region","biotype"),values = filterlist, mart = ensembl)

  genes
  hgnc_symbol chromosome_name start_position end_position 1
  KCNN3               1      154697455    154870280


I think the problem you're having is in the way you're thinking that all contracted muscle shortens, and all relaxed muscle lengthens. But the cilia is different. The ciliary muscle is a circular or radial muscle (like the orbicularis oris of the mouth.) Thinking of it like a sphincter muscle is much more helpful.

The ciliary muscle is attached at its periphery to the lens by suspensory ligaments (aka the zonules). Think of the the lens, the suspensory ligaments, and the ciliary muscle as a single unit with only two components whose length can change dramatically: the cilia and the lens. The length of the suspensory ligaments is more or less fixed.

This may be counterintuitive, but for seeing at a distance, the ciliary muscle relaxes, and the muscle in effect becomes "thinner" (think of the capitol letter O in a thin font, or think of a shpincter muscle; when the latter relaxes, it becomes thinner and more spread out). This means the "decreased distance" taken up by the ciliary muscle must be made up for by the suspensory ligaments and the lens: The tension on the suspensory ligaments increases, causing the lens to assume a flattened shape.

For near vision, the opposite occurs; The ciliary muscle contracts (think of the letter O now very bolded - it takes up more of the fixed distance.) This allows the ligaments to relax, allowing the lens to assume a more rounded shape.

Does that make any sense at all? I hope so, because it is essentially how it happens.

I did find a YouTube video; unfortunately it explains it pretty much like I did varying in a few details.

Morphological Study of the Accommodative Apparatus in the Monkey Eye Way way complicated; it's better to just believe me.


We might imagine living things that are very different from what we know. There is no conceptual reason for limiting life in its relation to water for example. Moreover, the definition of what is alive is really unclear. We classified more or less arbitrarily objects we know on earth as being living or not living but this does not give any clear definition of what is life and therefore it would not allow an exobiologist to even know what he's looking for!

But if you had to seek in billion of planets/natural satellite a living creature somewhere where what planets would start looking at? Probably those that look alike yours because you already know that life is possible the kind of conditions these planets offer. I think the answer is as easy as that.


It is a widely known spinal reflex arc which causes decapitated animals (even soldier without head) to move over some period of time after decapitation.

One of the arc representations:

see also The life after decapitation

additional video


Nicotine levels in non fruit/edible parts of plants (that are not tobacco)

Tomato leaves have something like 184 ng/g of nicotine, in the same ballpark as tomatoes (the fruit) and not close to tobacco.  I think this is not peer-reviewed, but it cites other papers that are: Nicotine Analysis in Several Non-Tobacco Plant Materials
And this is a PDF of a slide deck providing a simple presentation of the results from the same article: Nicotine Analysis in Several Non-Tobacco Plant Materials - PDF


Forest Succession 101

Pines are actually fast-growing, shade-intolerant, early-successional species. When land is allowed to lay fallow after being cleared by fire, wind storms, human land use or other major disturbance, the successional sequence will begin.

At first only herbs and grasses grow, but eventually these are shaded out by shrubs and tree seedlings. In this setting, the limiting factor is typically light. Because pines are fast growing in the sun, they usually take over a field and develop a relatively dense even-aged stand.

Because the seedlings grow so well and densely, they usually shade out and prevent most other trees and shade-intolerant plants from growing. The result: a dense stand of mostly pines:

I'll note here that early on in this process (before processes of self-thinning really get to take off), you can end up with what are sometimes called "dog hair" stands. Also, if you see clear rows in the pine stand, that's a good indication the pines were planted.

Eventually (80-120 years), most of these pines will die and fall out of the canopy (both due to "natural" causes and additional wind, ice, pest, or fire disturbance). As large pines fall and clear large enough canopy gaps, shade-tolerant sub-canopy hardwoods can take their place. Because pines are highly shade intolerant, pines do not regenerate again in that stand (without another major canopy-clearing disturbance). The result: a mostly hardwood-dominated forest (with perhaps a few remnant older pines):

So...

The all-pine stands you're seeing are early on in the successional sequence.
The few pines (that "don't look too happy" because of age) mixed with hardwood ("seasonal variety") trees are in a mid-to-late successional stand.


Why is weight gain a symptom of Cushing's Syndrome?

Cortisol is released when body goes through stress situations like while working out in gym, physiological activities outdoor etc. As you have already mentioned about what Cortisol does, it accumulates in the body after the stress situation and then with the intake of food and other nutrients it replaces the consumed carbohydrate and fat in the body i.e. a kind refueling. So this is how Cortisol maintains the body weight normally if our body gets enough exercise or has proper metabolism.

Whereas in Cushing' syndrome which comes usually by taking glucocorticoid drugs, or diseases that result in excess cortisol, adrenocorticotropic hormone (ACTH), or CRH levels. In this case Cortisol content will be more than the normal level which in turn requires more carbohydrate. So cortisol metabolizes the food and reefuels the body even when there is no requirement within the body. So because of excessive cortisol content body simply gets excessive fat accumulated in various parts which mainly results in obesity.

One more explanation from High level of Cortisol effects:

Chronically high levels of cortisol plays a big role in the development of obesity.

  Cortisol helps the body handle stress; so, when stress goes up,
  cortisol also goes up. Cortisol stimulates fat and carbohydrate
  metabolism during stressful situations. This leads to increased blood
  sugar levels required for fast energy. In turn, this stimulates
  insulin release which can lead to an increase in appetite.

  Adrenaline increases alertness and metabolism by helping fat cells release
  energy. When the immediate stress is over, the adrenaline levels
  return to normal. But, cortisol lingers to help bring the body back
  into balance after stress. One of the ways it gets things back to
  balance is by increasing appetite to replace the carbohydrate and fat
  used for the flight or fight response.

  The problem is that in today's society, stress-causing situations do
  not really require the body to use up a lot of energy. So, cortisol
  ends up causing the body to refuel after stress even when it doesn't
  really need to refuel. This excess fuel or glucose is converted into
  fat resulting in increased storage of fat.


What is "contigs" in Picard's ReorderSAM?

I'm not familiar with picard and their reorderSam function, but as far as I know/understand from their documentation they mean this:
The ordering of the contigs while using a reference sequence.
Like this:

   Figure 5: Anatomy of
  whole-genome assembly. In whole-genome assembly, the BAC fragments
  (red line segments) and the reads from five individuals (black line
  segments) are combined to produce a contig and a consensus sequence
  (green line). The contigs are connected into scaffolds, shown in red,
  by pairing end sequences, which are also called mates. If there is a
  gap between consecutive contigs, it has a known size. Next, the
  scaffolds are mapped to the genome (gray line) using sequence tagged
  site (STS) information, represented by blue stars. © 2001 American
  Association for the Advancement of Science Venter, C. et al. The
  sequence of the human genome. Science 291, 1304–1351 (2001). All
  rights reserved. (source)

ReorderSAM (Picard)
So in Picard you have your INPUT (File), the reads in this file are then mapped on the REFERENCE (File). This can also be seen in their code:

// write the reads in contig order
109
            for (final SAMSequenceRecord contig : refDict.getSequences() ) {
110
                final SAMRecordIterator it = in.query(contig.getSequenceName(), 0, 0, false);
111
                writeReads(out, it, newOrder, contig.getSequenceName());
112
            }

(code source)

  ReorderSam reorders reads in a SAM/BAM file to match the contig
  ordering in a provided reference file

Some more background
There are two main approches two obtain a genome sequence:

  there are two "main" approches for this:  g. Second-generation
  sequencing technologies produce millions of short(a few hundred bp)
  strings of nucleotides (reads), which is ideal for resequencing when
  reads are mapped to a reference genome (reference-based assembly). De
  novo genome assembly based on second-generation sequencing is
  challenging due to difficulties with GC- or AT-rich and homonucleotide
  DNA stretches, which are under-represented in the sequencing output (source)

The characteristics of these are:
de novo

  no bias towards a reference genome
  no template to adapt to
  the    assembly is normally more fragmented
  it normally works better for large-scale/median scale differences (source)

reference mapping

  less contigs
  in most methods the reads that don't map are not used in the final sequence (this is also the case with reorderSAM: Reads mapped to contigs absent in the new reference are dropped
  you look what is similar to your reference genome
  SNPs and very small veriations are more easily positioned and compared among groups (source)

I would highly recommend to watch this short animation to differentiate between these two and understand what reference genome mapping is.


How is color information transmitted from the eye to the brain via the optic nerve?

Color vision in layman's terms:

The eyes contain a photosensitive layer much like a digital camera called the retina. In the center of this layer is a 3 mm-wide spot called the fovea that contains high densities of photosensitive cells, called the cones. Cones are photon hungry and operate only in bright light (photopic vision). They are called cones because of their conical shape. Rods are abundant in the periphery and mediate gray-scale night vision (scotopic vision).

The cones in the fovea are present in three types: red, green and blue cones - hence they convey color images much like digital pictures, namely as a bunch of pixels with a mixture of red, green and blue.

The cones in the retina are the first nerve cells (called neurons) in a long chain of neurons. The cones are hence called primary neurons. They connect to secondary neurons, namely the retinal ganglion cells (RGCs). These cells have long protrusions called axons. These axons bundle together to form the optic nerve. Each cone in the fovea connects to one RGC. The optic nerve extends from the retina to the brain. Information is sent through the optic nerve in the form of electrical pulses, just like a photosensitive chip operates in a camera. The information from the optic nerve eventually reaches the primary visual cortex in the brain, also referred to as V1 or striate cortex (Fig. 1).

In the visual cortex, there is a retinotopic map, meaning that a topographic representation exists in the brain that matches the retinal image. In other words, images are projected faithfully on the brain's surface as neuronal activity. The brain's job is to process these images further and generate conscious perceptions out of them; we see with the brain, not the eyes (a famous quote from Bach-y-Rita).

Fig. 1. The visual system. source: IEEE

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


Can any organisms see non-electromagnetic radiation?

Some fungi have radiotropism; they grow toward radiation sources. Melanin-expressing (melanotic) fungi migrate toward radioactive sources, which  enhance their growth. According to this paper.

These Melanotic fungi inhabit some of the most extreme habitats on earth such as the damaged nuclear reactor at Chernobyl and the highlands of Antarctica, both of which are high-radiation environments.
Radiotropism was triggered primarily by gamma radiation, but it is possible that both alpha and beta radiation could be  “ sensed ” by the fungi as well.

It seems like these melanotic fungi can detect gamma and beta or alpha that they can use as energy source.


Fishers Geometric Model (FGM) is a theoretical prediction about the adaptation process in traits. There are a number of things to establish before attempting comprehend FGM. Firstly, shifts in an adaptive landscape, in natural scenarios, are generally quite small. Because populations have been evolving for such a long time and the small shifts in adaptive peaks it means that most populations should be near or on a local fitness optimum within the relevant landscape. The adaptive landscape comes from S. Wright, discussed in the Orr paper, where he spoke of a field of possible gene combinations" each with a fitness value, some combinations are fitter than others. Adaptive peaks represent the fittest combinations of all traits.

We can picture all of this using a single trait:

Here there is a local optimum (which is also global, Fisher assumed that adaptive landscapes are less rugged than Sewall Wright and had only one optimum) for the trait. The population starts at point A (the red ball), just off the adaptive peak for the initial fitness distribution (blue trace). Then selection alters (red trace), initiating a new bout of adaptation, making the population (green ball) further from the optimum.

From here lets imagine this is two seperate populations, the green population (A) wants to move along the red line to the highest point, the red population (B) along the blue line also for its own optimum.

If a mutation which has a very small effect arises then there is 50% probability in both populations that it will improve fitness (assuming no neutral mutation) because it will either be recessive or deleterious. This value is shown in box 2 figure 1 of the Orr paper.

Now if a large effect mutation was to arise in then there is less chance of it being beneficial for population B than for population A, this is because B is closer to its phenotypic optimum so a large effect mutation is likely to "overshoot" the optimum. (The black line illustrates where either population would end up after a large effect mutation in the direction of the adaptive peak). You can see this mutation would put population A very close to its peak (the red line) and population B would have a reduced fitness. This is summed up nicely in the opening to the Orr paper.

  "Precise adaptation is possible only if organisms can come to fit their environments by many minute adjustments"

So, descriptively, this is why we see a reduced probability of large effect beneficial mutations as we approach an optimum; we expect most bouts of adaptation to be due to small shifts in adaptive landscape and populations to start bouts near to the former adaptive peak.

The FGM expands this out beyond one trait (or, as Kauffman and Gillespie did, the sequence - with the latter seemingly being more successful than the former). As shown in figure 1 of the Orr paper,

This is a highly multidimensional space, with one dimension per trait, therefore more complex organisms by definition will have more complex spaces. The centre of this sphere is the phenotypic optimum, and each layer represents and adaptive movement, or substitution of the wild type as in the Maynard-Smith adaptive walks system. The red line shows the movement made by the population through this sphere.

And now for some math. (Refer to box two in the Orr paper). $P_a (\chi)$ is the probability that a mutation (of effect size $r$) is favourable. Thinking about what I discuss above, that is, $P_a (\chi)$ is the probability that a mutation will increase fitness, which must therefore be a product of the landscape complexity (the number of characters affecting the fitness), the distance from the population to the optimum, and the size of the effect. $\chi$ is the standardized mutation size, which accounts for the distance to optima, as $z$, the number of characters affecting fitness as $n$, and the effect size $r$. This means that $\chi$ = $r \sqrt{n} /2z$: therefore an increase in the distance to the phenotypic optimum ($z$) reduces the value of $\chi$ (thus increasing the probability that a mutation has a beneficial effect), whereas increases in $r$ or $n$ will decrease the probability that the mutation is beneficial (i.e. large effect mutations and high complexity). In the context of the above example, both populations have an $n$ of 1, and the values of $z$ vary - this means population A can tolerate a larger value of $r$, or in other words, population A is more able to make adaptive substitutions because it is further from peak fitness, thus more tolerant to large effects, than population B.

Difference between $r$ and $\chi$: $r$ is the raw value of effect size of a mutation, whereas $\chi$ is the standardized effect size. Assuming equal effect sizes the relative effect of mutations will depend on the number of traits affecting fitness (see the diagrams below), thus we have to correct for this.

How does complexity affect the probability of beneficial mutations? Look at the following diagram.

Each point represents a possible combination of traits when we have three traits affecting fitness, each with two possible incarnations (A or a [most fit and least fit respectively]). The outer green ring has one possible occupying combination (aaa) which is the least fit - it's the furthest from the optimal combination, the red point. On the green ring the probablity of increasing fitness with a mutation is 3/3 (because there are 3 possible mutations all of which increase fitness). Note, assume all changes are equal effect. If we change one trait to the A version we can have 3 possible outcomes (Aaa, aAa, aaA) which occupy the yellow ring. From the yellow ring a further single mutation has four possible outcomes, of which 3 can increase fitness so the probability of improving fitness with a mutation is reduced (3/4). In the blue ring there is a 1/4 probability of increasing fitness. Jumping to the red point, where all traits are A, every possible mutation will reduce fitness (0/3).

Bearing this in mind, lets change n (the number of traits affecting fitness) from 3 to 4. The least fit starts in the red ring (aaaa), from here there is a 4/4 probability of increased fitness via mutation. From the green ring there is a 6/7 probability. From the yellow ring there is a 4/8 probability of increasing fitness, and from the blue a 1/7 chance. Compare this to when n=3, from the blue ring there was a 1/4 chance, when n=4 it is 1/7 - there are more possible combinations and still only one fittest combination

Put another way; if we consider it in terms of single point mutations in a sequence, a mutation which affects 1 trait affecting fitness (n=1) then the probability it will increase fitness is drawn from the distribution of probable fitness effects. If the point mutation affects 5 traits then the effect is drawn from the distribution 5 times, and because we assume most mutations are deleterious and beneficial ones are relatively constrained to being small, there is a greater probability of reducing fitness when n>1.


Are chromosomal microdeletions passed on?

Of course. Just like any other type of mutation.

If a mutation (incl. a chromosomal microdeletion) happens in the germ line, then the mutation can be passed on.


What does the root "phyllum" mean used botanical binomial nomenclature

Binomial names often use of greek words. Phyllum means -- as you correctly stated -- "leaf", but is not derived from latin but from the greek φύλλον, 'phyllon'.

By the way, there are also lots of examples where the latin word 'folium' is used. To stick with the genus Acer from your example, there is another species named Acer gracilifolium. So don't be confused by the linguistic chaos in binomial nomenclature.


What is the difference between differentially expressed genes and deregulated genes?

Any gene whose gene expression differs significantly from some reference is considered to be differentially expressed. I think the most common representation of differential expression is the volcano plot, where you're plotting the fold change or log2 fold change against the -log10 p value assigned that gene.

This means a couple of things: One, you need a sufficently large sample size that you can actually get statistics, and two, you need a sufficient reference sample which will act as your baseline.

If a gene is degregulated, however, the expression is aberrant. In order to characterize aberrant expression you need a normal sample or accepted reference sample, and the sample of interest. This might be as simple as tumor vs normal tissue from the same patient.


Why is thrombin time (TT) normal range longer than prothrombin time (PT)?

This is a great question.

I'm going to hypothesize here because I haven't had a chance to test my theory and I'm afraid that by the time I get around to it, I may forget about this question.

The real question is, what is the variable that makes the thrombin time act differently than what you would assume? I’d wager the answer is temperature.

Protimes are performed at 37 degrees in order to simulate the in vivo environment, but also because most coagulation factors aren't active at room temp, or at least they are very slow-acting at room temp. Heating the environment speeds this process up so the test doesn't take all day.

Now, we know if you take a tube of warm normal plasma and add calcium and thrombin to it, it clots right away, right? But this is a problem because the thrombin time is a quantitative assay and we need it to be sensitive, especially for those super old-school clinicians who use it to monitor heparin instead of a more modern test like the APTT or Xa inhibition. We need to be able to tell the difference between a patient that’s gotten a bolus of heparin and a direct thrombin inhibitor. So, if you remove the heat, you slow down the conversion of fibrinogen to fibrin, and in the process you stretch the calibration curve, effectively increasing the sensitivity of the test. But this also has the effect of slowing down the conversion to where it takes 14–18 seconds rather than one or two.

If you change your test setup to have the thrombin reagent heated, my hunch is that your analyzer will give an error because the sample will have clotted by the time the analyzer reaches minimum threshold time. Or better yet, try this experiment on a fibrometer. I don’t have access to one so I can’t try it out as I’d like to.

I’d be interested in discussing this with any other experts out there, especially those that have played around in the coag lab. I may have occasion to test this out in the coming weeks; I’ll try to do it and update my answer with my results.


Chromosome 2 alternate explanation - apes gaining a set of chromosomes?

I guess part of the question is...what exactly are you bring up Chromosome 2 as evidence of, exactly?  It's evidence of that chromosomal rearrangements are possible, but that isn't terribly helpful to you, so I'm not sure why you are bringing it up.

I think the fusion is a rebuttal to a claim that the disparate # of chromosome is a problem for the claims of common ancestry between humans and other apes, but if they don't mention it, I'm not sure why you would need to use that particular fact.

Have you consulted talkorigin's 29 evidences of macroevolution?  Lots of good stuff there.

http://www.talkorigins.org/faqs/comdesc/


Single covalent bond is a shared pair of electrons. For stable bond there should be 2 atoms with unfilled higher orbitals and at least a pair of electrons that is "distributed" among those slots.

UC Davis have hilarious page on that.


Evolution of umbilical cord and reason of its elongation

The woman running bit is obviously a myth but that is genius.. Other than that the length of the umbilical cord has been found to be highly variable depending on each individual. Characterizing it as just long would therefore not be right. According to Wikipedia,

  The umbilical cord in a full term neonate is usually about 50
  centimeters (20 in) long and about 2 centimeters (0.75 in) in diameter
  (reference).

Some complications during birth are

  A number of abnormalities can affect the umbilical cord. The cord may
  be too long or too short. It may connect improperly to the placenta or
  become knotted or compressed (reference).

Why does it become too long has been associated with these factors.

  Long umbilical cords, defined as total length over 70 cm, have been
  significantly associated with:

  Maternal factors:

  Systemic diseases. Delivery complications. Increased maternal age.

  Fetal factors:

  Non-reassuring fetal status during labor. Respiratory distress. Vertex
  presentation Cord entanglement. Fetal anomalies. Male sex. Increased
  birth weight.

  Placental features:

  Increased placental weight. Right-twisted cords. Hyper-coiled cords.
  True knots (reference).

In conclusion, length of the umbilical cord has an average as mentioned before and being too long or short can lead to complications during birth. Regarding evolution of the cord, you could read this discussion.


All mammals have 4 limbs, and all fish have gills and fins (except for some, but I will get to that). What if that is because that is the perfect form for an organism in that kind of environment?

Different mammals species live in very different environments. We all have four limbs (except exceptions), not because it is adaptive to all of us for a specific environment but because there a strong phylogenetic signal. You should have a look at Why don't mammals have more than 4 limbs?.

All fishes have gills and fins (except exceptions). This is definitely because they inhabit a common environment. Gills allows fishes to get oxygen from water. Fins is a general structure that allows swimming. You will note that marine mammals also have fins (we often talk about convergent evolution) Btw, the post Do fish break a water molecule to absorb oxygen? might be of interest to you

  how much does the mindset and disposition of an organism affect its end body shape, and how much more random does it make the process of evolution?

I don't really understand what you mean by "mindset" and "disposition".

Nothing is random except in the consideration of unknowns. One can make sense of a probability only by consideration of a priories. While tossing a coin is often considered as the random event by excellence, a toss of a coin is everything but random if you were to know the exact forces that apply to the coin. So asking is something is random without stating what are the a prioris you consider knowing and not knowing makes no sense (although it may make some sense in quantum physics).

  say biologists were able to create organisms and watch them evolve quickly. If you took two single celled organisms that had no similarities, and put them in the exact same environment, would they evolve to look similar?

We are actually able to witness evolution in a matter of weeks in lab with organisms with short generation time such as yeast or E. coli.

The repeatability of evolution is a vast subject. The issue with such question is that it depends a lot. It depends typically on what evolution you are expecting to see and the size of the population. For example a simple change in allele frequency at a selected locus in a large population is typically very much repeatable. But if you think about larger time scale then, most think it is wise to consider that evolution would take a totally different path. There is a famous quote that says:

"If the tape of evolution were replayed a million times, a species like ours would not necessarily evolve" Stephen Jay Gould

You should have a look at Is evolution a predictive theory?.


What advantage do dogs have in clearly disclosing whether they are afraid or unafraid in a conflict?

It is better for animals to broadcast their qualities, and size one-another up before risking injury in conflict. As pack animals, dogs are particularly sensitive to where they are placed in a hierarchy. So it is better for them to telegraph their qualities than to engage in conflict that may hurt them.


Excess protein consumption effect on kidney

Short answer

The ammonia resultant from the protein metabolism is toxic to the body and specially kidney. (William V. et al.)

Long answer

Protein is a poly-peptide composed by amino acids. Each amino acid has an amine group (-NH2) in its composition. In the metabolism of the amino acids, this amine group is taken, and if it isn't needed is released the to blood vessels to be transported to the liver and be turned to urea.
Needless to say since the kidney filters the blood when there is excess of ammonia in the blood vessels the kidney is the first to suffer.

I've found some papers about the effect of ammonia in the kidney but none of them where about humans. (I may try to fetch some of them later.)

Why summer?
During summer water is lost through perspiration so there's less available for the excretion of urea.
I hope it helps.

References.

1.William V. McDermott, Jr., M.D. ,Metabolism and Toxicity of Ammonia


Where can I find a full genealogy of human cell types?

Wikipedia has a page listing cell types which classifies their origin as endodermal or ectodermal.

I haven't been able to find a source for a complete lineage of all cell types, and I have gained the impression that there is no complete picture, except in some specific cases such as the haemopoietic lineage.

Here is a TEDX talk by a researcher in the field, and here is a slideshow by the same person which lays out the problem and its importance.


Nice question! Nucleosome is quite a stable structure because of electrostatic attractions between the phosphate group of DNA and Lysine or Arginine of histone octamer1. In fact, both histone and DNA are known to protect each other from degradation: histone protects DNA from some kinds of damage2 and DNA protects histone protein from proteolysis3. Also, the histone protein gets modified whenever there is damage to nucleosomal DNA, so that DNA repair machinery can be activated4. Thus, nucleosome is not only structurally stable, but also tries to maintain its stability by its constituents protecting each other.

source

This stability has also been taken to a whole new level. In a research paper, scientists predicted that the reason for discovery of thousands of years old DNA, in intact form, is due to the stability of nucleosome5. They have even predicted that nucleosomal DNA can remain readable for even millions of years, because the time when histones start degrading is also the time when proteases and nucleases degrade, leaving very few chances for DNA to degrade.

But, nucleosomal degradation is not impossible. In a research, scientists concluded that the enzymes Caspase Activated DNase (CAD) or DNA Fragmentation Factor 40 (DFF40), together called CAD/DFF40, are indirectly required for degradation of nucleosome6. See this paragraph (I only pasted the main points):

  We report here that in response to apoptotic signals from a death receptor (CD95 and tumor necrosis factor-$\alpha$) or mitochondrial (staurosporine) apoptotic stimulus, the core nucleosomal histones H2A, H2B, H3, and H4 become separated from DNA during apoptosis in Jurkat and HeLa cells and are consequently detectable in the cell lysate prepared using a non-ionic detergent. The timing of this histone release from DNA correlates well with the progression of apoptosis...Taken together, these data demonstrate that CAD/DFF40 functions indirectly in mediating nucleosomal destruction during apoptosis...In this study, we have found that core nucleosomal histones separate from chromatin in apoptotic cells, but that this is not simply a by-product of DNA fragmentation. This event is indirectly related to CAD/DFF40 in the sense that CAD/DFF40 is required but is insufficient for the apoptotic histone release.

Thus, though it was the only paper I could find, nucleosomal DNA can also degrade in the same way as linker DNA if larger amount of CAD/DFF40 is present to degrade it.

References:

Histone structure and nucleosome stability; Leonardo Mariño-Ramírez, Maricel G Kann, Benjamin A Shoemaker, and David Landsman
Nucleosomal histone protein protects DNA from iron mediated
damage; Helen U.Enright, Wesley J.Miller and Robert P.Hebbel
Actin and DNA Protect Histones from Degradation by Bacterial Proteases but Inhibit Their Antimicrobial Activity; Asaf Sol, Yaniv Skvirsky, Edna Blotnick, Gilad Bachrach, and Andras Muhlrad
Histone - Wikipedia
Degradation of ancient DNA; Zvi Kelman, Lori Moran
Apoptotic Release of Histones from Nucleosomes; Dongcheng Wu, Alistair Ingram, Jill H. Lahti, Brie Mazza, Jose Grenet, Anil Kapoor, Lieqi Liu, Vincent J. Kidd and Damu Tang


How can two individuals of the same species have different chromosome numbers?

there are diverent concepts of definitions of species:

morphological species concept, distiguishes a species by body shape and other structural features
ecological species concept, distighuishes a species according to it's niche
phylogenetic species concept, smallest group which schare a common ancestor
biological species concept, a species is a group whose members can produce fertile offspring

the biological species concept is most commonly used, if we apply this on your problem, they still produce fertile offspring, so they are the same species.

If for example a mutation wil occur which causes polyploidy (more likely in plants, however it's possible in some animals). Let say the orginal species have 2n = 12, if polyploidy occurs(during meiotic error for example). We will have 2n = 24. If these species produce gametes n = 6 and n =12, fusion of those gametes will result in unpaired chromsomes, which in turn will lead to a reproductive barrière. The 2n =12 and the 2n = 24 species can only mate with each other to produce fertile offspring, so we can say these are different species.