Can hunting of large specimens of a species make the size and weight of the species tend to be smaller?

I don't know of any research about this on tigers or any other terrestrial predators, but this is a well-known phenomenon in "trophy" animals1 (i.e. big game hunted for sport) and wild-caught fish1-4.
1: Allendorf, F. W., & Hard, J. J. (2009). Human-induced evolution caused by unnatural selection through harvest of wild animals. Proceedings of the National Academy of Sciences, 106(Supplement 1), 9987-9994.
2: Heino, M., Pauli, B. D., & Dieckmann, U. (2015). Fisheries-induced evolution. Annual review of ecology, evolution, and systematics, 46.
3: Monk, C. T., Bekkevold, D., Klefoth, T., Pagel, T., Palmer, M., & Arlinghaus, R. (2021). The battle between harvest and natural selection creates small and shy fish. Proceedings of the National Academy of Sciences, 118(9).
4: Bowles, E., Marin, K., Mogensen, S., MacLeod, P., & Fraser, D. J. (2020). Size reductions and genomic changes within two generations in wild walleye populations: associated with harvest?. Evolutionary applications, 13(6), 1128-1144.


The best immunology book hands down is Janeway's Immunobiology. There is no debate among the immunology community.  The middle section is devoted to B cell development.


What chemicals can be detected in sweat?

Cystic fibrosis diagnosis. Here is a link to a paper describing the use of β-adrenergic sweat secretion as a diagnostic test for cystic fibrosis.

Anti-cancer therapy and its effectiveness. This report seeks to determine the levels of the anti-cancer drug sunitinib and its active metabolite N-desethylsunitinib in sweat.

I'll add others later.

Here's a 2004 study looking at a particularly unpleasant sulfury compound produced by bacteria in contact with sweat. It's interesting that the enantiomer of the malodorous compound had a grapefruit-like smell.

This paper puts forth the idea that sweat, which contains lactate, lactic acid, urea (of course) and amino acids, can be used in forensics.


Where does the energy required to turn ADP into ATP come from?

This is a common problem when asking about the explanations for things that happen in a biological context.  When you ask for why something happens in biology, the answer to that question depends on what, specifically, you want to know.  For example, the same question, "Why can humans see more colors than dogs?" can be answered using a physiological mechanism (Humans can see more colors than dogs because we have an additional cone type in our eyes), or an evolutionary explanation (Humans can see more colors than dogs because our ancestors were under selective pressure to be able to identify ripe fruit).  Both of these responses would be correct but they are answering from different perspectives.

The question of where the energy comes from to phosphorylate ADP is another one of these questions that can be answered in a couple of different ways.  The immediate mechanism for providing this energy is the proton gradient between the intermembrane space of the mitochondria and the mitochondrial matrix in the case of Cellular Respiration and the proton gradient between the Thylakoid Lumen and the Stroma in the case of Photosynthesis.  But where did the energy ultimately come from?  The sun.  In the case of Photosynthesis, it is energy from the sun that drives the photosystems that generate that proton gradient in the first place.  In the case of your own body, you either eat a plant or eat an animal that ate a plant that got its energy from the sun in the same way, and then use the chemical energy contained in that food to sustain your own proton gradient.  Either way, the energy ultimately came from the sun.  It's just that the proximate (immediate) explanation is a chemical one driven by a chemiosmotic gradient maintained either by sunlight and water in the case of photosynthesis or sugar and oxygen in the case of cellular respiration.


Single Nucleotide Polymorphisms and diseases

SNPs in all these regions will modify the DNA sequence. Effects will depend on where exactly the SNP is. I'll summarize the conditions in which effects can be maximum

Transcription Factors (TFs) binding sites: SNP in the nucleotide positions that bind to the recognition amino acids in the TF
Epigentic signals: C->X [x: A,G,T] SNPs can disrupt DNA methylation hotspots
Splicing variants: SNPs at splice donor/acceptor sites can cause intron retention
microRNA binding sites: SNP in seed region can abolish miRNA targeting
Coding regions: certain SNPs can create premature stop codons for e.g. CAG (Gln) -> UAG (stop)

there is a lot of work on SNPs. If you search in pubmed for all these categories, you'll get many research articles as well as reviews.


How do metal ions acting as enzyme cofactors "find" their respective enzymes?

The metal ions are transported across cell membranes by various mecanisms like channels, pumps or extracellular receptors for carrier protein.

The loading step mostly happens in the cell. Once transported inside, some ions just diffuse into their binding site on the protein; others, like iron, need a scaffold.

Some essential enzymes are metalloproteins, for example most ATP-using enzymes need magnesium; and the respiratory chain needs iron. Thus most cells will have transporters for these metal ions.


How is each region of the DNA replicated only once?

DNA Replication ensures it only occurs once by the use of licensing factors. These factors are released and bind to the origins of replication during one distinct phase. After the factors have been released and the first phase has ended, the actual replication initiates.

Information on the licensing factors:

The licensing factors used to create the pre-replication complex is the Minichromosome Maintenance (Mcm2-7) protein, Cdc6, and Cdt1. The Cdc6 and Cdt1 are required to load the Mcm’s onto the DNA and therefore, are highly controlled during the cell cycle. The Mcm2-7 hexamer is the actual DNA helicase that is used during DNA replication.

The way that the re-replication of DNA is prevented is that when the DNA replication starts, the Mcm helicase moves away from the ORC and the newly replicated DNA, meaning it then cannot be reinitiated. Along with the physical moving of the helicase, Cdt1’s activity is suppressed by the protein Geminin, which prevents the licensing of the helicase during times of non-replication.

Image from the article on the licensing.

More information on this topic:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688777/#!po=21.8085


They are tridimensional cell cultures according to H Ma et al. 2012.

  Multicellular tumor spheroids are one of the classic 3D culture models that can be applied to the development of anticancer drugs and treatments. By mimicking the 3D network of the cellular–matrix and cell–cell interactions, tumor spheroids resemble many aspects of the pathophysiologic environment within human tumor tissue.

Classical cell cultures are usually monolayer. Many of the differene between these cultures and real life tissues has been overcome by 3D cultures according to Carver et al. 2014.

  The multicellular tumor spheroid (MCTS), a three-dimensional model that closely resembles small avascular tumors and micrometastases, has been utilized as an intermediate between monolayer culture and in vivo studies for the screening of small-molecule drugs.

So is it a 'real life' entity or is it something that is computer generated? It is real life. Let's think of an organ. It's made up of a specific tissue(s) and a stroma that contains vascular, nervous and other components that supply nutrients and limit the organ's specific tissue. This structure develops in vivo in 3D. The blood vessels will follow tissue development in a tree-like 3D structure in order to reach to all cells. But what you do with lab cell cultures? There are no blood vessels there. How do you supply nutrients to all cells? That is why most in vitro cell cultures are developed in monolayer structure. Yet cells are 3D structures. They are joined together in a tissue by intercellular junctions. Monolayer limits this joining to a single plane. Moreover, when it comes to cancer cells which have specific properties (they lose junctions and start to move) the monolayer model becomes limited. This is how spheroids have become a better model for studying in vivo processes using in vitro cell cultures.


Is there any recent evidence for the aquatic ape theory of human evolution?

The Aquatic Ape theory has never gained wide acceptance. This is because it has never had strong evidential support.

The features supposedly supporting the hypothesis only do so under an extremely superficial analysis (e.g. the argument for bipedalism), frequently actually occur in other non-aquatic mammals (e.g. hairlessness in naked mole rats and rhinos, a descended larynx in red deer), show no sign of having arisen at similar times in the human evolutionary record (e.g. encephalisation evolved far later than bipedalism and bipedalism vastly predates hairlessness) and lack fossil evidence of having evolved near aquatic environments.


Gene knockdown vs gene knockout vs knocksideways?

Hello and welcome Adil Amchi.
In genetics and molecular biology there are differences between the terms knock-out, knock-down and (the lesser known term) knock-sideways.
Knock-sideways: Inactivates proteins. Could be done using small molecule inhibitors.
Knock-out: Gene removal, no gene expression. Could be done using CRISPR.
Knock-down: Gene expression is reduced. Could be done using interference RNA.
(Another reference for Knock-sideways:

"Importantly, the rapidity of the “knock-sideways” system allowed the researchers to observe a phenotype distinct from siRNA-mediated knockdown of the same protein...")


Is there any artificial species (in particular, an artificial species of animal)?

Artificial selection leading to new species - Domestication

As you talk about dogs in your intro, let's consider them.

You will fail to breed a great dane and chihuahua for obvious mechanical reasons. You will also fail to breed a chihuahua with a wolf. So, yes artificial selection have lead to reproductive isolation.

Artificial selection leading to new species - lab experiment

Artificial selection have also lead to reproductive isolation in non-domesticated species. See for example the post Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?

Concept of species

As a side note... Above, I consider the so-called 'biological species concept'. For a discussion on the definition of species, please have a look at this post.


Questions to ask to a panel of people that will be sequenced

23andMe is a company that provides sequencing. Before they sequence your genome, they ask you to fill in a couple of surveys, one of which is about your physical features. Here is a list of some of the questions they ask:

  How much hair do you have on your upper/lower back?
  When you walk, in what direction do your feet naturally face?
  Do you have a line or indentation (dimple) in the middle of your chin?
  Excluding any hair loss, does your natural hairline have a widow's peak (a V-shaped peak of hair at the front of the hairline)?
  Can you flip your tongue over so that the underside is on top?
  Can you lift one eyebrow while keeping the other eyebrow in place?
  Which is longer, your big toe or the toe next to your big toe?
  On your left hand, which finger is longer, your index finger or your ring finger?
  What is your shoe size in U.S. shoe sizes?
  How would you describe the arches of your feet?
  Can you bend down and place your entire palms on the floor while keeping your legs straight (see above image)?
  Which image best matches the natural shape of your face (with your hair pulled back)?
  ...

That's a small list of phenotype questions you can ask ;-)


Can you freeze an ATP assay sample for later use?

Pure ATP can be stable when stored frozen but I would be worried, perhaps unjustifiably, about storing a homogenized sample. You should try dividing a homogenized sample in half and assaying one half right away and the other half after freezing to see how the signals compare.


Why is a urea solution hypotonic relative to RBC?

I think you have the conceptual understanding down, but my guess is that the textbook is not representing the situation quite correctly.  Based on the phrasing of the statement, I can imagine they are describing one of two situations:

Imagine a dropping a cell in to a solution of 0.5 M urea with no other solutes.  Urea will diffuse across RBC membranes due to facilitated diffusion.  It won't really factor in to this situation much.  So, the RBC contains proteins and other solutes that cause water to flow in to the cell and the cell lyses.  I don't think this is what the textbook means.
Now, imagine a situation in which you precisely calculated the water potential of a RBC.  You mixed up an isotonic solution of urea and some non-penetrating solutes.  This solution is perfectly isotonic at first, but as the urea diffuses in to the cell, it alters the water potential of the cell and the outer solution leading to osmosis.  I think this is the situation the textbook is trying to describe.

Imagine a third situation now in which a RBC is at equilibrium with a solution.  If you just added urea to the solution, it would not affect osmolarity in the long term for the reason you describe.


That's not a Wolf Spider, although it's often mistaken for one.  The long, jagged-edged-banded legs, splayed out in a characteristic flat posture, and the large, round carapace are pretty characteristic indicators of a Dolomedes fishing spider - one of the terrestrial ones that have moved into drier, upland areas and hunt more like Wolf Spiders do.
There are two species this could be, but the fact that you don't see a full white underline beneath the 'w's on its abdomen tells you it's not Dolomedes scriptus, but its common relative Dolomedes tenebrosus.
These spiders are actually pretty mild-mannered and can make good pets (as spiders go), but they will bite if bothered too much (how much "too much" is seems to be different from spider to spider).  The bite can be painful because of their size and large fangs, but the venom is not particularly effective against humans.  I'd rate it as a lot less painful than even a mild wasp sting, although of course every individual spider and every individual human is different.
Here's a link to the Bug Guide page, which has more information and lots of photos..
https://bugguide.net/node/view/2011

I should also add that these guys eat beetles and other relatively large insects and small animals that you might or might not want to share your home, if that makes any difference.  I can't see its pedipalps clearly, but the large cephalothorax and relatively small abdomen make me suspect it's an adult male, just wandering around looking for love.  It's unlikely that you have all that many individuals living with you - unless you have a dirt cellar, of course; they seem to like places that are a bit cave-like.

I also forgot I'm supposed to include an image:


Are there more descriptive ways of naming genes and gene interactions?

Many gene names are descriptive, e.g. DRD1: dopamine receptor D1, TOP2A: DNA topoisomerase 2-alpha, or PTGS1: prostaglandin G/H synthase 1. These are examples of genes that have a clearly defined main function.

The genes you listed are involved in development, and there describing the function of a gene becomes much more difficult. E.g. sonic hedgehog is involved in patterning many organs, from brain structures to teeth. How would you assign a descriptive name?

The analogy to (programming language) functions does not work for many genes, because they were not designed to fulfill one function, but evolved to do many different functions. For genes that have many functions, we just need a unique name. The multitude of functions is catalogued elsewhere.

(Bonus descriptive gene family name: MAPKKK: MAP kinase kinase kinase)


Why natural selection leads to selfishness
Imagine a population of individuals. At a given locus, some individual carry the A allele and some others can the S allele (A for altruistic and S for Selfish). For simplicity, we will assume organisms are haploid. Individuals carrying the S allele are selfish and will take care of themselves only. The A allele are altruistic meaning that they produce behaviours (and non-behavioural phenotypes) that will reduce their fitness and increase the fitness of other individuals in the population.
As the altruistic behave as to reduce their fitness, they will be at a selective disadvantage and therefore, over time, only selfish individuals will remain.
How can altruism evolve then?
The study of the the evolution (and evolutionary consequences) of behaviour (and non-behavioural phenotypes) that affect the fitness of other individuals in the population is called social evolution. Social evolution is a wide field of knowledge and I will here attempt a very short summary of it so many concepts will be left out!
There are two main (non-exclusive) ways by which altruism can evolve:

Repeated interactions (False altruism)
Kin interactions (True altruism)

Repeated interactions
The concept is grounded within game theory. A good introduction to game theory is definitely out of the scope of this question but I just want to give a little bit of an intuition. I will over-simplified the concepts of game theory but you should definitely have a look at it. Those concepts are very enlightening for questions of evolutionary biology, economy, psychology, sociology and even philosophy.
If for example, the altruistic individuals are actually only altruistic to those
that have shown altruism in the past (via a Tit-for-Tat strategy for example or through the use of reputation), then altruistic individuals may end up have a higher fitness than the selfish individuals. Imagine for example that selfish individuals give nothing and receive nothing. Let's assume that all altruistic individuals, all make one good deed and receive one good deed. Giving a good deed comes at a cost of having, say 0.8 fewer offsprings on average. Receiving a good deed comes at a benefit of 1.2 extra offsprings. Overall and on average, each altruistic individual will produce 0.4 more offsprings than the selfish individuals and therefore, over time the whole population will become altruistic.
We often refer to these concepts as false altruism because altruistic individuals actually has a fitness increase over their life time. Let's now talk about true altruism where altruistic individuals really just give without receiving but yet, the allele coding for altruism thrives.
Kin interactions
Note first that any kin interaction follows within a give game theory scenario. As such kin interaction is just an add-on on what I discussed earlier. For those used to Hamilton's rule, please note that Hamilton's rule apply to Prisoner's dilemna (a type of game theory scenario) only.
So, imagine now that altruistic individuals are being altruistic with their family members (their kins) only (either because they direct their altruism or because there is a strong population structure). Note that such altruistic behaviour can pretty indirect as helping your partner (who we will assume is not part of your close family) will have for consequence that your partner may offer better parental care and therefore by being altruistic to your partner, you are actually being altruistic to you offsprings (which are your kins).
Because the kins of altruistic individuals probably carry the A allele, eve if the altruistic individual is experiencing a lifetime cost in fitness, the A allele may still thrive and the recipients of this altruism are likely also carrying the A allele. In other words, a truly altruistic individual is an individual that sacrifice itself for helping the allele A present in its kins to thrive. In yet other words, true altruism is when an allele is ensuring that copies of itself present in other individual will manage to get passed on.
And this is called Kin Selection. I can now clearly answer your question
Your question

What problem does kin selection solve?

Kin selection explains "true altruism"!
Only "true altruism" can yield to such separation of the reproductive task as that some individuals are perfectly steriles. In your post, you say

From the perspective of the sterile worker: Since it can't reproduce, no strategy will affect the number of offspring it has (will always be 0)

What is missing from this logic is that, 1) at a time workers could still reproduce and 'gave it up' and 2) in many (maybe most?) social species (honeybees, termites, ants and also in non-hymenopteran eusocial species), workers are still able to sometimes reproduce and are also able to overthrow the queen.


What are the ploidy levels in major groups of organisms?

Are all animals haploid (n=x) ?

No

  Are all fungi haploid (n=x) ?

No

  Are all plants diploid (2n=x) ?

No

  Are all Protists diploid (2n=x) ?

No

  Also, what is the ploidy of archaea and bacteria?

Generally speaking, Bacteria and Archaea don't have chromosomes (but have circular DNA). As such the question of ploidy does not really apply to them.

You might want to read about Biological life cycle to understand the terms haplontic, diplontic, haplodiplontic (and other similar terms).

Ploidy level can easily varies among species of the same family (typically in plants for which hybridization is common). There is no reason to expect that a taxon as big as "fungi" (for example) would all have the same level of ploidy.

Note that your question that all animals are haploids is surprising as you just described that humans are diploids.


Is there any research on how accurately people can follow a beat?

You might begin your search with the characteristics of Parkinson's disease. This degenerative disorder is precipitated by the death of neurons in the substantia niagra. This brain structure is composed of multiple neurological nuclei. Its function is to connect cortical regions and nuclei together, most significantly with the basal ganglia. The difference between nuclei and cortical brain circuits is important to your question.

The symptoms of Parkinson's are directly correlated with the function of nuclei in central nervous system: the integration of information. It's the integration of conscious thought, muscle memory, sensory-motor pathways that makes voluntary movement possible. Disruption of this network in Parkinson's degrades one's ability to voluntarily execute a movement.

The cerebellum also controls voluntary movement. As a cortical structure, it is involved more with the formation and maintenance of muscle memory than information integration. Damage here results in the loss of fine motor control as opposed to gross motor control in Parkinson's.

This problem has a sensory and motor component. It might be difficult to tackle your problem as a whole. Perhaps breaking it down into smaller pieces would shed some light on what you're looking for.

Here are 2 articles I found relating motor control with the cerebellum and substantia niagra.

Relating cerebellar damage with learning sequence information

Relating the substantia niagra with interval timing


Can a bacterium infect another bacterium?

Bdellovibrio bacteriovorus (BV) “infects” other bacteria:

Similar to a virus, BV attacks bacteria such as Escherichia coli (E. coli) by attaching to and entering its prey, growing and replicating within the cell, and then suddenly bursting out, releasing its progeny into the surrounding environment. — How bacteria hunt other bacteria


Breakpoint resolution for copy number variation analysis

It means that it is hard to tell the precise location on the chromosome where the structural variation event starts and finishes using only read-depth information.

Read depth is measured by counting the number of mapped reads that overlap targeted regions aka bins. These bins are typically many basepairs wide and are used to normalize coverage with respect to various parameters (e.g. GC content). Smaller bins can give better breakpoint resolution but have noisier statistics. Large bins have better statistics but can't be used to precisely call the SV boundaries.

The CNVnator paper discusses the topic
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106330/


This resource provides a short list of which general components of plumage are good indicators of a healthy bird.

Your pet's plumage should be. . .
Soft - feathers should be strong, yet flexible.
Smooth - no rough feather shafts; no uneven or split edges
Glossy - sheen extends over the entire coat
Full - thick, where it needs to be
Vivid - color should be deep, bright and uniform
Clean - free of dust, dander, waste, or soil
Parasite-Free - no lice or mites

Also, this website page discusses the signs of malnutrition or disease in plumage in more detail.
Stress bars, dark lines which transect a feather, are directly caused by an inefficient absorption or lack of required nutrients. Stress bars can be found on all feathers during the period of malnutrition, and remain even after this period.
Assymetrical moulting is also a sign of bad health. There should not be any bald patches present during the moult.
The resource states that if a moult is delayed due to malnutrition, an incorrect photoperiod or a metabolic problem, plumage will become depigmented. However, the appearance of "dirty" feathers can also be due to overpreening or damage done to feathers by physical contact.
Finally, a change in the usual plumage color of the bird in question is indicative of a lack  or oversupply of a particular nutrient.


How are long time periods measured in biological systems?

The short answer is: we do not know exactly, although we do have some insights.

I will take the example of puberty.

Although a clear definition of puberty is lacking, it is quite clear that it corresponds to a period where gonadal function starts.

This, in turn, is derived from the activation of the gonadotropin system, which consists of two main cell types:

a small number of neurons located in the preoptic area of the hypothalamus (a nucleus at the base of the brain) called the GnRH neurons. GnRH is the Gonadotropin-releasing hormone, a small peptide that stimulates the production of gonadotropins from the pituitary.
the gonadotrophs, a specialised group of cells in the pituitary (a gland located underneath the brain) which produce two hormones, called luteinizing hormone (LH) and follicle-stimulating hormone (FSH) which stimulate the gonads to produce various hormones, such as estrogen.

In mammals, the secretion of GnRH, and thus LH/FSH varies during the course of the menstrual/estral cycle. This cyclicity lasts several days (4-5 days in rodents, ~1 month in humans) and entrains the cyclical secretion of estradiol (E2) from the gonads.

Note that this is a sort of self-sustaining cycle, as cyclic levels of E2 will then allow for cyclic GnRH secretion and so on.

But, back to your question: how does the GnRH/LH/E2 system "wake up" at puberty?

The exact mechanism is still unknown, but recent work has found an important mediator, called kisspeptin, that is produced from two population of neurons in the hypothalamus, called the kisspeptin neurons.

Kisspeptin has been shown to be a very potent activator of GnRH neurons and work in the mouse has shown that these neurons appear at the time of puberty, their number increasing dramatically between 25 and 31 days (puberty is at around 30 days in mice).

Postnatal Development of Kisspeptin Neurons in Mouse Hypothalamus; Sexual Dimorphism and Projections to Gonadotropin-Releasing Hormone Neurons  - Clarkson and Herbison - Endocrinology, 2006

Similar work exist in the monkey:
Increased hypothalamic GPR54 signaling: A potential mechanism for initiation of puberty in primates - Shahab et al. - PNAS, 2005

In humans mutations in either kisspeptin, or its cognate receptor GPR54 results in disturbances of pubertal maturation because of underactivation of the system (hypogonadotropic hypogonadism) or hyperactivation (precocious puberty).

So, now the question is shifted: why do kisspeptin neurons show up only at puberty? We don't know for sure, but it looks like increased levels of E2 could be important for this.

Again, we get into a self-sustaining cycle. Growth of the body generates an increase in E2 production (possibly due to increased volume of the gonads?), which, when over a certain level permits the development of kisspeptin neurons, which will then stimulate the GnRH neurons, resulting in increased LH and E2. We then have more E2 and this makes kisspeptin neuron grow even more etc etc.

From: Postnatal development of an estradiol-kisspeptin positive feedback mechanism implicated in puberty onset. - Clarkson et al. - Endocrinology, 2009


Why does the thickness of the Loop of Henle have to be less than the convoluted proximal tube and the distal convoluted tube?

there is a bit more to it actually,

The Henle -loop only occurs in birds and mammals, giving them the ability to make the urine hyperosmotic in comparison to their blood, other vertebrates can't do this.

how does the henle loop achieve this further concentration of urea(= more resorption of H2O)?:

-> by using the physical principle of countercurrent exchange
Beware: the explanation follows the opposite direction as the flow of the liquid!

A potential is build up in the bigger upgoing part Pars recta by active Na+& Cl- resoption , the water cant go out because the membrane is impermeable here.

this leads to build up of osmotic pressure (positive osm. potential of 1200 mOsmol/kg)

The Henle -loop  loops back up as a thin part(!) the Pars ascendens

the downgoing part right after the PCT (pars descendens) uses the potential of the corticomedullary osmosis gradient to let water (resorption) out using passive osmosis while taking urea in (no ATP needed).

CONCLUSION: So why is the left and bottom part of this henle loop thinner?!  to resrobe H2O using passive osmosis ! (also, if the lowest bottom part would be thick, it would not loop so nice, therefore hindering the coutercurrence effect)


If Tumors have lots of mutations in them how is it the immune system can't detect them?

This is a good question and it gets to the most basic foundations of immunology. Your immune system is made to be flexible - able to adapt to almost any challenge. However, with so much flexibility comes the potential to generate immune cells that react against the 'self'. So, at the other extreme, the immune system needs to be limited.

In order to meet these two (potentially conflicting) goals, immune (at least lymphocytes) cells have a two-step development pathway. In the first step, the body randomizes its immune receptor specificity. In the second step, it ensures that these receptors are not auto-reactive.

Doing so means that immune cells are aware of their environment at the time that they are 'born.' Take a look at this review from the Fuentes-Panana lab to read about how tumors actively cultivate the immune system of their host in order to maintain a more favorable environment.


Issues with the post

I agree that the question is too broad. It is not the only issue, it is also primarily opinion-based (see below for explanations). The post is also somehow unclear (see below for explanations). But here is some kind of an answer that may help you.

If you google your question you will get tons and tons of hits. There is a whole lot of videos on youtube that address this question. You may want to have a look at those and come on StackExchange to ask a more accurate question because for the moment the question is too broad.

As a first short answer to the questions...

  At the present time it looks as if there is no other life in the Universe other than here on Earth

It sounds wrong (as a consequence your question would be primarily opinion based). We haven't found life. This doesn't mean that life doesn't exist elsewhere. Actually most people think that life exist elsewhere. Part of the issue behind this question is the definition of life. Often, people refers to Drake equation (you might want to read about it) which gives you the number of planets where life should exist. However, Drake equation is a speculation that has no solid grounds. It is actually pretty complicated (or impossible because we need to assume things about what the original conditions are) to calculate a probability that life occurs on a given planet. While it sounds pretty intuitive to many people (me, including) that life should exist somewhere else, there is really not much certainty.

  Is it possible for something to happen only once?

Well....yes, the death of Napoleon occurred only once.... I am not quite sure what you mean with this question, it is unclear.


Any relevant knowledge/studies about voluntary goose bumps

Recent studies prove that this involuntary phenomenon must be untrue. Obviously this is false, in order for research like this to take place people need to spend money. It would be interesting if we could create a crowd sourcing account maybe on kick starter to find ways to bring money into the research. I wish I had more information for you, I've been able to do it as long as. When you go to the dentist, just curious, you don't happen to have two bones underneath your tongue that is an anomaly as well? I've been trying to think of correlations for years. I can get the medical terms, if you like. Find me on Facebook Chris Azzy


When we look at the definition, Halophiles are just archaebacteria that require salt in their environment to live. Wikipedia states that they live in salt concentrations of 0.3 to 0.8 M (1.7 to 4.8% — seawater is 0.6 M or 3.5%).

According to The Saltwater Wetland bacteria in estuaries will get their food from dissolved organic mater in the water. An estuary can have a salt concentration of 0.5 to 35 ppt (according to google). This would be 0.05 - 3.5% salinity depending on the estuary, so obviously there are some estuaries would not be able to host Halophiles, but the concept is still the same. They would get their food from dissolved organic matter in the water.


Do men and women have the same number of genes?

It is true that the Y chromosome is shorter than the X chromosome and that there are more genes on the X chromosome.

  Do men have fewer genes?

One could (mis)understand three things in the expression "number of genes".

Number of gene copies (see Copy Number Variation)
Number of genes
Number of alleles

Thanks to @GerardoFurtado for correcting my semantic in the comments.

1. Number of gene copies

From the statement that there are fewer genes on the Y chromosome, one can conclude that men have fewer genes copies than woman.

This is the intuition the OP seemed to have.

2. Number of genes

Men also have an X chromosome. So men have the standard genes present on the X chromosome (but they only have a single copy of it while women have two copies; btw you might be interested in dosage compensation).

Because women do not have a Y chromosome and because there are a number of genes on the Y chromosome that are not present on the X chromosome, men have genes that female don't have at all. Therefore women have fewer genes than men.

3. Number of alleles

There is not much reason to expect that one gender would be more heterozygote than the other at autosomes (=non sexual chromosomes). Some may hypothesize that women may have more heterozygosity than men if there is stronger selection among sperm than among ovules or things like that but let's not get down this complicated path.

One one hand women have more gene copies and therefore might experience more heterozygosity, one the other hand, men have more genes and would therefore eventually carry more alleles. I don't know which side wins!

Did you mean number of genes per cell or per individual?

So far I assumed you were interested about the number of genes (or gene copies) per cells but if you want to compare whole individuals than it is a different story!

Men are on average taller and therefore have more cells. Therefore if you compare the body-wide number of gene copies, women will have fewer gene copy on average (Thanks to @JM97 comment).


Here's a partial answer, based more on common-sense then in-depth knowledge:

Physiological. One reason light is not required immediately is that many seeds are in essence bundles of stored energy (as carbohydrates, I suppose). This is what makes them attractive food for birds, squirrels, humans, etc. When they're able to escape that predation, the growing plant can use that stored energy, rather than relying only on sunlight.

Evolutionary. Seed dormancy can be a powerful tool for fitness – seeds that can remain dormant and germinate during favorable conditions could have a much higher survival rate. These conditions vary from simple: "spring" to more complex: "after having passed through the digestive system of a certain animal"; "after a forest fire"; "when there's a gap in canopy cover / less competition for solar energy". The cues that seeds "read" in order to try to break dormancy and germinate during these times therefore vary among species. Within species, there are probably often a number of cues, and as @Konrad Rudolph suggests these are probably all relatively "soft", or at least act in complex interaction with one another.


Sorry that my answer is not a real answer, but this would be a good starting point for some more science.

Several of the questions you might ask and could answer (with some more experiments):

Does this happen in plates without E.coli?
You have a contamination on the right side, perhaps also on the black part. Could this be the culprit? Only half the plate is black, the rest is (still?) red.
You used a paracetamol tablet with red dye and a lot of sweeteners, does the same thing happen if you use one without the red dye? A dye would be a likely source, because it already contains an absorbing moiety. It only needs to be slightly modified to absorb different wavelengths.
What kind of agar are you using exactly? There are many kinds, often selecting for certain types of micro-organisms, with indicators for pH or other colored markers to detect and identify strains.

For your metabolic question you can take a look at https://ecocyc.org/ where you can find a database with all known metabolic pathways for E.coli K12. Unfortunately I couldn't find anything for paracetamol (or synonyms) but you could try to see if it produces a colored product for any of the additives.


Resolution size of the gel simply means the distinction that can be made between molecules very close in size.

If you were looking to distinguish between a 100bp fragment and a 200bp fragment, then agarose will give you that level of differentiation.

But if you were looking to distinguish between a 190bp fragment and a 200bp fragment then you would likely want to us polyacrylamide. The PA gel has a higher resolution because you can distinguish between smaller differences on molecule length.

Think of it in terms of a simplified idea of a microscope, at 100X, you can probably distinguish between cells, maybe make out a well stained nucleus. where as at 1000X you can start to discern other organelles. You are seeing a finer degree of detail at the higher magnification. There are many factors that go into the resolving power of a microscope and the example based on magnification is simplistic and doesn't really address optical resolution, but it is an illustrative example of resolution in a gel. You can think of agarose as the 100X and PA as the 1000x, if that helps.


Well I sometimes use PDB files from proteins whose structure has been identified and study them. I use swiss PDB viewer software to do this and its pretty neat! I haven't looked at the biophysical data associated with a PDB file but I'm pretty sure they are there since you wouldn't be able to make the calculations and resolve the protein structure and confirmation without that kind of data. All you need is to download the software, go to Uniprot database and use the accession number of a protein you are interested in, see if its structure is resolved and either download the PDB file or use the accession number to download the file inside the software.


How do nicks in the DNA strand affect the success of Long Range PCR?

It is not unlikely that nicking is causing trouble. The question is if repeated freezing and thawing is causing the problem, there is an article which has been published in B.R.L. Focus in 1983 which disputes this effect. You can find the PDF with the article here, the article itself starts on page 10 in the PDF. On the other hand there is this paper ("Impact of long-term storage on stability of standard DNA for nucleic acid-based methods."), which shows that sstorage conditions do have an effect on the effciency of qPCR standards. Whatever causes nicking, it is a problem in (long) PCR. The following quote is from Sigma in their long PCR enzyme mix:

  Template High quality and adequate length of the template are
  essential for reliable amplification of larger fragments. Extreme care
  must be taken in the preparation and handling of the DNA target for
  long PCR. Nicked or damaged DNA can serve as a potential priming site
  resulting in high background. Avoid freezing, or, alternatively,
  freeze only once to minimize damage. The condition of the target DNA
  is critical. Depurination during cycling is minimized by use of
  buffers with a pH greater than 9.0 at 25 °C.

This paper ("Effect of Highly Fragmented DNA on PCR") shows that induced nicks affect the efficiency of PCR (although they do a much shorter amplification than you). So to overcome this problem I would make small aliquots of fresh DNA preps and then see, if this helps.


Hiding identical sequences in NCBI web interface

I'm not sure if there's a way on GenBank, but UniProt offers UniRef where you can cluster redundant sequences or specify a lower cutoff (like 90% identity).


We can actually use either depending on the specified convention, but a more convenient way to characterise the photosynthetic efficiency is:-

Considering the total incident solar radiation instead of that part which is absorbed (so that the calculated efficiency takes into account the total available solar energy on earth)
Using Net Primary Productivity instead of Gross PP.(so that the efficiency is characterised by the useful output (product) of photosynthesis by removing the non-useful respiratory losses of plant.)

I should also mention that using GPP instead of NPP was the practice followed in a large number of texts I read. But I think using NPP is not only the modern view, but also scientifically more convenient.

Here is the wikipedia page on photosynthetic efficiency and here is the book which houses the technicalities of these definitions along with several values of the various efficiencies.


Meta-analysis of fruits in blocking Cytochrome family

While I haven't found a list which is restricted to fruits, I found this page: P450 Drug interaction table. They list quite a number of substances which inhibit different isoforms of the P450 protein and also give the original references.

This list gives a large number of herbals which inhibit different P450 isoenzymes. The disadvantage is that they do not give further references so if you want to have a closer look you will probably have to spend some time with Pubmed.


Do all plant hormones of one group show the same qualitative effect with respect to their target pathway(s) and the biological response?

Preface: As @David says, the question is very broad. So, here, I'll take up the most common plant growth factors i.e. auxins to give you an idea.

Short Answer: We don't definitely know yet whether the pathways of two auxins (I take indole-3-acetic acid (IAA) and indole-3-butyric acid (IBA) here) are exactly same or not.

Background: We know that auxins have very similar functions1:

  Auxins are a class of plant hormones (or plant growth substances) with some morphogen-like characteristics. Auxins have a cardinal role in coordination of many growth and behavioral processes in the plant's life cycle and are essential for plant body development.

So much similar that2:

  genetic evidence has been found that suggests that IBA may be converted into IAA through a similar process to $\beta$-oxidation of fatty acids.

Now, when it comes to whether the exact mechanisms of how IAA and IBA work are similar or not then, as I said, we don't know yet.

When we talk about IAA, there is a theory known as Acid Growth Theory3 (though there are evidences against it):

  Plant cells elongate irreversibly only when load-bearing bonds in the walls are cleaved. Auxin causes the elongation of stem and coleoptile cells by promoting wall loosening via cleavage of these bonds. This process may be coupled with the intercalation of new cell wall polymers. Because the primary site of auxin action appears to be the plasma membrane or some intracellular site, and wall loosening is extracellular, there must be communication between the protoplast and the wall. Some "wall-loosening factor" must be exported from auxin-impacted cells, which sets into motion the wall loosening events. About 20 years ago, it was suggested that the wall-loosening factor is hydrogen ions. This idea and subsequent supporting data gave rise to the Acid Growth Theory, which states that when exposed to auxin, susceptible cells excrete protons into the wall (apoplast) at an enhanced rate, resulting in a decrease in apoplastic pH. The lowered wall pH then activates wall-loosening processes, the precise nature of which is unknown. Because exogenous acid causes a transient (1-4 h) increase in growth rate, auxin must also mediate events in addition to wall acidification for growth to continue for an extended period of time. These events may include osmoregulation, cell wall synthesis, and maintenance of the capacity of walls to undergo acid-induced wall loosening. At present, we do not know if these phenomena are tightly coupled to wall acidification or if they are the products of multiple independent signal transduction pathways.

However, there are evidences supporting this hypothesis, like this one4:

  When auxin stimulates rapid cell elongation growth of cereal coleoptiles, it causes a degradation of 1,3:1,4-$\beta$-glucan in hemicellulosic polysaccharides. We examined gene expressions of endo-1,3:1,4-$\beta$-glucanase (EI) and exo-$\beta$-glucanase (ExoII), of which optimum pH are about 5, and molecular distribution of hemicellulosic polysaccharides in barley (Hordeum vulgare L.) coleoptile segments treated with or without IAA. IAA (10–5 M) stimulated the gene expression of EI, while it did not affect that of ExoII. IAA induced gene expression of EI after 4 h and increased wall-bound glucanase activity after 8 h. The molecular weight distribution of hemicellulosic polysaccharides from coleoptile cell walls was shifted to lower molecular weight region by 2 h of IAA treatment. Fusicoccin (10–6 M) mimicked IAA-induced elongation growth and the decrease in molecular weight of hemicellulosic 1,3:1,4-$\beta$-glucan of coleoptiles in the first 4 h, but it did not promote elongation growth thereafter. These facts suggest that acidification of barley cell walls by IAA action enhances pre-existing cell wall-bound glucanase activity in the early first phase of IAA-induced growth and the late second phase involves the gene expression of EI by IAA.

But when it comes to IBA, all we have is this2:

  Although the exact method of how IBA works is still largely unknown, genetic evidence has been found that suggests that IBA may be converted into IAA through a similar process to $\beta$-oxidation of fatty acids. The conversion of IBA to IAA then suggests that IBA works as a storage sink for IAA in plants. There is other evidence that suggests that IBA is not converted to IAA but acts as an auxin on its own.

So, if IBA is converted to IAA before use then, obviously, it works the same way. But the article below suggests that either the mechanism or effectiveness of IAA and IBA is different5:

  We have examined in vitro rooting of apple ‘Jork 9‘ shoots exposed for three weeks to each of the three auxins commonly used for ex vitro rooting: indole-3-acetic acid (IAA), indole-3-butyric acid (IBA) and $\alpha$-naphthaleneacetic acid (NAA). During the initial five days of the rooting treatment, the cultures were incubated in darkness. In this period, the root initials are formed. Then, the cultures were moved to the light. NAA resulted in a low (ca. 8 roots), and IAA or IBA in a high (ca. 15 roots) maximal root number. The maximal root number was reached at a wide range of IAA concentrations (10-100 $\mu$M) but at only one concentration of IBA (10 $\mu$M) or NAA (3 $\mu$M). With NAA and IBA, growth of roots and shoots was much more inhibited than with IAA. For these reasons, IAA is the preferable auxin for in vitro rooting of apple ‘Jork 9’ shoots.

This suggests that IAA and IBA use different mechanisms or that IBA can't use the same mechanism as effectively as IAA.

References:

Auxin - Wikipedia
Indole-3-Butyric Acid - Wikipedia
The Acid Growth Theory of auxin-induced cell elongation is alive and well
Auxin-Induced Elongation Growth and Expressions of Cell Wall-Bound Exo- and Endo-$\beta$-Glucanases in Barley Coleoptiles
Effectiveness of indoleacetic acid, indolebutyric acid and naphthaleneacetic acid during adventitious root formation in vitro in Malus ‘Jork 9’


Wow, as an astrophysicist who has just logged into biology SE for the first time, I didn't think I'd have a question I could immediately answer.

You are correct about the Sun's output, so what about the lion.

If the lion is in its usual passive state, i.e. lying around as shown in your picture, then you would not go far wrong in treating them as black body radiators (well this will give you an upper limit, though the emissivity of human skin is quite high, so it should be a reasonable approximation.). To estimate a power I need a lion's temperature and its surface area.

According to this site the body temperature of a lion is 311.33 Kelvin.

I found a calculator that used the DuBois formula for surface area (for humans) and put in 440 pounds and 7 feet 10 for the weight and "height" of a (male, adult) lion - this returned a surface area of $3.6\ m^2$ (about twice a, male human, so sounds roughly ok).

Now using the Stefan-Boltzmann formula $P = \sigma A T^4$, I get the power output of a "black body" lion to be about 2 kW.

Thus $10^{12}$ lions have a power output of $2\times 10^{15}\ W$, which is 11 orders of magnitude less than the Sun.

But now take the question at its most basic. Compared to the Sun, the lion is a pretty effective power generation unit. The Sun only generates $2\times 10^{-4}\ W/kg$, whereas a lion-based power source weighs in with a massive $10\ W/kg$!

EDIT: Note that the calculation just assumes the Lion can produce this kind of power output whatever environment it is in. In practice a Lion absorbs a large fraction of this power from its surroundings and its internal metabolism does not need (and probably cannot) supply 2kW. Thus the 2kW should be reduced to some extent, though I'm not sure a simplistic $T^4 - T_{\rm env}^{4}$ calculation can be correct, unless one of you biologists tells me that a Lion's metabolism shuts down once the ambient (African) temperature approaches 311K (I guess in a human a lot of it goes in evaporating sweat?) Whatever, the order of magnitude of the answer is unchanged.


The computational study by Ehsani et al., 2011, argues that an ancestor metal-ion transporter gene ZIP served as the initial template for the prion founder gene, where the same author produced a 2012 paper that said this was probably a product of a spliced LIV-1 ZIP transcript that became reverse transcribed and inserted into the host genome. Thus, evidence in part points to a retrogene origin for prions (mediated by a retrovirus, especially since the gene is integrated into the host w/ no introns). They go on to state that two genomic rearrangements spanning hundreds of millions of years serve as the basis for the prion founder gene: A cysteine flanked core element inserted into the ZIP ectodomain, and then the insertion of a spliced, C-truncated ZIP transcript.

I don't think the evolutionary origin of prions are very well understood, yet, but I will try to find more recent data on the subject.


Why does Thiamine pyrophosphate have phosphates?

The diphosphate* part of TPP does not serve any catalytic function but, rather, helps bind the coenzyme to the enzyme. In this respect it is similar to the non-nicotinamide portions of NAD/NADP (think, why the P?), and represents a general theme, rather than a unique instance.

A pertinent paper that I found from an internet search unfortunately requires access to an academic library. This is P. Arjunan et al. J. Mol. Biol. (1996) 256, 590–600, and describes the crystal structure of yeast pyruvate dehydrogenase. I quote the following from it:

  The roles of Asp444 and Asn471 in binding the cofactor to the enzyme, observed in PDC and in their counterparts in transketolase (Lindqvist et al., 1992) and pyruvate oxidase (Muller & Schulz, 1993), conclusively establish the importance of a conserved sequence roughly 30 residues long (Hawkins et al., 1989) starting with GDG and terminating with NN (Figure 8). These residues are among the few highly conserved in all ThDP-dependent enzymes and form the Mg2+ binding site which assists in anchoring the diphosphate to the protein matrix.

And the Figure 8 referred to is a stereo-pair diagram (squint at the centre — with your specs off if you wear them — to see it in 3D):

￼
This also has a Pfam designation. The structure was deposited in the Protein Data Bank as 1PVD, where there is a useful diagram showing the interaction of the protein and magnesium ion with the phosphates:

*The paper quoted refers to the pyrophosphate part as “diphosphate”, which I assume is the standard chemical nomenclature.


Effect of cold showers after intense training

Taking cold showers(10-15 ℃) after training or workout have many benefits:

It helps in lowering the damaged tissues temperature by constricting blood vessels.
Cold helps numb nerve endings which provides instant localised pain relief.
Brings down heart rate and increases circulation.
It minimises inflammation and help you recover faster.
It is more effective in relieving delayed-onset muscle soreness,
which generally occurs one to four days after any physical activity.
It reduces uric acid levels, so it is beneficial for people suffering from gout.
It boosts glutathione levels in the body which is a very beneficial antioxidant.

Those who should avoid cold showers:

1] Those who suffer from heart diseases as constriction of blood vessels can lead to a heart attack.

2] People having high blood pressure, because blood vessels will constrict and can reduce the supply of blood to different organs, especially the brain.

Ice bath:

  In sports therapy, an ice bath, or sometimes cold-water immersion or cold therapy, is a training regimen usually following a period of intense exercise in which a substantial part of a human body is immersed in a bath of ice or ice-water for a limited duration. While it is becoming increasingly popular and accepted among athletes in a variety of sports, the method is controversial, with a risk of hypothermia, with the possibility of shock leading to sudden death. Many athletes have used cold water immersion after an intense exercise workout on the belief that it speeds up bodily recovery; however, the internal physical processes are not well understood and remain elusive. Generally research into the health effects of cold water immersion as part of an athletic training regimen is inconclusive, with some studies suggesting a mild benefit such as reducing muscle damage and discomfort and alleviating delayed onset muscle soreness, with other studies suggesting that cold water immersion may slow muscle growth and interfere with an overall training regimen.

[Source 1]

[Source 2]

You also maybe interested in:

[Question 1]

[Question 2]

References:

 - A cold shower maybe more beneficial to your fitness[Dr. Mercola].

 - Cold shower after exercise.

 - Effects of hydrotherapy on various systems of the body(NCBI)

 - The effects of cold water immersion and recovery of inflammation

 - Ice bath (Wikipedia)

 - 8 do's and don't's of Ice bath


Quinone A, Quinone B, Ubiquinone, Plastoquinone: whats the difference?

Difference between Ubiquinone (UQ) and Plastoquinone (PQ)
Structural Difference: Structurally, UQ and PQ are very similar. They only differ in a methyl group and 2 substituents on the benzoquinone ring (Liu et al, 2016). See the image for comparison:

Functional Difference: Functionally, PQ and UQ are very different. I'll give some differentiation points:

PQ is located on thylakoids of chloroplasts (Millner et al, 1984), whereas UQ is located primarily on the inner membrane of mitochondria, though it is found in all cells and membranes (Turunen et al, 2004).

Half-life of PQ is 15 hours while that of UQ is 30 hours in spinach cells (Wanke  et al, 2000).

UQ10 influences expression of hundreds of human genes involved in different cellular pathways, and UQ10-mediated gene-gene networks are involved in inflammation, cell differentiation, and peroxisome proliferator-activated receptor signaling (Schmelzer et al, 2011).

On the other hand, the redox state of PQ pool controls the NADPH dehydrogenase complex activity and further influences on cyclic photosystem I (Ma et al, 2008).

Although UQ has more widespread effects than PQ, most of their effects are restricted to their corresponding organelles i.e. UQ mostly influences mitochondrial activity whereas PQ mostly influences chloroplast activity. This can be understood on the basis of endosymbiotic theory since mitochondria appear to be related to proteobacteria whereas chloroplasts appear to be related to cyanobacteria (Mereschkowski et al, 1905). These two are thought to be taken in by cells about 1.5 billion years ago. We can suppose that at that time, both these organisms had similar carrier molecules (since they are very crucial for metabolism). This can justify why UQ and PQ are so similar in structure. Thus, your way of distinction can be considered as correct.
Difference between Quinone A (QA) and Quinone B (QB)
Structural Difference: In many cases, both QA and QB are structurally identical. For example, both QA and QB are ubiquinone-10 in Rhodobacter sphaeroides (Laszlo et al, 2004). Thus, the main difference between the two is functional difference.
Functional Difference: The distinct physical properties of QA and QB, including redox potential, are controlled by interactions with the binding site environment. Studies have shown that the 3-methoxy oxygen of QB interacts with the reaction center backbone (specifically amide of GlyL225). This interaction pattern serves to break the symmetry of neutral UQ between QA and QB by locking the 2-methoxy dihedral angle of QB in a position conducive to electron transfer from QA to QB (Vermaas et al, 2015). In short (not going in further details), QB interacts with the amino acid residues in reaction center in such a way that QA and QB acquire large difference in redox potentials. Apart from this, since QB is more loosely attached to the membrane, it is easily detached on being reduced to QH2 for transferring high energy electrons taken from QA to cytochrome bc1-complex8.
Thus, it is hard to differentiate QA and QB on structural basis, although QB and QA have different redox potentials due to different environmental conditions. Also, it is hard to tell whether QA and QB are structurally similar in all organisms; it is only known that they both are UQ10 in Rhodobacter sphaeroides. So, there is no simple answer (yet) on whether QB converts to plastoquinone or not. But since, in Rhodobacter, QA and QB are UQ10, thus it is not possible to convert QB to plastoquinone by this species. On the other hand, in a photosynthetic bacterium Rhodopseudomonas viridis, both QA and QB are plastoquinone molecules (Deisenhofer et al, 1994). Here, there is no need of conversion of QB to plastoquinone since it is already a plastoquinone. This finding only strengthens the fact that it is not easy to give a simple answer on whether conversion of QB to plastoquinone actually takes place or not. A much similar reaction center, from a thermophilic cyanobacterium Thermosynechococcus elongatus, looks like this (Ferreira et al, 2004; Loll et al, 2005; Umena et al, 2011):

Talking about replenishment of QB, when QH2 reaches the cytochrome bc1-complex, it is oxidized back to QB. This oxidized QB can again participate in the process of transfer of high energy electrons. Thus, QB easily gets replenished in cyclic photophosphorylation.
References:

Liu M, Lu S. Plastoquinone and Ubiquinone in Plants: Biosynthesis, Physiological Function and Metabolic Engineering. Frontiers in Plant Science. 2016;7:1898. doi:10.3389/fpls.2016.01898.

P.A. Millner, J. Barber, Plastoquinone as a mobile redox carrier in the photosynthetic membrane, FEBS Letters, Volume 169, Issue 1, 1984, Pages 1-6, ISSN 0014-5793, http://dx.doi.org/10.1016/0014-5793(84)80277-X.

Mikael Turunen, Jerker Olsson, Gustav Dallner, Metabolism and function of coenzyme Q, Biochimica et Biophysica Acta (BBA) - Biomembranes, Volume 1660, Issues 1–2, 28 January 2004, Pages 171-199, ISSN 0005-2736, http://doi.org/10.1016/j.bbamem.2003.11.012

Wanke M., Swiezewska E., Dallner G. (2000). Half-life of ubiquinone and plastoquinone in spinach cells. Plant Sci. 154 183–187. 10.1016/S0168-9452(00)00200-4

Schmelzer C., Niklowitz P., Jürgen G., Okun J. G., Haas D., Menke T., et al. (2011). Ubiquinol-induced gene expression signatures are translated into altered parameters of erythropoiesis and reduced low density lipoprotein cholesterol levels in humans. IUBMB Life 63 42–48. 10.1002/iub.413

Ma W., Deng Y., Mi H. (2008). Redox of plastoquinone pool regulates the expression and activity of NADPH dehydrogenase supercomplex in Synechocystis sp. strain PCC 6803. Curr. Microbiol. 56 189–193. 10.1007/s00284-007-9056-x

Wikipedia contributors. "Symbiogenesis." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 26 Mar. 2017. Web. 14 Apr. 2017.

Laszlo Rinyu, Erik W Martin, Eiji Takahashi, Péter Maróti & Colin A Wraight (2004). Modulation of the free energy of the primary quinone acceptor (QA) in reaction centers from Rhodobacter sphaeroides: contributions from the protein and protein–lipid(cardiolipin) interactions. Biochimica et Biophysica Acta (BBA) - Bioenergetics, 1655, 93 - 101.

Vermaas JV, Taguchi AT, Dikanov SA, Wraight CA, Tajkhorshid E. Redox Potential Tuning Through Differential Quinone Binding in the Photosynthetic Reaction Center of Rhodobacter sphaeroides. Biochemistry. 2015;54(12):2104-2116. doi:10.1021/acs.biochem.5b00033.

Wikipedia contributors. "Photosynthetic reaction centre." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 22 Oct. 2016. Web. 14 Apr. 2017.

Yocum, Charles Photosynthetic Reaction Centers, Univ. of Mich. 5 Sept 2008. Web. 14 Aug 2014


How does Cro protein expressed by lambda phage kill its host?

Have a look at the wikipedia page on lambda-phage (it is nicely illustrated and referenced).

See this map of the lambda-phage genome (Source).

Cro (Controller of Repressor's Operator) does not kill the host. It is a transcription factor that represses cI. cI, in turn, represses Cro and other pro-lytic genes (expressed from the PL promoter), thereby forming a positive feedback loop with Cro (some people also use the term "double-negative" feedback loop which in my opinion is incorrect).
During infection the virus just injects its linear DNA into the host via a porin protein (a sort of membrane channel). But at the peak of the lytic cycle many virus particles are formed inside the host cell (not just DNA but fully packed viruses). The viral proteins R and S cause breakdown of the cell membrane and the cell wall, which facilitates cell lysis.
As mentioned in the previous point, the virus is fully packaged while inside the host. This happens only during the lytic phase. During lysogeny, the viral DNA gets integrated with the host genome and remains dormant until triggered by some kind of stress such as UV (which actually leads to activation of SOS response protein RecA which by degrading cI tilts the balance towards the lytic cycle).


What is the difference between these two depictions of chromosome?

Here is the thing, chromosome refers to a lot of different things ( however, all are coiled up DNA).

Let me explain step by step.
You have DNA, it has a diameter of 2nm, it is coiled with histone proteins and make 10-11nm fiber. This is what we refer to as the chromatin fiber(Beads on a string). At this point we are in interphase where too much coiling is not required because a lot of transcription, replication going on. At the S phase of the interphase, DNA replication takes place and sister chromatids are formed or do they? The answer is yes and no. The thing is even though DNA has replicated and coiled upto certain extent, we dont call the replicated dna as sister chromatids because we only consider them to be sister chromatids when we can clearly see them as separated threads connected at centromere during the M Phase.
So, to put it in simple words, you have the sister chromatids formed (during the S phase) long before you are actually calling them as sister chromatids, you just wait for them to condense further and when you can finally see them as distinguishable threads you call them as sister chromatids.

Now, your real question can be answered. You have posted two chromosomes, one green and the other is red, red has two chromatids connected at centromere. Lets start with the red chromosome. The red one is the metaphase chromosome. Try to remember cell cycle. You have your DNA replicated by the S phase of interphase, then comes G2 and then M Phase starts with prophase, at this point your chromatin fiber gradually starts getting condensed and by the end of prophase, your 10nm coiled DNA (Chromatin fiber) ends up coiled to 700nm fiber but remember, you have two 10nm fibers connected at centromere after the S phase but they were so thin that you could not distinguish the two threads separately, now you can because they coiled in a very organized manner and now you have two 700nm fibers attached at the centromere, this is the maximum condensation achieved and as this final condensed version is observed at the metaphase it is named metaphase chromosome.

So, the red one is definitely a chromosome. What about the green one? That too is a chromosome. the green one is formed at the next step of cell cycle that is anaphase. Here the two sister chromatids split at the centromere and move towards the opposite poles of the cell as  new chromosome. but wait, haven't I called them sister chromatids throughout the answer and suddenly calling them chromosomes? Yes, the previously called sister chromatids are called as  individual chromosomes the moment they are separated from each other at anaphase.

So in summary, the thread like structure that you see in interphase are coiled DNA(Not called chromosomes), chromosomes are also coiled dna but the difference is that these are way more coiled. The red one is metaphase chromosome (1400nm) with two sister chromatids(700+700=1400). The green one is also chromosome but these are actually sister chromatids that got separated at anaphase(only 700nm), you can call them as daughter chromosomes

I hope this helps


Does the brain consume more energy when a person is stressed or anxious

The tiredness associated with depression/stress is not due to the 'brain power' increasing but due to a change in what parts of the brain are active and/or disrupted sleep. Anxiety can cause issues to the brain and body over time.
Brain power is relatively constant
For the average adult in resting state the brain consumes about 20% of the body's energy. It has been shown that the brain requires about as much energy at night when you are asleep as during the day. The increase of energy for 'hard thinking' is about 8% which is very little compared to the baseline usage (leg muscles can have a 300-400% increase when walking compared to sitting).
See this paper for more analysis.
Tiredness and Mental Health
Depression affects neurotransmitters associated with alertness and reward systems thus making you feel less awake, less motivated, and more tired even if you might have sufficient sleep. However depression and anxiety often also lead to disrupted sleep (trouble falling asleep, nightmares/poor quality sleep, waking up too early etc). This would lead to a feeling of constant fatigue. Unfortunately, the feeling of fatigue can also worsen feelings of depression and anxiety though it is often not the root cause of depression.
Effects of Anxiety Over Time
Repeated activation of the stress response (a cascade of stress hormones colloquially known as the 'fight-or-flight' response) takes a toll on the body. Research suggests that chronic stress contributes to high blood pressure, cardiovascular disease, and causes brain changes (including differences in the volume of gray matter versus white matter, as well as the size and connectivity of the amygdala paper) that may contribute to anxiety, depression, and addiction. Preliminary research also suggests that chronic stress may also contribute to obesity, both through direct mechanisms (causing people to eat more) or indirectly (decreasing sleep and exercise). Chronic stress keeps levels of cortisol in the body high.
Source
Another important factor is the effect of stress on the cortisol levels.
Stress leads to an increased release of the steroid hormon cortisol, which can lead to reduced bone formation, favoring long-term development of osteoporosis (progressive bone disease) source.
It transports potassium out of cells in exchange for an equal number of sodium ions. This can trigger the hyperkalemia of metabolic shock from surgery. Cortisol also reduces calcium absorption in the intestine source. Cortisol down-regulates the synthesis of collagen source.
Sustained stress can lead to high levels of circulating cortisol (regarded as one of the more important of the several "stress hormones"). Such levels may result in an allostatic load,which can lead to various physical modifications in the body's regulatory networks source.


What's the difference between Ki and IC50?

In biochemistry the Ki is the dissociation constant of a complex and molecules bound to it. It is a measure for the  functional strength of the inhibitor. This can for example be an enzyme and its substrate, the Ki defines the stability of the complex.

The IC50 on the other hand is the halfmaximal inhibitory concentration of a substance on a biochemical process. This can be an inhibitor of an enzyme.
See this figure (from the Wikipedia article on the IC50):

The Ki plays an important role in the calculation of the IC50, as it defines the strength of the enzyme-inhibitor complex.


You can find the sequence in the gene database, but it is perhaps easier to search the nucleotide database if you are only looking for the sequence of nucleotides.


What does uniprot consider "unambiguous" evidence for the subcellular domain of a protein?

Following your question, we have updated the documentation for topological domains in UniProtKB:
http://www.uniprot.org/help/topo_dom

I hope you will find it more informative now. Please don't hesitate to contact the UniProt helpdesk if you have any additional questions (or, if you prefer to discuss here, a short note to the helpdesk would help us spot your posting more reliably, since we cannot closely monitor all forums as you may understand).


What are these (eggs?) ? ( Location - India )

The group of insects called Neuropterans have several species that lay eggs on stalks. This group includes lacewings, owlflies and antlions, however stalked eggs are not a defining trait of the group. In addition to the Green lacewing, the Blue-eyed lacewing from Australia lays stalked eggs while owlflies do not. Mantidflies also have stalked eggs which are members of the Neuroptera order, but the stalks are relatively short compared to lacewings.

This thread provides some interesting discussion.

P.S. While not an arthropod, at least one Genus of Molluscs (Nucella), lay stalked eggs too.

These are certainly eggs from this order (Neuroptera). Incubation time for these type of eggs can be anywhere from 2-7 days so you may already be having hatching if there are less eggs than what was initially there.


Why does maintaining contraction of muscles require ATP?

Actually, it is not. ATP releases the myosin bonded to the actin, so when it is absent, the muscle remains contracted. This is, actually, precisely what happens during rigor mortis after death.

However, as long as you are alive, on a molecular level this is a dynamic process - actin release and bonding - and maintaining it requires energy. Moreover, muscle relaxation is not achieved by stopping the ATP flow, but incurrs additional ATP cost - it happens by actively removing calcium ions required to enable the actin to bind the myosin.


Action potentials are always based on coherent synaptic inputs. So dendritic processing means rewarding specific coherent subsets of synaptic inputs.

So to me it makes more sense to frame dendritic processing as allowing neurons to detect several different patterns (alternatively or at the same time).

In that case each dendritic spike encodes a different pattern. This allows a neuron to play roles (or maybe the same role) in several different contexts (or possibly in different combinations of contexts). If this is the case the neighbourhood mapping you describe doesn't have to exist (though it still might).


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

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

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

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

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


Inhibitory effect of GABA through GABA(A) receptors

Great question! This apparent contradiction has puzzled many neuroscience students before you.

Short Answer:

This is often called "shunting inhibition," in particular when excitatory and inhibitory conductances are out on dendrites.

Longer Answer:

The part that is wrong is this (emphasis mine):

  the internal voltage will increase, hence coming closer to the action potential. This would increase the probability of reaching an action potential, not decrease it, wouldn't it?

The idea that "hyperpolarization is inhibitory, depolarization is excitatory" is only partly true. It is very important to also consider what the spike threshold is, and to think in terms of reversal potential for a given ion channel (or more generically we can just call it a 'conductance'), and then you can revise the statement to say this:

  Conductances with reversal potential greater than spike threshold are excitatory, conductances with reversal potential less than spike threshold are inhibitory.

Most often, chloride-based channels fit into the second statement: their reversal potential is less than the spike threshold.

How Shunting Inhibition Works:

Any time you open a channel, you will shift the membrane potential towards the reversal potential for that channel. The amount of current that flows through a channel depends on the 'driving force': the difference in voltage from the reversal potential.

Let's consider a fairly typical textbook cell, with a spike threshold at -50mV, a resting potential of -65mV, and a chloride reversal at -60mV.

If the cell is at rest, and you open chloride channels (such as with GABA via GABA-A receptors), the resulting flow of current will tend to push the membrane potential towards -60mV, so the cell 'depolarizes'. However, no matter how big of a chloride conductance you open, you will never pass -60mV, so you will never reach spike threshold.

If, in that same cell, you instead opened AMPA channels, with a reversal of around 0mV, you also get depolarization, but in this case as you open more AMPA channels you can potentially depolarize the cell all the way to 0mV. Of course, unless you have blocked sodium channels you will get an action potential before you reach that point, but that's the key: you will cross threshold, therefore we call it excitatory.

Now let's consider a third case where we open both AMPA channels and GABA-A channels. As long as the membrane potential is <-60mV, both channels contribute to depolarization. However, as soon as the membrane potential is >-60mV, chloride ions will start flowing into the cell. We call this "shunting" inhibition because if you look at the sum current flow in the cell, it will look small, because you have chloride ions coming in at the same time as sodium ions, resulting in little change of the membrane potential despite lots of ions moving.

The result is that GABA-A channels, even if they can depolarize a cell that is at rest, will act to prevent the cell from depolarizing far enough to reach threshold. It's important to consider the dynamics of the membrane potential, rather than thinking of the membrane potential as something that is simply added or subtracted to instantaneously.

Important Caveats:

Ion concentrations matter! If chloride concentrations are not 'typical' or if the spike threshold is more negative than in a 'typical' textbook cell, then chloride conductances can indeed be excitatory! In fact, excitatory GABAergic transmission is important are certain stages of development. If cells have too much chloride in them, this can also cause GABAergic transmission to become excitatory (or at least limit the efficacy of the inhibition), and this can lead to epilepsy (see Cohen et al. 2002).

There can also be a time window where GABAergic transmission is excitatory even in a typical cell: this is the period where the GABA-A channels have closed, but the membrane remains slightly depolarized and has not returned to rest. Excitation that arrives during this time will sum with the residual depolarization, and there are no open GABA-A channels to 'shunt' the current.

Alger, B. E., & Nicoll, R. A. (1979). GABA-mediated biphasic inhibitory responses in hippocampus. Nature, 281(5729), 315.

Cohen, I., Navarro, V., Clemenceau, S., Baulac, M., & Miles, R. (2002). On the origin of interictal activity in human temporal lobe epilepsy in vitro. Science, 298(5597), 1418-1421.

Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A. S., McNamara, J. O., & White, L. E. (2014). Neuroscience, 2008. De Boeck, Sinauer, Sunderland, Mass.


How to explain the colour of these scots pines?

The bark of some pinus species, like pinus sylvestris and pinus pinaster naturally turns orange when they are a bit older. Other species stay grayisch black, like pinus nigra (hence the name).

By the way: I have never seen pinus sylvestris grow so straight. Is it possible this is another species, for example P. pinaster?

Sources: Den nya nordiska floran (Mossberg&Stenberg 2003) and Heukels' flora van Nederland (van der Meijden 2005).


Why and when did the misconception about the Panther being a species came to be?

Tigers, lions, jaguars and leopards are all different species. Panthera is a genus, a broader classification than a species. Tigers are Panthera tigris, lions are Panthera leo, and jaguars are Panthera pardus. In each cases the formal species name is the genus followed by the species identifier. Common usage rarely gives a hoot about the subtleties of biological classification.

Your initial impression was correct: any member of the Panthera genus that has a black coat is called a black panther. In South America they are jaguars, in Africa and Asia they are leopards.


Note that the query sequence you have provided matches the minus strand of your target sequence. That means not only that the target sequence will be reversed (as you have noted), but it will also be complemented as well. So in the GenBank record, you should not look for the sequence CCGACCGA... starting at position 10835, you should look for the sequence ...TCGGTCGG ending at 10835.

ccgaccga...    minus strand
||||||||
bbɔʇbbɔʇ...    forward strand

The sequence in the GenBank record contains spaces, so that complicates finding your sequence using the browser's "Find" function, but if you use the position indices at the beginning and end of each line of sequence, you will be able to find the reverse complement of the matched sequence reported in the BLAST results.


Why are fearful stimuli more powerful at night?

Short answer
The increased fear responses during the night are believed to be mediated by elevated corticotropin-releasing hormone (CRH) levels in the brain that drive the fear responses in the amygdala.

Background
Fear responses can be experimentally assessed by recording the startle reflex. For example, loud noises can evoke gross startle responses in rodents (whole-body startles) and more subtle responses in humans (eye blinks).

In nocturnal animals, it has been shown that startles are facilitated by bright light. In contrast, fear responses in humans, a diurnal species, have been shown to be stronger in the dark (Grillon et al., 2007).

In the rat, the light-enhanced startle is has been associated with the hypothalamic–pituitary–adrenal axis (Fig. 1). Specifically, light exposure has been shown fear mediated by corticotropin-releasing hormone (CRH) (Grillon et al., 2007).

Fig. 1. HPA axis. source: Wikipedia

The HPA-axis is affected by the circadian clock and therefore exhibits a pronounced daily rhythmicity. The HPA axis is activated by hypothalamic release of CRH, which stimulates the secretion of adrenocorticotropic hormone (ACH) from the anterior pituitary. ACH triggers the production of cortisol by the adrenal glands. Cortisol, in turn, provides negative feedback and shuts down HPA-axis activity by binding to corticosteroid receptors in various HPA-axis structures, e.g.the hypothalamus (Fig. 1). As a result, cortisol levels show a robust diurnal rhythm that runs in opposite phase with CRH. Cortisol in humans peaks at the time of awakening and drops to its lowest levels around bedtime, whereas the opposite is true for CRH (Miller & Gronfier, 2001).

The startle reflex shows a diurnal variation roughly opposite to the rhythm of corticosterone and in phase with CRH. Specifically, startle responses in nocturnal animals such as rats are highest during daytime (their passive phase) when CRH is peaking, and corticosterone is at its lowest. Conversely, startles are lowest during the night (their active phase) when CRH levels are lowest, and corticosterone levels are high. In man, a diurnal species, exactly the opposite pattern is observed. Hence, startle responses are thought to be endogenously modulated by the circadian system, most likely via effectors of the central pacemaker such as the HPA-axis (Miller & Gronfier, 2001).

In rats, administration of exogenous CRH enhances the startle reflex and blocking of the glucocorticoid receptors which produces a blockade of negative feedback, also increases startles. Conversely, blocking CRH receptors decreases the startle response, as does corticosterone administration (Miller & Gronfier, 2001).

CRH receptors are expressed at various brain centers, including the amygdala. The amygdala is a key structure in the limbic system, the emotional control center of the brain. The amygdala is specifically associated with anxiety and fear responses. Indeed, it is thought that CRH receptors in the amygdala are responsible for the fear-promoting actions of CRH (Grillon et al., 2015).

Hence, it is not darkness or light per se that mediate fear responses. Instead, it is the circadian control of the HPA axis that controls the daily variations in fear responses.

References
- Grillon et al., Biol Psych (2007); 62(10): 1183–6
- Grillon et al., Neuropsychopharmacol (2015); 40: 1064–71
- Miller & Gronfier, Psychophysiol (2006); 43(3): 297–301


cool pics!

Firstly, Formadahyde is a terribly toxic substance.

  Skin Contact: CORROSIVE. Contact can cause pain, redness, burns, and blistering. Permanent scarring can result. Can be absorbed through the skin.

Formaldehyde causes organ failure and scarring if ingested.

In this case, since you don't have burning or blistering, it seems like a reasonably low exposure. You should nonetheless call your doctor to check in or drop by the campus infirmary or what you have.

A good experience to remind you to wear gloves when working with chemically active reagents or solvents (DMSO for instance!)

I'm not a doctor, but as a non professional and informal opinion, your finger will probably become normal again, eventually all the cells will do their best to repair themselves.


In a normal cell, during each replication the telomere is shortened slightly due to the end replication problem, as you probably know. As mutations occur and a normal cell begins to exhibit cancerous characteristics, it needs a way to stop the self-destruction which happens when the telomeres become too short. In fact it is the cancer cells themselves which 'short-circuit' the shortening process and cause the telomeres to stay long enough.

90% of tumors do this by activating telomerase, an enzyme complex which elongates telomeres and keeps them from getting too short, so that the cell is effectively immortal from this sort of destruction. Usually telomerase is not active in most cells, except for stem, germ, and hair follicle cells, but cancer cells use this to their advantage and activate it to stay immortal. The other 10% or so employ a method called ALT, or Alternative Telomere Lengthening, a not yet thoroughly understood process which involves the recombination of tandem repeats between sister chromatids.

This page explains how cancer cells bypass the telomere shortening process well, and also provides a series of further reading on telomeres and telomere shortening.


Transposons, Viruses and RNA interference

Transposons and viruses don't "make siRNA". However, an endonuclease called Dicer can process dsRNA from these sources to produce siRNA which is then loaded to the RNA-induced silencing complex (RISC) to suppress propagation of viruses and transposons. The following papers provide a good overview:

Buchon N, Vaury C. 2006. RNAi: a defensive RNA-silencing against viruses and transposable elements. Heredity 96:195-202.

van Rij RP, Andino R. 2006. The silent treatment: RNAi as a defense against virus infection in mammals. Trends Biotechnol 24:186-193.


What's the difference between reaction norms and phenotypic plasticity?

Phenotypic plasticity, as you define in your question, is an ability or a property of the organism (a given genotype) to manifest different phenotypes in different environments (Pigliucci et al., 2006).

Reaction norm is an analysis of the pattern of phenotypes exhibited in different environments. In other words it is an analysis of the phenotypic plasticity.


Is there any evidence that any other species are "pre-intelligence"?

I don't exactly know, what the intelligence is, but i've got an idea what it can be.
I've read about smth similar before. I suppose, we can measure intelligence with working memory (don't mix with shott-term-mempory)  term (like registers of processor).
There were many experiments that was provided to check how big a working memory of humans and apes.

According to information people got from these experimence, average WM of humans equal to 7, apes - equal to 4 (count of terms subject can manipulate without any significant mistakes). So, apes can be considered as pre-intelligence this way. But anyway it is still controversial question.

You can also google articles like this:  http://www.pnas.org/content/110/Supplement_2/10371.full.pdf


Simply because it is ways more practical and there is no need to use a helicase. Heating is fast and convenient and denaturation is reversible. Also all the DNA is denaturated, so afterwards, primers can bind to their target sites, setting up the start point of the polymerase.

If you want to do this with and helicase, you need to make sure that you have a heat stable polymerase (at least at 72°C), you need to have the right places on the DNA unpackaged and finally, you need two enzymes in the reaction (which is more expensive than just having one).


Do the claims in this paper have any degree of validity?

I'm afraid I laughed a bit when reading that paper for the first time.

Why? Well, here's what they essentially did: They tried to model evolution by implementing an algorithm. They had a population of 10000 individuals, represented by their genetic sequence, and had an algorithm do mutations of those sequences and modeled selection and reproduction to get the next generation. They did that for a long time. Why did that make me laugh? I did both my BSc and MSc theses in the field of Evolutionary Bioinformatics. Almost every student there implements something like that when they first start, to learn to write that kind of program. It's not exactly novel. They even cite several other studies doing this kind of analysis.

Now, their result is basically that human evolution from human-chimpanzee ancestors couldn't have happened because it would have taken way too long. Not only would the whole difference between these two species have taken too long, every single difference of more than two nucleotides would have taken too long to get fixed.

Since this goes against established science, this algorithm better be good... The paper is lengthy and much of it isn't all that interesting or related, in my opinion. But here's the big problems, in my opinion:

  When natural selection successfully amplified the target string to the point of fixation (i.e., when the allele frequency reached 99–100 %),

Their target is for their target sequence to reach a frequency of at least 99 percent. That's unnecessarily high, and will of course take a long time, especially as they hold their population constant at 10000 individuals. They don't show a figure with how frequency changed over generations - I'd assume that 90 percent is reached a lot earlier than their threshold.

Holding the population size constant is of course also not a realistic model for human evolution. It wasn't at 10000 individuals for millions of years.

  initialization : initialize every individual to the same random or user-specified string (e.g., AAAAA)

Humans didn't start with random sequences and then mutated them to make them do something useful, we started with useful genetic material that then changed. If you start at AAAAA, expect a target of TAGGC, don't confer any benefit to intermediate steps (as they did) at a mutation rate of something like 1 per ten million nucleotides per generation, of course you are going to wait a long time. Mutation rate in genomes also isn't uniform, it varies by region. From what I can see, this was neither taken into account nor discussed.

There is also the problem of them only looking at single nucleotide mutation, not gene duplication, insertions, etc. that also make up a lot of the difference between humans and their ancestors.

Then there's random "mate-choosing", which is a valid simplification to make if you are just looking at some mechanisms of evolution, but not valid if you are going to use your model to estimate time needed for speciation.

They also only allow for one beneficial mutation to arise, then wait for it to be fixed, claiming that anything else would have just resulted in even longer times, without, as far as I can see, just implementing this and then testing that assumption.

At some points, their paper is just going to going for some kind of dramatic effect:

  waiting time was 500 million years – which is still extremely prohibitive. This amount of time approximates the estimated time required for the evolution of worm-like creatures into people

500 million years ago, we had the first animals emerging on land and the first chordates. Chordata and the "worm-like" phyla had already diverged.

Basically, in my opinion, they took a very simple model and drew sweeping conclusions from it. This kind of analysis is suited for looking at how evolution might result in speciation, what parameters might play a part, etc. but it is not suitable for estimating the time this takes.

But these are just my first thoughts, I hope there'll a more thorough review of this on the internet somewhere soon.


Do male animals visually perceive females as more/less attractive?

There are numerous examples of visual attraction in animals. An absolute classic of an experiment, taught to most/all evolutionary biology students, is the widowbird tail length experiment by Andersson. He experimentally manipulated the tail lengths of male widowbirds at random. Some tails were made longer and some shorter. From this experiment Andersson showed that females choose males with longer tails more preferentially. Another classic example is the lek mating system where there is a bias in reproductive success towards attractive males, in some cases 10-20% of the males get 70-80% of the matings.

  A lek is an aggregation of males that gather to engage in competitive
  displays that may entice visiting females who are surveying
  prospective partners for copulation. Leks are commonly formed
  before or during the breeding season. A lekking species is defined by
  the following characteristics: male displays, strong female mate
  choice, and the conferring of male indirect benefits. Although
  lekking is most prevalent among avian species, lekking behavior is
  found in a variety of animals such as insects, amphibians, and
  mammals

Beauty could be a an example of a an indicator trait:

  Indicator traits are those that signal good overall quality of the
  individual. Traits that are perceived as attractive must reliably
  indicate broad genetic quality in order for selection to favor them
  and for preference to evolve.

I'm sure there are some studies in fish, likely guppies or zebra fish, which gave individual fish the opportunity to visually assess potential mates (placing tanks next to each other and observing courtship) which would be very similar to your hypothetical duck example. Despite often being a paradox, female mate choice is well documented. Further, male mate choice is now coming to light, even in species where female mate choice and male-male competition exists.

I don't think selection on "beauty" would require some kind of particularly special neural system, obviously some visual capacity is necessary for visual attraction and some basic neural pathways linked to that. I have done experiments myself in Drosophila simulans which looked at good gene benefits of mating with attractive males (indirect genetic benefits of female mate choice) and another which assessed precopulatory selection (female mate choice) for a secondary sexual character in the same species. Even in such a small-brained species there appears to be some degree of (partially visual) mate choice going on.


Vision: what is the difference between on-off ganglion cells and lateral inhibition?

Short answer
Retinal center-surround receptive fields are an example of lateral inhibition. It occurs elsewhere in the nervous system too.

Background
Center-surround receptive fields are indeed an example of lateral inhibition, where the ON field suppress the OFF field through lateral inhibition. The center-surround connectivity in the retina (Fig. 1) is indeed the most well-known example of this kind of circuitry. However, lateral inhibition occurs in other sensory systems too, for example auditory and olfactory neurons (Bakshi & Ghosh, 2017). For more information on the retinal circuitry underlying center/surround inhibition see this answer.

References
- Bakshi & Ghosh (2017), Handbook of Neural Computation: 487-513.

Fig. 1. Retinal circuitry underlying On-OFF center-surround conncetivity in ganglion cells. source: New York University


What does "genetic correlations" mean as opposed to just correlations?

It is simply a correlation where one of the two variables considered is the genetic state at a given locus. In a GWAS, one loops through all loci and systematically performs a correlation analysis between the genetic states at this locus and the phenotypic trait of interest.

In the example of sentence you cite

  Genetic correlations of same-sex sexual behavior with various preselected traits

They looped through each polymorphic locus in their data set and at each locus they performed a correlation analysis between the two variables "genetic states at a this locus" and "same-sex sexual behavior" (whichever way this second variable is recorded).

A study might also be interested in more than one phenotypes. In such case, different phenotypic variables can either be considered separately or can be included in the same analysis through linear models. It is for example not so unusual to include one of the variable as a covariatiate in an ANCOVA type of design.


There's a fairly large misconception here. The huge amount of energy that's available from respiration, and which drives the synthesis of ATP, in fact comes from that reaction that you consider secondary, and that's the transfer of electrons to oxygen.

If you want to think of it as two separate reactions, then the first one
$$Glucose + 12\ {NAD}^+ + 6 H2O ⇌ 6 CO_2 + 12 NADH$$ releases about 10 times less energy than the second one: $$6 O_2 + 12 NADH ⇌ 12 NAD^+ + 12 H_2O$$

The reason you get something resembling 30 ATP from a glucose molecule is because oxygen is such a great electron acceptor.

Many microbes can in fact use molecules other than oxygen as the electron acceptor, but in general it is much less energetically efficient than using oxygen.

You could try equilibrator for estimating the free energy available from various chemical reactions. First reaction and second reaction from above as examples.


Its a Giant Gourami, Osphronemus goramy.
The giant gourami (Osphronemus goramy) is a freshwater species  believed to be native to Southeast Asia, and has been introduced to other parts  of the world.
This species is commercially important as a food fish and an aquarium fish.

(Source: tropical-fish-keeping)
Reference: fishbase