Applying saliva to mosquito bites Is it true that; when you apply your own saliva to a mosquito bite it would stop itching ?

There have been many personal experiences documented where people have experienced relief from itching of mosquito bites on the application of their own saliva to the itchy spot (reference 1, reference 2) It helps to reduce the itching because saliva has been proven to speed up tissue repair and has antibacterial properties. It also provides a moisturising effect on the itchy spot (reference). Salt is also known to provide relief to itching (reference) and the slight salt content of saliva helps in that respect too.


A study has found that cell phones cause infertility, is this something to worry about or is the study flawed? Is this a worrying study, or is it flawed?
A study has found that cell phones are detrimental to male sperm quality (Lower sperm motility and sperm concentration). It’s original goal was to determine if image content has a effect on sperm quality, but accidentally discovered that men who said they kept their phone in their pocket had worse sperm quality than those who didn’t have a phone in their pocket. As far as I can tell, from my limited knowledge, the study isn’t very flawed. What I do know is that they used 52 men, which doesn’t seem like a lot.
Another possible flaw is in regard to how they took sperm samples. Sperm parameters can vary amongst healthy individuals, the WHO recommends taking at least 2 samples to determine fertility. This study took one sample from all 52 men, then asked them if they wanted to participate the second time around and only 25 men agreed. So, they did take more than one sample but only for 25 men. I’m not sure, but this doesn’t seem like very good methodology as only 25 of the samples are representative.
Another issue is that the study had a variable that it changed from person to person. As stated, it’s original goal was to find out if image content affected sperm quality, and they concluded that it can. They gave different images to each mam, meaning that some of the images would have had a detrimental affect to the sperm quality. So, they could have gave a healthy cell phone user a type of image that causes poor sperm quality. However, it would be coincidental that cell phone use was still correlated with poor sperm, even if the study randomly gave out out different images to different people that could cause poor sperm in the analysis the ones with poor sperm.
I was wondering if certain lifestyle factors that tend to be associated with phone use where causing the infertility, not the phones themselves, but the study had a very extensive questionnaire and adjusted for many different factors from bathing habits to diet, so I don’t think that the study can be flawed in this are. What do you guys think? Is this something that we should be worried about and change our habits over, or is it scientifically limited and no cause for alarm until bigger and better studies conform their findings?

The study is basically worthless.
First, the study was not constructed to test this hypothesis, so it's just something interesting that may point to future studies. It does not provide sufficient evidence.
But the biggest problem is that the study was of 52 individuals with only one or two samples, which makes it statistically useless.
Any uncontrolled variable could account for all the difference detected. If one person had low sperm count because they wore tight underwear it would completely account for the difference.
This would barely qualify as an exploratory study, much less anything conclusive. This study would need to be reconstructed with a minimum of thousands of people, or control the participants' behavior (preferably both), to produce useful conclusions.
Any study with a really small N that deals with human behavior is basically worthless as far as any certainty goes.
The questionnaire is not any better — cellphone position is just binary: 1 belt and/or pocket, 2 anything else. Since most of the people are going to fall in the first category, there are very few degrees of freedom to work with. They just ran all the numbers hoping to get something. This is barn door statistics at its worst.


How pain can stimulate the vagus nerve I'm trying to find out why a prompt, severe, short pain is causing a stimulation of the vagus nerve. What could the physiological explanation be?

Is that because the pain is triggering the sympathetic system (Huge stress because of the pain), and directly after that the parasympathetic system is trying to balance it, but it's overreacting? and then the sympathetic system is going back to normal when parasympathetic stays high ?

Is there a physiologic explanation ?

Thanks

Short answer
Given your comments you are referring to the cause of fainting after being triggered by certain stressors. The reason is a sudden drop in blood pressure due to parasympathetic nervous system activation (vagus nerve activity). This leads to reduced blood flow to your brain, which results in a brief loss of consciousness (Mayo Clinic).

Background
There are various types of fainting (syncope) with various causes. The type you are referring to is neurally mediated syncope (Arthur & kaye, 2000). It is evoked by emotional activation due to stressors (pain, fear etc.) Stress responses are accompanied by the release of stress hormonses, most notably Adrenaline (epinephrine). Epinephrine release results in sympathetic nervous system arousal, resulting in increased blood pressure, increased pulse and sweating. It also increases amounts of blood being funneled to peripheral organs. These mechanisms aids in the fight,fright and flight response, as more blood in the periphery allows more glucose to be transported to the muscles (Agarwal, 2007). The funneling of blood in the periphery (venous pooling), however, can reach a point in which venous return of blood to the heart falls too sharply. This in turn can lead to a substantial increase in the muscle activity in the ventricles, as they are likely struggling to pump the small available amounts of venous blood into the heart chambers. The increased muscular activity in the ventricles is believed to activate mechanoreceptors that would normally fire only during stretch.

Stretch of heart muscle is normally associated with a high blood pressure. The warning message of a high blood pressure by the mechanoreceptors is sent to the medulla in the brainstem, which in turn leads to parasympathetic nervous arousal. As a part of the parasympathetic response, the vagus nerve is stimulated which reduces heart activity to reduce blood pressure.

However, when the mechanoreceptors are stimulated due to the overt contractility of the ventricles due to a low blood volume, they sent the same neural input to the medulla which normally signals hypertension, thus causing vagus nerve stimulation and hence a paradoxic parasympathetic arousal that results in low blood pressure (hypotension), low heart rate (bradycardia), and ultimately fainting (syncope) (Grubb, 2005).

References
Agarwal et al., Postgrad Med J 2007;83:478–80
Arthus & Kaye, Postgrad Med J 2000;76:750-75
Grubb, Circulation 2005;111:2997-3006


Why are there two abrupt changes in the genome sequencing price curve? In the price curve of the genome, from NIH:

NIH explained the abrupt drop at 2008 thusly:

  beginning in January 2008... the sequencing centers transitioned from Sanger-based (dideoxy chain termination sequencing) to 'second generation' (or 'next-generation') DNA sequencing technologies.

The NIH did not give any details as to why there was a similarly precipitous drop in 2015, or why there was such a saddening (for me!) plateau after that. Please explain them to me?

This graph from the Broad's Opinionome blog (ugh) is somewhat more annotated:

As noted elsewhere, the precipitous drop in 2007 is almost certainly due to maturing next-gen sequencing (NGS), in particular Illumina.  Illumina acquired Solexa in 2007, which offered gigabase-level sequencing ability.  In 2014, President of Illumina Francis de Souza essentially said as much:

  During the EmTech conference, De Souza said Illumina’s success was due to a “hard pivot” the company made in 2006, when it got into the DNA sequencing business by acquiring Solexa, a U.K. startup, and bet its fortunes “on a technology with no sales, that no one knew if it would work.”

Essentially, by 2007/2008 you had stellar technology+company hard-selling it = adoption

I'm less certain about the less-dramatic drop in 2014/2015, but I agree with Franck that it's likely largely be due to the introduction of the Illumina HiSeq X Ten in early 2014.  You can read some corporate spam, but it was indeed a big deal.  There were other technologies that probably played a role (new PacBio system released in 2013, etc.) but Illumina was and is top-dog.

None of this takes into consideration increased interest in such research, or the faster computers, larger SSDs, and expansion/normalization of multi-core systems that makes working with such data easier.


Near point and far point of myopic eye Suppose a person wears the specs of power -6D, the far point for that person is 16cm.
But the near point of normal eye is 25cm.

So, is the near point of a  person with myopia (having far point less than the near point of normal person) also changed ?

Let us say this myopic patient has amplitude of accommodation of 8D.  The patient accommodates 8D beyond far point, thus his near point is 1/6+8=0.07m (7.1cm).

If we compare the case with emmetropic eye with accommodation amplitude of 8D, the near point is 1/8=0.12m (12cm).

So, yes, near point of myopic person is different from an emmetropic one. But, you are wrong thinking that near point of "normal" eye is 25cm. The near point is age-and-lens dependent, thus near point is individual one and should be calculated considering amplitude of accommodation.

Look at this picture of age-related accommodation changes -

Look at the scheme of far/near points (near point here is just an example)


Are there any theories using thermodynamics/statistical mechanics or information theory principles to modelling in ecology? So far, I've only known one: the MaxEnt theory. It uses the maximum information entropy developed by information theorist, which in turn inspired by the thermodynamics from physics, to predict the number of organism in an area. This theory is developed by John Harte.
You can read about this theory in Quanta Magazine.

I also know the book Towards the Thermodynamics Theory for Ecological Systems, written by Jørgensen and Svirezhev.

I find it hard to find another theory similar with the two theories above. Do you know any theories using the thermodynamics or information principles to modelling in ecology?

I have opened a reddit discussion about this.

John Harte's work on applying the mathematical theory of maximum entropy to ecology is certainly one of the better known examples of the application of this area of mathematics to science, in part because he literally wrote the textbook: Maximum Entropy and Ecology: A Theory of Abundance, Distribution, and Energetics (Oxford Series in Ecology and Evolution)

To be clear, maximum entropy (also known as MaxEnt in some of the literature, though most/all researchers use the longer form in publications) is a mathematical tool stemming from the fields of probability theory, statistics, and information theory.  Its use is classically most often seen in thermodynamics, statistical thermodynamics, physics, and information theory, primarily because these were the areas in which E.T. Jaynes was working when he posited the idea. Wikipedia has links to his two seminal papers.But because of it's mathematical form, it can be applied in a multitude of areas, typically where one can utilize probabilistic methods.

If you're looking for additional areas of application, simply google the phrase "applied maximum entropy" and you'll find a wealth of areas including: econometrics, natural language processing, nuclear medicine, queuing systems, mass spectrometry, image processing, machine learning, and many others.

For ecology related work, a cross search on maximum entropy and "genetics", "evolution", "species", and similar words will provide a wealth of papers like "A maximum entropy approach to species distribution modeling".

Given the generic nature of your question, I might suggest that you'll find E.T. Jaynes' paper "On the Rationale of Maximum-Entropy Methods" (IEEE, 1982) useful.

Those generally interested in the broader applications of information theoretic methods to biology will likely appreciate some of the work that came out of last year's NIMBioS Workshop on Information and Entropy in Biological Systems (which Harte both attended and presented at), the BIRS Workshop Biological and Bio-Inspired Information Theory, and the 2014 CECAM Entropy in Biomolecular Systems. The NIMBios Workshop was organized by John Baez, a physicist, who has worked with MaxEnt methods and explored them on his blog "Azimuth".

Those with a more sophisticated mathematical background (including measure theory, functional analysis, etc.) may appreciate Henryk Gzyl's text The Method of Maximum Entropy (World Scientific: Series on Advances in Mathematics for Applied Sciences, Vol 29, 1995).

-- Additional thoughts after the question was edited --

First for those who don't have the background, I highly recommend reading the two seminal papers on information theory and statistical mechanics by ET Jaynes and the standard text on information theory Elements of Information Theory by Thomas M. Cover and Joy A. Thomas.

In addition to the information theoretic related areas, you might want to take a look at the discipline of complexity theory, which has primarily grown out of the Santa Fe Institute over the past several decades and which includes information theory as part of its disciplines. If you're unfamiliar with the broader topic, Melanie Mitchell has an excellent overview with her book Complexity: A Guided Tour. Also related to complexity is the area of cellular automata which one could view as a very base model of more complex ecological systems. Here, perhaps Stephen Wolfram's A New Kind of Science or Cellular Automata and Complexity will be enlightening. The broader theories coming out of these primarily mathematical areas may be useful to you.

In particular, given the types of models in ecosystems, I might suggest taking a look at some of the mathematical modeling going on at the intersection of complexity and economics. For a relatively simple introduction to this area, one could look at the relatively introductory text Complexity and the Economy by W. Brian Arthur which is very interesting. The economy is essentially a very specific type of ecology dealing with human beings, assets, and the monetary system.

Another area which I've seen a lot of literature over the last few years is applicable to the ideas of resiliency and complexity in cities, for assisting in designing more robust city planning. This really isn't that far from the naturally evolving systems being looked at in ecology settings.

For those looking for researchers in the area of complexity, I have a list of many who are on twitter in a variety of sub-areas. In addition to individuals, it also includes a number of institutes and related organizations as well.

I'd also suggest, that for the broadest theoretical setting, one could actually start with the topic known as "Big History" which takes the broadest approach of looking at history and the evolution of the cosmos over 13.7 billion years since the big bang. This conceptualization includes ideas like evolution, complexity, and emergence on the biggest scales, a set of theories that could be similarly applied to ecologies both large and small. For this viewpoint, I would suggest two works by David Christian including Maps of Time: An Introduction to Big History and Big History: The Big Bang, Life on Earth, and the Rise of Humanity.

In essence, with many of these topics and viewpoints, one is treating individual animals or even entire species as elementary particles and then using the mathematical models of statistical thermodynamics to tease out specific types of data or trends. As layers of overlapping "particles" interact with each other, they cause emergent types properties, and then these resultant emergent properties combine to create further layers of emergent properties, none of which might have been necessarily deduced from the initial conditions. Within Big History, these types of emergence go from the big bang and basic particles in the early universe to the ultimate evolution of humankind by way of a variety of stages.


Why eyes don't get heated while converging sunlight into retina? It is a common observation that a magnifying glass when used to converge rays of sun to a fine point in paper, the paper burns due to intense heat.

Why doesn't this happen in our eyes? Our eyes are also doing the same, they are converging the sunlight into our retina but our eyes don't get burned, or to say get heated.

Is viterous or aqueous humor absorbing heat? If so, then the tiny amount of fluid present in the eye shouldn't be enough to cool the eye for a longer period of time, but we can spend the entire day at sunlight without any eye stress or pain.

Size of eye lens small compared to magnifying glass? However a magnifying glass of the size of eye lens should also be able to produce significant heating by converging sunlight.

As far as I know, the heating effect is due to Infrared rays not because of UV rays so we can safely ignore them in this case, right?

If you look straight at the sun, you do burn your retina, in the same sense as you get burnt by contact to a hot surface: living tissue is full of water, so the burning process does not look the same as for dry paper e.g., and the harm will be done long before combustion.

To go a  little further, the first layer of retina in vertebrates is made of so-called Muller cells, which conduct the light as optical fibres do to the photoreceptor cells, but it has also been argued that they can in some measure filter too strong light in order to protect photoreceptors. See http://www.pnas.org/content/104/20/8287.full

These cells are also strongly vascularised, which allows to regulate its temperature. You can read http://creation.com/mueller-cells-backwardly-wired-retina-v-dawkins


Why does it take so long for the human brain to develop from an evolutionary point of view? I have read that it takes about 25 years for the brain to be fully developed.
  Coincidentally, humans from the Neolithic and Bronze Age had a very short life expectancy, in fact most of their life their brain wasn't fully developed.

My question is:
from an evolutionary point of view, is there a reason why humans spend so much of their life not being fully developed even long after being sexually fully developed?

We can say that brain and our nerve system is the first system in embryo that starts to develop and as you said this system is continuing to develop until after birth.
So here is a question that why our brain don't develop completely before the birth ?  Evolution has gone so far as to limit the development of the brain in the human embryonic phase and to allow it to continue into the postnatal phase. This helps the infant to be born and ease the birth both for mother and the new born because if the brain had fully grown, the size of the head would have made problem in birth. Now, after birth, the brain continues to grow and develop majorly between ages 2-3 and becomes more mature after that . The ability of the brain to grow over the years gives us the ability to adapt to different environments , learnings and new issues and other capabilities That happens with the subsequent creation and pruning of dendritic spines.


Cancer a method for early Earth Evolution? Something I have been wondering for a while is looking at cancer from an evolutionary standpoint.

It's easy to conclude (from observations today) that cancer is something we would rather avoid. However I kept asking myself what would be the purpose of cancer existing in the first place? In my experience of studying biology if a organism or mechanism in nature exists it is because there was a pressure to create it.

It has led me to think that perhaps early on, when cells were just beginning to clump together forming very very primitive organisms, that cancer was a way for a cell to proliferate very quickly and make their particular genomic sequence more common within what would have been organisms made of a lump of cells. Perhaps the different organs we have today exist not just because there was environmental pressure to have a specific organ with a specific function. Perhaps the cells descended from a "cancer" that proliferated faster over other cells in a primitive ancestor of that organism.

The answer that "cancer exists because our bodies make mistakes" doesn't satisfy me when everything else around us evolved and formed due to a multitude of different pressures.

In an effort to make this question less broad my question is basically this:

Is it plausible that cancer is a phenomenon that began to occur relatively early in Earth's evolutionary history as a form of survival for cells in primitive organisms or am I applying evolutionary theory incorrectly?

(I know there is a better word for "pressure" to describe the variables that guide evolution but right now my brain can't come up with anything better).

There is a lot of terminology, semantic and biology to be discussed if one was to fully answer your question and it would take a whole book. Below I am just trying to push you to reading more on the subject.

Evolution of cancer prevalence

The probability of getting a cancer is under selective pressure for sure. Citing cancer.net, here is some information on the genetics of cancer:

Many of the genes that contribute to the development of cancer fall into broad categories:

Tumor suppressor genes are protective genes. Normally, they limit cell growth by monitoring how quickly cells divide into new cells, repairing mismatched DNA, and controlling when a cell dies. When a tumor suppressor gene is mutated, cells grow uncontrollably and may eventually form a mass called a tumor. BRCA1, BRCA2, and p53 are examples of tumor suppressor genes. Germline mutations in BRCA1 or BRCA2 genes increase a woman’s risk of developing hereditary breast or ovarian cancers. The most commonly mutated gene in people who have cancer is p53. In fact, more than 50% of all cancers involve a missing or damaged p53 gene. Most p53 gene mutations are acquired mutations. Germline p53 mutations are rare.
Oncogenes turn a healthy cell into a cancerous cell. Mutations in these genes are not inherited. Two common oncogenes are:

HER2, which is a specialized protein that controls cancer growth and spread, and it is found on some cancer cells, such as breast and ovarian cancer cells
The ras family of genes, which make proteins involved in cell communication pathways, cell growth, and cell death.

DNA repair genes fix mistakes made when DNA is copied. But if a person has an error in a DNA repair gene, these mistakes are not corrected. And then they become mutations, which may eventually lead to cancer. This is especially true if the mutation occurs in a tumor suppressor gene or oncogene. Mutations in DNA repair genes can be inherited, such as with Lynch syndrome, or acquired.

Somatic Evolution in cancer

A cancer is a group of cells that proliferate. In other words a cancer is a group of cells having a higher fitness than other cells.

See Wikipedia > Somatic Evolution in cancer

Can a cancer be beneficial?

I am here attempting to answer your specific question.

We define a cancer based on the fact that it is detrimental to the organism carrying it. If a group of cells divide a lot more than the others and this is beneficial to the organism, then it is not a cancer but an adaptive developmental process.

Let's generalize the definition of cancer

To generalize the definition of cancer, one can say that a cancer is a group of individuals that proliferate to the detriment of the group. In other words, we need a social group of individuals (such as a multicellular organism) to get a cancer. Depending on your definition of a social group, one could consider a criminal organization as a cancer to human society.

If you push the definition a little further by either leaving out the need of a close phylogenetic relatedness between individuals of the group, one could say that "humans are a cancer of the earth". If you google this sentence you will get many hits!


Which steps occur in each phase of Meiosis and Mitosis MITOSIS

In mitosis am I correct in saying that the spindles attach to the centromeres at the end of prophase/prometaphase? (I read this in an answer to another question)

MEIOSIS

Does the nuclear envelope disintegrate during prophase (as occurs in mitosis), or during metaphase? (this is what it says on my textbook)
When do the spindles attach to the chromosomes during the first phase? (during prophase I, or anaphase I? On my textbook it says anaphase I)
And when do they attach to the sister chromatids in phase II? (on my textbook it says metaphase II).

Mitosis:
1. Yes, the spindle fibers attach to centromeres at the prometaphase

http://www.biology.arizona.edu/cell_bio/tutorials/cell_cycle/cells3.html

Meiosis:
1. The nuclear membrane breaks down in Metaphase 1 and reforms during Telophase. It breaks down again in Prophase 2, reforming after that in Telophase 2 in the daughter cells.

The spindles attach to the centromere is Metaphase 1
Yes the spindles attach to the sister chromatids in Metaphase 2

Check out this animation, it might be pretty useful


Why does the Vas Deferens detour over the pubic bone? I was surprised to learn that the vas deferens detours over the pubic bone instead of taking the obviously more direct path.

https://human.biodigital.com/widget?be=u1P&uaid=1ly5V

Because I would assume that the vas deferens is more prone to damage facing the front. Also its damage would put procreation at stake.

Hence my question: Is there a biological reason for this path? Some advantage which outweighs or balances its disadvantages?

The vas deferens following this seemingly odd path is just a result of the natural course of our evolution.  Millions of generations ago, our ancestors were quadrapedal (walked on all four limbs).  Similar to if you were to crawl on your hands and knees today.  In this position the pelvis is rotated forward by ~90 degrees from its position in humans currently.  The natural position of the testicles in this position would be to hang straight down due to gravity.  Which means the vas deferens would have a straight path up in front of the pubic bone.
Generation after generation, our taller and more upright ancestors were able to survive slightly better than their less upright siblings.  Meaning that many of the more quadrapedal siblings died while their more upright siblings survived and reproduced.  This process has continued for millions of generations, leading to our current homonid upright posture.
The path of the vas deferens was established long before our ancestors ever began this slow transition toward standing vertically.  So the vas deferens still follows the same path that it always has, but now our testicles have moved down because we stand vertically.  Which leaves the vas deferens with its seemingly odd route of going forward over the pubic bone and then down to the testicles.
Evolution is a continuous incremental process over the course of millions of generations.  There has been no point at which the vas deferens could be 'unplugged' and rerouted around the pubic bone.  So it now just loops in front of the pubic bone and then to its destination.
Richard Dawkins used the word "mistake" in his description because there is not necessarily an advantage to that particular route of the vas deferens(there may even be small disadvantages), but there was a LARGE advantage to our ancestors standing upright.  So as we evolved to stand more upright, the testicles moved down appropriately and the vas deferens just ended up where it is, simply because that's where it always has been.  Not really a mistake, just the way it worked out.
Hope this is helpful.


Neurons with thousands of connections: where are the extra connections coming from? If every neuron has only one Axon but can can have thousands of (or let's say, even just ten) incoming Axon connections via its dendrites, where are the extra connections coming from?

It seems to me that since neurons dont act as initiators (that is, decide to initiate signals) but rather act more as repeaters (that is, sending incoming signals forward to the neuron that their axon is connect to), then for every neuron, there must be at least one neuron whose axon is connected to it, and at least one neuron that its axon connects to (because without those two things, the neuron does basically nothing, right?), but since each neuron can only have one axon, I'm confused about where all of these extra axons are coming from.

Based on that understanding: 1 billion neurons means exactly 1 billion axons and one billion required inputs (axon -> dendrite connections), eliminating the possibility of any one neuron having more than one dendrite connection, since there can only be one billion axons to connect to those dendrites (and each neuron would require at least one input to function, right?).

But regardless, I've been hearing people talk about neurons having thousands of connections. And based on my understood model, the brain would have to be just one long linear chain of neurons, which makes no sense at all.

So clearly I've got something wrong in my understanding of neural structure. What is it?

As you say, a neuron can have thousands of inputs via its thousands of dendrites.  Each of those dendrites can have a synaptic connection to the (axonic) output of a different neuron.  So the neuron can take inputs from thousands of different neurons, not just from one other neuron.

At the other end of the neuron, the output of the axon can form synaptic connections with many distinct neurons; that's what the branching at the end of the axon is for.

Also, it's misleading to say neurons don't "decide to initiate signals".  Neurons in the brain do "decide" when to initiate an output.  The decision is a complicated function of the arrival of pulses at dendrites from different neurons.  Only some combinations of incoming pulses will cause the neuron to fire a pulse on its output axon while other combinations will not.  The specific combinations can change over time; this forms the basis of learning.

So a brain neuron is in the middle of a very complicated network of synaptic connections from many neurons to many other neurons.


Rabies virus mortality Why rabies virus has nearly 100% fatality rate in human (see this virology blog; thanks to @iayork for the link) if not vaccinated early, even some people have survived Ebola, then why does rabies doe not get extinct as its most virulent form will kill host and virus also?

It's a common misconception that pathogens "don't want to kill their hosts". In reality, pathogens don't "care" at all about killing their hosts. All pathogens "want" to do is transmit from one host to the next. (Taking out the teleogenic language: There's no natural selection on a pathogen to reduce virulence as such. The selection on a pathogen is for transmission.)

In some cases, transmission is optimized when the virus is less virulent. In other cases, transmission works just fine when the virus is highly virulent. Rabies is one of the latter cases.

If a pathogen is spread by, say, respiratory contact, then having a host that is ambulatory and seemingly healthy may allow the first host to contact many others, so reducing virulence may enhance transmission in that specific case.

If the pathogen is spread by sand fleas (as in myxoma in Australian rabbits), then rapidly killing the host is counterproductive, because fleas leave a dead body. But keeping the host healthy is also counterproductive because a healthy rabbit scratches away its fleas. Optimal transmission turned out to work with a virus that kills 50-75% of its victims, because that makes the host very sick for a long time, allowing the fleas to bite it unimpeded.

Rabies spreads by damaging the brain, making the host aggressive, and spreading through bites in saliva (among other ways, but that's an important one). Serious brain damage to the point of wildly abnormal behavior is really not compatible with a host living a long time, so optimal rabies transmission means very high host mortality.

Finally, humans are not natural hosts for rabies and rarely transmit the virus, so in any case there's minimal natural selection for any virulence changes in humans. But it likely wouldn't matter, for the reasons above.


Could there be a pathogen which does not activate an immune response? In order for the immune system to be stimulated to produce antibodies, there must be a surface protein of the invading pathogen which binds to a receptor on B cell surface somewhat loosely. We need this first step for the initiation of the somatic hypermutation phase to produce specific antibodies.
But what if there is a pathogen which does not have such a surface protein? i.e. its surface proteins, if it has any, do not bind with sufficiently high affinity to surface proteins on existing B cells to trigger further aspects of the immune response.
One may argue that this is unlikely to be the case because:
a) naturally occurring pathogens evolve from existing ones, so the changes in the antigens will generally be minor. A new strain will have surface proteins that are similar enough to those of an existing strain for some loose affinity to present antibodies in the host.
b) I think, though am not at all sure, that pathogens need to invade cells to be dangerous.I'm not entirely sure what the nature of a pathogen which cannot invade cells would be. Perhaps not a pathogen at all? In any case, if the starting assertion is true, the dangerous pathogens have a surface receptor which binds with surface proteins on cells to enter them. What if many antibodies are based on the same proteins? (Though I have trouble believing this because the natural agonists of these cellular receptors are some biologically relevant and useful proteins, which we would not want an immune response to. For instance, a generally accepted mechanism of entry of SARS-CoV-2 into cells is by binding the ACE2 receptor, which has angiotensin II- a vasoconstrictor peptide- as an agonist.
So my questions are:
a) Could we synthesise a pathogen which has no surface proteins but which nevertheless does harm in some way? How could it do this harm?
b) Can we make a pathogen which has surface proteins such that it can enter cells or do damage that pathogens normally do, but goes undetected by the immune system?
In the above I have assumed that surface proteins (or perhaps also other surface molecular- maybe carbohydrates will do- are necessary for activating the immune response. If this is not the case, please let me know.

"I think, though am not at all sure, that pathogens need to invade cells to be dangerous."
True in the case of viruses and some bacteria.
Hiding within the cells of the host is the intracellular pathogenesis.
But other "tricks" are possible. Four examples:

biofilms
surface proteins that "catch" antibodies
fast mutation of surface epitopes, like the (in)famous HIV
using host molecules (the HIV again)

Source: Extracellular Immune Avoidance (LibreTexts)
Also interesting: How bacterial pathogens colonize their hosts and invade deeper tissues (Microbes and Infection
Volume 17, Issue 3, March 2015, Pages 173-183).


Is there a difference between pig and cow anatomy that makes religious slaughter of the latter less painful? This question is not for the squeamish. I was told that non-Kosher animals like pigs have a different anatomy in their neck compared to kosher animals like cows such that the Shechita method of religious slaughter (a very sharp knife held on the neck only by the weight of gravity rapidly going back and forth in a single cut that drains blood and results in an "instant" drop in blood pressure in the brain), while causing pain in the non-Kosher animals, doesn't cause pain in the Kosher animals. Is there such an anatomical difference and thus difference in pain?

(If this would be more on-topic at Skeptics.SE, let me know.)

Difference between kosher and non-kosher animals

Rabbi Zamir Cohen, in his book The Coming Revolution - Science Discovers the Truths of the Bible, quotes modern day scientists that have made an incredible discovery of a major difference in the way the blood flows in the species that are kosher and those that are not. In non-kosher mammals, the vertebral arteries flow directly to the brain through the rete mirabile. However, in cloven-hoofed, cud-chewing mammals and permitted foul, the vertebral arteries drain into the carotid artery and do not have any direct flow to the brain. There will therefore be an immediate drop in blood pressure at the time of shechita that causes the animal to lose consciousness, thus feeling no pain.


Garden Hose Analogy for Blood Vessel Resistance I've been trying to reconcile the resistance component of Poisseuille's law with a mental analogy of a garden hose; specifically, I had assumed that the effects of reducing the radius of a blood vessel (of an arteriole in vasoconstriction for instance) would be the same as when you put your thumb over the opening of a hose, causing water to leave at an increased velocity. However, the law instead predicts that a decrease in radius like this would increase resistance, actually decreasing flow by a proportional amount equal to r^4. Why doesn't arteriolar flow actually end up increasing because of the pressure from the arteries, much like its "hose equivalent"? Does the hose analogy even work in this scenario? What am I missing that separates the two scenarios?

It comes down to the distinction between velocity and flow rate.
While you are right that the water would leave a an increased velocity if you put your thumb over the end of the hose, this is deceptive, because the water is exiting the closed system, so it can go absolutely anywhere.  So the fact that the velocity is increased could give one the impression that the flow rate is increased, but in fact it is the inverse.
Imagine that instead of putting your thumb on the end of the hose, you pinched the hose in the middle instead. This would result in the water flowing out of the end of the hose at a reduced flow rate (lower volume of water coming out per minute) and velocity (lower speed of the individual water particles).  Why?
It might help to take a snapshot of the place where you are pinching the hose.  the pressure behind the pinch zone goes up, causing the water to pass through the pinch zone at a faster velocity. However, because the hole is smaller, less water is able to pass through.  When it reaches the other side of the pinch zone, it slows down again because it has a very low pressure, and the smaller volume of water must fill the entire tube. However, because the flow rate was lowered because of the pinch zone, the amount of water at the end of the pinch zone is lower.  Consequently, the water flows slower and the flow rate is reduced simultaneously.
Another analogy that might help would be the comparison between a garden hose and a fire hose.  Let's say they have the same flow rate (same volume coming out of the hose per unit time).  You can immediately realise that for the garden hose to put out the same amount of water that the fire hose is putting out in a minute, the water would have to be flowing many times faster in terms of velocity.

Furthur reading

Grunwald JE, Petrig BL Riva CE, Sinclair SH. Blood velocity and volumetric flow rate in human retinal vessels. Invest. Ophthalmol. Vis. Sci. 1985;26(8):1124-1132. Available online: https://iovs.arvojournals.org/article.aspx?articleid=2159754
Baker M, Wayland H. On-line volume flow rate and velocity profile measurement for blood in microvessels. Microvasc. Res. 1974;7(1):131-143. Available online: https://doi.org/10.1016/0026-2862(74)90043-0


Why do different humans look different? Although farmers appear to be able to tell their cows apart, cows look very much alike to me. And this similarity in appearance seems to be a general trait across the animal kingdom: one individual of one animal species looks much like another.

Why do human facial and body shapes vary so much?

I understand that human beings live in many different environments (e.g. hot and cold) and have adapted to these (e.g. through lighter or darker skin color), but there seems to be much variation that has no apparent evolutionary purpose. So does the difference have a purpose in itself? That is, did we evlove to vary in appearance, and what is the purpose of this variation?

There is a substantial variation in some human traits: hair colour, eye colour, height, weight, skin colour, build etc. etc. HOWEVER there is also considerable variation within other species, to suggest otherwise is naive (though quite common). We often feel like there is more variation within our own species because we are more aware of the subtle differences within our own species (we have evolved to be able to recognise those that are more similar to us). Cows for example also have a lot of variation:

But to answer the question of why traits vary so much generally... There are two principle reasons that demographic patterns might evolve in traits (for example, "Why do Scandinavians tend to have blonde hair?" - [this is just an example, I'm not sure if blonde hair is actually more common in Scandinavia, it could just be a stereotype])

Firstly there is the selectionists view. This is the view that traits tend to evolve for some kind of adaptive reason, therefore most traits (and demographic patterns of variation) exist for some kind of purpose. A selectionist would argue that blonde hair offers some kind of advantage in Scandinavia, over other hair colours, that it doesn't in others. It could be a naturally or sexually selected advantage (perhaps blonde hair is more useful when hunting prey in snow, or there is mate preference for blonde individuals etc.)

In the 1960's though a scientist called Motoo Kimura proposed the neutral theory, a theory that most variation and traits have evolved by neutral processes. For example, scandinavians might be blonde because the humans that colonized Scandinavia were, coincidentally, blondes. Neutralists would argue that the demographic variance we see in humans, and within animal species, is due mainly to random genetic drift.

Here is some more on neutralist vs selectionist, and some on genetic drift. And just to show that other animal species also vary:

Here are some dogs (which have come under a lot of artificial selection specific to generating different physical variants)...

And here are some apes...


Have I identified this species correctly? Weird ocean blob I often comb the beaches in Santa Cruz (central California coast) for weird stuff that washes ashore. The waves have been a lot stronger than usual the last few days, and the today the beach was covered in a thick layer of kelp and other seaweed. There were even two dead seals washed up on the sand. Most intriguing however was this translucent oddity:

Reverse side:

It's about two inches across at its largest. I moved it to a concrete wall to photograph so I could turn it over without coating it in sand, but I found it down much closer to the water. It seems all but certain that it was ripped up from the seabed. I think there's a tiny snail attached to it, visible in the first picture.
Having done some digging, my best guess for the identity
of this species is some kind of ascidian tunicate. The closest comparison I find is this picture of Ciona intestinalis:

due to the orange hue and the distinctive black cord running through it. However it seems much fatter and I didn't notice a siphon on my specimen. Additionally, most images of the species show a much paler color and even more prominent siphon. My specimen might have shriveled from being out of the water though.
So, my guess is Ciona intestinalis. Can anyone confirm or refute?

A coworker of mine was able to identify the specimen as a Lightbulb Tunicate, Clavelina huntsmani. The distinctive "lightbulb filaments" that give the species its name can be clearly seen in the pictures I posted:

So it was indeed an ascidian.


Why does sexual selection evolve beautiful features? I have a very raw understanding of sexual selection:

Say a group of females of a certain species "like" some feature of a certain groups of males; by "like" I mean some behaviour that makes this group of females tend to mate with males having this feature, then the females are selecting their genes which make them feel appealed to males with the feature, and then this process becomes exponent since the group of females becomes bigger and forces the population of males to have this feauture, until an equilibrium is reached. I know this also happens with the roles interchanged.

My first question is, why do females tend to like males that have high amounts of these features, more than the average in the population?

My second question is, why do the end products of these selections are such beautiful features? Perhaps this may sound a little arrogant but I don't understand how an animal can appreciate this beauty, I suppose this is to make some sort of selection of healthy males.

Thanks

I think I can expand on the answer by @boo2060.

The evolution of female mate choice depends on females achieving higher fitness by choosing certain males over others. At the broadest scale, there are two mechanisms by which this can occur, direct benefits, and indirect benefits.

Direct benefits
These are material things that (surprise) directly benefit the female. This might be the provision of food by the preferred male, access to a good territory or shelter that is under the control of the preferred male, protection by the preferred male, that sort of thing. Females will accordingly favour male traits that advertise potential direct benefits. These might include male size/condition/colouration, or even built structures like those of the bowerbirds. Basically, these traits show that the male knows how to look after himself, and by extension, he knows how to look after her (as males in good condition generally inhabit the best habitats and will offer the best protection and parenting).

Indirect benefits
These don't do much for the female, but they increase the genetic quality (and thus potential fitness) of her offspring. This is a much more complicated area of mate choice, and can be split into a bunch of (non-exclusive) hypotheses (below). And of course, attractive males may well offer both direct and indirect benefits.

Sensory bias: Males may, by chance, possess a trait that holds intrinsic appeal for a female. The best explanation might be that it mimics the colour or shape of a food source (e.g. fruit) that the animal eats, and thus the animal has pre-evolved preference for that colour or shape (e.g. red patches). From that point, males with more of that trait, whatever it is, will tend to be more attractive, for no rational reason. This hypothesis is sound, but is currently lacking good empirical evidence.

Fisherian sexy sons: This can in fact lead on from an initial sensory bias. Females may choose males that they find 'sexy', because their offspring will also be sexy, and thus be successfull in reproduction. This can lead to 'runaway' selection for sexier and sexier sons, at considerable survival cost for males. In this case, natural selection and sexual selection work in opposing directions.

Indicator mechanisms: This is the handicap principle or 'good genes' principle. If a structure is costly to produce or maintain, or increases the risk of predation, and yet the male possessing it is still alive, he must have good genes to have withstood such a handicap. It may also advertise that the male is not infested with parasites. The extravagant plumes of birds may be largely explained by this one, but also sexy sons and sensory bias.

Genetic compatibility: Individuals seek partners that are genetically compatible. A certain proportion of the fitness of the offspring depends on the specific combination of genes (i.e. it's not additive), and individuals that can signal or detect signals in such a way that they can choose compatible partners will have an evolutionary advantage. The best example is scent (e.g. preference for dissimilar MHC immune genes - see the human t-shirt experiment).

These mechanisms are well known in theory, but not always well-supported by evidence (yet). This is probably the best reference.


Clinical Microbiology Books I am looking for a good book about Clinical Microbiology, particularly good in Bacteriology and Bacteria Diagnosis (medium, plates, type of colonies...). With good photos. What are the bests in your opinion?

Thank you.

Manual of Clinical Microbiology.

My version is old, but it is an excellent reference considered gold standard in the clinical science industry and by educators.   It has been used by clinical microbiologists for many years and is still coming out with updated revisions. It comes as a two volume set due to comprehensive content. Published by the American Society for Microbiology.

http://www.asmscience.org/content/book/10.1128/9781555817381


Why does mud therapy work by some pain related diseases? Apparently, some users here agree there is no ion exchange through the skin. Mud therapy has some therapeutic effect for pain related diseases. As an anecdotal example, I experienced pain relief by treating my sport injury using mud therapy. If it is not ion exchange, then what is the mechanism behind mud therapy?

The answer on the linked question is apt: transdermal administration of medications or other compounds include exclusively lipophylic compounds, i.e. uncharged 'fatty' materials, such as nicotine, opiate-bases and steroids. Minerals, like those found in clay, are highly hydrophylic and are therefore unlikely to be taken up by the skin.

A search through a bunch of articles makes me believe that mud therapy has mainly a thermal effect, i.e. a mud pack heats the underlying tissue and thereby relieves muscle spasms and pain (Espejo-Antúnez et al., 2012; Liu et al., 2013).

References
- Espejo-Antúnez et al., Rheumatology (2012); 258: 1-10
- Liu et al., J Int med Res (2013); 41(5): 1418–25


Why use a logarithmic scale when plotting pharmacodynamics/kinetics? I've seen the plots and they don't look drastically different. Why do this?

Why use a logarithmic scale when plotting pharmacodynamics/kinetics?

There could be several reasons for this. You mention in the comments that your plot of interest is the concentration-time profile. As you can see, plotting the logarithm of concentration vs time yields a very different plot for a drug administered intravenously.

The reason this is done is because the two plots yield different information. The slope of the log(C) vs t plot actually yields the elimination constant, Ke. The logarithmic plot can also be used to assess if the drug is distributed into one or more compartments. If the drug is distributed into two or more compartments, the initial slope would be different than the remainder (but this is not pictured here).

In terms of pharmacodynamics, its often useful to assess how a 10- or 100- fold increase in concentration affects the effect.


Could we have endless pleasure? Are there any studies that point out that we could have a device in the future  or drug that could give us endless amount of pleasure by stimulating or blocking processes in the brain or nerve system?

Drugs and alcohol end up saturating receptors in the brain. Is it known inside out how this mechanism of rewards / saturation / abstinence work in the brain and how it relates to consciousness?

It is well known that you cannot have the same amount of pleasure by repeating the same action over and over again but is it truly known how that works? Would it be possible to reset the receptors in the brain to accomplish this?

Of course.

There is a famous set of experiments (Milner & Olds) in biology that basically started modern behavioral research in which a wire was inserted in to a rats brain allowing for direct electrical stimulation of the pleasure center. as long as the current continued the rats experienced extremely high levels of pleasure. To the point they were unwilling to engage in any voluntary behavior, including seeking food and water, even when right next to them if it would interrupt the pleasure. You could keep stimulating the pleasure center until the rats died of thirst.


Why are there nail growth differences  between humans and other mammals? When a cat is growing, his nails are growing with him to some extent. A grown cat has a fixed nail length that is not extending.

By contrast, human finger nails just keep on growing, so we have to cut them to keep an aesthetically pleasing look.

Nature clearly has a mechanism to control nail growth.

What is the most probable reason as to why this is not implemented in humans?

Cat claws are growing all the time, like horse hooves, or human nails. However, cats and horses usually use their claws/hooves, so they get shortened through mechanical action.

An indoor cat may need their claws trimmed if it doesn't use them enough (that's why cats will want to scratch everywhere), or if has supernumerary toes that don't normally touch the ground. Similarly, cattle that doesn't get to move will suffer from hoof overgrowth, which appears to be very uncomfortable to the animal.

Consequently, if you were to use your fingernails more often for digging and scratching, you wouldn't have to trim them all the time.


How can bobcats feel the mice under the snow? I've just seen the Planet Earth II's second episode "Mountains" where they shock us with these North American bobcats that can feel mice from the distance of several meters, sneak to them and kill them with a single jump. What is their biggest source of information about them? The smell? Feeling of the quiet rumbling of the earth? Hearing it? Any of it seems almost impossible to me, with regard to the conditions of the polar regions.

You can smell roughly where your pan is cooking, but you can hear it with more precision, in order to pin point something you would tend to use your ears, especially if it is under snow.

Cats use all their senses and experience to hunt. The mice have tunnels under the snow to get around and they mark their territory randomly, so the smell doesn't provide a very precise coordinates for tracking: it propagates via wind, through snow, and takes a lot longer than sound to be sensed by the cat. Smell can travel further amd mouse piss smells strong, and freezes. Freezing temps prevent aromatics from diffusing outwards and from reacting with other chemicals. Snow is a very good thermal and therefore airflow insulator. Wind doesnt go through snow very fast, and aromatics take a while to get through (aromatic molecules can even travel through steel and glass)

Cats can hear higher-pitched sounds than either dogs or humans, detecting frequencies from 55 Hz up to 79 kHz (a range of 10.5 octaves) and dogs hear from 67 Hz to 45 kHz, a range of about 9 octaves.

To compare the hearing of a cat to that of a bat, the most sensitive range of bat hearing is 15 kHz to 90 kHz. A human adult hears up to 16-18khz and a child up to 20-22khz.

Sound arrives at the cat nearly instantaneously and provides a direct triangulated reference to the mouse position... One sound arrives slightly later than the other depending on the position of the sound source, and the entire sound spectrum is used in the brain to construct a clear image of the mouse position... shuffling sounds and percussive grey noise generated by animal movement tends to have peaks of energy distributed over a wide range. If the mouse is out of it's den in the middle of winter, it means that it's mostly searching for food, forageing, actually quite noisy activities.

Snow dampens the propagation of sound, so in winter you may notice that ambient sound is different in snowy conditions. That cats can pin point a mouse under snow is not that suprising, given the ambient silence of mid winter, the foraging of rodents, and the olfactory and auditory faculties of felines. it's a good quesiton because you wonder what cats do near mole hills, they are probably sensing a lot of activity there that we don't think about.

https://upload.wikimedia.org/wikipedia/commons/thumb/5/5d/Animal_hearing_frequency_range.svg/512px-Animal_hearing_frequency_range.svg.png


How do nerve impulses travel so quickly? Nerve impulses must travel incredibly fast to achieve the functions they do. However, I have been taught that sodium ions move down the axons by diffusion (thus causing depolarisation of the next part of the membrane etc, and this is the action potential).

However, I was under the impression that diffusion is a very slow process? How can this be the case?

There is a large gradient created by selective permeability of Na channels and as you're probably aware the speed of diffusion is proportional to the electrochemical gradient.

Very small numbers of ions actually cross the membrane during depolarisation and subsequent AP events.


Is it possible to estimate how much variation in common phenotypes is predicted by genetics? Phenotypes such as; skin color, eye color, nose shape, lip size, limb proportions, and skull shape.

Im trying to find a source for this quote.

"If you ask what percentage of your genes is reflected in your external appearance, the basis by which we talk about race, the answer seems to be in the range of .01 percent," said Dr.

Harold P. Freeman" From - http://astro.temple.edu/~ruby/opp/racesnyt.html

Height

This is just a single example, but "height" has received a lot of GWAS (genome-wide association study) attention, and last year the GIANT consortium published results of an analysis on 250,000 people looking at the genetic influences of height [1].

Using just 2,000 genetic variants they could statistically account for 20% of the phenotypic variation in height. Using 9,500 genetic variants this rose to 29%.

What this emphasises is that common traits (such as height) are highly polygenic; there is no "height gene" that controls it - instead it is the combination of many small-effect variants that cumulatively give rise to an individuals final phenotype (height, in this case).

Pigmentation

Pigmentation (of eyes, skin and hair) on the other hand is not nearly as polygenic. A 2013 review [2] discussed the known genetic variation for these traits. Prediction of eye colour using genetics, for instance, requires only six genetic variants "to be suitable to predict blue, intermediate, and brown colors with an overall accuracy of 0.91, 0.72, and 0.93, respectively".

So in contrast to height where even with 9,500 variants measured you would still only have 29% accuracy, you can be 91% sure that someone will have blue eyes if you know the individuals genotype at only 6 positions.

So in short the quote you reference is incorrect - we can predict many common traits with reasonable accuracy - although for some phenotypes the individual predictive capability of a specific genotype may be around 0.01% (e.g. some of the height variants).

Wood, A. R. et al. (2014) Defining the role of common variation in the genomic and biological architecture of adult human height. Nat Genet 46, 1173-1186, doi:10.1038/ng.3097
Liu, F., Wen, B. & Kayser, M. (2013) Colorful DNA polymorphisms in humans. Seminars in Cell & Developmental Biology 24, 562-575


Is there are practical lower limit to gene length in E. coli? Question is rather self-explanatory.

Putting aside other post-transcriptional factors like rate of degradation of transcript, what is the smallest gene ever reported to have successfully been transcribed in E. coli or other similar prokaryotic systems? Why couldn't this gene be any smaller?

Note that in the context of this question, I am disregarding factors like promoters, operators and terminators. Also note that this gene does not necessarily need to code for a protein.

In terms of naturally-occurring "genes" I think that the record is probably held by the attenuator peptides.

In bacteria, the regulatory mechanism known as transcription attenuation involves the ribosomal biosynthesis of very short peptides. In the trp operon, where the phenomenon was first described by Yanofsky's group, the peptide, MKAIFVLKGWWRTS, consists of just 14 amino acids. Other examples, described subsequently, are of comparable size.

Now that I have written this answer, I have reread your question and I see that you are really interested in transcripts. In the case of the attenuators, the peptides are encoded by the 5' end of a much larger transcript, so they probably don't count for you.


Fish ID? Small, yellow-finned, tropical fish in Thailand I have not had any luck finding the yellow fish shown in the photo in any of my fish books. I saw them in many places, so they are fairly common. This observation was at around 15 meter depth.

I hope someone here knows it.

With a little Google search I found similar fishes. Says it is golden or yellow damselfish or possibly lemon damsel but I'm not sure because there are some different names for this picture or different pictures for searching same name can be found on Google.

Also, I found a fish identification page on which this fish can be found.

Is this your fish?


Why does Nature use a 4-level system to encode information in DNA? First, I am not a biologist, so this question might be naive:

Computer information processing and storage is based on 2-digit system of bits with values 0 and 1. Now, DNA stores the information in a 4-digit system: A, C, G, T. Three base pairs form a codon and can encode 43 amino acids.

Is there a good reason why a 4-level system (which can store 2 bits per encoding entity) evolved rather than a 2-level or a system with a larger number of symbols in the alphabet?

Put differently: Why was a binary system not preferred for storage and processing of data? In computing, binary is much easier, and the very few tests of exotic higher-level data processing have not really been successful.

The current hypothesis is that RNA came first, DNA and proteins came later. So the reason that four bases are used might be related to the initial RNA world, and then DNA just reused the already existing RNA bases in a slightly modified form. In the RNA world, all functions had to be performed by RNA. Having more bases available than two would likely be important to be able to adopt various structures and create binding pockets or active sites for ribozymes.

You can't really think of the genetic code as an abstract data storage device. There are physical and chemical consequences to the choice of encoding. For example, proteins have to be able to bind to DNA and recognize particular patterns. With your binary code, the recognition sequence would have to be longer, because each basepair contains less information. The tRNA anticodons would have to be larger for protein biosynthesis to work with the binary code. Another issue that plays a role in some processes is that GC base pairs are more stable than AU/AT base pairs.

These are all just hypotheses. Evolution doesn't necessarily choose the best option, sometimes it is just the most convenient one that still works well.

I also found a review titled "Why are there four letters in the genetic alphabet?" that makes a similar point as my first one.

  All present models to explain the fact that we have four base types in
  our genetic alphabet hinge, in covert or overt form, on the assumption
  that the genetic alphabet evolved in an RNA world

Another factor I didn't think of that is mentioned there is that while more bases make better ribozymes, more bases also decrease the accuracy of  replication.

  In summary, two-dimensional RNA-like structures (and, presumably also
  the three-dimensional structures) become better defined as alphabet
  size increases, whereas the accuracy of replication decreases.


What does the evidence suggest about how Neanderthals became extinct? According to "Neanderthals: Facts About Our Extinct Human Relatives" (Szalay, 2013), Neanderthals dominated Europe during the last Ice Age, but may have died out before the arrival of Homo Sapiens (according to research detailed in "Radiocarbon dating casts doubt on the late chronology of the Middle to Upper Palaeolithic transition in southern Iberia" (Wood et al. 2012).

There are a number of theories floating around in the literature - everything from inability to adapt to climate change  to dietary deficiencies.

What does the latest research suggest as the cause of the Neanderthal extinction?

(refereed papers would be appreciated)

This is one of those active areas of research where there isn't a lot of consensus among researchers. There isn't even consensus as to whether it was an extinction in the strictest sense, because we now have evidence from genomic research that Neanderthals interbred with modern humans. Research is still being done on a lot of different hypotheses.

This article by K. Harvati is a decent short summary of the current state of the field, and includes references to recent articles.


Homework question on chemically defined medium Why would the following medium not be considered a chemically defined medium:

Glucose, 5 grams (g); NH4Cl, 1g; KH2PO4, 1g; MgSO4, 0.3g; yeast extract, 5g;
distilled water, 1 litre

I am unsure why it is not a chemically-defined medium considering all measurements and grams are given and such is required for it to be one. Therefore I am unsure why it would not be a chemically defined medium.

A chemically defined medium is, according to this Wikipedia article:

  ... a growth medium suitable for the in vitro cell culture of human or
  animal cells in which all of the chemical components are known.

Four of the five components fit this criterion precisely, as they are chemical formulae (and of course a common name for a compound whose formula is well known).

However, even though you know exactly how much yeast extract was added to the medium, you do not know its exact chemical composition. To be sure, assays of the chemical composition of yeast extract have been run, and one could come up with approximations of it's makeup. But the bottom line is that there is no precise chemical formula for yeast extract as there are for the other components of the medium.


Is COVID-19 more deadly than swine flu? I have a question about the novel coronavirus and swine flu.

How do the death rates compare between the two diseases?
How do the transmissions and rate of transmission compare?
Was a vaccine developed quicker for swine flu?

I ask because I don't recall this level of global disruption during the swine flu outbreak.

“Swine flu” is an obsolete name.  The official name for the virus that was briefly called “swine flu” is “H1N1pdm09”.

H1N1pdm09 has a mortality rate of around 0.01-0.1%. That’s roughly 10- to 20-fold lower than COVID-19. Its R0 was estimated at between 1 and 2, which is roughly half the estimates for SARS-CoV-2 (the virus responsible for COVID-19].

A vaccine for H1N1pdm09 was available in the fall of 2010.  It was possible to make it that quickly because it’s just another influenza strain, and the normal techniques for for vaccines against influenza strains worked fine.

Most importantly, H1N1pdm09 never went away.  It is still one of the main influenza strains circulating today, and if you were vaccinated for influenza since 2010 you received a vaccine against it.

CDC info here: 2009 H1N1 Pandemic (H1N1pdm09 virus)
WHO info here: Evolution of a pandemic:
A(H1N1) 2009, April 2009 – August 2010, 2nd edition


What is the difference between floral primordia and floral buds? As we know an axillary bud differentiates to form a floral bud, but what is a floral primodium?

A primordium (plural: primordia) is the first recognizable manifestation of a biological structure. In the case of a flower this will be a small meristematic bump typically at the periphery of a shoot apical meristem.
In contrast, a flower bud is generally used to describe the entire structure including the meristem and any associated structures (such as bracts) that can develop into a flower. This structure often goes through a period of dormancy.
Another way of saying this is that, in the context of a flower, a primordium is a group of meristematic cells that has not yet formed any lateral structures, while a bud contains a meristem and its associated lateral structures. Note however, that I believe I've seen bud used as a synonym for primodium in some cases.
Another difference is that primordia are (usually) microscopic structures, while buds are (usually) macroscopic (visible to the unaided eye) structures.


How do animals contain and dispose of bacterial endotoxins (lipopolysaccharides)? Gram negative bacteria naturally release endotoxins which are lipopolysaccharide molecules. These molecules are toxic to many eukaryote cells, including macrophages. My question is how animal organisms locate, isolate, contain these toxic molecules. For example, if a lipopolysaccharide attaches to a macrophage, thus neutralizing it, does this actually kill the macrophage or just render it inert? In any case, the ineffective macrophage must now be removed as waste. How does that occur?
In the Wikipedia article on endotoxin it reads "Normal human blood serum contains anti-LOS antibodies..." without further describing them. I find this statement strange because normally when I think of antibodies, I think of them attacking cells or organisms, not individual molecules like lipopolysaccharides. What are these anti-LOS antibodies and how do they function?

There are too many questions embeded here to cover in a single answer. I'll summarize and answer what I interpret to be the "central" question.

How do animals A) locate, B) isolate, and C) contain/eliminate bacterial endotoxins?

LPS in the blood stream is rapidly bound by LPS-binding protein (LBP) and localized to the liver for detoxification and excretion (1).
A) LBP recognizes and binds the Lipid-A region of the LPS molecule (2),
B) At this point LPS is released from bacterial cell membrane and sequestered into complexes with high-density lipoprotein (HDL). This is also the stage at which free LPS can activate CD14+ monocytes, triggering an acute inflammation response (3). However, additional HDL reduces monocyte activation, suggesting that these complexes inactivate LPS by "isolating" it from CD14 (4).
C) Finally, the LPS-HDL complex is taken up by the liver, either into Kupffer Cells (~25%) or liver sinusoidal endothelial cells (~75%), where enzymatic inactivation of LPS occurs either by dephosphorylation of the phosphates or deacetylation of the primary acyl components of lipid A (5)
Given the hydrophobic characteristics of LPS lipid-A and the fact that it's processed in the liver, I suspect that LPS and its metabolites are eliminated from the body via excretion into the bile ducts, but I haven't found a reference in the literature to confirm that suspicion.
References:

Wassenaar and Zimmermann, Eur J Microbiol Immunol. 2018 Sep 28; 8(3): 63–69.
Tobias et al., J Biol Chem. 1989 Jun 25;264(18):10867-71.
Vesy et al., Infect Immun. 2000 May; 68(5): 2410–2417.
Flegel et al, Infect Immun. 1989 Jul; 57(7): 2237–2245.
Yao et al. J Immunol. 2016 Sep 15; 197(6): 2390–2399.


Variation of fixation probability over time in Wright-Fisher model In Wright-Fisher model of population size N and initial mutation frequency of 1/N, how does the fixation probability vary over generations. So, mathematically, what is the function that maps the generation to its fixation probability?

The function probably look like $r(t) = A + B e^{-C t}$, where $r(t)$ is the rate of fixation at time $t$ (in generation). The reason for this exponential is that the probability that a mutation happens after $t$ generation is given by the exponential distribution.

As the rate of fixation at equilibrium must be at $2N\mu \frac{1}{2N} = \mu$, $A=\mu$, that is $r(t) = \mu + B e^{-C t}$

As at $t=0$, the rate must be 0. As $e^{0} = 1$, you should have $B=-\mu$. Hence,

$$r(t) = \mu - \mu e^{-C t}$$

$C$ here represents the steepness of the curve. I don't know how you could calculate it a priori but it must depends upon your population size $N$. As the expected time to fixation starting at frequency $p_0$ is (from Kimura and Ohta 1968)

$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0)$$

For $p_0 = \frac{1}{2N}$

$$\bar t\left(\frac{1}{2N}\right)=-4N\left(2N-1\right)\ln\left(1-\frac{1}{2N}\right)$$

or

$$\bar t\left(\frac{1}{2N}\right)=\left(4N-8N^2\right)\ln\left(\frac{2N-1}{2N}\right)$$

if you prefer. Maybe $C = \bar t\left(\frac{1}{2N}\right)$ leading to

$$r(t) = \mu \left(1 - e^{-\left( \left(4N-8N^2\right)\ln\left(\frac{2N-1}{2N}\right) \right) t}\right)$$

Let me know if it matches (I'd pretty amazed)!


Significance of the resequencing of the chimpanzee genome Introductory remark: I am not a biologist, but a somewhat knowledgeable layperson.

I have been told that sequencing of chimpanzee DNA until recently has been done almost exclusively using human DNA as a “template” to help piece together short DNA sequences. The similarity that emerges to human DNA could then perhaps be somewhat misleading, as the structure of human DNA affects the end result obtained for chimpanzees.

However, recently (2018) a new study was performed in which the assembled DNA fragments from various apes were assembled completely separately from human DNA, giving a better estimate of the similarities and differences between the DNA of humans, chimpanzees and other apes (Kronenberg et al. Science vol 360 issue 6393, eaar6343).

What new information has emerged and to what extent does it alter previous results?

The effect of re-sequencing the great ape genomes (orangutan as well as chimpanzee) without the use of a human genome as a guide to assembly has in general been to correct mistakes and improve the ape genome sequences so that they can be compared better with the human genome.

As far as I am aware, it appears that in a broad sense the same genes are present in humans and great apes, i.e. each will have a similar (orthologous) gene for, e.g. insulin, trypsin, keratin, generally at the same position on the chromosome. As the species are different these differences are thought to come from differences in these orthologous genes or in the regions of the genome that control their expression as RNA and then protein. The differences could also affect their activity, where they are expressed in the body or whether different variants occur (by differential splicing of transcripts).

So with improved and independent genome sequences it was possible to identify a greater number of variants in these orthogonal genes.

The focus of this work was on genes that are expressed in brain cells, because a key feature that distinguishes man from the great apes is brain size. The interest was in genes that were found in separate experiments to have significantly different expression when glial or neuronal cells of human or non-human species were compared. The authors report mutational variation in 252 genes with such differences in glial cells and 123 in neuronal cells.

To quote the discussion:

  These improved genomes yield a comprehensive view of intermediate-size
  structural variation among apes. As we focused on SVs (structural
  variants) that potentially disrupt genes or regulatory sequences, we
  began to address potential functional effect. Differential gene
  expression, especially in cortical radial glia, has been hypothesized
  to be a critical effector of brain size and a likely selective target
  of human brain evolution. Nearly 41% of the genes down-regulated in
  human radial glia, when compared to chimpanzee radial glial analogs
  from cerebral organoids, associate with an fhSV (fixed human-specific
  structural variants) and most often as a deletion or a retroposon
  insertion. These findings are consistent with the “less-is-more”
  hypothesis, which argues that the loss of functional elements
  underlies critical aspects of human evolution.

So, they haven’t found what makes us human yet, but have laid the foundations for studies that may at least find out why we have bigger brains.


How long is saliva viable? Does anyone know if saliva can stay viable for about 5 days, before it gets suspended into a DNA genealogy vial for testing?

Background: My brother wants to do a DNA genealogy test at a US testing facility. The country he lives in doesn't allow it, however. For some reason FedEx has no problem with shipping his saliva to me in the U.S. The fastest they can do is 4 days. Will it still be viable to test? Or will it have gone bad somehow? He wants to ship it tomorrow.

Saliva buffer usualy provides stability at RT for month or even years. Genotyping companies like 23&me use collection kits like Norgen's (https://norgenbiotek.com/product/saliva-dna-collection-preservation-and-isolation-kit) which allows to store the sample up to 5 years.

So my advice would be: get the spitting vial at your place, send it as regular mail to your brother, and then ask him to send it back to you once filled with saliva. By doing so you won't have to worry about temperature.

Sending fresh saliva should be ok if your brother sends it refrigerated (4°C). I keep fresh cells up to at least one week in the fridge in proper medium, and saliva is a pretty decent buffer and has some antimicrobial properties.


Neisseria meningitidis transformation into a pathogen I read the wikipedia article about Neisseria meningitidis, and it says that

  N. meningitidis is a part of the normal nonpathogenic flora in the nasopharynx of up to 5–15% of adults

In some cases however, it infects the bloodstream, creating a Meningococcemia disease which is highly lethal. It may also create a meningococcal meningitis.

The article also says that this disease is somewhat infectious. Not as infectious as common cold, but it is known to cause epidemics in Africa and Asia.

My question is: How can it be so abundant in its non-pathogenic form (up to 15% of adults) yet cause epidemics? It seems that it's transmitted from nose to nose somehow and doesn't cause a disease, yet when it does cause a disease it also causes a disease upon transmission.

It's not like a strain of E. coli that may cause disease in immunosuppressed individuals yet is a part of normal microbiota for other people. Because then it wouldn't cause epidemics, since the majority of the population is immune to it as evidenced by the fact that it's part of their microbiota.

Does N. meningitidis mutate to become pathogenic? Do the nasal strain and the pathogenic strain have different genotypes?

I tried searching for an answer but didn't find any.

Thank you very much.

It's not like a strain of E. coli that may cause disease in immunosuppressed individuals yet is a part of normal microbiota for other people.

Well, actually, it is kind of like that.
The answer is complicated, but can be boiled down to, virulent serotypes of Neisseria meningitidis infect susceptible populations. For the short answer, just read between the highlighted boxes.

Invasive meningococcal disease results from the interplay of: (1) microbial factors influencing the virulence of the organism, (2) environmental conditions facilitating exposure and acquisition, and (3) host susceptibility factors favoring bacterial acquisition, colonization, invasion, and survival.

Virulent serotypes have capsules that help them evade detection and destruction; they have an outer envelope that helps them invade and infect susceptable individuals.

The virulence (14) of N. meningitidis is influenced by multiple factors: capsule polysaccharide expression, expression of surface adhesive proteins (outer membrane proteins including pili, porins PorA and B, adhesion molecules Opa and Opc), iron sequestration mechanisms, and endotoxin (lipooligosaccharide, LOS). N. meningitidis also has evolved genetic mechanisms resulting in a horizontal genetic exchange, high frequency phase, antigenic variation, and molecular mimicry, allowing the organism to successfully adapt at mucosal surfaces and invade the host.

The most susceptible populations are infants/babies (most frequently), young children and unvaccinated young adults (during outbreaks). These are the populations most likely to have no to low antibodies against the bacteria.

The meningococcus remains a common cause of bacterial meningitis in children and young adults in the USA (132), now mostly affecting children less than 2 years of age (102, 133). Two-thirds of meningococcal disease in the first year of life in the US occurs in infants less than 6 months of age (134). Worldwide, the rates of meningococcal disease are also highest for young children due to waning protective maternal antibody, but in epidemic outbreaks, older children and adolescents can have high rates of disease. Fifty percent of cases in infants in the US are due to serogroup B; serogroup C is mostly seen in adolescents and serogroups B and Y in older adults. Even though peak incidence occurs among infants and adolescents; one-third to one-half of sporadic cases are seen in adults older than 18 years.

Carrier state isn't lifelong or even year long, in fact, it can last as little as a few weeks.

When approximately 10% of individuals from the general population at any time were carrying N. meningitidis in the nasopharynx (Cartwright et al., 1987), the carriage rate was shown to be <3% in children younger than 4 years and increased to 24–37% in the age-group 15–24 years... Then carriage rates decrease to less than 10% in older age-groups.

and

Meningococcal carriage increases rapidly among university students in the first month of the academic year and much of this increase probably occurred during the first week (Neal et al., 2000). The study, performed at the University of Nottingham, UK, showed the carriage rate increased in the first week of term from 6.9 % on day 1, to 11.2 % on day 2, to 19.0 % on day 3 and to 23.1 % on day 4. High social mixing probably caused this increase.

Carrier state is influenced by protective antibodies, local mucosal factors, and lower virulence of the bacteria in carriers. Smokers, for example, are more likely to be carriers than non-smokers. The type of N. meningitidis  also influences carrier vs. infected individuals.

In Norway, approximately 9% of the carriage isolates belonged to two of the known hypervirulent clonal complexes...

That is, of 100 carriers, less than 10% carry a very virulent type. Non-virulence or low-virulence is the norm.
A non-virulent strain can become virulent to others by sharing of DNA.

Because of mixed colonization with other bacteria and because of its duration, the carrier state is an ideal condition for horizontal gene transfer between different strains of meningococci, and between meningococci and other commensal bacterial species. The human nasopharynx may harbour diverse pathogenic bacteria, like N. meningitidis, H. influenzae, S. pneumoniae, as well as non-pathogenic bacteria, such as N. lactamica and the moraxellae.

Again, carriers ave protective antibodies.

Immunity to invasive meningococcal disease is dependent upon the presence of serum immunoglobulin G (IgG) which elicits bactericidal activity toward the infecting organism. Infants may be protected from meningococcal disease by the presence of maternal IgG which is obtained passively during gestation and lactation. Maternal immunity will be replaced by acquired immunity. Exposure to non-pathogenic Neisseria and other cross-reacting species in the nasopharynx increases the level of specific antibodies during childhood (Sanchez et al., 2001, 2002; Troncoso et al., 2000).

And

Carriage of commensal Neisseria, especially N. lactamica, is associated with a high titre of antibodies against N. meningitidis. Highly homologous structures are present in N. lactamica and N. meningitidis (Troncoso et al., 2000, 2001). Sera from mice immunized with N. lactamica and boosted with N. meningitidis have been shown to kill meningococci.
...Mucosal immunity is not able to prevent the colonization of the nasopharynx by meningococci, but it plays an important role in preventing the invasion of epithelial cell (Griffiss, 1995).

If that answers your question, that's what I hoped for, because the rest is a mystery  to me. But remember, you aren't a lifelong carrier. You might be a weekslong carrier, and every exposure to a non-virulent serotype increases your immunity.
Neisseria meningitidis: Biology, Microbiology, and Epidemiology
Neisseria meningitidis: an overview of the carriage state


What is the scientific name of such a fungus? Several days ago, in a bush I found the fungus as attached which is about 25cm in height and does not look like an edible mushroom:

Any one has an idea of its scientific name and other details?

This looks pretty much like a Coprinus comatus (also known as: shaggy ink cap, lawyer's wig, or shaggy mane) to me. You can see the characteristic ring around the stipe of the fungus (see image below from Wikipedia). The fungus is edible and is also cultivated in China for this purpose. See here for more details.


What is the minimum number of clades necessary to partition Vertebrates while maintaining the classical groups of Birds, Mammals, and Amphibians? At school I was taught the Linnaean view of vertebrate life - that vertebrate animals consisted of 5 distinct groups: mammals, birds, reptiles, amphibians, fish.

I learned later however that this was phylogenetically inaccurate, with birds being 'closer related' to crocodiles than other reptiles are, for example.

As such I am curious - since the idea of these groupings is so strong in popular conceptions of animals:

What is the minimum number of clades we would need in order to partition 'Vertebrates', maintaining 'Mammals', 'Amphibians', and 'Birds' as clades?

Phylogenetic taxonomy of the Vertebrates (mun.ca) has the following graphic (14 clades total, minimum of 12 collapsing Amphibia):

Here, what was preivously 'Fish' (the paraphyletic group of non-tetrapod vertebrates) becomes 6 clades, and 'Reptiles' (the paraphyletic  group of non-avian Sauropsids) becomes 3.

It seems the question is equivalent to asking "what is the minimum number of clades necessary to partition Vertebrates while maintaining 'birds' as a clade?".


Disease causing variants and Hardy-Weinberg Equilibrium Is it true that many disease causing variants/mutations do not follow Hardy Weinberg Equilibrium?  If so, then please elaborate on why this may be true (or not) and provide examples.

I am interested in single-gene disorders or those linked with single nucleotide variants.  I was told that many disease causing variants/mutations do not follow Hardy Weinberg Equilibrium, but I cannot find any documentation showing this (so I am looking for a reference on this matter).  In particular, I have considered Huntington's disease, Sickle cell anaemia and Hemophilia, but have not found any special relationships with these diseases and HWE.

Thank you.

Hardy-Weinberg law makes a series of assumptions. One of them is the absence of selective effects. As you talk about disease, this assumption of neutrality is obviously not met.

At the moment of fecundation

Imagine for example that at the moment of the fecundation, the genotypes AA, Aa and aa are at Hardy-Weinberg equilibrium. Let x be the frequency of the allele A at the moment of fecundation, the frequencies of the genotypes AA, Aa and aa are $x^2$, $2x(1-x)$ and $(1-x)^2$, respectively.

After selection

As all genotypes aa die off, you're left with the A allele being at frequency $y=2x^2 + x(1-x)=x(1+x)$ and the frequencies of the genotypes AA, Aa and aa are $\frac{x^2}{x^2 + 2x(1-x)}=\frac{2x-2}{x-2}$, $\frac{2x(1-x)}{x^2 + 2x(1-x)}=\frac{x}{2-x}$, and $0$, respectively.

Expressing the genotype frequencies in terms of the new allele frequency

You can as well plug $y$ into those genotype frequencies to get the expression in terms of the genotype frequencies at birth ($y$; after selection). It gives you $\frac{1-\sqrt{4 y+1}}{\sqrt{4 y+1}-5}$, $\frac{2 \left(\sqrt{4 y+1}-3\right)}{\sqrt{4 y+1}-5}$ and $0$ for the genotypes AA, Aa and aa respectively. So, obviously, it is not at Hardy-Weinberg equilibrium.

Assumptions

You can make some more interesting calculations by leaving out the assumptions that all aa genotypes die at birth and you could use a Leslie matrix to describe the probability for an individual of each genotype to make to the next age. I also assumed that the a is completely recessive. You might want to release this assumption as well by computing the death of a fraction of the Aa genotypes.


Why do some people burn and others tan? Connected to What is happening when we get a tan? - Why do some people burn while other people tan?

Very pale people tend to just burn while other people tan very nicely, what causes this difference?

I assume it has something to do with pigmentation - so what is the pigmentation in our skin actually doing in order to protect us from getting a sunburn?

There are two things happening: First melanin absorbs the energy from the UV radiation and releases it as infrared energy and thus protects the cells in the skin. This happens in all people, the deeper the skin color is, the better is the protection.

What is different between people is the amount of pigment they produce, the number of melanocytes is approximately the same. This depends on their genetic backgroud and is influenced by mutations in the pigment production pathway. As this is relatively complex, there are numerous positions which can influence the ability to tan, so I will only name a few.

The rate limiting enzyme for the pigmentation is Tyrosinase which catalyzes the first step of the melanin biosynthesis and oxidizes the amino acid tyrosine into DOPA. Without tyrosinase humans are not able to make any pigment at all which causes albinism. This is pretty drastic and doesn't happen too often. See reference 1.

Other possibilities are mutation in the signalling towards pigmentation, more specifically mutations in the MC1R gene which encodes on of the receptors. These mutations affect the ability to tan and are associated with red hair color, pale skin and freckles (most of the red-haired people carry at least one mutation in their MC1R gene). See reference 2.

Then there are mutations in the tyrosinase gene, which results in an enzyme with a lower processing rate. Because of this, less pigment can be made as the amount of materials is limited. See references 3 and 4.

The diversity of the human pigmentation is influenced by all these (and much more) genes. Have a look at references 5 and 6 for details.

References:

Analysis of tyrosinase mutations associated with tyrosinase-related
oculocutaneous albinism (OCA1).
Red hair is the null phenotype of MC1R.
Mutations at Critical N-Glycosylation Sites Reduce Tyrosinase
Activity by Altering Folding and Quality Control
Mutational mapping of the catalytic activities of human tyrosinase.
Molecular genetics of human pigmentation diversity
The genetic architecture of normal variation in human pigmentation:
an evolutionary perspective and model


How can I set micropipette volume with decimal separators, for example 109.5 in p200? And how can I set:

150.1 in p200
871.3 in p1000
840.5 in p1000?

It doesn't make sense to set volumes of decimals of microliters with a P200, since usually the accuracy of these pipettes is in the order of a few microliters. So even if you set your pipette at 190 uL, you may still dispense a volume ranging from 187 to 193 uL. For a P1000, due to higher volumes the inaccuracy is of course higher, usually +/- 10 uL or more. Some brands are more accurate than others, like Eppendorf or Finnpipette. I suggest you check the specs of your pipettes and see how much accuracy you can achieve.


How reversible is DAT upregulation from long-term ADHD medication use? A mechanism for ADHD stimulant medication tolerance has now been found. See http://neurosciencenews.com/adhd-medication-patient-brains-adapt-dat/.

Here's the thing though: what exactly is the "signal" that the body uses to interpret whether or not it needs to upregulate the amount of DAT (dopamine transporter) that exist? Is it a dopamine-based signal  that somehow then gets carried to a transcription factor that gets carried to the nucleus for additional transcription?

First the boring (but most important part) looking at the study:

It is important to critique the study design FIRST to see what kind of information we can actually obtain from this study. This is a meta-analysis of cross-sectional studies (meaning there is no record of change over time) that include a variety of age ranges of ADHD patients (some on treatment, some not) who were compared with age, gender and IQ-matched non-ADHD people to measure DAT levels in the stratum measured with PET and SPECT.

What they found:

There were very heterogeneous results from all the studies, there was no statistically significant difference between DAT in ADHD and normal (note that they use the word "trends"). The only thing statistically significant that they found was that there was a wide spread of DAT in the ADHD population, and that exposure to treatment accounted for half of this spread (variance).

What can we say about this?

This is not a very conclusive study, but studies like this are often necessary to merit doing higher resource intensive studies.  This study did not reach statistical significance in it's primary outcome, and on further search was able to only find a single outcome of significance. My summary of this would be: maybe this could represent a method of medication tolerance.

To answer your question
If hypothetically this was the cause and I had to make up a possible method of transcription control, I would say something similar to your answer. I would guess there is some transcription factor that is inhibited by dopamine in the cell. When there isn't dopamine (b/c it is being blocked from returning), it would somehow become active and start transcribing the gene for DAT.

Disclaimer
I am not a neurobiologist, this is my opinion after reading the article. Feel free to add to my comments

  Reference:

  Fusar-Poli, P., Rubia, K., Rossi, G., Sartori, G., & Balottin, U. (2012). Striatal dopamine transporter alterations in ADHD: pathophysiology or adaptation to psychostimulants? A meta-analysis. American Journal of Psychiatry, 169(3), 264-272.[Link]


Skeletal muscles in clam Although skeletal muscle fatigues fairly rapidly, clams have a protein called paramyosin that allows them to sustain contractions for up to a month. What might be the role of paramyosin at the molecular or cellular level, which results in this peculiarity?

Older papers initially presumed that it was part of a mechanism called "catch" in invertebrates like molluscs which is a "sustained contraction."  However, paramyosin was also found in insects.  There is a very detailed review on invertebrate muscle from 2008 that you should read through (or, you know, search through) points out that recent evidence has shown that paramyosin is not involved in catch; that review also has this to say on the subject (emphasis added):

  Furthermore, paramyosin’s presence in almost every invertebrate muscle (including those with relatively small thick filaments) suggests that paramyosin should not be considered a ‘special’ molecule whose presence needs explanation. Paramyosin is instead an everyday constituent of invertebrate muscles, similar, for instance, to the giant sarcomere associated proteins (see Hooper and Thuma, 2005). Indeed, a more salient question might be why vertebrates do not have paramyosin.


Calculation of extinction coeffcient of GFP I want to convert the absorption of a protein into concentration. Hence ı need to calculate the extinction coefficient of the protein (GFP). ı found the formula (nTrp)5500+(nTyr)1490 on the internet but not able to use it since ı dont understand what n in front of the amino acids stand for and how ı reach to the n value

Only the number ("n") of the aromatic amino acids Tryptophan (Trp) and Tyrosin (Tyr) in your protein contribute significantly to its absorption at 280 nm (and Cystein (Cys), albeit to a lesser extend), see also here.

You could retrieve the protein's amino acid sequence from uniprot (see GFP here). Looking through the GFP sequence, one can identify n=11 (4.6%) Tyr and n=1 (0.4%) Trp. Now you can insert those in your formula and end up with an extinction coeffient of 21'890 M^-1 * cm^-1. This formula is only valid if all Cys are reduced (GFP has n=2 Cys that could form a disulfide bridge).

If you want to avoid all the formulas I suggest you copy the sequence of GFP and paste it into ExPASy ProtParam. This way you get a nice overview of the amino acid distribution of your protein and also retrieve the extinction coefficient under oxidizing conditions, which BTW is 22'015 M^-1 * cm^-1.


Hiding identical sequences in NCBI web interface Sometimes there are identical sequences in Genbank/Genpept, most often coming from the same species but different strains. Ie if I look up "bacteria chitin synthase", the 624-aa protein from Dickeya dadantii shows up three times. There even is an "identical proteins" link.

Is there any filter that I can use to get only one sequence from every group of identical ones? I mean, other than parse downloaded file on my own computer.

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).


Why do we make T4 if we only use T3? So, recently, I learnt that T4 and T3 are both released into circulation but only T3 is the active form. Why then, do we make T4 in the first place? I read that T4 has a higher half-life, which might be the reason. Also, my professor said that it might be because thyroid peroxidase is not specific enough to control if it adds one Iodine or two. So, what is the actual reason?

It sounds like what you read and what your professor mentioned are different types of causation.

T4 is the primary form produced by the thyroid; T3 is metabolized from T4 in other tissues and more strongly activates thyroid hormone receptors. Metabolism from T4 to T3 then allows tissues to have control over how much active thyroid hormone there is - multiple levels of control are very common to hormones, and other signaling pathways as well.