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Oxygen uptake with gills from water vs lungs from atmosphere
The concentration of oxygen in water tends to be around 6.5-8 mg/L. In the atmosphere, it is 21%, one liter of air weighs roughly 1.25 gram, so, oxygen concentration is 0.25 g/L or 250 mg/L. So, lungs can access 50x higher concentration of oxygen than gills can. This suggests, sort of, that maximum oxygen uptake possible should have a significant increase when lungs evolved. Is that trend observed and a topic that is often talked about?

The assumption in the question was corroborated by this article here, and is correct. The downvote is unnecessary, it is a valid question, and was easily answered with strong scientific consensus.

As a precondition for the coevolution of eurythermy and life with high energy turnover, oxygen availability had to be maximized and the
  capacity of oxygen supply mechanisms selected high (Fig. 2). Such
  preconditions were met with atmospheric oxygen levels always above a
  minimum of 13%–15% during animal evolution (Fig. 4). Moreover, such
  preconditions were most ideally met in terrestrial environments since
  breathing air rather than water implies a reduction by one order of
  magnitude in the energy cost of ventilation at 30–35 times higher
  levels of ambient oxygen and about 103 times lower viscosity of the
  respiratory medium. However, new and largely different ventilatory
  systems had to be developed in air (lungs instead of gills in
  vertebrates) in most cases (except for terrestrial crabs) to exploit
  the excess amount of oxygen. At the same time, thermal conductivity in
  air is more than 20 times less and specific heat about four times less
  than in water, reflecting that thermal buffering is much less in the
  968 H. O. Po¨rtner terrestrial than in the aquatic environment. As a
  consequence, temperature changes occur on shorter timescales and at
  larger amplitudes in terrestrial than in aquatic environments.
  Therefore, terrestrial organisms at the same latitude are likely to
  experience much larger temperature fluctuations than aquatic
  organisms. Opposite to the marine realm, where temperature
  oscillations are less in polar and tropical than in temperate areas,
  those in air increase at high, especially Northern, latitudes, as
  estimated for mainland locations in the Americas (Gaston and Chown
  1999). According to these considerations, extreme stenotherms
  comparable to Antarctic marine species are highly unlikely to exist in
  (cold) terrestrial environments. Eurytherms will predominate instead.

Pörtner, H. O. (2004). Climate Variability and the Energetic Pathways of Evolution: The Origin of Endothermy in Mammals and Birds. Physiological and Biochemical Zoology, 77(6), 959–981. https://doi.org/10.1086/423742

A mammal would have to breathe 800 times more volume to throughput the same weight of medium, so, in a given time, the fish puts through more oxygen than the land animal.
Considering salmon and tuna and sea iguanas and turtles, reptiles aren't more active than fish, and air is inefficient to lift against, so sharks and mammals move at around the same speed. Great white sharks and humans have the same hemoglobin concentrations, 14g/l.
We can also compare a great white shark and a killer whale, a tuna and a wolf.
Yes the maximum available oxygen is higher on land, although the limiting factor for energy throughput can be measured through food consumption and metabolism temperature:
Dolphins consume 4-10% of their bodyweight per day
Tuna consume 5-15% of their bodyweight per day.


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Energy produced from respiration
Why is the amount of ATP Produced from anaerobic respiration is less than the amount produced from aerobic respiration?

Anaerobic respiration does not completely oxidize the glucose, and as a result, pyruvate is not completely broken down, yielding fewer ATP molecules, and there are leftover molecules: lactic acid in animals and ethanol in yeast. This is because anaerobic respiration does not utilize oxygen, which is required for the electron transport chain, where most of the ATP comes from in aerobic respiration. In aerobic respiration, the glucose molecule is completely oxidized, and so (through the Krebs cycle and the electron transport chain, which requires oxygen and which produces the majority of the ATP) is completely broken down into carbon dioxide and water.

source: Stack Exchange

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Viruses. Alive or Not?
I saw this fascinating article today about how HIV moves through a mouse host in real time.
http://www.engadget.com/2015/10/02/watch-hiv-spread-through-mouse-in-real-time/#continued
It's common to hear a virus' activity described in the way the article does: with intent.
I have a hard time understanding this. Something is considered alive when it has a metabolism, takes in nutrients and expels waist.  It has to have some kind of respiratory system and it's own reproductive mechanism. Although locomotion is optional, most forms of life have some form of getting around.  Some plants are able to move somehow...
Viruses have no sensing organs and no method of locomotion.  They cannot smell or see or move on their own.  This means they have to be carried inside a cell or if free floating in a host's fluids, rely on random motions to get about.
In order to invade, as far as I understand this; they must essentially wait until they come into physical contact with a compatible target.  At this point, their protrusions (I call them "keys") attach to a host cells "door" and they then inject their DNA.
Most (or all?) cells use Mitochondria for "power" so they can do things - like metabolize and reproduce.  I've never seen a diagram of a virus that shows where it get's it's energy to power the 'injection' part of it's 'life cycle'.
How is this done?
In the mouse video, the HIV virus looks like it has a "plan" and that it knows how to select which initial cells to invade and then how to pick a good method of remaining hidden.  How can this be when they have no sense organs?  How can they "know" of other virus particles are being successfully attacked by the host?
This is incredible and incredibly complex.
I'm not a medical professional. I'm just a fascinated by-stander.

I don't think it's a duplicate, given the specific questions.

The questions posed here are neither answered nor asked in the question which this supposedly duplicates.

So in terms of finding ways to infect a host, a virus is entirely passive?  Like I mentioned before; without sense organs or locomotion of it's own, it would not have any method of seeking targets.  Is this correct?

If you think about the sheer number of viruses that probably enter at once, all they have to do is tumble into a cell for which their binding receptor has something to bind to, and adhere. Then, either the cell senses something and engulfs the virus, or another viral protein makes it favorable for the virus to get into the cell (for example).

You cannot expel your waist, because it is stuck in the middle of your torso.

When we're thinking about cells that get infected with viruses, we have a two of subgroups to consider, often denoted susceptible or permissive. In essence, a cell which a virus is meant to successfully infect must not only possess a receptor to that virus for adhesion, but also the ability to replicate the virus (so it needs the machinery!). So these cells must be susceptible and permissive!
After adhesion you end up with an entry phase, this differs by virus, but you can essentially break it down into endocytosis, membrane fusion, or injection. You can get an idea of injection from something like lambda phage, outlined here. Enveloped viruses can fuse with the host membranes because these envelopes are often derived from ER, golgi network, or another plasma membrane. (Remember, viruses are essentially coding 3 basic sets of genes: for structure, replication and binding. It can't just code for everything it needs, either, so viruses hijack the host cell machinery to replicate.) Naked viruses, those that are just a protein coat and nucleic acid in essence, enter the cell through endocytosis and end up uncoating in a vesicle. And to stress it again, if the cell didn't have a receptor for the virus, it probably didn't get it. Portal of entry does make a difference, but I'm trying to keep it simple for our purposes!
Being said, when we're considering most viruses, membrane fusion and endocytosis aren't really using any energy but the host cell's, right? And then when the virus gets in there, they continue to use the host's resources becauase they really didn't bring a lot of baggage, either!
On the matter of "knowing" what they're doing, viral particles really don't do anything themselves. What I'd argue is that they've evolved methods of becoming particularly good at being viruses, many of which make it seem like they're making conscious choices, but suppose the following: Most of the time, viruses are probably just reproducing in such great numbers that it's just faster to get lucky and produce a strain with a better overall fitness.
Mind you, this whole time your body is attempting to fight off the virus, as in HIV, for example, eukaryotic cells have methods at each stage of attempting to protect themselves,

Source: Cellular Self-Defense: How Cell-Autonomous Immunity Protects Against Pathogens
You also have NK cells and macrophages responding to IFN produced by cells distressed by viruses, and eventually the presentation of viral antigens which result in effector T cells and antibodies unique to the virus in question. Another article here shows some methods by which some inhibitors of HIV infection can be evaded by the virus, as well, and just as likely, you also see that HIV has mechanisms of evading innate/active immunity as well! For example, if your antibodies recognize a viral capsid protein, what do they have to bind to if there's a lipid membrane in the way, as in HIV? What if the receptor composition changes?
In closing, viruses are obligate intracellular parasites. They need you to survive, but their objective is to replicate, so sometimes they do end up killing their host, but they aren't really communicating with each other in a fashion like: "I wonder how those other viruses are doing?" They really don't have a means of responding like that, so the end goal? Just keep moving from host to host and keep replicating, in the most basic sense.

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Does the human body metabolize what it smells, even in trace amounts?
I conjectured to a friend that some small amount of anything we smell is likely metabolized by the body. He disagreed. My thinking is that, if you are smelling something, some portion of molecules are being sensed by the olfactory tissue and some portion is taken into the lungs. Of the portion taken into the lungs, some portion is exhaled and some portion remains. I didn't propose a mechanism for the part that "remains" at the time, but it seems reasonable that some of it gets caught in mucus, some of which is then swallowed.
Obviously, a very, very small portion of whatever we're smelling would go through this process if my conjecture is even correct. For context, we were discussing people who have elected to restrict their diets for ethical or similar reasons. I was comparing what I proposed to when food products are labeled with "may contain trace amounts" due to "shared equipment".
So I guess my questions are these: was I right in my guess, and if so, was the mechanism correct or not?

Olfaction is the result of the neuronal impulse of ligand / receptor binding. To smell something requires 1) Specificity between the receptor and the ligand, 2) Concentration of the ligand molecule, and 3)The receptors that are on the surface of neurons in the olfactory bulb.
As for metabolize, then you need to be much more specific in defining what you are considering metabolism. Is the molecule broken down further; does it pass into the cells directly; does it need to be the unaltered molecule to qualify as metabolizing the molecule that you sensed as a smell.
The majority of our mucus in our airways is moved to the digestive tract as the result of ciliated epithelial cells "sweeping" the mucus and everything trapped in it to our esophagus, where it goes into the stomach and is digested. It is hard to say whether or not the molecules that you detect as smell are reactive, and if they are, whether or not they would chemically react with something else before it got to your stomach.
Also the volatile chemicals which you sense as an odor, aren't necessarily what would constitute the substance that they emanated from. So I would probably argue against your conjecture that someone who decides to be vegetarian or who has a peanut allergy is metabolizing something just because they inhaled it. It is likely the proteins in a peanut that cause an allergy, and that is not what you are inhaling, and as for the vegetarian, I think the justification is that it would be the protein that constitutes the consumption of a meat and not the molecules that come from the cooked or uncooked tissue.
If you want to broaden what you are calling metabolize, then you would only need to look at inhaled medicines such as corticosteroids or compounds to bronchodilate, to make a case for the fact that you are metabolizing what you inhale.

Thanks, @AMR. Can you clarify what you mean about volatile chemicals not constituting what they emanated from? Also, are you saying that the stuff we smell is non-nutrative and non-caloric? And since the precise context of the discussion was where an ethical vegan draws lines, can we define metabolism as breaking down the molecule and using its components? I apologize for any casual or incorrectly used language. I'm rather far afield of my discipline here. I appreciate the interest in such facile and impractical question.

What I meant by volatile chemicals are just chemicals that easily enter the gas phase are the molecules we are smelling. This article might clarify a bit, though if you are interested further I would suggest a Google Scholar search of Volatile Compounds in Food. https://en.wikipedia.org/wiki/Volatile_organic_compound To the extent they may not be used by the body as an energy source then you may or may not want to classify them as a undergoing metabolic processing. To the extent that they initiate a cellular response, i.e. the olfactory nerve impulse, then they do initiate a metabolic process.

I also think that an ethical vegan needs to draw the line at their choice of what they ingest and not inhale. If they are claiming that their right to be a vegan is being violated because they have to inhale compounds from animal products, then they are going overboard, in my opinion. And if they are arguing that they are vegan even if they inhale compounds from animals, then I would say that their argument is valid. The difference between what we inhale and what we ingest are very different things, which is why municipalities have a much easier time passing no smoking laws than soda taxes.

In the end, you are really defining the terms of the debate, my suggestion was that you clarify what your terms and conditions are. Like I said, inhaled medicines can even go as far as to turn on or turn off the transcription of genes in your cells, which is a metabolic process of the cell, so you need to specify the rules in order to get a definitive answer.

It sounds like, basically, the chemicals that enter the gas phase during cooking are VOCs and cannot be used as an energy source, though they might have other effects. So I'm going with I was wrong! This really was a hypothetical debate, since I wasn't suggesting people not breath in restaurants. Thanks again!


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"Antibiotic resistance" equivalent in archaea for selection during cloning
I'm beginning to work with halophilic archaea and I'm trying to figure out a good way to select for cells that have taken up a plasmid.  Obviously, one can't use antibiotic resistance since they are not bacteria.
Is there anything equivalent I could use for + selection in cloning experiment for halophilic archaea? Usually I would use NeoR and Neo plates but that won't work...

Obviously, one can't use antibiotic resistance since they are not bacteria.

This is not so obvious. Some common antibiotics are active against archaea.1 The Halohandbook, an indispensable document for the propagation and transformation of Halobacteria, includes a list of selectable markers and their concomitant plasmids:

NovR, MevR, and TmR are genes conferring resistance to novobiocin, mevinolin, and trimethoprim, respectively.

Usually I would use NeoR and Neo plates but that won't work...

Without knowing the specific organism you are trying to clone, we can't know if neomycin resistance will work as a selectable marker. Indeed, the bacterial neomycin resistance gene Neo (encoding aminoglycoside-O-phosphotransferase) can be utilized by mammalian cells to reduce aminoglycoside toxicity2, so it's not a huge logical jump to assume that archaea could similarly use Neo.  If you are working with Methanococcus, you can take advantage of vectors encoding aminoglycoside phosphotransferases native to Methanococcus voltae to select for neomycin resistance.3

References

Khelaifia S, Drancourt M. Susceptibility of archaea to antimicrobial agents: applications to clinical microbiology. Clin Microbiol Infect. 2012 Sep;18(9):841-8.
Dulon D, Ryan AF. The bacterial Neo gene confers neomycin resistance to mammalian cochlear hair cells. Neuroreport. 1999 Apr 26;10(6):1189-93.
Argyle JL, Tumbula DL, Leigh JA. Neomycin resistance as a selectable marker in Methanococcus maripaludis. Appl Environ Microbiol. 1996 Nov;62(11):4233-7.

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Normal TSH Levels in Hyperthyroxinemia
When it comes to hyperthyroxinemia, how is it possible for TSH to be normal when there is an elevated thyroxine concentration? What I know so far is that it is caused by a mutation in the Human serum albumin (P02768)that carries normally around 10% of the thyroxine.The mutation apparently makes it have a higher affinity for thyroxine, but how does it allow the TSH levels to remain normal?

bound thyroxine in the plasma is different from the "free" thyroxine in the plasma - it is for the most part the free T3/T4 that is able to feedback to regulate TSH secretion

Differential diagnoses of hyperthyroxinaemia with non-suppressed TSH levels include secondary or tertiary hyperthyroidism (e.g. due to TSH-secreting pituitary adenoma, resistance to thyroid hormone or paraneoplastic TRH production, respectively, all of them being very rare) and transient activation of the feedback loop in situations of type 2 thyroid allostasis1. In the context mentioned by you, elevated concentrations of T4 are most likely caused by increased plasma protein binding (which leaves free T4 normal)2.

Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood A, Klein HH and Dietrich JW (2017) Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming. Front. Endocrinol. 8:163. PMID 28775711 doi 10.3389/fendo.2017.00163
Bianchi R, Iervasi G, Pilo A, Vitek F, Ferdeghini M, Cazzuola F, Giraudi G. Role of serum carrier proteins in the peripheral metabolism and tissue distribution of thyroid hormones in familial dysalbuminemic hyperthyroxinemia and congenital elevation of thyroxine-binding globulin. J Clin Invest. 1987 Aug;80(2):522-34. PMID 3112186.


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Why is living on land beneficial?
When fish started developing the stronger limbs needed to walk(Slither?) onto land how was this beneficial? I cannot think of any form of food that would be helpful that would not be plentiful in water, but it must have been so as from what I can tell most beneficial mutations tend to be either a better way to either survive or obtain nutrients.

No competitors, no predators, lots of new niches to conquer. Isn't this enough?

Welcome to Biology.SE. What have you found so far? There are a large number of hits that talk about the role of the serosa when insects came out of the water but I am not sure this is what you are looking for. Maybe @JayCkat answer is what you are looking for but it sounds a bit like common sense and will be hard to find any peer-reviewed paper on the subject.

https://www.newscientist.com/article/2124873-these-fish-are-evolving-right-now-to-become-land-dwellers/

Related: How many times did terrestrial life emerge from the ocean?

Insects were the first animals to conquer land. Vertebrates followed later. So there may not have been an absence of a food supply. Also, the ability to leap to land for safety to avoid a predator is useful if said predator cannot follow. similar in manner to flying fish.

Also lots of plants to eat.

Walking developed before fish moved onto land. Fish that live in shallow water crawl along the bottom instead of swimming, because it is easier to sneak up on prey and hide from predators that way and it disturbs the water less than swimming. There are several modern fish that do this.
Like many brackish water fish they also could already breath air. Brackish water tends to be low on oxygen while air is always high.
Resources may have been plentiful in water but so was competition and predators.
For vertebrates there were no predators on land, there was food that no other fish were eating, there was access to new pools of water, etc. It was a completely open environment full of resources that had not evolved alongside them (thus had few defenses), no competition (the advantage of being the first vertebrate on land) and it was completely free of predators that is the like eden for an organism. There would be a huge selective advantage in exploiting it. You may want to familiarize yourself with adaptive radiation in general if you don't understand this.
Further reading:
https://academic.oup.com/icb/article/53/2/192/806098/Vertebrate-Land-Invasions-Past-Present-and-Future
https://en.wikipedia.org/wiki/Vertebrate_land_invasion


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What are proliferating, but "normal" (non-cancer, non stem) cells of the human (mouse)?
What are proliferating, but "normal" (not cancer, not stem, not differentiating) cells of the human (mouse) ?
Typically after differentiation process finished the cells stop proliferation.
But as far as I understand some cell types still proliferate.
But I cannot find much information about what types exactly and what is known about that.
I have heard about fibroblasts, but details are welcome.
Some pair (but slightly different question) is here:
https://www.biostars.org/p/9476880/

Gut epithelial cells have the highest proliferation rate in the human body (and probably mice too). They are essentially proliferating constantly, with complete turnover of the gut epithelium every 3-5 days.
One caveat, regarding the biostars question, is that these cells are also maturing (i.e.  differentiating) into at least 5 different cell types that I can think of off the top of my head. However, I think the proliferation should only be occurring among the epithelial stem cells at the base of crypts, which differentiate as they mature and migrate towards the villi, so it might be possible to use single-cell sorting techniques to separate them for experimental purposes.
Another cool thing about the gut is that the entire structure of the epithelium (crypts, villi, cell differentiation, etc.) can be grown in vitro with various different primary cell culture systems.
References:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7211432/
https://www.frontiersin.org/articles/10.3389/fbioe.2019.00144/full

Interesting, so the epithelial cells produce senescenting cells on a weekly basis. All those cells are evacuated?

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What is happening at the electrode interface when the electrical field is modified due to the change of ion concentration after an AP?
I have been working for quite a while now on electrophysiology and electrode fabrication.
I studied what is happening at the neuron level during an action potential (polarization/depolarization, change in ion concentration inside/outside the cell membrane) as well as the interface electrode/electrolyte (double layer, electrical model of an electrode, etc...), but I am still struggling to tie all of those principle together.
My question is, what is actually happening when an electrode is recording an AP (extracellular recording). To my knowledge, this is what is happening:

AP triggered, change of ion concentration outside the cell membrane.
As the ion concentration is modified, electrical field is modified around the cell

My question is now, how does the electrode record this change of electrical field? In almost all of the literature, a simple, but unexplained, shortcut is usually done: the authors usually speak about the change in ion concentration and then directly link it to a "change of potential at the electrode", but how can we explain this change of potential? What is happening at the electrode interface when the electrical field is modified due to the change of ion concentration after the AP? Is there any current flowing inside the electrode?
Thank you in advance

I’m voting to close this question because it seems to be about the details of what happens within an electrode (probably Physics or possibly Chemistry) rather than anything biological.

This is the field of biophysics and is on-topic here.

@AliceD — I could be wrong, but after rereading the question it still appears to be asking about what is going on inside the electrode. If that is on-topic for biology, then what isn't? For example why wouldn't a question about the details of NMR be on-topic (since MRI is used to study biology)? It seems to me that encouraging tangential questions is a disservice to the asker (since they are less likely to get a good answer and that answer is very unlikely to be properly scrutinized due to lack of expertise by this sites users).

@tyersome - the fact there may be a better stack to ask is not a reason to close the question. A comment to OP with your suggestion about a more promising stack is awesome. Also tell OP that cross-posting is discouraged and that if they decide to ask the question elsewhere, they should delete their first post. But again, many questions fit at multiple stacks. Many, if not all Neurosci questions here at Bio also fit at Psych&Neurosci.SE and vice versa. Some I see appearing here would receive better answers there, and vice versa. That is not a reason for migration.

There is an art to expressing the nature of any kind of uncertainty in writing, and especially in experimental literature, to stating no more than has been empirically shown.  An electrode interface only measures a one dimensional trace of what actually happens during an action potential cycle or spike, and it could be that in most of the literature, the precise mechanism by which the spike is measurable takes lower priority than the existence (or non-existence) of a particular signal.
According to Hodgkin-Huxley theory, the action potential is controlled through changes to the ionic permeability of certain membranes.  The precise mechanisms by which this happens depend on the molecular structure of channels through which sodium and potassium ions flow.  However, it is not hard to explain how a change in the permeability of a membrane can cause changes to an electric potential gradient (over 'large' length scales); the "deep concept" at work here is the second law of thermodynamics.
Let's suppose that you have two ions, one positive and one negative, confined to one side of a box as shown:

You might notice that there are more negative ions than there are positive ions, so there would be a nonzero electric potential gradient between the left and right hand sides of the container.
Now let's suppose that the confining membrane is replaced with one that allows only negative ions to pass (through the purple or tapered channels.)  You might expect a fraction of the negative charge to flow over to the other side of container where the potential is slightly higher (as shown):

The result is that the original potential gradient (from left to right) is dampened slightly.
The OP is probably aware of this, but it turns out that replacing the membrane with one that allows positive charge to pass through results in a fraction of the total positive ions moving to the left side of the chamber (even though it would be attracted to the right hand side by the net negative charge)*.  The reason for this is that the entropy gained by the first positive charge to move into the (log-macroscopically large) empty chamber vastly outweighs the (microscopic) entropy cost of leaving the occupied chamber with fewer positive ions to offset the negative ones.

This results in a slightly larger potential gradient than in the first (impermeable) case, as there are now positive charges in the region of higher electric potential.
The electrode can pick up on changes to the potential gradient by "grounding" the circuit at several points.  In particular, this requires a circuit that is soft or sensitive enough that it does not disturb the ambient potential significantly (a tape measure or height rod adapts to your height, not vice versa.)  That is, whatever current flows between the electrodes should be weak enough that it does not completely drain or equilibrate whatever local potential difference might exist, and other circuit elements should be weak enough that they do not cause flooding or, in a sense, drought of the natural electrodynamic state.  Beyond this, the complex and densely packed environment of neurons would make it a challenge to place electrodes to isolate a single action potential, or even a potentially useful signal across several action potentials.  Also, there is inevitably a certain amount of excessive unnatural current flow below a certain length scale (the scale at which the electrode starts to look like a bulk conductor.) Because of this, neuroscientists probably care more about the presence or absence of noise at this point than about the precise physiological origin of the signal, except insofar as the disturbance from the electrode is correctable and within tolerance.
*If the experiment is performed at nonzero temperature, which seems to be unavoidable.

Welcome to Biology.SE! While this looks like it may be a good (or even excellent — I lack the background to judge) answer, it is to a question that isn't about biology and thus is off-topic for this site. It would be better to leave such questions unanswered or have them migrated to an appropriate site. Second, for future posts please provide complete reference information since links can (and do) break. ——— You may also wish to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!

@tyersome not about Biology? I don't agree -- It's about action potential generation, i.e., the field of biophysics, neurophysiology, neuroscience etc.


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Evolutionarily, why do male rats and horses lack nipples?
Developmentally male rats don't have nipples because (reddit)

Testosterone release in the fetal male rat happens before the stage of mammogenesis where the teat is formed whereas other species halt that same process after the teat is formed.

According to the same page, male rats and horses (and mice) are unique among non-monotreme mammals in not having nipples.
Male humans have nipples because there's no evolutionary pressure for them not to. (Why do men have nipples?) Then, why was there selection for males to lack nipples in the case of mice, rats, and horses?
(Apparently, male horses lack nipples because "female horses have their nipples between their hind legs, and in males, that real estate is used for other purposes". (Straight Dope))
Evolutionarily, why do male rats and horses lack nipples?

Your question is interesting +1. I just want to note that the post "Why do men have nipples?" currently has an accepted answer (that is pretty highly upvoted) that is wrong (to my opinion at least)! Or at least that pictures a set of work (neutral theory) into something that it is not.

For rats at least, the answer is in your quote: because developmental sequences evolve. I don't think one need to posit an evolutionary reason for losing nipples, because in all likelihood that change was associated with some other developmental difference. And there is probably no way to know what the reason for the alteration of the timing of testosterone release.

For those wanting a paper instead of reddit: Hotchkiss, Andrew K., et al. "Prenatal testosterone exposure permanently masculinizes anogenital distance, nipple development, and reproductive tract morphology in female Sprague-Dawley rats." Toxicological Sciences 96.2 (2007): 335-345.

Male mice lack nipples too. Mice are frequently used for embryonic research as they are small and reproduce quickly. It is thought that male mice do develop nipples, but that they regress during development (Wysolmerski, 1998).
In general, it is thought that mammalian organisms develop as females by default when there is no male (Y) chromosome present (Hughes, 2004). Notably, X_ individuals and XY individuals with certain Y-chromosome deletions also develop as females. Basically, it is testosterone that suppresses female features. Hence, also boys with testosterone production, but without the appropriate receptors also develop as females.
Hence, men have nipples because females do (Simons, 2003).
The development of nipples is a pretty complex process (Wysolmerski, 1998). Disruptions in the process cause regression. Indeed, in mice, the tissues typical for nipples do develop in males during embryogenesis, but degenerate within a few days, leaving no trace of nipples at birth.
Hence, given the mouse example, I think that every mammalian male species develops by default nipples somewhere in development like mice, but that development is halted at various stages across species. The later in development it halts, the more it resembles female nipples. When it is stopped very early after gestation, they regress completely, like in mice.
Why is there a difference between species as to when the nipple development halts? Because the nipple developmental sequence is complex (Wysolmerski, 1998), and because evolution typically prefers losing things over gaining them, it is likely that by happenstance one of many crucial genes was lost in males, but selective pressure was simply too small to be of any significant advantage over males with slightly better-developed nipples. But from here on, it is guessing.
References
- Hughes, N Engl J Med (2004); 351(8): 248-50
- Lawrence, Nature News, August 1999
- Simons, Sci Am, September 2003
- Wysolmerski et al., Development (1998); 125: 1285-94

So that means for some reason rats and horses may have a gene similarity at some level for exhibiting this kind of phenotype? (Anyway, best answer! Bounty rewarded.)

Thank you @DevashishDas - you have been investing quite a lot of rep into expensive bounties of late! Good work. This is my first received bounty -- Thanks! Regarding your question - they may, or may not. These why questions are all kind of guess-away questions. Given the fine bounty I tried to add some elements backed up with proper citations and make a coherent theory, but it is still a guess. My theory is they share a developmental similarity, that may, or may not be reflected at the DNA level.

Good to know. :)

That female development is the default pathway is perhaps not entirely accurate, though often stated. This is evidenced by XX sex reversal in r-spondin 1 and Foxl2 mutants. See here. Not trying to nit-pick, it's just too fascinating of a topic not to bring up. Good answer, +1.

@canadianer - I tried to be on the safe side of things by saying: "In general, it is thought that mammalian organisms develop as females by default...". There are pretty much always exceptions to a rule and I will check out your linked information for sure. Interesting! Thanks for upvoting :)

I just realized the same is likely true for Bos taurus, as well. Cows have udders and bulls and steers have, nasty bits....

Stallions/Geldings don't have nipples because a mares "udder" ,so to speak, is underneath her flank area. A stallion's/Gelding's penis is also as well underneath their flank. Their evolutionary genes keep male horses/donkeys/zebras from having these nipples.

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Wearing sunglasses during a solar eclipse
Note: I had asked this on Physics, but it is off-topic there due to being about safety.
On the BBC's guide to eclipse-watching, Dr Lucie Green says:

Watching an eclipse with normal sunglasses provides virtually no protection. In fact, they trick your eyes to let in more light, so they can cause even more damage.

This doesn't seem right, because proper sunglasses should block UV to a safer level. Surely wearing proper sunglasses at any time is safer than not? Whilst I can understand staring at the sun with sunglasses on still allows too much UV in, why couldn't someone just glance at the eclipse from time to time?

Your eyes can dilate behind sunglasses, especially when the main source of light (the sun) is blocked, and ambient light decreases. Regular sunglasses offer some protection against certain UV wavelengths, but not enough to protect your eyes when looking directly at the sun (or, during an eclipse, the corona). Most sunglasses are mainly designed to, first and foremost, look good. After that, there is some protection against UVA (400-315 nm) and UVB (280-315 nm) light. Some sunglasses also offer "UV400" protection, which is short-wavelength blue light longer than 400 nm. Polarized sunglasses do not protect against UV at all, only reflected light (such as shining off the water or from an automobile's body or glass) and glare. Different sunglasses tints (or colors) also do not protect against UV, but they can affect color perception.

Surely wearing proper sunglasses at any time is safer than not?

That is true, it is safer, the question is to what degree? Sunglasses offer some protection from indirect UV and visible light that has been scattered by the atmosphere and reflected off of things around us. However, the number and energy of photons (the "particles" of light) reaching your eyes when looking directly at the sun is dramatically greater, and so much more dangerous. Eyes can be damaged quite quickly by high-energy light of many wavelengths, including UV and visible, with the magnitude of the damage correlating to the energy of the light. Damage is also cumulative, accruing over a lifetime. Even small peeks directly at the sun will contribute to your overall lifetime risk of eye damage, and may cause permanent, irreversible harm very quickly.
There are a number of much safer alternatives for watching solar eclipses, including pinhole projectors, welding goggles rated higher than 14, various solar filters for cameras, telescopes, and binoculars, and fully exposed and developed black-and-white film (good luck finding that nowadays), among others.
Above all, make sure you're safe, and if you have any doubts consult with an expert, such as a science/natural history museum or local university's astronomy department.

So, if this answer http://biology.stackexchange.com/questions/34286/is-it-safe-to-look-indirectly-at-the-sun is correct, then we should avoid looking in the general direction of the sun at all times?

@BrianFunt yes, that is correct.


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How difficult is it to make a shRNA/miRNA/siRNA to silence/knockdown NaV1.7 voltage gated sodium channels in humans?
There have been various research projects that experimented with shRNA/miRNA/siRNA to specifically silence/knockdown NaV1.7 voltage gated sodium channels in small animals like rats & guinea pigs. (Example; my previous question: Is HSV-vector-mediated miRNA expression in dorsal root ganglia stable?
But I can't find any that's been done for humans... So I think it means scientists have not gotten to that stage (if they are interested in doing so), and I was wondering,

technically, how difficult do you think it is to make a shRNA/miRNA/siRNA that can silence/knockdown NaV1.7 in humans, given that they already know how to make it for NaV1.7 in small animals?
financially, how much money is needed to invent such a thing (and how hard to get a grant for it?)
if technically not too difficult, and not very expensive to invent just a sample, is this something not necessarily a professional researcher, but a student could try making as their research project?

Why should any ethics comittee approve such experiments in humans?

Because especially when it is a partial silencing/knockdown, people who are suffering from pain after failed pain therapies or people with pain disorders can benefit from it, I think

What about potential negative side effects? Life is usually more complex than people think.

That's true, there could be side effects, although no serious ones seem to have been reported so far (but only in animals...).

Knockdown experiments in humans are almost always carried out on cell lines. In fact, I am doing a few such experiments myself at the moment (using U6 promoter expressed shRNAs introduced by lentiviruses). Doing it on humans would be extremely problematic for ethics committees due to the host of possible side effects.

The major hurdle for novel treatments to make it into humans is the assessment of its merits and added value over existing, proven treatments. And more importantly, the safety for humans has to be validated to a sufficient extent. The notorious from bench to bedside (Goldblatt & Lee, 2010) bottle neck. To answer your questions:

Technically, going from animals to humans may be a small step. Just increase the dose according to body weight. However, ethically it is a giant step. In fundamental research, lab animals are typically investigated only for the positive effects (e.g., amelioration of symptoms). In preclinical research, the animals have to be tested on side effects. Systemic injections, and even localized administration of potentially harmful virus vectors carries considerable risk. What if it returns to an infectious state? What are the side effects? Further, while animals can be treated systemically via iv injections, humans don't like needles. The FDA will put every possible danger and every possible discomfort to the patient into the spotlight.
Getting grants is hard. Going from bench to bedside is even harder, as the FDA, institutional review boards and the scientific community at large will scrutinize the plans.
To undertake clinical trials with humans is a team effort involving medical professionals, review boards, patients or healthy volunteers, an independent monitoring committee and so forth. It's not something you'll be doing in a few months. It can take years or decades to bring novel treatments to patients. It doesn't take one grant - it takes many, and development costs easily run into the tens of millions.

Reference
- Goldblatt & Lee, Am J Transl Res (2010); 2(1): 1–18

@pewiwe - If you appreciate the answer, an upvote can help to show others that it's a useful answer. Thank-you comments are great, but SE works with a voting system. Thanks!

Aw sorry i can't seem to upvote it because I registered as a guest :(

@pewiwe - perhaps consider converting to a real account?


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Does more ATP present mean that a microbe can ferment more and decrease the pH?
I noticed that EMP produces 2 ATP and EDP produces 1 ATP. Does that mean that if more ATP is present that would give more energy for fermentation and lowering the pH of a system?

You need to explain clearly what you are talking about, avoiding abbreviations. Why do you think fermentation requires energy? What type of microorganism are you concerned about? What is the relevance of the pH? At the moment your question is incomprehensible.

I'm thinking about the oral community and if utilizing the Embden–Meyerhof–Parnas Pathway more than the Entner–Doudoroff pathway could result in a lower pH.

To repeat, why do you think fermentation requires energy? It produces it.

@David I guess he/she meant more fuel/substrate for fermentation, or more free energy to drive the process...

@O.rka An underlying question would be what is the limiting factor that would stop fermentation assuming a closed system. Or maybe the question is about the balanced pH in a chemostat when one or the other pathway is imposed?


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What is meant by "the degree to which a gene is expressed" in an individual?
Here is an excerpt from a text that I was reading,

Here is an example of microarray data. The idea is to take a group of
  different individuals and for each of them, you measure how much they
  do or do not express a certain gene. Technically, you measure how much
  certain genes are expressed. The colors in the graph, like red, green,
  grey etc. show the degree to which different individuals do or do not
  have a specific gene.

The data they are talking about is this:

But a gene is either expressed or not expressed right? It's one allele is expressed or another allele is expressed, or yet another one is expressed. It is a discrete thing.
Then what is meant by the extent or the degree to which the gene is expressed? Can a gene be expressed more in certain individuals and less in others? Please explain with example.

It is true that a gene is either being expressed, or not being expressed. However, the degree to which a gene is expressed can vary tremendously. "Degree of expression" basically means the number of times the gene is read by the transcription machinery, which (generally) correlates to the number of copies of mRNA present in the cell, which (generally) correlates with the number of protein molecules being translated. Essentially, the degree of expression of a gene corresponds to how much of the gene's product is being produced. (Of course, this being biology, things aren't always quite as simple as that, but this is the general trend.)
Here's an example. All nucleated cells express housekeeping genes that are required for the normal function of the cells. These are often involved in maintaining metabolism in the cell, sensing and processing nutrients, maintaining the cell's structure and shape, etc. These genes are expressed to a very high degree, meaning they are always "on" and being transcribed. On the other hand, there are many many genes that are not needed in "normal" situations, and are only turned on at certain points in development, during pathology, during a certain point of the cell cycle, or other similar situations. These genes have a very low degree of expression, and in fact may be turned off altogether in some cells.
So, the degree of expression can be described as the rate at which the gene is being transcribed. In a study like the one illustrated in your question, the number of copies of each gene's mRNA in the cell is quantitated, and compared to the expression of a housekeeping gene that should have the same degree of expression regardless of the sample. The relative amounts of each mRNA are then compared among individuals, and scored accordingly. This numerical score is then turned into a color for the purposes of generating the heatmap image.


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Summarising ChIP-seq and controls needed
As part of my study I have to present on a method of discerning binding sites of proteins to DNA, for which I have looked at ChIP-seq. This is a brief overview of what I have so far, and was wondering if there are any particularly glaring omissions that I have made so far.

Cells treated with formaldehyde to cross-link proteins such as transcription >factors (i.e. HIF) covalently to DNA and incubated for 2-30 minutes. After >incubation glycine is added to terminate the cross linking and dissipate the >formaldehyde.
Cells are lysed, and sonication (application of sound waves to agitate a >sample) is used to fragment the DNA into sizes between 200-1000 base pairs.
HIF–DNA complexes are selectively immunoprecipitated by using antibodies >specific to the HIF protein of interest, complexed with a matrix of either >agrose or superparamagnetic beads.
HIF-DNA-antibody-matrix complexes are isolated through the use of either a >centrifuge or magnetic field (depending on the matrix employed). Several >washings take place to further purify the sample.
Cross-linking of the protein to the DNA is reversed by way of heating, >separating the DNA and protein-antibody-matrix complex. Proteinase K is used to >digest proteins, leaving only the DNA.
Oligonucleotide adaptors (primers) are then added to the small stretches of DNA >that were bound to the HIF to enable rapid simultaneous sequencing.
DNA sequences are then mapped to the reference genome to determine the binding loci.

I would also like to discuss controls that are used in these procedures. So far I have found limited mention of negative controls, positive and negative control loci, non-template control and positive control antibody, but am having trouble discerning what any of this actually is referring to.
I would seriously appreciate any help available on this topic!

The most stringent antibody control is the pre-immune serum from the same animal that was immunized with the Transcription Factor, but if you are purchasing the antibody from a company that control is almost never available. A non-specific serum from the same species can usually be purchased (e.g. Sigma), and is often used as a negative control. Some people just leave out all antisera and use that (with the beads, etc) to see what is pulled down. If the antibody recognizes an epitope tag then you can use that Ab on a cell that does not contain the epitope.

Full disclosure: I am a co-author on this paper:  ChIP-seq guidelines and practices of the ENCODE and modENCODE consortia http://genome.cshlp.org/content/22/9/1813.full

Good experiment! ChIP-seq is good for a whole genome look at transcription factor binding. KEY POINT:  The data generated are only as good as the antibody. Considerable effort needs to taken to prove antibody is specific for only the protein of interest.  It is for this reason, that some TFs still haven't been characterized by ChIP-seq.
As far as controls for your experiment:
The breaking of DNA from sonication isn't uniform from experiment to experiment, and sonication will preferentially break at some regions of open chromatin more often.
Controls for this:

Isolate DNA from cells that have been x-linked and fragmented under same conditions but don't use antibodies to IP.  This is "Input" DNA.
You can conduct a "mock" ChIP using a control AB that reacts with some non important non-nuclear protein, such as IgG.

Then sequence these samples to same depth as the Immunoprecipitated DNA.
Here is a good paper that is a little dated, but still relevent: Go to Control Sample Section
Here is a link to the guidelines for ChIP-seq for ENCODE PDF
Last but not least, if you are working on a much smaller scale, don't forget about things like DNA footprinting and EMSA to identify the ACTUAL binding site.


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Are the kind of mutations different in an antibiotic setting than they are in a non antibiotic setting?
Hy everyone!
I'm looking for experiments that deal with the kind of mutations that arise in antibiotic environment, as opposed to non antibiotic environment. As far as I understand, AB (anti biotic) doesn't change the kind of mutations that arise, it only gives advantage to the lineage that's already resistant. However I cant find an experiment that deals with this directly. What google brings up is only the Lederman experiment, however I can't find an experiment that deals with the aftermath.
What I'm imagining is this:

we create a replica from bacteria and put one of them in AB environment (or preferably many replicas from both groups
at every generation (or at least at certain times) we check the genetical makeup of bacteria in both of the AB and non-AB populations

Will the groups of bacteria at the same place (the "same" lineages) have almost the same genetical makeup with a comparable genetic drift? Or will there some specific mutations arise repeatedly in the AB group as opposed a non selective environment? I understand this can only be tested up to a few generations because after a while we are only testing selection and not mutation itself. However Im curious if there is such an experiment out there and if there isn't, why?
Thanks in advance!

This is essentially the same as the Luria-Delbrück experiment. They were interested more in phage resistance than antibiotics, but there is no theoretical difference. (https://en.wikipedia.org/wiki/Luria%E2%80%93Delbr%C3%BCck_experiment) Similar work has been done in antibiotics, even earlier it seems, though not so famous. A recent theoretical treatment with many relevant citations is here: https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1007930

Thank you for the answer, sorry for responding so late. Maybe I'm misunderstanding but it seems to me that the Luria Delbruck experiment deals with preexisting variations, before they are introduced to the virus. What I'm curious about is whether once a line of bacteria is introduced to the environment with the virus and it survives, will it start to develop a different group of mutations compared to a line that wasn't introduced to the virus? Maybe it is a pointless test, as the underlying mechanism is supposed to be the same as the L-D experiment, but I'm curious if it has been carried out.


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The Effects of Large Static Magnetic Fields on the Human Nervous System
How do static magnetic fields impact the nervous system?
I imagine with sufficiently intense magnetic fields the Lorentz force is going to change the behavior of nerve impulses, but at what field intensity do these issues occur? Which parts of the nervous system are most impacted by these fields? What specifically does the magnetic field interfere with? Are motor nerves more impacted than sensory nerves?
The WHO has some guidelines which suggest that fields of high intensity cause nerve issues, but this seems more related to MRI tech safety and doesn't really go into the biophysics of the situation. Additionally, they talk about issues which appear while moving through the fields, which seems to imply they're talking about low frequency field variation because an MRI field isn't spatially uniform.

I’m voting to close this question because whether or not something is safe for humans is more of a biology question.

Biophysics questions on PSE should be primarily about the physics. I agree that MRI is an important biophysics topic, but since this is Physics Stack Exchange the biophysics problems here need to mainly be about the physics.

I agree, physics is extremely relevant in this system. I am sorry if I gave the impression I thought otherwise. I am saying that determining whether something is safe is more of a biology question. Physics will not tell you what is biologically safe.

I don't have any power to migrate anything. You can raise a flag on your question to see if a moderator thinks it should be migrated though.

I don't know anything about long term health effects. The guidelines mentions that noticeable effects begin around 2 Tesla. This is in line with what I have heard. On the other hand, this mentions public exposure limits of 40 milliTesla. Here is a paper from the NIH that discusses health effects of neodynium magnets, but doesn't mention field strength.
Keep in mind that 2 Tesla is an extremely strong field. You are not likely to find it except right next to a large superconducting magnet. Or possibly between the poles of an exceptional research grade non-superconducting electromagnet.
Keep in mind that even if a strong magnetic field has no direct effect on a normal person, it could be harmful to a person with, say, a pacemaker.
Also, a field that strong can turn a stray piece of metal into a dangerous projectile.
Motion in a magnetic field matters because it exerts a force on moving electric charges. $\vec F = q \vec v \times \vec B$. This means for example, a copper wire feels no force, unless an electric current is moving inside it. In people, nerve impules are small brief currents. This may be why people feel effects in large fields. Walking means charges are moving faster.

@Triatticus - Thanks. I was not aware of that. I updated my answer.


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What fish is it?
I bought this 2 weeks ago, but i forgot to ask the seller, what fish is it.
Currently the size is 1 inch.

it is one of the 1300 types of cichlids,i do not know what type you have in your tank other than it is definitely a cichlid.

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Do you have any clearer photos of it? It's pretty blurry.

An African cichlid. Because it is apparently albino you may not find an exact match.  Start looking under "apistogramma".

it is a poor picture,over exposed and out of focus so i am not sure it is an albino cichlid.


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Have scientists tried to communicate with Sperm whales?
I see lots of passive studies of sperm whale click "language", usually focused on fingerprinting to identify groups and individuals. There's application of deep learning, and all sorts of advanced analysis. However, I haven't found any examples of scientists actively producing their own clicks and trying to elicit responses from whales. It seems to me that successful interactions would push our understanding of the clicks forwards much faster with a bit of a debug/test cycle.
Have studies like that ever been done? If so, can I please have links/references to the papers? Thanks!!

There has been a study / rescue attempt of a group of male sperm whales a few decades ago, where female sperm whale codas (a type of rhythmic communication clicks) where played from an underwater transducer in order to entice the males and lure them from an area of confined waters and into deeper water.
According to this study1, the playback was not successful in terms of getting the whales out to deeper water, but on one occasion, one of the sperm whales made a close approach to the playback sound source. A variety of sounds were produced by the sperm whales, but no codas were recorded.
References:

Goold, J. (1999). Behavioural and acoustic observations of sperm whales in Scapa Flow, Orkney Islands. Journal of the Marine Biological Association of the United Kingdom, 79(3), 541-550. https://doi.org/10.1017/S0025315498000666

You're right that there have been few playback studies assessing the response of sperm whales to sperm whale clicks. A couple of studies have shown a response (reduced foraging, returning to surface[1,2]) when killer whale vocalizations are played in the presence of sperm whales.
As an acoustician focused on odontocete echolocation clicks, I field a lot of questions about communicating with whales and when we're going to "get there" or "figure out what they're saying". Based on the title of your question, I'm not sure whether you envision the end goal of playback experiments to be getting us to the level where we could communicate specific messages to the whales themselves. If that is what you mean though, I think we're probably a long way off from that, and I'm not sure whether or not it's possible. It is not a guarantee that the way we use language and the way sperm whales using vocalizations are compatible enough for us to truly communicate.
If you mean communicate more in the context of understanding what types of clicks mean by playing them at the whales and observing their response, i.e., when we play clicks of type A, the animals always come to the surface, so clicks of type A must be some sort of surfacing cue, that's also very complex. For one thing, to draw conclusions you'd likely have to conduct experiments in a wide variety of locations/different groupings of animals, which gets expensive fast. Additionally, as animals are difficult to observe at sea in most cases, you have to factor in the added expense of equipment such as satellite tags that would be required to understand the animal's response to the sound, as you likely couldn't rely on simple visual observation. I'm not saying these efforts wouldn't be feasible, but to my knowledge these are some of the reasons why they may not be more common.
References:
[1] Curé, Charlotte, et al. "Responses of male sperm whales (Physeter macrocephalus) to killer whale sounds: implications for anti-predator strategies." Scientific Reports 3.1 (2013): 1-7.
[2] Isojunno, Saana, et al. "Sperm whales reduce foraging effort during exposure to 1–2 kH z sonar and killer whale sounds." Ecological Applications 26.1 (2016): 77-93.

Project CETI (Cetacean Translation Initiative) is designed precisely to understand sperm whale vocalizations. https://www.projectceti.org/
Check out recent talks by Ellen Garland and Shane Gero about Project CETI with the SETI institute. Note - SETI is trying to find intelligent life in the universe, while CETI is focused on whales here on earth.
https://www.seti.org/event/seti-talks-whales-their-song-their-culture-another-intelligence-earth


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Do bears have killer instinct?
For example, all big cats have killer instinct.
They go straight for the throat or neck of their prey, killing it before consuming.
I've seen videos of bears and wolves hunting prey. I've never seen any where they bite the throat or neck deliberately.
Bears just bash their prey till they die or eat them alive.
Wolves eat their prey alive when the prey literally exhausted all of their energy.

I'm a bit confused by your question. Are you asking "why do some species kill by biting the throat and some use other strategies?" A beat beating its prey to death still sounds like an instinct to kill to me...

A bear usually kills its prey by biting it on the back or neck. The bear uses his forepaw to strike very hard, usually breaking the prey's spine so this is why usually his killing instinct is on the back part of a prey. Bears also bite their prey on the snout.
this information can be found at the end of this article: http://www.largecarnivores.fi/species/brown-bear/bears-diet-and-hunting-behaviour.


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Can mold grow on copper pipes?
Couple months ago noticed something was literally, for lack of a better term, eating paint off of lead pipes.  And I noticed joints in copper pipe seemed to be "leaking" flux. Now all the water in my house causes lips and tongue to feel as if they have cold sores or anesthesised.  taste could be rusty.

Not mold. But you may be getting metal poisoning, get good advice. Seriously.

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text:
Calculating approximate dose of UVs received by a virus
I am making a very approximate calculation to determine the dose of UVs received by a virus standing at 1.5 cm from a UV source during a certain amount of time. Please let me know if my train of thought is incorrect.
Suppose I use an LED that emits 2mW of radiant flux. Side comment: I found one that with that draws 20mA of current when a forward voltage of 6.5 V is applied, which leads to a power draw of 130 mW. Thus LED efficiency is 2mW/130mW= 1.67%. I though LEDs are very efficient...)
To avoid making complicated calculations, suppose that 80% of all the flux is concentrated in 45 degree cone. In addition, supposing that the flux per cm2 is constant (I don't know the name for that value) on a flat circle area at a 1.5cm distance from the light source and where the virus will be placed. The LED will be switched on for 5 seconds. As such, the dose received by the virus is:
$$
Dose = 80\%* \frac{2mW}{(pi*(1.5cm)^2)}*5sec
$$
Is that equation correct?
Thanks

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, this question doesn't seems like it is a good fit for this site since it isn't directly about biology. Thanks!

I'm voting to close this question as off-topic because it about estimating a physical parameter (radiation flux) rather than biology.

which SE site should I post this to?

Maybe [Physics.SE] or [Engineering.SE]? I'm not familiar with either of those sites, so please make sure you read up on the standards for each site and check them for similar questions before reposting.

To avoid making complicated calculations, suppose that 80% of all the flux is concentrated in 45 degree cone.

The actual distribution of light is probably nothing like that.  Diodes tend to put significant amounts of power at higher angles so that way less than 80% ends up in the center, and within the central spot they peak at the center and then gradually drop off:  https://photonsystems.com/wp-content/uploads/2017/03/280nm-LED-performance-informationV3.pdf
Usually beam patterns are either simulated from manufacturer ray data or measured.  Since you're looking at low power and very low efficiency diodes, and given how much UVC LEDs cost, I'm guessing these are surplus or below-spec parts being sold on ebay or similar and you don't have access to the underlying datasheets.  In that case this is a reasonable way to estimate.


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How much of the genotype-phenotype map do we understand in HIV?
From what I understand, viruses have very small genomes relative to those of standard model organisms used in biological research. For example, according to Wikipedia, "the HIV genome contains nine genes that encode fifteen viral proteins". This is several orders of magnitude below the complexity of the mouse genome for example, with over 20,000 genes encoding over 50,000 proteins.
As a bioinformatics student (from a non-biological background) working with mammalian genomes, I often find the link between genotype and phenotype quite abstract and I'm unable to fully get an intuition for concretely how genomes can encode the instructions (or recipe using Dawkins' analogy) for creating complex phenotypes.
With this in mind, I wondered whether viruses, in particular HIV, which I know has been well studied, provide the simplest models for understanding the principles of how genes can encode the complete phenotypes of a functioning biological entity. Having such a small number of genes, I assume it is feasible to follow the transcription, translation and interaction of all genes and proteins? If so, is it the case that we understand how all of the genes and proteins work in HIV? If not, what is the main barrier in our understanding?
Apologies for this poorly-defined question. I am having a hard time getting my head around how molecular/cellular biology fits in with the complex phenotypes I've been studying in developmental biology/physiology and hoped that a simpler species/biological system could help to illuminate how it all comes together! Any pointers to further resources would be much appreciated.

I'm sure HIV is well studied since as you know it has a small genome and is highly relevent to therapeutic research, but virus regulation can be complicated and not representative of what happens in normal cells. This is why model organisms exist. The yeast Saccharomyces cerevisiae has about 6,000 genes and researchers have systematically deleted nearly every gene and looked at what happens to the cell. This information is available on the saccharomyces genome database. For example if you search SNF1 (which has a human homolog) on SGD (https://www.yeastgenome.org/locus/S000002885). You can see the phenotypes associated with deletion, overexpression, as well as a summary of what it does and how it's regulated (with original references). I don't think it gets any better than that. A lot of what is known about genetics and molecular biology comes from studies in yeast so I think it is worthwhile learning about yeast genetics to get a better understanding of what goes on in cells.


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Anticoagulation of black beans extract
How many ml of lithium heparin do I need to use on 2 ml blood to prevent coagulation for over 15 minutes?
I am comparing it to the 4 different dosages of black turtle bean extract that has polyphenols which I think have an anticoagulant effect.

At the very least, you will need to supply the concentration of lithium heparin, or work in milligrams rather than ml.

Thank you for responding. I only have  the lithium heparin from Vacutainer, which has 75 units and 4ml. Do you think I can use that as a control?

Is that Howell units, USP, etc.?


text:
How to mark nest area in double bridge experiment?

In my setup, I am lacking a nest. I'd need some way of telling the ants to bring food back to a first container, instead of just accumulating at the food source.

Presumably you have a queen, or at least some larvae?

Ah yes that might work, or maybe I could put one end of the setup close to a nest outside

Could you please explain what this is all about and what your question about biology is.


text:
Why would E. coli cultures suddenly start to slow down?
My E. coli cultures used to take 13.5 hours to reach stationary phase. I have not changed any of the parameters like temperature, shaking speed, media formulation/components or inoculation volume. However, the cultures now take 15.5 hours to reach stationary phase. What could be causing this issue? Is there any chance there is a phage/fungal contamination in the lab?

Fungal and phage contamination could both be checked by plating the culture. If you see plaques or multiple colony morphologies, you have your answer

If you resolve your question experimentally @JohnFlamour, please be sure to answer your own question here so that others can learn from your experience!

Are they sequential, you may have a mutation.

Several questions that might help diagnose the problem. How are you standardizing your inoculum? Using overnights or colony suspensions can be less consistent than back diluting from log-phase growth, leading to variable lag times. Are you starting from the same freezer stock for each experimental replicate, or just using subcultures? Subcultures can accumulate mutations. Has the maximum growth rate changed as well, or just the time to reach stationary? If it's contamination, I would expect the max growth rate to change (mutations from sub culturing could also cause this).

Have you considered the culture that you are using as inoculum is old and less active, resulting in a longer lag phase?


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Why does the Corpus Luteum produce more Progesterone than Estrogen?
In the human ovarian cycle, follicular cells produce only Estrogen in high concentrations (to my knowledge). Yet after ovulation and formation of CL, which should be the remnant follicular cell mass, it is seen that Progesterone is secreted in higher concentration, along with some estrogen. Is this due to some structural change, or is it the effect of LH, or something else entirely? This may have an obvious answer, so I apologize in advance for my ignorance, since it is my first time using this website.

Welcome, Sriram! What did you find when you googled this? You need to show an attempt to answer this. (Hover over the down vote arrow.) Some people take offense at this. Isn't this a Q&A site? Yes, but it's an "advanced" Q&A site, so to speak. This requirement is puzzling to many, but it is not personal or meant to make you feel "less than". We do (often gladly) answer even basic questions that show research. Every site has a culture; this is ours. We're not trying to be unwelcoming. Please edit to include what you found. It's a good question, basic for an endocrinologist, but hey... ;-)

@anongoodnurse 8 months late, but still haven't found any good information. The internet is telling me the purpose of the change in hormones (to prepare the endometrium for implantation), but not the actual cause - as in some physiological change in the Graafian follicles, or external stimulus etc. However, there are articles that mention how and why an LH surge occurs and promotes ovulation, but that's not the hormone that I'm interested in.

Sriram, I would love to help you, and will, but you must provide a quote and a link to a relevant article. I googled, "Why does the Corpus Luteum produce more Progesterone than Estrogen?" and got a perfectly good scientific article that discusses all aspects of the corpus luteum high up on the first page.


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The animal with the fastest hair growing rate
we know that human hair usually grows about 1/2 inch a month.
My question is what is the species with the fastest hair growing rate? (including fur for example).

Welcome! What did you find when you googled this? You need to make/show us an attempt to answer this. (Hover over the down vote arrow.) Many people take offense when informed that they need to show their attempt to answer this question first. Isn't this a Q&A site? Yes, but it's an "advanced" Q&A site, so to speak. This requirement is puzzling to many, but it is not personal or meant to make you feel "less than". We do (often gladly) answer even basic questions that show research. Every site has a culture. This is ours; we're not trying to be unwelcoming. Please edit to include what you found.

I'd love to be able to give some info on that topic, unfortunately it's an overlooked field of science. I found that hair growth speed depends on the area of the body and is regulated by cortisol, and that Asians have faster growing hair than Africans.


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Why are drug dosages so high in some mice studies?
On reading through some research on the effects of certain drugs I often come across staggeringly high dosages such as in this paper:

Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A.,
Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits
adult hippocampal neurogenesis in male mice. Pharmacopsychiatry,
43(05), 174-178.

The paper says:

After 2 weeks of acclimatization all
mice received at an age of 12 weeks an identical treatment with
either finasteride (100 mg/kg) or 2-hydroxypropyl-ß-cyclodex-
trin as vehicle [32]. A single daily injection was administered
subcutaneously during 7 consecutive days.

To give context, a standard dosage of Finasteride for androgenic alopecia is 1mg per day orally and 5mg for benign prostatic hyperplasia. The dosage listed in the paper would be equivalent to me taking 7200mg per day via injection.
I see this sometimes in drug research and I imagine this is done to force an effect and see what that effect is. Are they inferring that the effect scales linearly and that the standard dose has 1/7200th the effect?
What is the reasoning behind this approach?

Mice are simply different from humans; they have different metabolism, different lifespan, different body size.
Generally, for a first order approximation, one might scale simply by body weight to account for body size, expressing dose in units of "drug/body weight". Among humans, that can work fairly well, though fails in several cases:

Kids, and especially young children/infants, whose metabolism differs a lot from adults

By sex, since body fat percentages differ on average between men and women

For the obese, especially for drugs that partition differently in different tissues.

It fails for mice, too; most typically the dose per weight to get the same level of effect in mice is much higher than for humans.
An alternative is to adjust based on body surface area, though that isn't something easy to measure, so typically we still express and adjust doses among members of the same species by weight. However, you can use a rough estimate to come up with some constant cross-species conversion factors. Nair and Jacob, 2016 recommend a 12.3X higher dose per weight to adjust for surface area differences between mice and humans (they have a whole table for other species, too).
Ultimately, the appropriateness of any adjustment depends on precisely what drug you're talking about and how exactly that drug is metabolized. Drugs may also have different affinities for target receptors in different species, which may lead to additional conversion factors. These things can only be worked out with specific study.
There can also be experimental reasons. When doing a study for safety, it may be preferable to study doses much higher in animals than expected for use in humans, both because the sample sizes in an animal study are going to be far smaller than the population sizes exposed to a pharmaceutical drug that is approved, and because the tolerance for risk in humans is far lower than the tolerance for risk in the animal study. If you give a drug at 10x or 100x the effective dose and it doesn't cause problems, you can be far more confident going into clinical trials that there isn't a lurking disaster (of course, bad safety results still happen). You may also plan to give the drug to people for years on end; a mouse can't live nearly that long, so a higher dose over a shorter time might help build an understanding of the safety profile, or at least an approximation. It of course isn't quite as simple as giving a drug at 100X the dose for 1/100th the time, but moving in that direction may be preferable to testing a drug in a mouse for only a week that is used in humans for years.
Additionally, when screening drugs for some effect, it may be easier to test a lot of drugs at high doses in small samples, find which ones do something like what you're targeting, and then experiment further with the dose.

One more point that applies to the specific example you gave is that bioavailability can vary depending on how a drug is administered. Generally, IV is the most direct route with the highest bioavailability. For mice, intraperitoneal injections are also used that typically have high bioavailability, since IV injections can be a bit complicated. Oral bioavailability is typically lower, since the drug may be modified to inactive form in the digestive tract, especially in the acidic stomach environment, or through liver metabolism before reaching systemic circulation. Subcutaneous typically has the least bioavailability and slowest systemic uptake. Of course, for drugs that are intended to be modified, the effects of different administration routes can be opposite (for example, a drug that is more potent after liver metabolism, or a drug that reacts with stomach acid to its active form).

Nair, A. B., & Jacob, S. (2016). A simple practice guide for dose conversion between animals and human. Journal of basic and clinical pharmacy, 7(2), 27.


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Where can I find a global life expectancy table?
I've found good information on specific countries and demographics, but I can't seem to find global numbers.  I know that the world life expectancy is around 71.0, but I'm trying to get a percentile breakdown in the form of something like an actuarial life table.

Not surprisingly, the WHO has a lot of data, I think especially interesting for you is this interactive figure, which you can find here:

Other data on this topic can be found on the WHO website here, in the Wikipedia or from the Worldbank.


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What happens to deep sea creatures if they reach the surface?
Since deep sea creatures are adapted to incredibly high pressures, I would assume they would not be able to survive in the low pressure environment of the surface.  What exactly happens physiologically to a deep sea fish if it reaches the surface?  Would cell walls rupture?

What if you opened a door in a spaceship without a spacesuit? and wiki > Space Exposure are related.

It varies depending which creature is considered. The faster they are made to lower the pressure and raise the temperature, the worse the effects are. Some animals have a liver, which can help to counteract toxic effects at lower pressures, and some fish at 2000m have an air bladder, so they explode if they are hauled up.
Deep sea fish sometimes arrive at the surface with their inner organs popped out of their mouth.

They have different lipid types than us, because lipids are packed together differently at high pressures, and lowering the pressure on their lipids can make them malfunction.
Chemicals can act differently at high and low pressures, so a chemical that can be inert at a low pressure, can produce a different reaction at high pressure, producing gas, precipitating into component chemistries. Urea can be toxic at high pressures and fine at low pressures.
Proteins fold and change shape under pressure, so deep sea animals can use different proteins that may chainge their shape and function at lower pressure.
Dolphins can get the bends if they are scared back to the surface by deep sea exploration industries, too fast for their bodies to adapt.
here are some info sources:
http://www.deepseanews.com/2016/03/under-pressure/
https://www.quora.com/Do-deep-sea-animals-experience-decompression-sickness-if-brought-to-the-surface


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What is the global average BMI?
I have been looking for hours trying to find this number, and can't seem to get a straight answer.  I've seen some studies that calculate the change in BMI, but for some reason they don't give you the actual numbers, just the rate of change.  I've also found information for individual countries, but I want the global average, and would prefer not to do a calculation with 196 different sets of data.

The answer might be a little late, but it was published after you asked the question. See the following publication for estimated global BMI averages from 1975 to 2014: http://thelancet.com/journals/lancet/article/PIIS0140-6736(16)30054-X/abstract

World Health Organization data
World Health Organization (WHO) is your friend for this kind of question. You can find loads of data on BMI per country, per region, per sex and even see the individual data points on here on the WHO website. They also have maps and graphs. Have a look!
Graphics from daily.co.uk
Daily.co.ok have an article (there) with some interesting graphics that I am reporting below. Please note that they made a mistake in the header of each graphics, so just look at the bars below the map and not the range indicated above the map.
Here are some countries with...
...the highest BMI:

... average BMI:

... low BMI:

... the lowest BMI:

BBC applet
You might also want to play around with this applet on the BBC website who allows you to compare yourself with the average in your country for your gender  and age and the world wide average for your gender and age. For example, I entered my personal data and it allows me to see that 69% of the world-wide (my age category and gender) population has a lower BMI than me and 64% of the population of the country I am living in (my age category and gender) has a higher BMI than me. This number goes down to 56% when considering the country where I grew up.
Average BMI
I don't think that knowing the world average will tell you much. What is important is to consider variation within countries, comparison between countries and consider age category and gender. The WHO data set indicate the percentage of individuals that is in a given BMI range per country but not the average value from I got so far.

The table is showing population, not BMI.

Oh I just understood how the data works. So apparently, the WHO don't show average per countries but only the fraction of the population in a given BMI range for each country. Thanks for your help

I looked through this data before, but unfortunately it doesn't really give me what I'm looking...I just want a single number on the estimated global average.


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How sterile is working next to a bunsen burner?
When I was still doing lab work, many people would just wear gloves and work next to a bunsen burner because the clean benches were all in use.
This was mostly for plating bacteria like Bacillus subtilis. The equipment had been autoclaved, of course, but is just having the bunsen burner next to you without working in a clean bench really enough to avoid contaminating your plates?

Nice question. Although the upward flow of air does likely reduce the chance of falling something on your plate, I always wondered if it doesn't equally increase the chance of sucking something into it from below :/

For doing bacterial work on an open bench, this is standard "Sterile Technique." The updraft from the heat generated by the Bunsen Burner should create a relatively sterile field with which to work, so long as you aren't breathing directly on your plates.
Also part of sterile technique is to "flame" all of your pipets, agar plates, and the openings of bottles to remove any contaminants from those areas, and also to protect them from getting into sterile mediums. Every time you uncap or cap a media bottle or test tube you are suppose to quickly pass it over the flame. Obviously these days, plastic equipment makes that a little less practical, but it still can be done if you pass quickly and aren't too close to the flame.
Disposable serological pipettes should remain covered until just before use and then the "banana peel" method of removing the wrapper should be used. If the tip touches anything it should be discarded.
The true test of your sterile technique is whether or not you are getting contamination. Some labs that work with recombinant bacteria don't even bother with sterile technique for bacteria work as they are using antibiotic selection, and contamination becomes much less of a concern. That being said, an ounce of prevention is worth a pound of cure, so if you keep your work space clean, and there isn't a risk of fire, i.e. you don't have organic solvents in the area or the stack of lab reports you are supposed to grade spilling over onto your bench, then it doesn't hurt to light up a burner even if you are using selection.
You are also supposed to have cleaned your work space prior to lighting the burner with 70% ethanol, which will rather quickly kill most bacteria on the surface. Wearing gloves and proper glove technique also helps keep contamination to a minimum. Keeping hair tied back and wearing a clean lab coat can also help, though lab coats are usually more for your protection and for the protection of others (not transmitting hazardous materials on your personal clothing) than to prevent contamination.
Most people get the false impression about BSL-2 Laminar flow cabinets or glove boxes are suppose to be sterile and prevent contamination. Their real purpose is to keep things in, not really to keep things out. Laminar flow hoods will keep aerosolized particles within them from getting to you, so long as you keep the hood area fairly clear and do not block vents, but as you pass your hands through the flow, you are bring whatever is on you and has tagged along for the ride into to work field. Glove boxes can maintain a sterile field, so long as it, and everything going into it, other than your samples have been sterilized, and your sample hasn't already been contaminated.

you must work near a lit Bunsen burner when culturing microorganisms because it helps stop your results from getting contaminated because heat sterilises (kills bacteria). Also, the upward flow of air reduces the chance of anything falling onto your plate and contaminating it. this is the best way to get true results if you don't have lots of fancy equipment.


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What are these flowers on Kerguelen?
What are these plants, which resemble short pink sunflowers, in this photograph from Kerguelen island?

This is acaena magellanica which is also called "Buzzy Burr" or "Greater Burnett". See these images for comparision (from here and here):


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How do I identify and then isolate a Gene that codes for a particular observable phenotype
How do I identify and then isolate a Gene that codes for a particular observable phenotype. It is a novel bacteria and I do not know the gene sequence or the protein that it codes for.

This sounds like a homework question. Finish reading the Tour (you haven’t) and read our policy on homework questions. The repost when you can satisfy the criteria for allowable homework questions.

https://en.m.wikipedia.org/wiki/Forward_genetics


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Why are P and T waves curved and not straight (ECG)
The P and T wave are in shape of a curve while the QRS complex is in straight lines.
What is the reason this is happening?

P wave represents atrial depolarization (hence atrial contraction).
Atrial depolarization takes only a split second, therefore its corresponding wave will be smooth and rounded.
Variations from this shape could be consequences of various heart diseases: for example,a spiked P wave is called P pulmonale and suggests right atrial enlargement.
T wave represents ventricular repolarization: a normal T wave looks like an

upright low amplitude broad hump following the QRS complex.

Abnormalities in T wave could be the signs for multiple heart diseases, varying from myocardial ischemia to hyperkalemia.
In particular, peaked T waves suggest an hyperkalemia diagnosis.
T wave abnormalities are well documented here
The QRS complex corresponds to ventricular depolarization, which is faster and more intense than atrial or ventricular repolarization: hence a normal QRS complex is peaked.
In conclusion, P wave and T wave are rounded because these correspond to low-intensity electrical events while the QRS complex is provoked by an intense electrical event.


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Is there any disease in common between human and insects?
I am not asking about disease transferred by insects.
I am wondering is there any disease that commonly make both human and insects sick?

Welcome to Biology.SE! Many human pathogens are transmitted by insect vectors and these pathogens often also have deleterious effects on the insects — are those kind of examples of interest to you? (If so, please [edit] your first line to make this clearer.) Thanks!

@tyersome, Many thanks. I mean only the common pathogens that are very serious on both human and insects eg. making their life paralized, disrupted or cause death.

What research have you done to answer this question yourself?  You can search for insect viruses for starters. A better approach would be to educate yourself on the general features of virus diseases — what determines their host specificity and how they spread. The major differences in this regard between humans and insects should lead you to the most likely answer to your question.  Learn to save your own life.

@David, I searched google and the websites talk about everything but not the thing I want. Do you have any answer to this question? BTW, I am not a biologist but an engineer.

Patience. We have some virus experts here, who I would have expected to answer you. They may be busy saving the world from the coronavirus at the moment, as you can imagine. I’m busy too, but will get back if nobody answers. Why do you ask, anyway?

@David, asking mostly for fun. But, I am curious to know if a human virus from a sick human can kill insects too? Also, I am curious about the similarity of human body and insects when affected by a common virus/bacteria.

Been very, very busy, and had difficulty finding the sources I hoped for, but finally found time to honour my promise.

It is always difficult to prove that something does not happen, so I will restrict myself to saying that I know of no examples and think it unlikely that there will be a common viral or bacterial disease of human and insects.
Viruses are not limited to a single host, but the typical host range of mammalian viruses would not appear to extend to insects, as far as one can tell from the literature — see e.g. the Wikipedia entry on Virus.

Viruses are by far the most abundant biological entities on Earth and they outnumber all the others put together.[134] They infect all types of cellular life including animals, plants, bacteria and fungi.[3] Different types of viruses can infect only a limited range of hosts and many are species-specific. Some, such as smallpox virus for example, can infect only one species—in this case humans,[135] and are said to have a narrow host range. Other viruses, such as rabies virus, can infect different species of mammals and are said to have a broad range.[136] The viruses that infect plants are harmless to animals, and most viruses that infect other animals are harmless to humans.[137]

Likewise for the host range of bacterial pathogens, judging from articles such as an article by Baümler and Fang in the Cold Spring Harbor Perspective on Medicine.
One general molecular reason for expecting a limited host range that would exclude insect/human pathogens relates to the means by which the pathogens enter the host cells. Quoting, for example, from the abstract of an article by JM Casasnova:

To initiate the infective cycle, the viral genome must therefore translocate from the viral particle to the cytoplasm. Via distinct proteins or motifs in their outermost shell, the particles attach initially to specific molecules on the host cell surface. These virus receptors thus mediate penetration of the viral genome inside the cell, where the intracellular infective cycle starts. The presence of these receptors on the cell surface is a principal determinant of virus host tropism.

The membrane proteins that act as receptors generally differ between related members of a species, but mutations can allow the viruses to cross species barriers. However the extreme difference in cellular structure and biochemistry between insects and humans make it unlikely that this could happen, even if the cell type and protein still exist in common. Consider, for example viruses such as Hepatitis A, B and C which infect the human liver. My own favourite insect — Drosophila melanogaster — does not have a liver as such, its functions being served by the insect fat body.
I am less familiar with other aspects of the viral life cycle that relate to physiology (my background is chemical) but these clearly differ and would affect modes of transmission, for example respiratory and sexual.
These latter considerations will also apply to pathogenic bacteria. As an anecdotal conclusion to an imperfect answer, I would mention the bacterial diseases of silkworms that affected the French silk industry in the 18th century. There are several accounts of Louis Pasteur being called in to eradicate the disease but these contain no suggestion that the workers breeding the worms contacted the disease.

Tribute to Pasteur for ‘saving’ the silk industry at Ales, nr. Nîmes, France

Flaviviruses are an important group of virus, including yellow fever, dengue, zika, west nile, japanese encephalitis, tick-borne encephalitis. These viruses spread through the human population via arthropod vectors. The vectors have separate tubes for pulling blood in and injecting saliva; so in order to infect a vertebrate, the virus has to get from the blood meal in the arthropod vector's gut to its salivary glands where it can be injected into the next vertebrate host. This can only be done by infecting and reproducing in the tissues of the 'vector'. They can perhaps be more accurately thought of as a class of arthropod viruses which use a vertebrate vector in some cases:

the wide diversity of flavi-like viruses found in invertebrates, as well as their deep phylogenetic positions, suggests that they may represent the ancestral forms from which the vertebrate-infecting viruses evolved.

from  https://jvi.asm.org/content/90/2/659
For west nile and Japanese encephalitis, humans are a dead-end host, that is, an infected human doesn't produce enough virus for a mosquito to get infected from feeding on them.
As for how sick the arthropods themselves get from these infections, I wasn't able to find much information. West nile gets into the brains of infected mosquitoes, so I would expect significant pathology. However, if the mosquito is incapacitated it cannot bite a second host so there is evolutionary pressure for milder disease.

Few bacteria infect both humans and insects - though not many people care about keeping insects healthy.
Yersinia pestis causes plague in humans (and some other mammals) and in the Oriental rat flea can block the foregut. I don't know how bad that is for the flea, or whether this counts as a disease of insects.
There are some similar genera (groups) of bacteria living in and on both hosts; Clostridium, Lactobacillus, Enterococcus, Staphylococcus, Pseudomonas. The last has species on plants as well.

Though quite a lot of people care about making insects sick, as for instance biological pest controls such as Bacillus thuringiensis: https://en.wikipedia.org/wiki/Bacillus_thuringiensis