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Why do horses recycle their endometrial lining while humans don't?
How does not recycling the endometrial lining of the uterus benefit humans (and other organisms that menstruate), while recycling it is beneficial to horses (and other organisms that undergo estrus cycle)?
So the question linked by user137 gave me some useful points to work from. Bear with me though, because I learned alot of new jargon just by reading it.
Helps immunity:

"forces loose not only the endometrial lining but sperm-borne pathogens contained therein."
"menstruation delivers immune cells to the uterine cavity, triggered by the mechanical pressure exerted via the shedding of endometrial lining."

Energy efficient:

its simply more energy efficient to shed. saving 6 days worth of food per 4 cycles.
for individuals/species with high fecundability shedding of the lining is less useful
larger uterus = increased likelihood of menstrual shedding (from the answer I learned humans have a larger uterus -- relative to body size -- compared with other mammals who don't shed.)

Miscarriage discardation?:
the comment section also had an interesting reason saying that sloughing off the lining regularly helps get rid of dead embryos.
All of this is very useful and interesting but I'm still confused as to why horses don't shed. I would think horses have low fecundability since their awkward bodies would make it hard to mate. And if shedding the lining is more energy conservant, then why don't horses? I want to know why it is evolutionarily better for horses to fully reabsorb, compared to humans?

What do you mean with help?

I don't have the source right now, but human women do reabsorb much of their uterine lining during menstruation. However, there is so much of it, and the duration of menstruation is so short, that it can't all be reabsorbed in time, so it leaks out instead. EDIT: here is a related question that might be more informative.

@JordiZambrino When I say help im assuming its better for human females to do it this way and i'm wondering why.

@user137 thanks but that source doesnt say anything about humans reabsorbing their lining . at least nothing that I could find. it really useful though thankyou

Horses do not undergo menstrual cycle; they have estrus.


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Are heterozygotes always fitter than homozygotes? Can inbreeding be beneficial?
Inbreeding is mostly not very good because when there is a 'disease' in one allele, the other could/would take over the function. But when you have two of the same genes/alleles, do they, or could they have advantages? Can inbreeding be beneficial?

Certainly it is not necessarily the case that having two of the same allele is a bad thing - if there is a "bad" allele then there is a "good" allele. It can be that the heterozygote is equal, better than, or worse than either homozygote. When the heterozygote is fitter than both homozygotes it is called heterosis and, when this is the case, outbreeding/hybridisation is advantageous.
The process of inbreeding can actually improve fitness because it increases the rate at which deleterious mutations (bad mutations) are expressed, and therefore the efficacy of selection. If the population avoids fatal inbreeding depression it can have positive effects. This process of removing deleterious variants by inbreeding is called genetic purging.

A good example of homozygotes being more fit might be Polled Cattle. The allele that makes horns on cattle is actually recessive, so a cow needs two copies to have horns. A cow with horns is better able to defend itself in the wild. It also allows them to outcompete other cattle for food on the farm, and can be a safety issue for the farmer. By breeding bulls to be homozygous for the dominant no-horns allele, you can easily remove horns from a herd and avoid costly, and potentially harmful, surgical horn removal.

The phrasing in quite unclear and I would not be able to comment on it.
In short: yes, hybridization can cause offspring to have either particularly low or particularly high fitness. Hybrid depression refers to cases where hybrids have low fitness while heterosis or hybrid vigour refers to cases where hybrids have a higher fitness than any of the two parent lines.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

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Has a restriction enzyme ever been tagged?
As part of an experiment that I am preparing, it would seem necessary for me to tag a restriction enzyme (HaeIII to be exact) with GFP. I began researching its domains to determine whether to tag the GFP to the N- or C-Terminus, but I was unable to find any previous studies where this restriction enzyme was tagged. As I got asking around, it would seem that no one has ever tagged any restriction enzyme at all.
It appears that this is only the case with restriction enzymes, because I very quickly found several articles where the HaeIII methyltransferase was tagged with GFP.
So, does anyone here know if a restriction enzyme has ever been tagged before? Is there something that I am overlooking that would inhibit the tagging of a restriction enzyme?
Thank you.

I don't see a reason why it should be generally impossible to GFP-tag a restriction enzyme. I suspect, that simply nobody has had the need to do so until now. I suggest you simply try both N- and C- terminal variants simultaneously (including a flexible linker) and test their activity.

Just out of curiosity, why are you tagging a restriction enzyme anyway?

@Thawn, I had the same thoughts. I'll just make both constructs and see which works better. I was just wondering if anyone has ever done it before. Like I said, I found several articles that tagged GFP to the N-terminus of HaeIII methyltransferase, so I was able to make one construct that worked well. I was hoping to do the same with the restriction enzyme, but it's alright, it won't be too much of a hassle to make both.

@MattDMo, just to make sure the cells are transformed properly. Of course, I need to introduce the methyltransferase before the restriction enzyme, so I need both to be tagged with a fluorescent protein to select whichever cells express both. Additionally, we will be observing the concentrations of both the methyltransferase and the restriction enzyme in different parts of the cell, so fluorescent tags are a win win.

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Relationship between lifespan and reproductive age?
I remember reading a while ago that there is a "general rule" in biology between an animals lifespan and when they reach reproductive age.
In other words, an organism that reaches sexual maturity after a short amount of time (for example, less than a year) will have a short lifespan (for example, 2-3 years) and an animal that reaches sexual maturity after a long time (elephant, 10-12 years) will have a much longer lifespan (40-60 years in case of elephant).
Is there a special name for this "law" or "rule"? Are there any major papers/theories supporting it that also attempt to propose why (perhaps from an evolutionary perspective) this trend exists?
Some quick supplemental questions:
1.) Is there also a trend between lifespan and animal size?
2.) Is there also a trend between lifespan and base metabolic rate?
3.) Do the two aforementioned "trends" or "rules" have technical names that I could look up as well?

Don't forget that some species (most notably humans) used to live for a lot less time, therefore we reach sexually maturity early in our lives which is not related to our current lifespan.

Actually, I'm not sure that is completely true. The average lifespan was certainly lower, but there are records of people living to ripe old ages of 80+ in ancient civilizations if they managed to avoid getting sick/being killed. Anyways, I think its fair to leave humans out of this question since we have developed ways of artificially extending our lifespans.

@Nova is right, people tend to mistake "lifespan" for "life expectancy at birth". Lifespan in late palaeolithic was quite high, and in the Roman empire was almost the same as today. Life expectancy at birth, on the other hand, was way lower...

I think the only "general rule" in biology is that there are no "general rules". Take for example the central dogma of molecular biology where it was for a long time believed that RNA could not be reverse transcribed into DNA - until they found retroviruses.

The sort of thing you're talking about would be called a Life History Invariant: a dimensionless ratio between two life history traits $A$ and $B$, such that although the traits themselves vary widely between species, the ratio $\frac{A}{B}$ is relatively constant.
Eric Charnov has written a lot about this, including a book.

One of the invariants which has been suggested is the ratio of age of maturity $\alpha$ to adult lifespan $E$. Charnov claims that it is relatively invariant within taxa, but has a different value for eg. fish vs. mammals vs. birds vs. reptiles.

From Charnov and Berrigan, "Dimensionless Numbers and Life History Evolution: Age of Maturity Versus the Adult Lifespan", Evolutionary Ecology (1990).
(If the ratio $\frac{A}{B}$ is invariant, then plotting $A$ vs. $B$ for different species on a regular graph will give you a straight line passing through the origin. The slope of the line gives you the value of the invariant.
Sometimes, in looking for an invariant researchers will instead graph the quantities on a log-log plot: they then look for whether the curve is a straight line with slope 1 (whose height gives the value of the invariant), with a good fit. This method has been criticized: the fact that some quantities are just about necessarily a fraction of other quantities (eg. you can't really lay an egg bigger than yourself), together with the fact that log-log plots "squish down" variance about the regression, opens the possibility of observing artifactual yesses. I tried to give an intuitive explanation of this criticism in a quora answer. Charnov and company have dismissed it as not applying to the invariants they found, however.)
This invariant is slightly different than the one you describe, in that they deliberately ignore pre-maturity deaths. (If infant mortality were high enough then it would be possible for average lifespan to be less than the age of maturity.) Also, they measure the ratio of pre-maturity lifespan to post-maturity lifespan $(\frac{\alpha}{E})$ instead of the the ratio of pre-maturity lifespan to total lifespan $(\frac{\alpha}{\alpha+E})$. These are just two different ways of talking about the same thing, but the former has an upper bound of 1, while the latter has no upper bound.
Finally, it's important to note that even if a quantity is relatively invariant, it can't be expected to be perfect; you have to decide how much noise you want to allow while still finding an approximate invariant interesting.

There certainly is a general trend of later reproductive age and longer lifespan. This is simply because the organisms need to live at least until their reproductive age to be able to reproduce. However, other than that I think there is no definitive correlation that animals normally live approximately eight times as long as their reproductive age (as your Elephant example seems to suggest). For example, many Insects such as the Mayfly only live until they reproduce and then die quickly (speaking of a "magical first time").
To your supplementary questions:
1) Similar to the above there is a general trend of larger body mass and longer lifespan. This is because a larger body requires longer to grow. Again, beyond this very basic correlation, I would be careful of trying to find rules there as you will find very different lifespans in animals of similar size. Take for example the mole (lifespan 6 years) and the naked mole-rat (31 years).
2) No there is no general correlation between body size and metabolic rate. Metabolic rates vary greatly with habitat, warm blooded/cold blooded animals etc. If you restrict yourself to a certain family of species, such as mammals, you may find a weak correlation. For example, many smaller mammals have a higher metabolic rate, because their larger surface to volume rate requires a fast metabolism to keep their body temperature up. However also here you will find many exceptions (think of hibernation).
To summarize: It is tempting to try to find "general rules" in biology. However, while you will find many trends and correlations, particularly within certain families of species, calling them a rule is dangerous as it may lead people to believe they are generally true which is usually not the case because you will find exceptions everywhere. This is also the reason why you will not find names for such "rules" in reputable scientific literature.

When I say "general rules" I am obviously referring to named observations of trends like Cope's Rule, Von Baer's Law, Allen's Rule, Mendels 'Rules' of Inheritance, Dollo's Law, etc etc.

Most of the laws and rules you are quoting have since been found incomplete, inaccurate or plain wrong.

I can't find a very fine writings/documents to support this or satisfy your question.
I think, it's related somehow. Let's take a sample: (It's not super accurate but you can make a search)
 ------------------------------------------------------------
|  Creature        Lifespan              Reproductive Age    |
 ------------------------------------------------------------
  Butterfly        7 week           Until become a butterfly
     Dog        around 14 yrs            around 9 months
    Human       around 80 yrs            around 10 yrs
   Whale        around 80 yrs             around 8 yrs
  Jellyfish    can be immortal        depends on a situation

The data above is some-kind the "usual" but still it's not the 100% of proof. There are other factors that affects the lifespan and reproductive age relationships like:

Usual/Common ability to produce no. of offspring/s --- Like whales or elephants, they can't produce a ton of offspring in one shot so their lifespan can be longer. Or those cockroaches, they have short lifespan but they can produce a ton of baby roaches in one egg.
Environment Capability --- If one can survive longer in one place, then there's a possibility of late reproduction maturity but when a creature has less of percent of survival in one place then there's a possibility of early production of offsprings. It all depends on the environment.
Lifestyle --- Bad habits and unhealthy foods can shorten ourlives but good habits and healthy foods can help use for longer lives.


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Validity of measurements of respiration in isolated mitochondria
I've recently read a couple of papers on exercise and mitochondria, in which state 4 and state 3 respiration rates and ROS production are assessed in vitro after exercise has been performed (i.e., rat heart mitochondria are isolated).

Question:
Given that it takes 1 hour for the mitochondria to be removed from the animal and isolated, that additional (saturating) substrate is added before respiration parameters are measured, and that the medium is saturated to the ambient oxygen concentration (much higher than in vivo), are this type of experiment valid to assess mitochondrial function in vivo in active animals? Opinions and/or pointers to resources that clarify how useful these measurements are would be helpful.

What type of cells are these mithocondria being extracted from?

Heart tissue in the case of the above, but also skeletal muscle.


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how to quantify toxicity
When going through this link, Table 1, what are the numbers mentioned there? How is one quantifying toxicity?

Usually, toxicity is given in the units of mass of the substance per unit mass of body mass of the organism that will kill 50% of the organisms in a species if those organisms ingest the toxin at that dose (e.g. mg/kg, ng/kg). This measurement is called the median lethal dose, and is often abbreviated as LD50.
In your table, they only provide the mass of the (average) dose of the substance needed to kill the organism listed, as can be seen by the (mg) after the words "Toxic dose". They likely multiplied the LD50 of the toxin by the average mass of the organism to obtain those numbers. Based on Google's estimation that a mouse has an average weight of 0.68 oz (0.019 kg), and on this table of murine LD50 measurements, I calculated that for tetanus toxin, the lethal dose in the average mouse is 3.8x10$^{-8}$ mg, which is basically what your table provides, which supports my guess on how they obtained their numbers.
The other values listed under "Lethal toxicity compared with" appear to be ratios, given by the formula [lethal dose of toxin above]/[lethal dose of toxin on left]. Using Wikipedia's LD50 for Strychnine in mice (2 mg/kg) and the tetanus toxin LD50 from my previous source, I obtain the exact ratio that they do (1x10$^6$). The lack of units makes sense, as ratios are unitless.
Source on LD50

"needed to kill 50% of the organisms of a species tested", what does this mean?

It means that when they were testing the drug on animals, 50% of the animals tested died when given the dose. So, if the LD50 of X is 1 mg/kg in mice when ingested orally, then 50% of mice can be expected to die if they consume 1 mg of X orally for every 1 kg of their own mass.

no  my question is whichever value is the correct value, how can one get that correct value. How is the quantity of the toxin related to the functionality of the host?

@Rishika I am not sure I quite understand your question. If you want to know how LD50 is calculated, the LD50 value is obtained experimentally. If you want to familiarize yourself with the methods used to calculate LD50 values, I would read some articles that report research doing that. Here is an article I found with a quick pubmed search where the LD50 of several compounds was calculated in silkworms: https://www.jstage.jst.go.jp/article/ddt/10/1/10_2016.01025/_pdf. If this does not answer your question, I would encourage you to post it as a new question on stack exchange.

A small note: There are some other measures too such as Maximum Tolerated Dose, Minimum Lethal Dose, therapeutic index etc.

@Rishika How is toxicity experimentally measured is a different question. Your comments are not actually asking for clarifications but asking new questions. Either edit your question to add these aspects or ask another question. Moreover, try reading about LD50/Lethal dose on wikipedia or other online resources instead of simply asking a user to explain it.


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Why does the wavelength in curly hair differ?
Different people and animals have different wavelengths in the curls in their hair. I understand what purposes hair serves in protecting the skin from light and bugs. I am wondering about the eventual physiological consequences of curly vs straight hairs.
Do the curls help in cooling, blocking light or catching wind over flat hair? Does the wavelength in curly hair have intrinsic properties that physically would give an animal advantages in climates where straight hair would not?
I will be happy to accept another answer.

http://physics.stackexchange.com/questions/261308/why-does-the-wave-lenght-in-curly-hair-differ

My hypothesis when the curls are left ungroomed they will form knots. These knots form a barrier that works similar to woven wool. Unlike strait hair the mat of knots (dreadlocks) collect dirt and form denser material that insulates against direct light and mosquitoes better than strait material. The wave length does play a part as well. The smaller the wavelength the tighter the knot. The tightest knots are commonly found in places that have the most sun light per year.
Strait hair tends to keep heat in more and ice builds up less on it.


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Species Identification: Coniferous tree, Italy
I noticed it close to the place where I work, I live in Italy
Could you tell me the complete name of this tree?
Particular of the leaves

To me, it looks like a species of Taxus (Yew), for instance Taxus baccata. This is based on the flat needles, "flat" apparence/growth of the branches and the red berries. It's a bit hard to see what the red things are in your 3rd picture though (berries, shoots, flowers??). It should also have reddish bark where you can easily peal of loose scales. They can become very old (>1000y), have been used for many human purposes (woodcarving, medical purposes, bows), and all parts except for the berries are toxic.
Abies alba might be an alternative (if the red things are flowers), but then the needle underside should be relatively white and they also look to broad, soft and shiny to me.
Some pictures:

(from wikipedia)

(from http://linnaeus.nrm.se/flora/barr/taxa/taxus/taxubac.html)

(from wikipedia, a 1200-year-old tree in Poland)


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Is there a biological explanation for perceived altered cognition whilst on cannabis?
Cannabis has been associated with literature, arts, and culture for centuries. There are a few features of the drugs affect on the human mind that account for this, however it remains illegal in most countries.
In a very tangible way, cannabis causes a few alterations of perception, such as an altered sense of time and this is often exploited by police to see if a potential felon is intoxicated. Other psychoactive alterations that are attributed to a cannabis (AKA marijuana or weed) include a temporary sense of deeper metacognition, depersonalization, & derealization.
Whilst I'm aware that this is probably the result of the active compound THC, it's unclear how is this deeper feeling of cognition achieved from a physiological perspective? What is this process in the brain that changes the perception of reality?
Ideally studies mirroring the recent Cahart-Harris et al., 2016 paper would be ideal (but focused on THC rather than LSD). That paper identified key physiological features that correlated with the feelings of being "high" such as changes in brain blood flow, electrical activity, and network communication patterns.
Note I am not talking about long term IQ alteration, but rather the temporary affect the drug has on the brain's cognition.

I'm not ready to answer a perception-of-reality statement, but endocannabinoids such as anandamide need to be mentioned here.  These escaped notice right up until the 1990s - political motivations led the NIDA to deny permission for mechanistic studies and for a long time preserved the very peculiar notion that cannabis was a psychoactive drug without a specific receptor.  But a search for the terms above will yield much useful biomedical research.

There has only been little research on the neurocognitive and neurophysiological effects of cannabis. There have been introductory neuroimaging studies in mainly non-psychotic populations, which show that cannabis does not affect gross brain anatomy. On the other hand however, it has been proved that cannabis does acutely increase cerebral blood flow (temporarily; in the right hemisphere) on the long run, exposure will cause an overall reduction in cerebral blood flow.
There have been studies with animals where they used an active cannabinol called delta-9-THC to demonstrate enhanced dopaminergic neurotransmission in brain regions which are usually associated and known to be implicated in psychosis.
In humans the delta-9-THC causes psychotic-like states and memory impairments. The effect of a CNS cannabinoid system, on humans is still tested by neuroimaging studies.
The endogenous cannabinoid system is sensitive to contact with exogenous cannabinoids such as the delta-9-THC, which is known to impair memory in humans.
In a further study is was examined what impact chronic cannabis use has on memory-related functions by examination of the subsequent memory effect (SME) of the event-related potential (ERP). The study concluded that comparing the group to the control group that chronic users of cannabis have an altered memory related brain activation in the form of dysfunctional SME production which may also go hand in hand with reduced neural efficiency.
Several investigators studied the acute effects of cannabis specifically on attentional processing. Hart et al. (2001) studied the effects of placebo, light (1.8%), and heavy (3.9%) THC cigarettes in chronic, daily cannabis users and found no significant differences in the accuracy of response to attentional tasks. However, performance on a tracking task, which requires sustained attention, was found to improve significantly after the high dose of THC, relative to the other conditions.
In one study of 37 adults with a history of light cannabis use, acute intoxication with a high dose of THC resulted in significant impairment on a measure of impulsivity (McDonald et al., 2003). Another study (Ramaekers et al., 2006) found similar impairment on a task of inhibition in intoxicated, chronic cannabis users. The results measured where in a timespan from 0-6 hours after consumption.
In another study from 2010, researchers investigated "semantic-priming".

Under the influence of cannabis, users showed increases in both automatic semantic priming and schizotypal symptoms compared with controls. When abstinent, cannabis users exhibited hyper-priming at long SOAs.

References and further reading:

Linszen D, van Amelsvoort T. Cannabis and psychosis: An update on course and biological plausible mechanisms. Curr Opin Psychiatry. 2007;20:116–20
de la Serna E, Mayoral M, Baeza I, Arango C, Andres P, Bombin I, et al. Cognitive functioning in children and adolescents in their first episode of psychosis: Differences between previous cannabis users and nonusers. J Nerv Ment Dis. 2010;198:159–62.
Bossong MG, Niesink RJ. Adolescent brain maturation, the endogenous cannabinoid system and the neurobiology of cannabis-induced schizophrenia. Prog Neurobiol. 2010;92:370–85.
Battisti RA, Roodenrys S, Johnstone SJ, Respondek C, Hermens DF, Solowij N. Chronic use of cannabis and poor neural efficiency in verbal memory ability. Psychopharmacology (Berl) 2010;209:319–30.
Hart CL, van Gorp W, Haney M, Foltin RW, Fischman MW
Neuropsychopharmacology. 2001 Nov; 25(5):757-65.
McDonald J, Schleifer L, Richards JB, de Wit H
Neuropsychopharmacology. 2003 Jul; 28(7):1356-65.
Ramaekers JG, Kauert G, van Ruitenbeek P, Theunissen EL, Schneider E, Moeller MR
Neuropsychopharmacology. 2006 Oct; 31(10):2296-303.
http://druglibrary.org/schaffer/hemp/general/mjeff1.htm

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What can saliva tell about ones health?
I was wondering if I d want to analyze something related to my current health based on my saliva. What could it be?
I mean e.g. by putting a thermometer in your mouth you can know your body temperature and know whether your immune system is eventually fighting some disease. But as you already have that apparatus in your mouth I think it would be usefull to prelevate some saliva (hit two birds withone stone) or other stuff in order to eventually easily investigate ones health.

If there was broadly relevant information about one's health available by sampling saliva, tests would already have been developed. There are some specific assays that can be performed by analyzing saliva, such as looking for the presence of certain pathogens and proteins, but you won't be able to get anywhere near the broad-spectrum indicator of health (or disease) as you would be able to from a carefully-chosen panel of blood tests.

@MattDMo: Sex hormones analysis, for hormonal disorders specific to females and males by saliva tests. Correct?

there do exist tests for that, yes. And I mentioned that some clinical salivary tests exist in my above comment, but the point remains that the broad range of assays available for blood isn't even distantly approached by how many and what kind are available for saliva.

Well, saliva (or the rate of production of saliva in your mouth) can tell you a lot about health, but the information you acquire is extremely general, so it won't really give you an entire health analysis in terms of diseases, sugar levels, body temperature, likewise.
As for what saliva does tell about your health, here is an extract from a source:

"Dr. Stuart Froum, president of the American Academy of Periodontists, says: “If the eye is the window to the soul, the mouth is the window to the body.” Saliva in the mouth is one of the best indicators of health. If something is off, there is a good chance your saliva will change as a direct reflection.
Saliva is produced around the clock and is affected not only by every bite of food you take, but also every other thing you put in your mouth. If you notice your saliva is too stringy or thick, your body might be having a hard time producing saliva. This could be because of the prescription and over-the-counter medication you are taking.
Studies indicate that an imbalance of the ‘stress hormone’ cortisol in saliva points to emotional sensitivity to stressful situations...the measurement of cortisol in saliva is becoming increasingly acceptable as a screening test for hypercortisolism, such as depression, hypertension and diabetes.

Source: http://healthtoday.com/5-things-your-saliva-can-tell-you-about-your-health/
http://www.medicaldaily.com


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Does denaturing proteins lead to loss of epitopes?
I am doing an experiment where I have to do both Immunohistochemistry and SDS-PAGE. I am assuming that the native conformation of the protein is maintained in the IHC. But during the blot, we heat the protein (at least in our lab) at 95oC in mercaptoethanol to denature the protein by breaking the disulphide bonds thereby destroying the tertiary structure.
My question is when we are using the same antibody against the protein in the tissue (intact for IHC) and isolated (denatured for SDS-PAGE) protein, how can it bind both? So, the antibodies bind to the epitope based on the AA sequence or the 3D conformation? Wouldn't there be a lot if cross reactivity if it binds just based on sequence (since you could have the same sequence in many proteins, having the same conformation is much less likely)?

Short Answer - If the same antibody works both for IHC and SDS-PAGE it either means it is monoclonal against a surface linear epitope or a polyclonal antibody.
Long Answer -
Starting off, there are broadly two kinds of antibodies based on the type of the epitopes. The epitope can either be linear or conformational. Here's a couple of pictures that should clarify.

Now coming to the techniques, in IHC although there is little denaturation, one can expect the conformation to be intact. On the other hand, SDS-PAGE requires the protein to be drawn into linear structures so that they can pass through the gel.
When the manufacturer says that the antibody is monoclonal and can be used both for IHC and the blot (manufacturers do mention the compatibility of the antibody with different techniques and species), it is most probably derived against a linear peptide on the surface of the protein. This means that it would work for IHC (since it needs a surface epitope) or SDS-PAGE (which needs a linear one). May you keep in mind that, a surface epitope can either be conformational or linear. Monoclonal Abs are produced by the hybridoma technique.
On the other hand, if the antibody is polyclonal, it is much more likely that this set contains some IgGs that bind linear epitopes and some that bind surface epitopes. Thus a polyclonal antibody is much more likely to work on both SDS PAGE and IHC. It is also somewhat easier to produce, since it is essentially only purified antisera from an animal that was immunized with the antigen of interest.

Many but not all B cell epitopes will be destroyed by denaturing.  Those that are conformational will be destroyed, but there are also many B cell epitopes that are linear, based on amino acid sequence only without strong conformation dependence.
Also, depending on your IHC protocol, there's often a fixation step that involves a certain amount of denaturation, though rarely as drastic as in immunoblotting.  Conversely, some proteins are capable of at least some restoration of native conformation after they bind to your blotting substrate.
Bottom line, it's unpredictable, but it works often enough to make it worth trying.

Thanks! So, does it mean that when the Ab manufacturer says it would work both for the blot and IHC, it is a linear epitope it is binding against?

Probably, though there are also epitopes that are not linear that can make it through denaturation (I've heard; I don't know what happens with those), and as I say IHC often leads to some denaturation and blotting substrates can partially restore conformation.  Another possibility, of course, is that the manufacturer is mistaken.


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If targeting a certain daily water intake, do you have to compensate for beverages that promote diuresis?
Please forgive my ignorance on the topic and I hope this is a "on topic" question here. It was a toss up between this SE and Physical Fitness SE but I want a more scientific answer.

I came at a impasse in a conversation with another fitness enthusiast. They stated that if you are targeting your water intake during the day then drinks with a diuretic effect (tea/coffee) count negatively towards that water intake total.
So, is it true that one should over-compensate if drinking these diuretics? Or does the water content of drinks like coffee and tea balance out or even positively hydrate you?

The notion that tea and coffee are diuretic and don't count in your daily waterbalance, is an urban myth. At most, both are mildly diuretic (if any).
The assumption is based from an old study from 1928 with only three participants. While the small number of participants alone is a good reason to reject the study (it would never get published today) because the findings would lack any statistical power, the design is also questionable. You can find this story in reference 1 if you want to read it.
It is known that large amounts of caffeine indeed have a diuretic effect by increasing the blood flow to the kidneys and inhibiting the reabsorption of sodium. This leads to the outflow of water and an increased production of urine. See reference 2.
However, reference 3 found that this diuretic effect (which is only present at high concentrations of caffeine) diminishes due to tolerance when people regulary drink tea or coffee. They do not see any diuretic effect from normal tea, coffee or caffeinated beverages.
The explanation for this effect is most likely a misinterpretation of our observation. We seem to produce more urine when we drank tea or coffee, but we wrongly compare it to a time when we drunk nothing. If we would compare it with a time, when we drank the same amount of water, the effect (you have to pee more when you drank something) would be the same.
Drinking tea and coffee will therefore help to keep our waterbalance, as would water, juice or softdrinks.
References:

TOLERANCE AND CROSS-TOLERANCE IN THE HUMAN SUBJECT TO THE DIURETIC
EFFECT OF CAFFEINE, THEOBROMINE AND THEOPHYLLINE
Caffeine and the Kidney: What Evidence Right Now?
Caffeine ingestion and fluid balance: a review.


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Bee identification
Can anyone help identify this UK bee? The picture was taken in June 2016.
Doesn't have to be exact, really just want to know if it's a honey bee or a solitary bee.

Thanks.

When was the photo taken (time of year)?

@fileunderwater This week

It's useful info since species and/or sexes (males) can sometimes be eliminated based on flight time. Either way, its not a honey bee but a solitary bee. They have an orange band across the abdomen and they have a pollen basket on their hind tibia (scopa).

And I'm in the North East, if that helps.

BTW, if you'd use facebook the UK Bees, Wasps and Ants group by BWARS(  bees wasps and ants recording society) is focussed on questions like this and holds many experts.

I am sure it’s not a honey bee – the eyes are different. It could be a solitary bee of the genus Colletes. According to Wikipedia, their nests
... are lined with a cellophane-like plastic secretion, a true polyester, earning them the nickname polyester bees.

+1 for introducing me to 'polyester bees' - how have I never heard of these before?

Thanks.  There seems to be a few of them going into my walls.  Any idea if it's something I should be worried about?

You are right this is not a honey bee, but I doubt it to be a Colletes. It lacks the stripes at the abdomen and the abdomen is hairy. I think is is Osmia rufa, see my answer for details.

It is indeed not a honey bee, but I don't think it belonges to the genus Colletes. They have a striped, not hairy body. The bee shown seems to have stripes but these are hair bands. I think this is a Mason bee, Osmia rufa (=bicornis). Osmia rufa is one of the most common bees in Northwestern Europe.
Osmia rufa uses holes to lay eggs with some pollen and then closes the hole, usually with clay or loam, hence the name Mason bee. It is probably looking for nesting space. But they live solitary so every nest will give only a handfull of bees next year. They are completely harmless, will not defend their nest. I have them in my garden a lot. Don't worry but enjoy them!

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Are there available fluids that can be used in place of blood to facilitate oxygen and carbon dioxide exchange during major surgery/trauma?
Are there any available fluid alternatives that can be used instead of blood replacement that adequately exchange oxygen and carbon dioxide?

I'm not sure I follow your question - - - are you asking if another fluid can be used in the airways to help exchange oxygen and carbon dioxide?

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

No sir. I meant are there alternative IV fluid that can help to transport oxygen in the cardiovasular system in cases like major sugery where parallel blood infusion can't  meet up with the rate of blood loss. Thanks


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Can we infect with "bad" genes other organisms?
We know that some organism's DNA stay with human for life (Herpes) and we also can, i think, design such "gene" that can interact with human's DNA-polymerase very intensive.
If we attached this gene to herpes virus and after that it infected human, would our "artificial gene" be produced and replicated by human DNA-polymerase and how it can affect infected human? Is it possible? What are difficulties we can face?

Perhaps you may want to rephrase your question as "can virus mediated lateral gene transfer happen in higher eukaryotes/animals". That would be a good question. Avoid asking open ended questions like "what difficulties can we face".

It is common in biology to use a virus to deliver new genetic information to a cell. Such a virus is called a viral vector. Retroviruses can be used to enable the viral DNA to be incorporated into the cell's genome. Usually viral genes are removed, making the virus unable to replicate once the cell is infected 1. Using viral vectors in vivo to "correct" disease-causing genetic mutations is a commonly studied aspect to gene therapy 2.
For obvious reasons, people for years have been considering how genetic engineering and gene therapy may be used as a bioterrorism weapon, and ways to ensure our safety if it is used as a bioweapon 3.
1 - http://www.ncbi.nlm.nih.gov/books/NBK19423/
2 - https://ghr.nlm.nih.gov/primer/therapy/procedures
3 - http://dujs.dartmouth.edu/2013/03/genetically-engineered-bioweapons-a-new-breed-of-weapons-for-modern-warfare/#.V1hdeJMrKN8


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Taking care of Birds: Unwanted species scaring away a less common one from a birdhouse
Near my house, I have set up a birdhouse, which has become home to a pair of Oriental Magpie Robins. They are not a common species in Delhi, India, and are generally shy of human interaction and avian conflict (territory disputes with other species):
However, the birdhouse is constantly visited by a pair of Common Myna. This bird is notorious for being an invasive species and had chased away a pair of Oriental Magpie Robins in the past.
Is there some way for me to get rid of the Mynas without scaring away the Oriental Magpie Robins? The bird is a real menace and I'm afraid it'll push away the Oriental Magpie Robin and other species of smaller birds that visit my locality. It is already considered an invasive species in Australia and South Africa. I don't want to kill the Myna, and trapping is out of the question as well. I just want to scare it off or restrict access to the birdhouse. Is there some way to make the birdhouse and surrounding area more appealing to the Oriental Magpie Robins?

^Oriental Magpie Robin. The darker one is male, the lighter one is female.

^Myna.
Update: The Mynas seem to be guarding the bird house from a distance, since I have been shooing them away. The Oriental Magpie Robin hasn't showed up since.

The best way to foil Mynas is to use an Anti Myna baffle over the nest box. Since Myna always fly directly into the nest box hole, this baffle prevents that while allowing other species to enter the box.


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What is the transcriptome in layman's term?
I am new to the bioinformatics field and am trying to understand a research paper that includes some terminology without definitions. The term transcriptome in particular is banded around in the literature, but is not clearly defined.
Can someone provide a reference or source to guide me to some learning material where I can get the basics.

Hi, welcome to Biology SE. Can you please clarify and refine your question? I`m not quite sure what you're asking, although I believe you would like to know what Transcription in RNA is.

Doesn't googling "transcriptome", help?

I've given a layman answer. With that information in mind you'll see that this is a big field and without the specific paper you had in mind, answering this question in the most helpful way isn't possible.

I would strongly recommend getting an introductory textbook such as Bruce Alberts' Molecular Biology of the Cell to help you understand all the various terms you are going to come across.

There are three "omic" definitions that might help you.
The DNA is the long term storage of the information. You're probably familiar with this concept, and the study of this type of information is genomics.
One of the major functions of DNA is it's use as the blueprint for the production of proteins. Proteins carry out all sorts of structural and functional roles in the cell. Which proteins are present at a certain times and locations is known as the proteome. This is studied in proteomics.
Inbetween the DNA and the protein is an intermediate step. The DNA is transcribed to RNA, and then the RNA is translated to the protein. During the transcription of DNA to RNA, certain sequences of the DNA are not transcribed to RNA for a variety of reasons. The study of what exactly is transcribed at what time in which locations is transcriptomics.

Also to include RNAs that do not give rise to proteins, DNA also serves as a blueprint for their synthesis.


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Identify this smooth-cocoon worm from Southern India
I couldn't identify which species these worms belong to. I believe they're insect larvae.
They measure approximately 5 to 10 mm in length, and are common in the southern states of India. They carry cocoons, open at both ends, which the worms can wriggle inside and alternate their direction of movement. These cocoons are perfectly smooth except for the openings.
Another post shows something similar, but the cocoon of that worm looks more woven, while this one doesn't.

It's a larva of moth: https://en.m.wikipedia.org/wiki/Phereoeca_uterella . Not exactly this species in the link, because this one is from the Americas.

It will probably be easier to identify the adult. Try to keep this in a jar or something and see what it becomes.

Probably a moth and here is an earlier similar question

i see these all the time and have tried finding information online a few times but never found an answer. this is the only photo i have seen that matches. i'm in eastern india. i really want to know the exact species!

I see them in Pakistan too. I personally call them "dust worm" Because they only exist in places where dust is available and there is no cleanliness for a long time.

This is definitely the larvae of one of a many number of case-bearing moth species. As noted in comments and elsewhere, these case-bearing moths show up fairly frequently on Bio.SE (e.g., see here, here, here, here and here for some examples).
Most of these moths are members of one of two families: Coleophoridae (the case bearing moths) or Tineidae (the fungus moths).
Some of these species even build cases that they carry around with them.
Your specific example is possibly Tinea pellionella (case-bearing clothes moth).
[
T. pellionella has a cosmopolitan distribution and occurs nearly worldwide (Cheema 1956). As the Wikipedia article summarizes, the larva feeds mainly on fibrous keratin (e.g., hair and feathers) as well as carpets, furs, upholstery, and woolen fabrics. The larvae remain inside a case it constructs from debris such as hairs and fibers (e.g., from clothing, upholstery, carpets, etc.).


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Previously frozen papaya seeds sprouted. How will it affect the plants?
I thought about asking this on Gardening SE, but it seems to me as a technical subject which requires biological expertise to answer. This is not something that usually occurs for gardeners, so I don't think anyone there would have experience with it.
A bunch of seeds from a papaya fruit were put in the refrigerator. They were taken straight out of the fruit, along with pieces of pulp, sarcotesta and all.
The seeds ended up below zero. Probably only by a few degrees, at worst. They would have been in that state only for a few hours, at most. However, ice crystals had formed on them, and the pouch had hardened a little bit. I then thawed them. All that happened on May 19.
Well, I decided to plant them, as an experiment. And a few days ago, they started sprouting.

I actually have more seeds from the same fruit, which have not been exposed to below zero temperatures.
Now my question is: If I let these plants become large trees, will they in any way be different from the normal seeds? (Assuming they get equal treatment.)
I thought the seeds would die, so I was surprised when they sprouted. But since this is a tropical plant, could the negative temperatures have damaged their DNA in any way? Or had some other detrimental effect on them? Or can I expect these plants to be exactly like the other group? (Except for individual variations unrelated to the freezing, of course.)

Seeds are generally made in order to stand dry/cold conditions.
I don't see any reason to believe that the DNA got damaged during freezing (that could cause mutation and phenotypic changes). So, if they have germinated, the plants should not be any different from the controls.

How does the "made to withstand cold" part differ between seeds from tropical plants vs those native to colder climates?

The strategy to stand extreme environments is roughly the same, the seeds tend to have very little water inside them. This is an advantage in many situations including low temperature so that ice crystals will not be able to form and destroy the cells. For sure there are differences in the strategies used by tropical plants and alpine plants, but overall they reach the same goal, to make a strong and long lasting seed.

Have a look at this Wikipedia's article to get some more info about it. https://en.wikipedia.org/wiki/Seed_dormancy


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Can a chicken really be hatched outside of the egg?
This YouTube video (screenshots attached) claims to show Japanese schoolchildren breaking an egg into a kind of clingfilm "hammock in a cup", and then growing and hatching a chick from it in an incubator.
Is this really real?
My first immediate thought is, "If this can happen, why don't the eggs in my cupboard at home sometimes hatch? Why do I never see an embryo in my frying pan?"
Obviously the egg has to be fertilised, but depending upon where you get your eggs (like an "organic home farm" or something) this might happen.
If it's more a matter of temperature, how warm do the eggs have to be? For how long? (ie, Could a warm kitchen cupboard in a hot summer do it?)
What other biological requirements are there to make this work?

It is perfectly clear what the question is, and it is not a subjective answer. I'm not sure why this question was flagged for closure. @WYSIWYG's answer covers it comprehensively.

The eggs have to be kept warm for the embryo to develop. They're removed from the nesting boxes as soon as they're laid so the embryo never has a chance to develop.

Yes it is real, in the sense that this protocol has been through a peer reviewed journal.
Note that the embryo is developing outside the shell, not outside the egg. It is the fertilized egg that develops into the embryo. The shell only provides protection and allows exchange of gases. You can replace the shell with any other material that does the same job. Embryos of non-placental animals can grow in a petridish as well. Someone seems to have done this back in the 1980s (Scadding, 1981).
You can see a video along with the detailed protocol of this process in this article published in the Journal of Visual Experimentation.

Why do I never see an embryo in my frying pan?

Because it has probably become an omelette.

how warm do the eggs have to be?

37-39oC is the ideal temperature and usually hen eggs hatch in 21 days (common poultry facts). However, the incubation time can depend on other factors (including temperature) such as humidity and air composition.

At first glance, this seems like it might be a good way to monitor embryonic development in the chicken, since you could see the whole process in real time. But you point out that this was probably done in the 80s. Any thought on why it never caught on?

@user137 I don't have a great knowledge of history of embryology but as far as I know chick embryo was a model system for embryology since long ago (and for quite some time). So I guess people would have actually used this technique. Possibly people started working on other model organisms later on.


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How does DNA organise a cell's physical position within a body?
How do cells "know" where they are supposed to be in relation to other cells, in forming the physical shape of the body?
If you have ever tried to organise or choreograph the physical positions of a group of people on a field, for example for a dance or display, or even just to stand on stage at a graduation, you will know it takes a bit of communication and working out between the people, and the choreographer (who could be considered a kind of "central intelligence")
Analogy: If you give each person on the field a simple diagram or map (DNA) which shows where the final positions should be, they may or may not be successful, but they would definitely have to talk: "You stand here; I'll be next to you; Jo you need to turn a bit; etc, etc..."
How do cells do this, given than cells could attach and clump in any direction? Especially, how do cells coordinate with other cells quite distant? (Given how small cells are in relation to the shapes & structures of the body)
For example, in my diagram here, 4 cells are forming a specific shape (let's say they're building the corner of an ear or something.) Does cell A "know" where cell C or cell D is?

Please, I'm not after specific chemicals names or in-depth mechanics of cell physiology. I'm after a layman's description or a general principle that is at work.
Bonus related concept: Why/how does the body build a bone of such exact shape the first time around (in the womb) but when you break that bone later, the body seems to just slap bone material around all over, like a bad plasterer?
I've appended a list below of articles I've read (or attempted to read) to try to answer my question.

https://www.reddit.com/r/askscience/comments/3ln201/how_do_cells_know_where_they_are_in_the_body/
http://www.newswise.com/articles/how-do-cells-know-what-to-do-and-when-to-do-it
http://www.thenakedscientists.com/HTML/interviews/interview/1000544/
https://www.sciencedaily.com/releases/2014/10/141027085032.htm
https://www.ucsf.edu/news/2014/05/124831/how-do-our-cells-know-where-they%E2%80%99re-going

I think this might help.

I found this related question after I posted. http://biology.stackexchange.com/questions/21881/how-does-an-embryo-know-where-to-grow-limbs-etc

Does that post answer your question or you have some confusion?

Still reading it ...  :)

OK, so I get that my map analogy is flawed. DNA is not a map, it's directions on "how to get there." But still in my diagram, all 4 cells have exact copies of these instructions. How does cell A get to execute different instructions to cell B or C ?

Stewart, read about Hox genes. @another'Homosapien' Quora is an abomination!! :D

Its related to transcription factors. Transcription factors are important to determine which genes are switched on in cell A and switched off in cell B. There is a complex mechanism behind why cell A has transcription factor while cell B doesn't.

@another'Homosapien' Thanks! You've given me a specific terminology which I've never heard of before, which I can look into. That's a very definite starting point!

@WYSIWYG yeah but since there were references in its answer, so I thought it would be useful ;) BTW OP wants layman answer, so hox genes would be a bit difficult to them :P


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Does prokaryotic transcription have activators / enhancer regions involved?
I am designing a biosensor, and I need to know whether prokaryotic transcription involves or can involve (if a gene needs to be regulated) enhancer regions. Also, where are enhancer regions located (how far away from the promotor), and when isolating a promotor region, how do you make sure you are also isolating these enhancer regions?

This question is too broad. Prokaryotic also have enhancers and repressors, of different kinds, their distance from the promoter may vary a lot. If you can list a particular gene you are interested in then I can have a look. In general, however, the right choice of promoter is often enough for a biosensor.

I am deriving the promotor from a silver resistance mechanism found on plasmid pMG101. The SilE is transcriptionally controlled by enhancers known as silS and silR (they are sensor / enhancer responder units). What I need is this promotor with neighbouring enhancer regions. I am not sure how to do this....

Good, you should edit your question then.

You can find the sequence of the plasmid, with all the detailed coding regions, here: http://www.ncbi.nlm.nih.gov/nuccore/AF067954 . Once you have the sequence you should design a pair of PCR primers to take out what you need.

Dang it, primer design. Thanks for your help!


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Partial pressure of gases in the alveoli
The atmosphere has a partial pressure of oxygen of 160mm Hg, but in the alveoli it is 105mm Hg. The partial pressure of carbon dioxide in the atmosphere is 0.3mm Hg, but 40mm Hg in the alveoli.
How are these difference maintained, and what is the mechanism behind it?

There are two main reasons for the pO2 in the alveolar air being lower than the atmospheric pO2. First, the diffusion of CO2 from the blood lowers the alveolar pO2. Secondly, there is a lot of water vapor inside the lungs, and all this vapor lowers the alveolar pO2 as well.
This is the equation:
PaO2 = FiO2(Patm - PH2O) - PaCO2[FiO2 + (1-FiO2) / R]

Source: https://en.wikipedia.org/wiki/Alveolar_gas_equation

Many different factors contribute to this difference being maintained. These include long, thin airways, big lungs, and homeostatic mechanisms.
The alveolar air in the lungs is connected to the outside air by long, thin tubes (the trachea is about 11 cm long). Because of this, there is almost no diffusion between the outside air and the alveolar air. To fill our lungs with fresh atmospheric air and get rid of stale, alveolar air, we need to breathe.
Breathing creates pressure gradients between the alveoli and the atmosphere. During inhalation, fresh air from the atmosphere is "pulled" into the lungs. During exhalation, stale air from the alveoli is pushed out of the lungs. If we are not active, each breath pumps only a small amount of air in and out of the lungs. The average volume of a breath (inhalation or exhalation) is about 500 milliliters. 150 milliliters of air get "stuck" in the airways during inhalation and are exhaled into the atmosphere during the next exhalation. Likewise, 150 milliliters of air get "stuck" in the airways during exhalation and are inhaled into the alveoli during the next inhalation. Only 350 milliliters of fresh air are inhaled into the alveoli in each breath, and only 350 milliliters of stale air are exhaled into the atmosphere. Since the lungs are big (about 2.5 liters), pumping 350 milliliters of fresh air in and 350 milliliters of stale air out doesn't make much of a difference to the overall composition of the alveolar air.*
Homeostatic mechanisms in the body try to keep the partial pressure of carbon dioxide in the blood at about 5% of atmospheric pressure. If our carbon dioxide levels change and chemoreceptors detect the change, the respiratory center in the brain alters our breathing rate and depth to bring carbon dioxide levels back to normal.  For example, we usually generate about 250 ml of carbon dioxide every minute, which corresponds to 17 ml every four seconds (the duration of a breath.) The homeostatic mechanisms make us breathe about 500 ml of air in every breath so that every exhalation contains 17 ml of carbon dioxide from 350 ml of alveolar air. This keeps the ratio at 5%. Homeostatic mechanisms also increase respiratory rate and volume during exercise.
*During exercise, however, the alveolar air composition changes rapidly due to large and fast breaths.


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Use of western blotting
I ran across this paper recently.
http://www.ncbi.nlm.nih.gov/pubmed/21151122
I am confused on their use of Western blotting. Their unmodified protein (no PTM group) has a band and their modified protein (succinylation of Lys) has no band, yet they use this as evidence of successful identification of the PTM. Can anyone see what they are doing here?

They are doing a peptide competition assay (see abcam protocol).
The antibody is incubated with a purified sample of the antigen and used in a normal Western-Blot of cell lysates. Any cross-reactivities of the antibody would still be visible as only the interaction with the epitope of interest is blocked. So all bands that disappear after such treatment are indicators for the substance that was used for blocking. A Western-Blot with non-blocked antibody is normally used for comparison.
In the experiment you mentioned, they vary the principle a bit, as they are comparing two blots - one blocked with a succinylated library, one with a non-succinylated one. As the band disappears after treatment with the succinylated library, they confirm that their antibody is specific against succinylated proteins - at least in these three cases.

So the the succinylated library blocks the binding of the antibody?

Right! And only the succinylated one, as the antibody does not recognise the Lys as such as you can see in the blocking with the non-succinylated library

Why do it in the negative this way? Why not have an antibody that recognizes SucLys and then show that it's positive for the PTM and negative for the unmodified?

Or do such antibodies not readily exist?

I think its just an experimental problem: They have three proteins that contain SucLys and they have those libraries as they are commercially available. For a comparison as you propose, they would need a SucLys and a Lys version of their protein that would have to be (reliably) created beforehand.

I see, that makes sense, but wouldn't you also need to test against all other PTMs here...or was that the point of the final part of your post...you can only prove that it isn't the other PTM if the band doesn't disappear? (So many negatives I get confused : ) )

You are right, they only show that the AB does not recognize unmodified peptides, but succinylated ones. There is no information on the reactivity towards other PTMs in this experiments. But it may be hard to show this, as you would need whole cell lysate without any SucLys.


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Why does azithromycin not affect human mitochondria?
Drugs like tetracyclines, macrolides and aminoglycosides bind to prokaryotic ribosomes. It is interesting that our body too having mitochondria, which have prokaryotic ribosomes, there is little(?) effect seen. It can not be ruled out that the effect may be lesser due to them being organelles. Azithromycin's effect on parasites like Toxoplasma and Plasmodium is due to its effect on the plastid that these Apicomplexans have (Castro-Filice et al. 2014).

Azithromycin is a macrolide, but it also inhibits bacterial protein synthesis. I'm not sure if its effects are studied but aminoglycosides like streptomycin are known to cause mitochondrial toxicity.  The overall toxicity would depend on the pharmacokinetics. I did look up some articles that do say that azithromycin has an effect on Toxoplasma. Added a reference for you. As per the reference, azithromycin seems to be acting via many different mechanisms. It seems macrolides in general, have different pharmacological effects.

those drugs target the bacterial ribosomes, but not human ribosomes. Even though the mitochondria have 'bacterial' DNA-origins, I'm fairly certain that they don't express bacterial ribosomes. The genes the originate from the mitochondrion are transcribed to RNA and then translated by eukaryotic (i.e. human) ribosomes

@Vance L Albaugh, human cells have two kinds of ribosomes: those in the cytosol which translate nuclear mRNAs and those in the mitochondria which translate mitochondrial mRNAs.  The latter are derived from the bacterium which became the mitochondrion.

the ribosomes of bacteria are NOT the same as the ribosomes of the mitochondria, even though mitochondrial ribosomes have a distant prokaryotic ancestor - which is why drugs like tetracyclines (etc) that target bacterial ribosomes do not effect human mitochondrial ribosomes...Here is a link to a open access manuscript that discusses the differences in human, bacterial and mitochondrial ribosomes... http://onlinelibrary.wiley.com/doi/10.1080/15216540310001626610/abstract;jsessionid=28D286AFDEAEC35928908AAACDFFFB31.f02t03

There are two general points that should be appreciated in relation to this question:

Your statement that mitochondria “have prokaryotic ribosomes” is a misleading simplification. Although mitochondria and plastids are thought to be derived from eubacteria — and their ribosomes have some similarities  in antibiotic sensitivity — the structures of their large rRNAs differ (as indeed do those of their small rRNAs and their ribosomal proteins). This is important because the large rRNA (the equivalent of 23S rRNA in E.coli) is the target of many antibiotics, including the macrolide antibiotics, of which azithromycin is a member.
Experiments in vitro have shown that human mitochondrial ribosomes are not sensitive to some of the macrolide antibiotics that inhibit eubacterial ribosomes, whereas those of some lower eukaryotes are.

Therefore it should not be particularly surprising that macrolide antibiotics do not affect human mitochondria, or that they do affect Toxiplasma etc., the ribosomes in the apicoplasts of which are sensitive to these antibiotics in vitro — presumably because of their rRNA structure in the specific target region.
An answer to the question in your title would seem to require an explanation of the molecular basis of these different sensitivities. It is thought (although not, I gather, definitely proved) that this is the identity of the base at the position equivalent to 2058 of E.coli 23S rRNA: those ribosomes that are sensitive to the antibiotics have the base A in that position, whereas those that are resistant have the base G.
References
Böttger, E.C. et al.(2001) EMBO Reports vol 21, pp. 318–323. Structural basis for selectivity and toxicity of ribosomal antibiotics.
Greber, B.J. et al.(2014) Nature vol 515, pp. 283–286. The complete structure of the large subunit of the mammalian mitochondrial ribosome.

The endosymbiotic theory states that eukaryotic mitochondria were once freely-living bacteria that somehow migrated into the cell and began a symbiotic relationship.
However, just because the mitochondria within human cells have prokaryotic origins, these are distant relationships that are exceedingly old. The ribosomes of current day bacteria (on which some classes of antibiotics target) are NOT the same as the ribosomes of the mitochondria. The structures and physical properties of the mitochondrial ribosomes, as well as many of the genes within the mitochondrial DNA are significantly different than their previous prokaryotic ancestors. Here is a link to a open access manuscript that discusses some of the differences in human, bacterial and mitochondrial ribosomes.

but still, how does it explain azithro targeting apicoplast ribosomes in human mitochondria? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085955/


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How likely is it that a person's progeny has an inheritable disorder based on this pedigree?
Case study:
A person (let's just call him "John") had 3 aunts that died back in the 1950's in early childhood due to an unknown form of neuromuscular disorder. One died at birth, one at 2 years and one at 3 years. John's father was the only surviving descendent of John's grandparents. John and his brother do not show any symptoms. John's brother has a daughter who shows no symptoms. John has two sons, one does not show any symptoms and his other son is a 4 month old who is exhibiting signs of some sort of neuromuscular problem.
John has provided me with a pedigree that he believes is correct (note, the ones with the blue square are the ones that exhibit the symptoms):

I took a bit of genetics in university, but basically I am just trying to understand the genetics here. These are my assumptions. Please correct me if any are wrong:

Since the disorder appears to prevent developing past childhood it must be autosomal recessive because everyone who exhibits symptoms is not be able to reproduce due to their early death.
Both of John's grandparents must have been carriers.
The probability of John's dad and any aunts and uncles having the disorder is 25%, and the probability of being a carrier is 50%. The 3 aunts who died must have just lucked out.
John, his dad, and his wife must all be carriers of the disorder.

However I really feel like I'm wrong about these assumptions since the math really doesn't add up. The likelihood that so many carriers for a relatively rare disorder all coming together and the fact that 3 of the 4 offspring of the grandparents died with only a 25% chance all seems improbable.
It could be that John's son doesn't have the disorder and what he has is something completely different. What do the geneticists say?

Although your question is actually about genetics (and not personal medical advice), I would still recommend that you remove personal references and make the question as general as possible.

@WYSIWYG Why exactly would you recommend removing personal references?

Things are often not as clearcut as simple mendelian inheritance suggests, and you might be interested in this wiki article on penetrance. It includes a couple of concepts you might need to consider when trying to reconstruct the pedigree.

@Mike I meant you can say that this is a case study in which an aunt of a person is affected.. and so on, instead of "my aunt" and "my son" etc.

@Mike personal medical questions are off-topic on this site, which is why you need to remove any and all personal details from these types of questions.

@fileunderwater Thank you for the information.

@MattDMo I did not realize that it was against the rules. I have removed any references.

The probability of carriers for a genetic disorder mating is higher than you think. Without knowing the specific disorder you're asking about, we can't look up prevalence rates, but as an example, about 1 in 30 caucasians carry an allele for cystic fibrosis. So any two caucasians have about a 0.1% chance of both being carriers.

Please state the condition generally or somehow so we can somehow understand. I do have access to appropriate databases but need to understand about condition. Vascular? Tissue growth? Which genes do you think? Any findings of genes?

@Masi I have a feeling it was spinal muscular atrophy, but I can't be certain.

@Mike Please, put it then Suspected Condition: Muscular atrophy. Differential Conditions: ... [here comes all other possibilities] ..., excluding life-threatening conditions first based on gene tests, imaging, history, ... Please, provide us gene tests if you have them generally. Etc evidences.

@Masi I don't have any of the information you are asking for.

This is a very rough draft about the case, not verified, and should not be used for any medical conditions. Ask your own doctor. It is just for demonstrating some Mathematics and genetic passing generally.
Condition: Muscular atrophy
Differential conditions: TODO
Support: history of genetic passing in -1 and -3 generations
Disease
Muscular atrophy as a condition jumps over a generation. The environment/living of your greatgreatgrandfathers determine your grandfathers future, as a rough estimate.
The disease's common feature is recessive autosomality.
Assumptions

Autosomal recessive disease because everyone who exhibits symptoms is not be able to reproduce due to their early death.
TODO genetic passing
What is the genetic profile? Is there any other autosomal recessive diseases in the gene map?

Proposed probabilities where the random variables $X = disease$ and $Y = carrier$ such that the subscript 0, -1, -2 and -3 is about new children's, John's, parents' and grandparents' status, respectively.
Both of John's grandparents must have been carriers
\begin{equation}
P(Y_{-3}) = 100\%
\end{equation}
The probability of John's dad and any aunts and uncles having the disorder is (TODO think this again with the correct genetic passing)
\begin{equation}
P(X_{-2}) = 25\%
\end{equation}
The probability of being a carrier is for dad, aunts and uncles (TODO think this gain with the appropriate genetic passing)
\begin{equation}
P(Y_{-1}) = 50\%
\end{equation}
Disease as a process

$X \sim P_{i}(\mu, \sigma)$, $i = -3, -1, 1, ...$  where I propose the mean $\mu$ and the variance $\sigma^2$.

To understand this better, we should know how the generation $-5$ lived.
Can you get it?
Assumptions

Assume the events of individual probabilities independent i.e. (-3) events do not affect (-1) events in the series.
...

Test if the two independent statistics $X_{-3}$ and $X_{-1}$ are from the same population.
If you assume it, put it to assumptions.
Probability Density Functions in Generations -3, -1, 1, ...
Probability density function

At $X_{-3}$, the 3 aunts of 4 died. The mean $m = 0.75$ (=3/4).
You cannot use Binomial because sampling is not with replacement, not Poisson because occurrence probability is not less than 10%, ...
...

Conditional probability and Bayes theorem

Consider the conditional probability $P(X | Y)$ that is what is the probability of getting the disease for the generation when given the carriers ...
...

You propose 25% probability for generations series $-3, -1, 1, ...$.
You can test this. Select the statistical significance $\alpha = 0.05\%$. Select the appropriate probability density function or teach neural network to it.
False assumptions

John, his dad, and his wife must all be carriers of the disorder. Why wife should be a carrier?

Literature

Blythe, Peter.  Mathematics for the international student Mathematics HL (Options). Haesa & Harris Publications. I recommend this for beginners.
TI-84 and TI-86 have good manuals about the statistics.
Some publications about teaching a neural network doing some of the genetic analysis.
...

About "why wife should be a carrier?", it seems clear that "Me"'s son must have inherited the disease gen from both parent's. If he hadn't, he wouldn't show the symptoms. Am I missing anything?


text:
Enzymes and Reversibility of Reactions
Richard Feynman mentions in the third chapter of The Feynman Lectures:

So the real system is in the GDP-GTP transformation; in the dark the GTP which has been stored up during the day is used to run the whole cycle around the other way. An enzyme you see, does not care in which direction the reaction goes, for if it did it would violate one of the laws of physics. 1

Which law of physics is Feynman referring to and how would it "caring" violate it?
Chapter 3 Vol. I of The Feynman Lectures, just search for "violate"

I think Feynman is referring to the second law of thermodynamics.
The entire statement is this:

The most important feature of the cycle of Fig. 3–1 is the transformation from GDP to GTP (guanosine-di-phosphate to guanosine-tri-phosphate) because the one substance has much more energy in it than the other. Just as there is a “box” in certain enzymes for carrying hydrogen atoms around, there are special energy-carrying “boxes” which involve the triphosphate group. So, GTP has more energy than GDP and if the cycle is going one way, we are producing molecules which have extra energy and which can go drive some other cycle which requires energy, for example the contraction of muscle. The muscle will not contract unless there is GTP. We can take muscle fiber, put it in water, and add GTP, and the fibers contract, changing GTP to GDP if the right enzymes are present. So the real system is in the GDP-GTP transformation; in the dark the GTP which has been stored up during the day is used to run the whole cycle around the other way. An enzyme, you see, does not care in which direction the reaction goes, for if it did it would violate one of the laws of physics.

Now, there are some mistakes here. For instance, GTP is not used in the muscle contraction but ATP. Perhaps this was not quite known during Feynman's times. Coming to the point, I think what Feynman means is that external work has to be done by the enzyme (that catalyses the GTP-GTP exchange) if it is actually moving the chemical equilibrium towards one side (against what would happen in an uncatalyzed condition). Some enzymes can actually do that (shift equilibria and catalyse one sided reactions), by using energy from ATP hydrolysis or other energetic transformations but since they are performing work by using energy from an external source, they are also not violating the second law.
That's the essence of the second law of thermodynamics: you cannot move heat from a cold reservoir to a hot reservoir unless external work is done. We don't have "heat" here but there concept is the same for chemical energy and reaction rates.

Whilst I think this is a good answer, I don't think Feynman has in mind the second law precisely. See my answer. The reason I say this is that the issues discussed in my answer are a fairly big, well known theme in physics and were being heavily debated in Feynman's time too.

Actually I don't think Feynman is referring to the second law. Although he is wandering some way off topic in this piece, I believe he's referring to the fact that for all fundamental building-block physical theories, such as electromagnetism, quantum mechanics and Newtonian mechanics, any solution to the relevant equations can be reversed in time to find another solution. That is, fundamental physical laws don't know the difference between past to future and future to past time progression: they work in exactly the same way in both cases. The same holds for general relativity although it is less relevant there because people most often tend to think of the spacetime manifold rather than time evolution. So if the enzyme "cared" or "knew" which way the reaction were going, its behavior would tell against at least one of these fundamental theories of physics which are all reversible.
Imagine a glass falling from a table, hitting the floor and shivvering into thousands of shards. That process conforms with all the fundamental physical theories that govern it: the mechanics of motion and the solid state physics that governs how objects stay together as a whole. Now imagine that we could freeze the time evolution, and change the motion state of every glass shard flying off the impact so that its velocity vector were pointed exactly in the opposite direction, before letting the physical process keep going. You would also have to reverse the direction of the wavefronts of all the acoustic waves travelling off into the floor and air as well as the wavefronts of the electromagnetic radiation produced by the impact. We would see all the shards coming together at the impact site, the glass reassembling itself (the edges would line up so that the chemical bonds would all reform) and jumping back onto the table unblemished! This, believe it or not, is a valid solution to all the relevant equations of physics here, just as valid as the one where the glass falls and shatters.
Feynman here is alluding to something in thermodynamics known as Loschmidt's Paradox: the problem of explaining why physical processes seem to have a preferred direction when the underlying laws are time-reversible. The answer is the second law of thermodynamics whose modern accepted explanation seems to be that the universe, somehow, began in an exquisitely low entropy state such that any "random walk" in phase space undergone by a physical system will increase the system's entropy with overwhelming probability. The same would not be true if the universe began in or near a maximum entropy state. This leaves the mystery as to why the universe began in that state; a highly readable account of these ideas is to be found in:
Roger Penrose, "The Road to Reality: A Complete Guide to the Laws of the Universe", Chapter 27 "The Big Bang and its Thermodynamic Legacy"


text:
The human has 46 double chromosomes or simple chromosomes?
What I mean: does the human cell have 46 of these:

or 46 of these:

Thank you in advance.

Are you asking about the actual structure of chromosomes ?

the second one. 23 pairs.

Do you mean single chromosomes in your title?

Your first picture shows a chromosome that has been (1) condensed and (2) undergone DNA replication. During G1 interphase (normal cell activity; not dividing), your chromosomes actually do not look like either of the pictures. They look more like a mass of noodles (called chromatin; look at the image provided below); it is only during prophase (step 1 of mitosis, where the cell undergoes division) that the chromosomes condense into the form you have depicted in picture 1. Now, in G1 interphase, you only have single chromosomes. You have 46 of these, which can be grouped into 23 pairs—23 from your father, and 23 from your mother. Remember they aren’t condensed during this stage.

I have also included a diagram of the cell cycle:

In S interphase, DNA undergoes replication, and each of the 46 chromosomes create a double. This double sticks to the original chromosome at a point called the centromere. So long as the two “chromosomes” are conjoined at the centromere, the two “chromosomes” are considered as one chromosome, consisting of two sister chromatids (each like the “single chromosomes” you had previously). Again, in S interphase, chromosomes are not condensed, and look more like noodles than either one of your pictures.
During prophase, the chromosomes look like picture 1. Picture 2 depicts a sister chromatid during prophase (and metaphase), which is considered a chromosome after anaphase (when the two sister chromatids are separated from their centromere). Remember that when the chromatids are not conjoined at the centromere, they are considered each as their own chromosome.
Thus, the human body always has 46 chromosomes. They are “double chromosomes,” as you call them, during S phase of interphase to the beginning of anaphase of mitosis. They are “single chromosomes” from anaphase of mitosis to the beginning of S phase of interphase. As most cells spend the most time in G1 interphase (normal activity), you can say that most of the time their chromosomes exist as single chromosomes. Again, note that most of the time they don’t look like your pictures, except for the times that I mentioned above.

EDIT: To answer the question in your comment:

If during interphase the DNA is not yet condensed and looks like a mass of noodles, then how can we know that there are 46 chromosomes (single ones in this case)?

During interphase, it is indeed difficult to tell how many chromosomes there are. It is only when they condense that they become visible to the eye and can be observed through a microscope. Chromatin, in its noncondensed form, is considered as euchromatin—that is, true (noodly) chromatin. When it is condensed, it can be referred to as heterochromatin. We can only count the number of chromosomes when they are in heterochromatin form; euchromatin is invisible to us. If we align all the chromosomes present, we will get something called a karyotype. Look below.

(You can see each chromosome in each of the 23 pairs are “double chromosomes.” These chromosomes were likely documented during prophase. Some karyotypes show "single chromosomes," most likely taken during anaphase or early telophase.)
In any case, double or single, we can observe that there are 46 chromosomes at all times. If we see "double chromosomes," we would find 46 chromosomes. If we see “single chromosomes,” we would still find 46 chromosomes. In both cases, we would find 46 centromeres, and ergo, 46 chromosomes.

References

Reece, Jane A., Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, and Robert B. Jackson. "The Cell Cycle." Campbell Biology. 10th ed. Glenview: Pearson, 2014. 232-50. Print.
https://micro.magnet.fsu.edu/cells/nucleus/images/chromatinstructurefigure1.jpg
http://www.everythingmaths.co.za/science/lifesciences/grade-10/03-cell-division/images/d62a6708a4a3942f21e003500ddf9664.png
https://study.com/cimages/multimages/16/karyotype_karyogram.png

Can you please add some citations (even wiki links will work), especially for the images you used?

Thank you! However, I don't quite understand this: If during interphase the    DNA is not yet condensed and looks like a mass of noodles, then how can we know that there are 46 chromosomes(single ones in this case)?

@MattDMo I have redacted my answer.

@Diego I have made an edit to my answer to answer your question.

The first picture you posted represent a pair of chromosomes. The second one represent a single chromosome. Humans have 46 single chromosomes that can be paired in 23 pairs. In this picture, https://en.wikipedia.org/wiki/Chromosome#/media/File:NHGRI_human_male_karyotype.png, you can see the 46 human chromosomes grouped in 23 pairs. Note that the last pair is formed by different chromosomes, X (the long one) and Y, so you are looking at the chromosomes of a male.

Answer: Both are images of chromosomes. Before a cell divides, we have 46 structures of Image 1. After cell division, we have 46 structures of Image 2 in each daughter cell. They are structures of chromosomes at different phases of cell division.
When the human cell is not dividing we have Interphase, during which chromosomes inside the nucleus look like a network of threads, called chromatin.
Cell division takes place in four phases,abbreviated: P-M-A-T

Prophase: during which stage the chromatin condenses and duplicate themselves. each of this is two chromatids attached at the centromere.

Metaphase: the chromosomes align themselves at the equator
Anaphase: The chromosomes are pulled towards the two poles, each at opposite ends of a cell. Each of this is a single chromatid.

Telophase: contractile ring (a cleavage) starts to separate the two daughter cells.

@Bantu Manjunath - I know a term for it . It's called "chromatid". If it simplifies your answer , you can use it.

When a cell isn't dividing , the DNA is decondensed. So, you can't say what type of chromosomes are present in non-dividing human cells.
But just to clarify ; it can be said if a human cell's DNA condenses into chromosome(without replication) , it will look like 46 chromosomes of image 2.
If it condenses after replication,  it will look like 46 chromosomes of image 1.
And to clarify your next doubt of what's a chromosome-
A chromosome is a structure with centromere present in it. It can have many chromatids in it .
For eg- both of your images are a single chromosome.  The 1st image has 2 same chromatids in it and 2nd image has one.
A chromatid refers to a single DNA molecule.


text:
What is an interaction motif with respect to protein sumoylation?
While am reading about protein sumoylation this morning I got stuck on sumo interaction motifs and consensus motif line. I heard the the word motifs for the first time. What does motifs mean in this context and What does canonical Sumo consensus motif ΨKx(D/E) mean also? Would you please elaborate the formula and thanks in advance.

A motif means a pattern. Since nucleotides and proteins have a sequence, they can have some patterns of sub-sequence that may serve some kind of function. For example TATA box in DNA serves as a promoter element. Similarly proteins can have some sequence motifs that can serve as recognition sites for binding partners (amongst other functions). Similarly there can be structural motifs in proteins, network motifs in big networks etc.
In this case the motif is a sequence motif.
From Gareau and Lima (2010):

Many SUMO-modified proteins identified contain an acceptor Lys within a ψKX(D/E) consensus motif, where ψ is a large hydrophobic residue

This motif serves as a recognition site for the SUMO-Ligase.
Here,
K=Lysine
X=Any amino acid
D=Aspartic acid
E=Glutamic acid
From the below figures (Rodriguez et al., 2000), you can observe that ψ can be leucine (L) (original residue in Ran GAP1), isoleucine (I), phenylalanine (F) or valine (V).
I am not sure about the effect of double hydrophobic residues on rate of SUMO conjugation.

@Meti If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.

@WYSIWYG I did not understand what the plus signs mean in the figure. So could you please explain the figures more in detail. Thanks

@Meti It is just an arbitrary symbol to denote affinity; more plus signs means higher affinity. You can have a look at the paper for more details.


text:
doubt with a multiple choice question
Permanent decrease in population would occur due to-
A) Migration B) Natality C) Emigration D) Mortality E) Territoriality .
It's obvious that C) & D) options are possible . But I'm confused about which one is more correct and what is the cause ?
The answer is given : C

please see this post and this post

Emigration is a permanent phenomenon. Mortality, on the other hand, is dependant on various factors such as epidemics, health, life expectancy, etc. A change in these factors leads to a consequent change in the mortality rate. For instance, if an epidemic plaguing a country is eradicated, then the rate of decrease in population would slow down. Hence, it can lead to an increase in population as compared to the population during the epidemic.

Aside the fac that the post is off-topic, It is definitely a poorly phrased question. Is it really the way the exact way the question was phrased? There was not even the term "size" after "population"? Both C and D sounds equally correct.

@ Remi.b : The question was on my MCQ book & i didn't commit any changes as i had doubt with the answer . If you have problem , Do an edit or don't give advices

I don't know if this is just me, but I'd consider this a pretty badly worded question. For models of population dynamics, the rate at which the size of a population changes over time is normally accepted to be the net balance of four fundamental processes: Birth, Immigration, Death, and Emigration ('BIDE'; see for example here). Birth and immigration increase a population, death and emigration decrease it. Unless you exterminate a species then it's going to be pretty difficult to assert that a population decrease from either source is 'permanent' - new individuals are likely to be born into the local population and/or immigrate eventually.
An example that specifically refutes the assertion that 'emigration results in a permanent decline in population size' would be a source-sink metapopulation, in which emigration repeatedly/constantly occurs from the 'source' population but it doesn't permanently decrease in size.
As a lesser quibble, although 'migration' can be taken to refer to temporary movement/resettling, it is pretty common to consider immigration and emigration to each be components of migration.
So I would certainly argue that for the question as asked, 'D' is at least as valid an answer as 'C', but in both cases it is impossible to say a permanent decrease would occur. At the same time, if it was changed to 'could occur', you could make a case that 'A' could be a valid answer (since 'migration' includes emigration).

A and C is more obvious answers.
Mortality and natality are two sides of the same coin there is a balance between them and are dependent on several factors.
Migration is temporary (Wiki: An instance of moving to live in another place for a while), whereas emigration is to permanently move and populate that area.

Through Migration , i tried to mean Immigration

anyways, I feel the question is incomplete.


text:
Why don't animals need filtered water?
Almost 10 years back when I was a kid, we had a picture in our school text of wild buffaloes drinking water from a river - which was visibly muddy. I asked my mother of why we need to drink filtered water when they needn't. The question still persists now!
Do wild animals have better immunity? Has the potency of the human immune system reduced in the course of evolution due to better hygiene (different from hygiene hypothesis?)? Do animals also suffer from infections (like giardiasis which are known to spread by drinking contaminated water) and hence lesser life expectancy (due to lesser hygiene?)?


text:
Why can't we find a broad spectrum antiviral drug to viruses like antibiotics to bacteria?
Antibiotics have a very broad spectrum because they attack the metabolism pathways many bacteria share. For example, penicillin inhibits peptidoglycan synthesis, which is vital for formation of cell wall of gram-positive bacteria, so penicillin can be used to treat gram-positive bacteria infections. Streptomycin inhibits protein synthesis of bacteria. Because all the bacteria need protein synthesis, streptomycin has a very broad spectrum.
Why doesn't such strategy work on viruses? For example, nucleos(t)ide analogues can inhibit the RNA synthesis of RdRp. Most riboviruses (except hepatitis D virus) require a viral RdRp to replicate their genome. But why can't nucleos(t)ide analogues be used as broad spectrum anti-riboviral drugs even we have found very good drugs such as Sovaldi?

One of the main issues with nucleotide analogs is that they can also affect the host replication and transcription (though they have a higher affinity to the viral polymerase), and can therefore have adverse side effects. On the other hand, the broad spectrum anti-bacterial antibiotics specifically affect prokaryotic cellular machinery.
(Note that some antibiotics like streptomycin do affect the host mitochondria and thereby cause toxicity. Ototoxicity and nephrotoxicity are known side effects of streptomycin.)
Nucleotide analogs are actually used as broad spectrum anti-virals: For example, Lamivudine is used for both HBV and HIV, which are different types of viruses.