How does discontinuous distribution provide evidence for evolution? One of the evidences for evolution is bio-geographical evidence.

In it,'discontinuous distribution' is mostly cited as an evidence.

For example,

Alligators are found only in south-eastern US & eastern  China; elephants are found only in Africa & in & around India; lung fishes are found only in South America, Australia, Africa.

Their distribution is discontinuous due to possible changes like continental drift etcetera.

But, I am not understanding how these discontinuous distributions prove evolution.

Can anyone help me explain how they provide evidence for evolution?

There are probably several relevant perspectives. Since you mentioned continental drift, consider a taxon (i.e. species, family, etc.) that evolved when all the continents were joined together to form the supercontinent Pangaea.

If it was a successful species that continued evolving and expanding its range, then we might expect to find its fossils - or maybe even living descendants - on multiple modern continents. In fact, dinosaurs evolved on Pangaea, and their fossils are found on every modern continent.

On the other hand, imagine a taxon that evolved after Pangaea broke up into Laurasia and Gondwanaland. If this taxon evolved in Gondwanaland, then its fossils and descendants will likely occur only on the southern continents. (Gondwanaland broke up into Africa, South America, Australia and Antarctica.)

In fact, you mentioned a good example - lungfish. On closer inspection, lungfish fossils have been discovered in North America, however. So we might guess that lungfish evolved in Pangaea but died out in the northern portion (Laurasia) for some reason.

Elephants belong to the order Proboscidea, and proboscideans were once widespread in Eurasia and North America, and they even ranged into South America for a time. The familiar mammoths and mastodons were apparently exterminated by changing climate and/or human predation. This tells us more about extinction than evolution.

But the fact that proboscidean fossils are found only in the Northern Hemisphere and South America tell us that they evolved in the Northern Hemisphere, spreading into South America only after it was connected to North America.

I'm not sure when proboscideans first evolved, but it was probably long after Pangaea broke up. However, North America and Eurasia have connected and reconnected at various times, making it possible for species to migrate between the two continents. The most famous link is the Bering Land Bridge, which existed during the last "ice age" (Pleistocene).

At any rate, elephants today survive only in the tropics, which, like the sea, are a sort of refuge for "living fossils."

There are a number of taxonomic groups - living and extinct - that are found only in the Northern Hemisphere, only in the Southern Hemisphere, or only on particular continents that are evidence of both evolution and changing environments (including climate change and continental drift).


Under what circumstances does Batesian mimicry evolve? Batesian mimicry is a form of biological resemblance in which a noxious, or dangerous, organism (the model), equipped with a warning system such as conspicuous colouration, is mimicked by a harmless organism (the mimic). An example would be unrelated species such as Myrmarachne plataleoides, the spider, and the weaver ant Oecophylla smaragdina.

Given that evolution is a random process that doesn't have any pre-defined targets the probability of such convergence in evolutionary history should be nearly zero. My argument is that the search space for a 'nearly optimal' Batesian mimic would be too large and hence any search algorithm would be unable to avoid the curse of dimensionality. Even the sampler, which would
need to sample from a wide variety of valid phenotypes in the parameter space would run into serious problems.

The problem of the curse of dimensionality for optimal sampling can be intuitively explained in the following way:

Let's say you have a straight line 100 yards long and you dropped a penny somewhere on it. It wouldn't be too hard to find. You walk along the line and it takes two minutes.
Now let's say you have a square 100 yards on each side and you dropped a penny somewhere on it. It would be pretty hard, like searching across two football fields stuck together. It could take days.
Now a cube 100 yards across. That's like searching a 30-story building the size of a football stadium.
The difficulty of searching through the space gets a lot harder as you have more dimensions.

Here are additional points to clarify what I mean:

My question is whether the Batesian mimic would need to initially be quite similar in morphology to the different species that it's converging to in morphology. In mathematical terms, if the parameter space for the visible morphological features is $(x_1,x_2,...,x_n) \in \mathbb{R}^n$ then convergence is probable if and only if the initial condition lies in a small enough neighborhood of the solution $(q_1,...,q_n)$.

One of the features of the fitness function is that I think there should be exponential payoffs in terms of reproductive success near the solution $\vec{q}$. Further, I think there are probably other very important environmental factors that might lead to such convergence. An arboreal jumping spider of similar size that shares the same environment as leaf-cutter ants is a good example. They would already have similar color among other features in order to blend in the same environment.

While the attempt to consider this in a mathematical framework perhaps isn't so useful, it seems that the biological essence of your question is along the lines of:

  Does a Batesian mimic initially need to be initially quite similar in morphology to the different species which it evolves to mimic?

The answer is no, morphology does not need to be similar, but it does help make mimicry likely. The only requisite to evolution is the presence of heritable genetic information with the potential for change, and this prerequisite is the same for any trait. Selection is not a prerequisite but mimicry is more likely to evolve by adaptive evolution than random evolution. Given that phenotype is often strongly affected by the DNA and that DNA has a potential to mutate, then any distance in phenotypic space can be covered so long as sufficient mutations occur. Sufficient mutations are more likely to occur when

a) the distance in phenotypic space between the two initial species is small (the ancestral form of the mimic species is similar to the species it will mimic)

b) a large amount of time is allowed to elapse (more mutations can occur)

The first of these is simply stating that there are fewer (or less extreme) mutations required to get the species to be perfect mimics. The latter simply states that time allows for a greater number of mutations to occurs, making it more likely that large phenotypic spaces can be bridged.

Consequently, allowing identical time, mutation rates, mutation effect sizes, and selection coefficients, two species that initially look similar are more likely to evolve mimicry than two species that initially look very different, because fewer steps need to be taken for convergence of phenotypes.

This is the same for any trait. One could ask can humans evolve to be ten feet tall, the answer is yes, as long as the genetic variance arises. One could ask can humans evolve to be 20 feet tall, and again the answer is yes. However, the latter is less likely because it requires a greater movement in phenotypic space. More time also makes both results more likely.


Why is there no cure for Dandruff? It looks like a simple problem, affecting almost half of the population at the post-pubertal age and of any gender and ethnicity [wikipedia]. What is so complex about finding a cure? Also, if you know some of the most effective treatments, they're welcome.

For dandruff caused mainly from dry scalp, I imagine that there is a delicate balance between moisturizing the scalp and getting oily hair. In my uninformed opinion, this is what shampoos like Head and Shoulders attempt to do.

Taking a more general look at skin health, growing research suggests that the right compilation of microbiota dictates lots of skin health issues. Just like your bowel has an endless supply of mutualistic bacteria, so does your skin. Disruption to this ecosystem (whether genetic, by way of a pathogen, or environmental) could have various negative effects. Dandruff, I imagine, is one of them. It is unfortunately very difficult to understand what a healthy ecosystem looks like, as every person is different both in genetic and environmental factors. This is part of the reason why other dermatological conditions like acne are difficult to treat.

You may be interested in research done through the Human Microbiome Project. Additionally, this article includes some discussion of the fungi mentioned above in the comments and postulates the role of microbiota in determining their success.


Can living cells be imaged with electron microscopy? According to this article from October 2009, http://news.mit.edu/2009/electron-microscope

  "Electron microscopes are the most powerful type of microscope,
  capable of distinguishing even individual atoms. However, these
  microscopes cannot be used to image living cells because the electrons
  destroy the samples."

  "Now, MIT assistant professor Mehmet Fatih Yanik and his student,
  William Putnam, propose a new scheme that can overcome this limitation
  by using a quantum mechanical measurement technique that allows
  electrons to sense objects remotely. Damage would be avoided because
  the electrons would never actually hit the imaged objects."

Is it possible yet to image living cells with an electron microscope? If not, has there been any advance in this direction?

While it may not be possible yet to image live cells with EM, it is possible to image live animals. For one example, Ishigaki et al. (2012) imaged live ticks (Haemaphysalis flava) with scanning electron microscopy. They could even see the ticks moving their legs inside the microscope for about 1 min after they went in the chamber. The ticks were still alive after they were removed from the vacuum inside the microscope. Half of those exposed to the vacuum and the electron beam died within the next two days, but the rest remained alive for at least two more weeks. Apparently, ticks that were only put inside the vacuum all survived just fine. It was only when they were blasted with the high-energy electron beam that their chances of dying increased.

Live ticks in SEM
Notice that the scale bars in panels B-F should be in $\mu m$, not $mm$

This is not the first study to succeed in imaging live organisms with electron microscopy; that was Pease et al. in 1966. It appears that in some insects the ionizing beam induces the polymerization of "extracellular substances" into a thin (~5 $\mu$m) membrane that acts as a protective "nano-suit" (Takaku et al. 2013). Takaku et al. (2013) could induce the formation of a similarly protective thin membrane by using polysorbate 20, a broadly used surfactant. Artificially inducing the formation of similar "nano-suits" may be a more promising way to image live cells with electron microscopy rather than relying on quantum mechanical measurements. Takaku et al. (2013) even go as far as to speculate that the natural formation of similar "nano-suits" may have acted as a protective shield for prokaryotic extremophiles that could have invaded the earth during early evolution (panspermia hypothesis).

References

 - Ishigaki Y, Nakamura Y, Oikawa Y, Yano Y, Kuwabata S, Nakagawa H, et
   al. (2012). Observation of Live Ticks (Haemaphysalis flava) by
   Scanning Electron Microscopy under High Vacuum Pressure. PLoS ONE
   7(3): e32676. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0032676
 - Pease, R.F.W., Hayes, T.L., Camp, A.S. and Amer, N.M., (1966). Electron microscopy of living insects. Science, 154(3753):
   1185-1186. http://science.sciencemag.org/content/154/3753/1185
 - Takaku Y., Suzuki H., Ohta I., IshiiD., Muranaka Y., Shimomura M., and HariyamaT. (2013). A thin polymer membrane, nano-suit, enhancing
   survival across the continuum between air and high vacuum
   PNAS 110 (19): 7631-7635. 10.1073/pnas.1221341110


What type of flask should I use to culture NTERA2 embryonic cancer stem cells? I'm just starting my MSc research and I am in the process of making a list of equipments/consumables to order. Is there a specific flask in which I can culture NTERA2 (NTERA2/D1) cell line?

I found a protocol by ATCC for NTERM2 cells, and it didn't mention any specific flask, so any cell culture flask would do. Since ATCC is basically a cell culture bank I trust that their protocol is valid.


Which information can be obtained from a list of gene names? Lets say I only have a list of gene names. I know they are up regulated and I know they are related to cancer.

What information can I obtain from having only the names of genes? For example is there any way to find a gene-gene interaction, or anything else? Is it possible to retrieve any information by having only the name of the genes?

I would suggest searching the name in any trusted genetics database such as NCBI's GenBank (http://www.ncbi.nlm.nih.gov/genbank/). You can just Google search it, but it may take a little longer to find useful information that way.

I hope this helps and good luck with your research,

CDB


Mutation in pre-mRNA sequence Has there any mutations been recorded which cause harmful effects due to change in the part of pre-mRNA responsible for proper m-RNA splicing ?

Yes, you can find mutations in the genomic DNA which affect splice acceptor sites. Wikipedia lists the following outcome:

Mutation of a splice site resulting in loss of function of that site.
Results in exposure of a premature stop codon, loss of an exon, or
inclusion of an intron.
Mutation of a splice site reducing specificity. May result in
variation in the splice location, causing insertion or deletion of
amino acids, or most likely, a disruption of the reading frame.
Displacement of a splice site, leading to inclusion or exclusion of
more RNA than expected, resulting in longer or shorter exons.

The article lists two interesting papers:

Lim KH, Ferraris L, Filloux ME, Raphael BJ, Fairbrother WG (2011). "Using positional distribution to identify splicing elements and predict pre-mRNA processing defects in human genes". Proc. Natl. Acad. Sci. U.S.A. 108 (27) 11093–11098.

Ward AJ, Cooper TA (2010). "The pathobiology of splicing". J. Pathol. 220 (2) 152–163.

Both papers are open access.


How can a plant resist glyphosate (Roundup) herbicide? In my area, the most common weeds that strongly resists (N-(phosphonomethyl)glycine) (glyphosate) are the horseweed, or mare's tail, Conyza canadensis, and Canada thistle, Cirsium arvense There are several other weeds with similar resistance. I use the brand Roundup on jobs where a complete kill is necessary. However, I sometimes have to go through again, with glufosinate, to control these weeds. I'd prefer not to, as the glufosinate lingers much longer in the soil.

Glyphosate inhibits an enzyme used in the synthesis of the aromatic amino acids tryptophan, tyrosine,  and phenylalanine. It is taken in by the stomata in the leaves, and is moved throughout the plant to all the points of growth, acting fastest on those plants which are undergoing fastest growth.

I can't seem to find an article on how the weeds mentioned can tolerate this treatment. How do these weeds resist the glyphosate?

I found a paper investigating the mechanism of glyphosate resistance in Conyza canadensis. They used 31P NMR to investigate the fate of the glyphosate in vivo. What they found is that the resistant plants are able to transport glyphosate into the vacuole:

  The following view of horseweed resistance to glyphosate emerges from
  the data presented herein. Glyphosate enters the cytoplasm of both R
  and S plant variants at the same rate. Within hours, however,
  glyphosate begins to occupy the vacuole in the R but not the S
  biotype. The identical pH values of R and S vacuoles speak against the
  possibility of a pH-driven process. This, coupled with the
  preferential movement of glyphosate from the cytosol to the vacuole in
  R tissue but not in S, suggests the presence of a transporter for
  glyphosate either specific to R or at a substantially greater
  concentration in R than in S tissue.

Another paper titled "Two non-target mechanisms are involved in glyphosate-resistant horseweed (Conyza canadensis L. Cronq.) biotypes" found a different mechanism for glyphosate resistance in addition to the sequestration into the vacuole.

  Glyphosate was metabolized faster in the R (C004) biotype than in the
  S biotype. The herbicide disappeared completely from the R (C004)
  biotype by conversion into glyoxylate, sarcosine and
  aminomethylphosphonic acid within 96 HAT.

The resistant plants seem to be able to metabolize glyphosate more effectively.

It is of course not guarenteed that these are the only mechanisms for glyphosate resistance, there are likely more variations.


Molecules responsible for reading amino acid language The molecules responsible for reading the language of amino acids and nucleotides is:

  RNA polymerase enzyme
  mRNA
  tRNA
  DNA

I don't actually understand what "reading amino acid language" means!
Does saying nucleotides refer to those on the DNA molecule? If so then RNA-polymerase is then responsible for synthesizing mRNA molecules which carries the same genetic code of the amino acids; or is it something else?

Clarifying the premise

As mentioned in my comment, the term “amino acid language” doesn’t really make sense as far as I’m concerned. Worse: nothing, to my knowledge, is ever reading an amino acid sequence in living systems.

Yet here we are. The term “amino acid language” itself is definitely used (though, once again, I’ve never heard of anything “reading” this language).

So, to answer the question, let’s define a meaning for the term “amino acid language”:

  The amino acid language is a language written by amino acids. In other words, a set of sequences consisting of amino acids.

The candidates

Now, your question is multiple choice so it’s sufficient to go through all possible choices and see if they fit:

  RNA polymerase enzyme

RNA polymerase reads either DNA (DNA-dependent RNA polymerase) or RNA (RNA-dependent RNA polymerase) and produces RNA. There are no amino acids involved. This is clearly not the right answer.

  mRNA

mRNA is an information-carrying molecule. But it does not “read” anything (at least not in its canonical function). Note that other RNAs are involved in recognising/reading things, but not mRNA. So, not the answer.

  tRNA

tRNAs (transfer RNAs) are RNAs that carry individual amino acids. Each individual tRNA recognises a codon on an mRNA via complementary base pairing and thus “translates” the codon into a specific amino acid by the rules of the genetic code. In the context of this question, it’s fair to say that tRNAs (in combination with other molecules) are writing the amino acid language.

  DNA

DNA, like mRNA, is an information-carrying molecule that does not read anything. Moving on.

The answer

tRNAs do not read amino acids in the conventional meaning of the phrase. But it’s the closest candidate here: not only does it indeed read a language, it translates symbols into amino acids. This is therefore almost certainly the expected answer, unless an acceptable answer is “none of the above”.


Converting unit/mg or unit/ml into ng/ml, or vice-versa I am working with the enzyme Cu/Zn Superoxide (SOD1) and i am quantifying them in ng/ml.
However, most past studies has SOD1 quantified in unit/mg or unit/ml, and i need to compare the SOD1 level of my study with those past studies. Is there a way to standardize these units?

Thank you!

There is no archaism in measuring enzyme amounts in units. Unit definition for SOD and a protocol can be found here (from Sigma): https://www.safcglobal.com/technical-documents/protocols/biology/enzymatic-assay-of-superoxide-dismutase.html :

"One unit will inhibit the rate of reduction of cytochrome c by 50% in a coupled system, using xanthine and xanthine oxidase ..."

I don't think, there is a good way to convert ng's to units, since one measures either mass or enzymatic activity, and the correlation between them is not always consistent. Units should be much more reliable in terms of comparisons with other studies, if you are not considering your enzyme as, e.g., a nutritious substance.


How are T cells transported? T cells are formed in bone marrow and mature in Thymus. How are they transported from bone marrow to thymus ? Through the lymph vessels ?

The progenitor cells of T-cells (they do not develop into T-cells and show their characteristics before reaching the thymus) are mobilized into the bloodstream and enter the thymus from it by crossing the endothelial barrier. The figure shows schematically the development of the precursor cells from hematopoietic stem cells (HSC) and the migration of the precursor cells (it is from the paper linked below):

See this review for the details (if you have problems accessing the article, let me know):

The long road to the thymus: the generation, mobilization, and
circulation of T-cell progenitors in mouse and man.


Can photosynthesis take place if the plant is kept in ice cold water or not? Can photosynthesis take place in a plant even if the plant is kept in ice cold water? I have googled this question, but so far have not found a satisfactory answer.

Biochemically, it appears it can, as some Algae can. The question is then whether there are any real plants who do it.


What concentration of table salt is needed to kill bacteria in sweaty gym clothes? My gym clothes retain an unpleasant musk even after washing them with warm water and detergent. I've experimented with soaking my gym clothes in salty water before washing them. My hypothesis is that the high salt concentration will cause plasmolysis in the cells of the bacteria. It has worked with mixed results; I'm never sure how much salt I should add or how long to soak the clothes.

I've looked for answers but I can only find papers with highly technical results.

(1) Can the odor-causing bacteria be killed with a salt treatment?

(2) If so, what concentration of table salt is needed?

(3) How long does the treatment need to last for plasmolysis to occur?

Short answer
Toxicity of salt depends on contact time. 50 g NaCl per liter kills nearly all bacteria in 2 days. 100 g NaCl/L may do a quite thorough job in 30 minutes.

Background
Body odor is caused by bacteria that feed on the fluids produced by the apocrine glands, mainly present under the arm pits and other areas with abundant hair follicles. Bacteria in the skin feed on the products of the apocrine glands and convert it into odorous compounds. Skin microfauna includes Staphylococcus, Micrococcus, Corynebacterium, Dermabacter and others. As pointed out by others in the comments, treating your cloths against bacterial growth may not be the most efficient approach, as the bacteria are residents of the skin. Nonetheless, the following studies addressed the antimicrobial effects of salt.

A study using the gut bacterium E.coli showed that survival in 5% NaCl (50 g NaCl per liter H2O) was <0.01%. In 2% NaCl survival survival was 8%. The contact time was 48 hours (Carlucci and Pramer, 1958).

Another study examined the effects of salinity on E. coli using a shorter contact time of 30 minutes, and concluded that 10% salinity killed 80% of organisms (Somani et al., 2011).

Sea water, which has a salinity of about 3.5% contains low numbers of bacteria (Carlucci and Pramer, 1958), suggestive of toxic concentrations of NaCl, the major salty constituent in sea water.

Although E. coli has been associated with skin fauna and body odor, I must note that Gram negative gut bacteria as used in the two studies above may not be representative of the mainly Gram positive microfauna found on the skin (Strauss & Kligman, 1956).

References
- Carlucci and Pramer, Am Soc Microbiol (1958)
- Somani et al., J Eng Res Studies (2011): 40-43
- Strauss & Kligman, J Invest Dermatol (1956); 27: 67–71


All or none phenomenon Let's say that the threshold potential of a neuron is +40 mV to make a muscle twitch. Now suppose we have two signals of +20 mV. So, this signal will cause the twitch in muscle because it has reached the threshold potential.

Suppose that we have many signal of +20 mV. Will this cause a lot of twitch, the same twitch or no twitch at all in the muscle? In other words, how will the twitch be greater?

Please be a little simple.

I think you are asking about cooperativity.  In many biological systems the action of many individuals are coupled together such that when an individual is activated, the others are more likely to act as well.

The classic example of cooperativity is hemoglobin a protein which has four sites to bind oxygen (one in each of four protein subunits).  When there is enough oxygen present for a single binding site to bind oxygen, the other three will have an increased affinity for oxygen.  This makes the binding curve relatively steep.  Take a look at the graph.

When one oxygen is bound, three others also become bound. The more individuals in a cooperative system, the sharper the curve becomes until a very small change in a few individuals creates a very large effect very quickly.  "all or nothing" as you say.

Muscle contraction also is cooperative.  In this case there are many individual muscle fibers, both the myosin thick filaments, and the actin thin filaments.  Each fiber consists of chains of interwoven individual proteins.  When a myosin individual protein acts against a thin filament other myosins in that filament and those on other thick filaments that are bound to the same thin filament will react to the change in tension and also be more likely to activate and pull.  This causes the entire muscle to quickly start to contract together.  Most researches feel that all the various other factors contributing to muscle contraction, calcium release and uptake, other proteins that are associated with the thick and thin filaments etc, are cooperative as well.  A search for 'muscle contraction cooperativity' will give many references like these.


What kind of a microscope do I need to see cell organelles? I would like to study cells and looking for a microscope that would allow me to see:

groups of cells
individual cell
cells organelles

I would like to target insects and mammal tissue.
I would be very grateful for info in magnification ranges that I need and maybe some popular models of microscopes.

Is there a difference between digital and non-digital microscopes for that purpose?

groups of cells

A normal light microscope. 4x-20x magnification

  individual cell

Lo resolution: Light microscope with 40x magnification.

High resolution: Confocal microscope with 40-100x magnification.

  cell organelles

Low resolution: Confocal microscope with >=60x magnification.
Note: some organelles are easier to visualize while others are difficult. With confocal you can manage to see almost all of them with low resolution i.e you will be able to detect their location and distribution but wont be able view their fine structure.

To view the structure of organelles you would definitely need an Electron Microscope.

  Is there a difference between digital and non-digital microscopes for that purpose?

If you are not too much into the optics of it then I guess it wont matter. I prefer if it has an analog mode along with a digital mode. Image acquisition is anyways digital.

Popular models: Leica, Zeiss and Olympus are popular brands. You select the model as per your requirements.


Book recommendation: protocols and recipes handbook for molecular biology / biochemistry I'm a 5th-year PhD student in chemical biology. I've mostly been doing computational work, so my bench skills are rusty. To help me, I'd like a handbook of common techniques -- transformations, ELISA, protein purification, DNA extraction, SDS-PAGE, column chromatography, etc. I'd especially like a collection of recipes for buffers, etc.
I can find some protocols, but it's hard to find ones covering the more basic methods, and I'd like something cohesive. And there's something satisfying about an actual book.
I found these (and browsed through them in an HHMI library once):

https://www.amazon.com/Kathy-Barker/dp/0879697083/
https://www.amazon.com/Lab-Ref-Handbook-Reagents-Reference/dp/1936113791/

But they're pretty out of date! Most of the techniques are still valid, but I know many have been superseded. There are still a lot of radioligand assays (which are now uncommon in most labs).
So, can anyone recommend a book that could help someone relearn basic techniques?

My experience is that techniques are almost most often taught by hands-on, one-on-one training -- you find someone who knows the technique and ask them to show you, but COVID-19 distancing protocols make that nearly impossible. (The good news is that I often have the lab to myself and an underused supply of chemical stocks and reagents.)

I know you are asking for books, but for up-to-date basic overview of how some methods work - I would try websites or YouTube instead of textbooks...
One good website is BiteSizeBio. They have their own section for 'how to articles' and educational webinars. Otherwise I would also try YouTube. If you search in YouTube for basic techniques like 'how does the ELISA method work?' or 'principles behind SDS-PAGE' then you will find a lot of instructional movies. There is also the 'the protein man's blog' for purification of proteins, some analysis but also some DNA things.


How efficient is the human body at metabolizing food? My friend and I were having a discussion over how "efficient" human digestion is. If a human ate a 1000 calorie hamburger, how many of those calories (how much energy) does the body process into usable energy (i.e. fat or other stores). I've heard things like "it's better to workout on an empty stomach because you will burn fat instead of energy from the food you just ate" - so from this I presume that storing energy as fat is less efficient than using the energy from digestion immediately (though in all honesty I'm not sure if that even makes sense.)

So, to summarize: how many calories of food does your body turn into usable calories via digestions? Percentages would be nice.

Bonus question: If the body does not process at 100%, does the FDA take this into account when labeling food products on their calorie content? If my Basal Metabolic Rate is 1800 calories a day, do I need to eat more than that since my body won't process all of the calories into usable energy?

I suspect that what you are actually looking for is the following:

- 1 gram of fat = 9 kcal
- 1 gram of protein = 4 kcal
- 1 gram of sugar = 4 kcal
- 1 gram of alcohol = 7 kcal

Those are general and inexact values. They're just often used to give a rough idea of the amount of energy we get from different types of food.


What is this creature I found on my house? What is this creature and what species is this?

I found this on my balcony.

Well, your question ended up being closed... If I understand it correctly, you simply asked "what is this creature?" and, after that, you asked "what species is this?". That being the case, the question seems to be clear enough to me.

Therefore, let's see:

What is this creature?

It's a caterpillar of a moth from the Genus Orgyia.

What species is this?

The Wikipedia link above lists more than 40 species. Here is, for instance, Orgyia antiqua:

And Orgyia leucostigma:

But my guess is that your specimen is Orgyia australis (specially if you live here down under):

Adding your location will greatly improve the chances of defining the species inside that genus.

Conclusion

That's simply a caterpillar (larva) of a moth from the Genus Orgyia. Narrowing it down to the species depends on you adding more information to the question, specially geographic location.


What protocol does the nervous system use? I just read How does an inhibitory synapse communicate to the cell body of a neuron? and found myself asking this question ... hopefully I'm not asking the same thing

Any body possessed of a nervous system probably has hundreds of neurons. At one end of the neuron is the nervous system, at the other - the organ.

A neuron is connected to several others in the vicinity through it's dendrites.
When a 'signal' (for want of better word) is put on the system bus - how does a neuron know whether it has to act ( contract/relax it's associated muscle/organ ) on the signal, or pass it on ( forward ) after amplification of the signal, if necessary?

Is there something like a chemical protocol to identify the target neuron/group-of-neurons that form the destination?

An analogy to a computer bus can easily mislead you. Neurons do not communicated via a multiplexed "bus" with different targets; rather the complex connectivity of the neurons itself works as a computing device as a whole. The area study for understanding the communication among neurons is called "neural coding".

If you are talking about just the motor and sensory peripheral nerves, they innervate specific targets.


Where do birds and squirrels go to die? This may sound like a silly question, but I have been wondering about this for a while. I live in a suburban neighborhood with a lot of trees. A lot of trees means birds and squirrels. You can hear them all day and cant leave the house without seeing them.

So why dont we see dead birds and squirrels more often? I only really see them after they have been hit by a car.

My first thought was that nature was just really efficient at cleaning them up. Flies, foxes, and maybe birds of prey get to them before I notice. But that would have to be awfully efficient. When I see a dead squirrel in the road it can take weeks for the sun and the flies to remove it entirely. A fox would have trouble getting in to my backyard (lots of trees but it is fenced in), and I rarely ever see a hawk or a falcon in my area.

My second thought was that there may not be as many birds and squirrels as i think. Yes, there are a lot of them, but maybe I am seeing them same ones over and over again? Squirrels dont really travel THAT far from their homes so maybe I just see the same 10 squirrels all of the time, which makes me overestimate their numbers.

There is a store near my house that always has hundreds of pigeons hanging out in the parking lot. They fly up to the power lines and occasionally fly down for what I assume is left over food or trash. Im guessing they arent there at night, but during the day you can always see them. Why wouldnt you see more dead pigeons in an area with so many pigeons? I know they have relatively long lifespans but still, some of them must die of unnatural causes

Does anyone have any idea where they go?

A major cause of squirrel death is predation:

Survival and mortality of the Arizona gray squirrel (Sciurus arizonensis)
Causes of red squirrel (Sciurus vulgaris) mortality in England

You won't see those bodies, for obvious reasons.

Disease, starvation, and harsh weather are other major causes of death. Squirrels dying in these ways are probably likely to die in their nests or otherwise hidden places. Again, no visible bodies.

So that leaves being hit by cars as the major cause of mortality where you'd have a chance of seeing bodies. You've already noted that you do in fact see these bodies, so there's no contradiction there. I'll add that depending on where you live, roadkill can be cleaned up by scavengers more or less quickly -- in areas where buzzards, coyotes, crows, etc are common, they can be cleaned up quickly, but in more urban and/or colder areas they may last longer.


Phylogenetic algorithms: How to interpret multiple ML trees from the same dataset? There's still something that confuses me about how many of these algorithms work, and how results are presented in the literature.

Let's consider a Maximum Likelihood based algorithm like MrBayes or RAxML: Users set a random number seed which generates the starting tree. For many of our datasets, different seeds which result in different ML results, as the algorithms are initialized with different trees.

I'm not entirely sure how one is supposed to interpret this, especially as my experience with ML methods is that the initial step is irrelevant to the global/local min/max in parameter space----the chains just take longer to converge.

How should one interpret these results? Are users to run 1000s of trees at different parameter values, and then chose the most optimal likelihood value? That seems rather ad hoc, as does bootstrapping, etc.

Is the dataset fundamentally flawed?

In short, you have chosen two examples that do not use maximum likelihood as you know it in other contexts. In most statistical contexts, the ML is a single number which can be calculated analytically, so it it always the same for a given data set. This is not the case for either MrBayes or RAxML but for different reasons.

MrBayes

The likelihood criterion in MrBayes is the marginal likelihood of the posterior, given effectively the data conditioned on the priors. This likelihood comes from a stochastic MCMC sampling of the parameter space. If all is well behaved, then the chains and/or runs will converge in the same general location. But then the different possible topologies need to be summarized in some way.

RAxML

RAxML generates essentially random starting trees by random sequence additions to build up trees. The subtrees are then rearranged to find a "best" tree. Again, different starting points may lead to different best trees. But if all goes well, analyses will end up with the same tree. This process is described in this chapter.

In both cases, if you start in a different place, you may end up in a different place. There may be many trees that are, within some criterion, equally likely. If you are familiar with parsimony methods, the analogy is that of multiple equally parsimonious trees.


How are Moluccan cockatoos so loud? They say a Moluccan cockatoo's screech has a decibel level of around 129 or even more (e.g., 135). That is almost as loud as a jet engine (140 dB at 100 feet).

How are they able to emit a screech that loud? Don't they hurt themselves?

I was able to find a reference to the book Good Parrotkeeping by Robin Deutsch (©2009) from a forum post which purports to list several species' call loudness level (sorted by dB):

Nanday conure, 155 dB
Moluccan cockatoo, 135 dB
Mealy amazon, 124 dB
Quaker parrot, 113 dB
Mustached parakeet, 111 dB
Macaw, 105 dB
Mitred conure, 100 dB

I don't have a copy of the book so was not able to check the author's sources. However, I can answer a more general question about how birds are able to make loud noises in general.

Birds have a syrinx instead of a larynx as in mammals. This is situated at the bottom of the trachea, instead of at the top. Given this, birds can take advantage of acoustic resonance, which can allow for some extremely loud calls.

In a 21 Oct 2019 article in the New York Times titled "The Loudest Bird in the World Has a Song Like a Pile Driver" (paywall), the South American white bellbird is said to be the loudest bird in the world at 125 dB. (With the screaming piha now in second place). The study, "Extremely loud mating songs at close range in white bellbirds" was conducted by Dr. Jeffrey Podos and Dr. Mario Cohn-Haft in 2018. Unfortunately, it does not seem to cover the biological mechanics that produce such loud calls, but rather focuses on the evolutionary and sexual pressures that have led to such outliers in avian acoustics.

Edit:

Note that decibels are a measure of acoustic sound pressure, and vary greatly depending on the distance from the source they are measured. In order to be scientifically sound, the loudness of something should be measured from a fixed distance under controlled conditions. Note that the table of examples of sound pressure levels contains a "distance" column, which is extremely important for comparison purposes between sounds. I have no idea whether the parrot measurements were conducted using the same criteria as the white bellbird study (very likely not). Therefore, the higher dB values listed there may be due to measurements with much smaller distances.


Why do bad smells make us vomit? According to my understanding, vomiting happens when the body wants to get rid of something that we have ingested or put in our mouths to get it out of the body.

So why is it that when something smells really bad our bodies make us vomit even if we have not ingested the food, or not even put it in our mouth yet? Is this something psychological?

Thanks!

It is not really making you vomit not directly, it is making you nauseous if you become too nauseous you vomit.(nausea has multiple triggers but for this I will stick to smell) Nausea exist to keep you from eating toxic food and to help you get rid of it if you do, the reflex is a balance between the biological cost of a meal(minimal) and the cost of being poisoned(extreme) so you can see why it might favor vomiting and losing a meal vs not vomiting and dying of poisoning than it would the two costs were not so drastically different.

Now your body can't really tell the difference between a smell coming from inside your mouth and one from outside, they both reach the nose by a roundabout course, and your mouth cannot smell. The closest your instincts can come is assuming a stronger scent is coming from the mouth since it is close and enclosed. That's why a stronger disgusting smell results in a stronger feeling of nausea. the stronger the smell the better the chance it is coming from inside your mouth.

Combine these two concepts and you can see how the stronger the smell and the more disgusting it is the more likely it is to make you nauseous it is the best protection our anatomy allows for. Now of course this is only the the current hypothesis, Nausea is not easy to study nor is it a in high demand for research.

Additional sources


How long can Cholera bacteria survive in a dead host? How long can cholera bacterium survive inside a dead host? Can they remain dormant in such conditions?

BACKGROUND

On a hill not far from where I live, there was a hospital operating since 16th until 19th century, for cholera patients, and a cemetery for those, who didn't make it. It was closed in 1st half of 19th century and until 20th century not even ruins of the hospital remained; the gravestones got lost under a layer of soil.

Currently, the area is being built over. Large amounts of soil are being excavated for foundations and basements of new houses. Rainwater falling on the piles of excavated soil floats down through driveways, backyards and gardens of houses down the hill, including my own.

Should I worry?

No, I don't think so.

Mostly estuaries (brackish water) and marine biofilms on submerged surfaces are a reservoir for Vibrio cholerae. Vibrio cholerae is isolated from rivers, creeks, washes, irrigation ditches, hulls of ships, etc. (Indeed, cholera spread rapidly throughout the world after the 1817 epidemic, largely due to the inadvertent transport of contaminated bilge water, mainly from British ships.)

  Transmission is by the fecal–oral route. Infections are particularly common after ingesting contaminated water or food. Cases are occasionally seen in people who have eaten raw or undercooked shellfish, particularly oysters, from contaminated waters. V. cholerae is excreted in the feces and vomitus. Viable organisms can be found in feces for up to 50 days, on glass for up to a month, on coins for a week, in soil or dust for up to 16 days and on fingertips for 1 to 2 hours. Bacteria survive well in water and may remain viable in shellfish, algae or plankton in coastal regions.

In 1855, a wave of cholera hit London. Thousands became ill and died before John Snow identified the Broad Street water pump as the single point source of that outbreak. Today, patrons of the John Snow Pub (built on the site) can enjoy local ale, and more importantly, a glass of crystal clear, pathogen-free water.

  V. cholerae [is] an autochthonous aquatic bacterium rather than a human pathogen that is a transient resident of the aquatic environment. V. cholerae has over 200 serogroups, with O1 and O139 being the causative agents of cholera, due to their carriage of the genes encoding cholera toxin (CT) and the toxin co-regulated pilus. ...[A]ssociations with the human host is only one small aspect of the V. cholerae life cycle and is not necessary for environmental persistence. ...[T]his bacterium is a cosmopolitan aquatic species that is capable of causing illness in humans.

Vibrio cholerae attachment is mediated by pili, which promote surface attachment and subsequent biofilm formation. It is rather difficult to believe that an aquatic biofilm was preserved on the hill for all those years, even in a dormant stage.

  ...they could transform into a unique dormant stage that was able to survive for months in the sediment of the estuary. ...These exciting new data enabled investigators to now integrate information regarding the seasonal nature of events surrounding an outbreak in populations living near estuaries.

I have found nowhere that the dormant stage can occur outside of water.

Environmental reservoirs and mechanisms of persistence of Vibrio cholerae

Medical Ecology Main Page

Cholera

 Something goofy going on with these, sorry.


If you suspended your DNA like a rope in its 6ft full length, could you feel it if you waved your hand through it? Maybe a silly question but I was wondering about this.  Trying to understand how small things are.

I have read that the DNA in a single cell if stretched out, would be about 6 feet long.

If you actually stretched it out and had something hold it - so that it was n a vertical line from about 6 ft to the floor, and then

would it cast a visible shadow?
if you waved your hand through it, would you be able to feel it?

Research on tactile detection has found humans can detect wrinkles in a surface on a nanoscale. One could argue that we may be able to feel a strand of DNA.

However, this research found only wrinkles of 10 nm were detectable. Therefore it is unlikely we would detect a DNA strand by simply touching it, considering DNA has a radius of one nanometer radius (10 ångströms).

We still may feel a pull of the strand depending on the tensile strength and bond strength but I'm not sure how those values relate to human perception.


How does being afraid or nervous affect mental performance? It's known that when somebody is not relaxed (nervous,worried....) , they can't concentrate , what exactly in being nervous is the problem?

I will try using logic, but that might only just get you on a lead:

Concentration means being focused on a specific task.
Consciously, you want to focus on a specific task, but there are other process that may want to claim ressources and that you cannot repress.
Anxiety, but also fear or worriness are symptoms that basically translate an unconscious (or conscious) proccess that requires your attention.
Therefore, two concurrent psychological process require focus from your conscious mind. Ergo, you cannot concentrate on either on them. Usually, the emotional part will win since it involves brain structure (such as the amygdala) that are specialized in shunting more evolved brain structures. That is when you are afraid of something, it is very hard to repress that feeling with logical thinking.
In psychoanalysis, Freud introduced something called as "The pleasure principle" (I hope that's a good translation). This principle is one of the few basic principles that rule human behavior. Now, anxiety is an indicator of displeasure. Your mind will try its best to settle that issue before settling anything else. That is why usually you cannot isolate anxiety.

Here's an example:
You hate spiders. You need to measure the surface of an old mannor. You've seen some spider webs. Odds are you will have much trouble to concentrate on measuring any room's surface, because one task your brain will perform for you is checking in every corner whether a spider can be seen, so you'll be able to identify a potential threath as soon as possible and react appropriatly (usually, get the hell out of there if you're really affraid of spiders.

Here's another example that doesn't use fear:
Your girlfriend texted you before an exam, and she said "We need to talk". Since you are emotionnaly bound to your girlfriend, you might get anxious: what does she want to talk about ? Your mind will begin scanning for every possibility, emphasizing on the worse ones (the ones that will disturb the "Pleasure principle" the most for instance). Now that you identified that she might break up with you, this thought will just keep popping up, even if you manage to think for a minute about the exam you should be thinking about right now.

Fact is this is a matter of autoconservation for your psychee. A breakup will certainly harm you more than a failed exam. Your brain is very smart about processing important stuff before, and any attempt from your conscious mind to shunt this will most probably fail.

By the way, there is a psychology stackoverflow. I guess you should have posted this question there.

Hope this helped !


How do other primates treat their fingernails? Do all primates have to trim their fingernails in some way, or do some primates' fingernails wear off through natural use?

Also, is constant nail growth common to all primates?

Both. Many primates bite their nails. Some do not. It's not species specific.

Chimpanzees, for example, usually bite their nails; some prefer to leave them alone. They do grow continuously, and nails not kept trimmed probably break off (looking at the thickness of those nails, I get the impression that this might be rather painful if they break too short.)

The caption for the picture below (taken from a chimpanzee sanctuary) states

  Annie likes to pick Missy’s nose. Missy tolerates it but doesn’t seem to enjoy it. I don’t blame her – Annie doesn’t bite her nails down like the other chimps do.

They bite their toenails as well.


What do the qualifiers used in botanical species names mean? These are all the qualifiers I've come across so far. The first 3 were quite easy to google, but the other 4 have me stumped.

I also can't say I'm completely clear on the nuances of s.s. vs. s.l..

agg.
s.s.
s.l.
cf.
cv.
auct.
ined.

agg. means aggregate and is used when species have been grouped together.

s.s. stands for sensu stricto and is used for a strict or narrow usage of definition.

s.l. stands for sensu lato and is used for a wide or broad usage of definition. these two pop up a lot in paleontology since species definition can be vague.

cf. stands for "conferre" and is used for provisional names when an organism is not completely known, such as when a variant is found and they are not sure which species to place it in.

cv. stands for cultivar and is usually followed by the unitalicized name of the cultivar.

auct. means "of author" and means the name is used in a different way than it is currently or in a different way than the paper using it does, such as quoting a incorrect name from another author or a debate between two possible usages. (used a lot with overturned or contested names) it is often followed by a qualifier giving more information about usage.

ined. means undescribed, and is used for a new proposed species before it has been formally described (common in paleontology when many papers about the same new specimen may be released at the same conference or where a specimen might not be identified yet still yield useful information in other ways.)

if you put the exact form of the epithet (include the period) followed by the word "species" in google it will usually return the usage, failing that you can search this site.


Are all enzymes proteins? So throughout my education and research career I have been taught that all enzymes are proteins. This makes sense when you consider enzyme denaturing and folding/shape etc. However, I was recently told by a biology professor that in fact, not all enzymes are proteins -- and he alluded to the RNA world hypothesis and rRNA's.

Could someone explain further how exactly an rRNA (or similar) could be (or not be) considered an enzyme, and whether or not all enzymes are proteins etc?

Thank you!

Until the late 1980's all enzymes* were believed to be proteins, and were often defined as protein catalysts, often in textbooks which are often not perfect representations of science. At that point every macromolecular biological catalyst known was a protein so they thought all macromolecular catalysts were proteins. But the discovery of ribozymes (RNA strands that act as catalysts) changed that. The discovery that one of the most well known enzymes ribosomes had their functional components made of RNA and not protein also played a factor.

NOW enzymes are generally defined as macromolecular biological catalysts and include ribozymes. But older works or outdated textbooks will still refer to enzymes as only proteins but newer works will not. Don't feel despondent I was taught the same thing initially, and it persisted for a several years in college. Part of this is each successive step in education tends to lag behind and/or get over simplified in scientific knowledge. Textbook manufacturers are not overly concerned with poor phrasing or outdated definitions and are rarely writtten by scientists.

*in its object form, originally and for quite a long time enzyme referred to the process not the agent responsible becasue the agent was unknown.


How do individual plants adapt to changes in temperature? If you grow a plant from seed in your nice warm house, then plant it out in your temperate garden, it will stop growing for a while, possibly die, and if not, subsequently resume growth. Standard gardening practice is to 'harden off' plants, moving them to an area of intermediate temperature for a while before planting them out.

Why does this happen? What is the difference between a plant adapted to a warm environment and one adapted to a cold environment?

Expression of cold-tolerance genes? Levels of some secondary metabolite? Thickness of cell walls? Density of root hairs?

An unidentified author on the Royal Horticultural Society website states that
"The effect of hardening off is to thicken and alter the plant's leaf structure and increase leaf waxiness", which is not quite detailed enough to satisfy.

As far as I know, the main challenges the plants have to face in cold environment are metabolism reduction and membrane fluidity. If the temperature is even lower, they may face freezing.

Increasing the metabolism is quite hard, because plants usually are unable to increase their temperature by its own. Plant may produce more pigments in order to absorb more sunlight; grow trichomes and other structures that may generate an air layer which acts as an insulator or simply reduce its metabolism by, for instance, hibernation. The amount of stomata is also related to temperature, and a plant growing in low temperature needs less stomata.

In bacteria sometimes there exist isoforms of many enzymes that are expressed during different conditions, and since plants usually have large genomes with tons of duplications, it's reasonable that some plants may express different genes for the same processes in high and in low temperature. One group of genes that are certainly expressed in cold exposition are membrane desaturases, which introduce unsaturation in the lipids, increasing the fluidity of the membranes. Some plants also protect themselves of freezing by accumulation of some substances, such as glycerol or proline, avoiding the formation of ice inside the cells.


How do cellular conditions change the Gibbs free energy of a reaction? How do cellular conditions change the Gibbs free energy of a reaction?
Taking glycolysis as an example, how exactly would cellular conditions affect the free energy released from this reaction?

To understand that, you must have a basic understanding of Gibbs-Helmholtz equation. it states-
$\Delta G'=\Delta G^{'o} +RT\,ln\,(Q) $
Here, $\Delta G'$ = biochemical free energy change & $\Delta G^{'o}$ = standard biochemical free energy change.
Suppose you have a reaction,
$x+FADH_2\rightleftharpoons xH_2+FAD $
So, $Q=\dfrac{[xH_2][FAD]}{[x][FADH_2]}$
Now let's assume that $\Delta G^{'o}>0$.
Hence the spontaneity of the aforesaid reaction (in forward direction) will be dependent on the $\Delta G^{'o}$, which is a function of reaction quotient (Q) as well as temperature (T).
Now, if the body is in lower energy state, i.e. fasting; $\dfrac{[FAD]}{[FADH_2]}$ ratio will be high. So, in order to make $\Delta G'<0$, the following condition must be satisfied $-$
$RT\,ln\,(Q)+\Delta G^{'o}<0$,
or, $RT\,ln\,(Q)< -\Delta G^{'o}$
or, $RT\,ln \dfrac{[xH_2][FAD]}{[x][FADH_2]}\,< -\Delta G^{'o}$
With this reasoning, be it any metabolic pathway; we can predict its spontaneity.


Difference between going against and going down a concentration gradient The difference between facilitated diffusion and active transport is that facilitated distribution occurs down a concentration gradient and active transport occurs against a concentration gradient. I understand that, as a result of these differences, active transport uses ATP so that it can bind to the carrier protein, however I don't know what is meant by going against a concentration gradient or down a concentration gradient.

In short, I would like to know the difference between going against and down a concentration gradient. A definition of what a concentration gradient is might clarify things a little further as well, since the definition I have doesn't help much.

"Concentration" is "how much stuff is there someplace?" "Concentration gradient" is "how much is concentration changing from point A to point B?"

Imagine a terrain where concentration is represented by height.

"Down" a concentration gradient means from high concentration to low concentration - this is the direction things would move via simple diffusion.

"Up" or "against" a concentration gradient means from low concentration to high concentration. Moving in this direction requires some sort of energy input, such as active transport using ATP, or an electrical gradient, or something else.


How it is possible that blood group shows that a person is not the son or daughter of their parents? I see a family in which it has only one daughter. The blood group of the mother is AB positive and the father is B positive, but the blood group of the daughter is O negative.

When she was young, they apply to shift abroad permanently. When the Embassy test their blood group, the doctor said "She is not your daughter because of her blood group".

How is it possible? Why is she not the daughter of their parents?

Each person has two alleles for the blood type. The two A and B alleles are dominant. So, you don't need A/A to end up with blood type A, it could also be A/O. Having both A and B results in blood type AB. Having none of these, results in blood type O.

Following these rules, from parents being AB and B (genetically either B/B or B/O) you would expect these possible blood types for their children:
- A/B
- A/O
- B/B
- B/O

The Rh factor (positive or negative) is inherited similarly. The positive allele is dominant, so genetically +/+ or +/- would be positive, only -/- is negative.

There is a rare case of a "cis AB" mutation, where the A and B antigens are in just one allele (wiki, paper). Then the genetic alleles of an AB type could be AB (in one allele) and O.
The children of the couple could then be
- AB/B
- AB/O
- B/O
- O/O

So, there would be two possibilities for the case you describe.

The parents are not the biological parents of the child.
The mother is cisAB/O +/- and the father B/O -/-

edit: or a third way would be of course some de novo mutation in the child, resulting in the loss of A/B from the mother

edit2: maybe to answer your actual question "How can a child not be the child of its parents?".. adoption, in-vitro fertilization with donated eggs and/or sperm from other people, mix-up in the hospital..


Do spermatozoa have mitochondria This is something that I have heard/read so many different contradictory claims about over the years.

In high school I was taught that sperm cells have a lot of mitochondria because they need a lot of energy quickly. This made sense to my adolescent mind.

When I was an undergrad, my one microbiology lecturer swore up, down and sideways that they did not have mitochondria. She never gave any reason or evidence, but I had gotten used to the idea that high school info was often out of date and, sometimes, completely incorrect, so I let it slide.

Then I was reading an article for a paper several years back and it said that, not only did sperm cells have mitochondria, but they did not lose them all. That in fact, some were preserved and engaged in genetic recombination with the mitochondria belonging to the ovum (the maternal ones). This contradicts another rule that so many treat as certain, which is that while nuclear DNA is 50% from each parent, mitochondrial DNA is exclusively maternal.

To sum up: Do spermatozoa contain mitochondria or not? And if so, is the recombination I described above likely?

The midpiece has a central filamentous core with many mitochondria spiralled around it, used for ATP production for the journey through the female cervix, uterus and uterine tubes. This is a good article explaining more about this topic: http://genetics.thetech.org/ask-a-geneticist/mtdna-comes-only-mom


Is there nutrient absorption in the large intestine of hindgut fermenters? In hindgut fermenters, plants are digested in the caecum by microbes. I want to know whether hindgut fermenters can absorb the nutrients obtained from the digestion in the large intestine because the absorption of digested materials is not the main function of the large intestine in other animals. I know some hindgut fermenters reingest the materials created in the caecum, but I think not all hindgut fermenters perform this behavior. I want to know the main site of absorption after the caecum.

I have divided this answer into a section on horse and rabbit. While there are many other hindgut fermenters, these species are good illustrations of  different ways hindgut fermenters can digest and absorb nutrients from their food.

Horse

As you know, absorption of "nutrients" occurs along the intestines, but at varying degrees at different sites. Most compounds are primary absorbed in the small intestine of the horse. This includes protein, glucose (soluble carbohydrates), fats, calcium, and magnesium.

Any carbohydrates that are not absorbed in the small intestine reach the hind gut. Here they are fermented by bacteria to short-chain volatile fatty acids  (VFAs) and lactic acid. Horses can use the VFAs (propionate, butyrate, and acetate) as an energy source, but a diet too high in grain can also lead to excessive lactic acid production in the hindgut, and as a result the horse may experience colic.  As your question pertains to the hind gut, a nutrient of main concern is therefore volatile fatty acids.

The hindgut of the horse is very long and developed. To review with the anatomy of the horse hindgut, it consists of the caecum, ventral colon, dorsal colon, transverse colon, descending colon (or small colon), and rectum.

In a study in 1974, RA Argenzio et al. determined that among the parts of the horse hindgut, most VFAs were produced and absorbed in the ventral colon, 8-12 hours after feeding. This is depicted by the graph below, which shows a large negative net production of VFAs after 8-12 hours (i.e. more VFAs absorbed than produced). Note that the caecum and dorsal colon are also important sites of VFA production and absorption.

The hindgut is also an important site for phosphorus absorption in the horse, unlike many other species that primarily absorb phosphorus in the small intestine. This is thought to be because most of the dietary phosphorus in the horse in phytin phosphate, which must be exposed to the enzyme phytase produced by the microbial flora in order to be absorbed. Studies such as Schryver et al. (1972) and T. Matsui et al. (1999) have shown that most phosphorus is excreted by the small intestine and caecum, and most is absorbed in the dorsal colon and small colon. The figure below from Schryver shows the net absorption of phosphorus on the various experimental diets. Note that this is oriented opposite to the VFA figure above; absorption is positive rather than negative on this graph.

Rabbit

To begin with the rabbit anatomy, you will note that the colon of the rabbit is much less developed than that of the horse. However, both are hindgut fermenters, and what they do have in common is a very large caecum.

As in the horse, much of the digestion and absorption of nutrients occurs in the small intestine. This includes protein, fats, and simple carbohydrates (glucose), as well as some vitamins.

Also like the horse, the digestable material not absorbed by the small intestine passes to the caecum, where it undergoes fermentation by the microbial flora. The large fibrous material passes directly to the colon, where water is absorbed and forms hard faecal pellets, while the small digestible material passes through reverse peristalsis into the caecum. What is different in a rabbit to a horse, however, is that the about 8 hours after feeding, the caecal material is packaged into a small pellet called a caecotrophe. As or shortly after the caecotrophe is excreted, the rabbit re-ingests the caecotrophe. As this food has been digested once already, the small intestine is better able to absorb nutrients from it.

As an example, important nutrients that are able to be absorbed due to caecotrophy in the rabbit are the B vitamins such as niacin, riboflavin, folate, and cobalamin (vitamin B12). One of the early studies on this topic is Kulwich et al. (1953).

Summary

The reason for the difference between the horse and rabbit is fundamentally an anatomical difference. Both species have a large caecum which enables fermentation of plant matter. However, the horse has a long, voluminous colon in which it can absorb many nutrients, but they will lose protein and other nutrients in this process because the colon is less adapted to absorb them. In coprophagic (rat) or caecotrophic species (rabbit), they do not have as long a colon, but can absorb vitamins and proteins lost in the faeces during the second pass through the gastrointestinal tract.

An excellent and very detailed review of the gastrointestinal tracts and nutrient absorption in a variety of species is this freely accesible paper by Stevens and Hume, "Contributions of Microbes in Vertebrate Gastrointestinal Tract to Production and Conservation of Nutrients."

References

Argenzio, R.A., Southworth, M., and Stevens, C.E. (1974) Sites of organic acid production and absorption in the equine gastrointestinal tract. Am. J. Physiol. 226:1043-1050.

Bugaut, M. (1987) Occurence, absorption and metabolism of short chain fatty acids in the digestive tract of mammals. Comp. Biochem. Physiol. 86B(3):439-472.

Hornincke H., and Bjornhag, G. (1980) Coprophagy and related strategies for digesta utilization. In Digestive Physiology and Metabolism in Ruminants, 707-730. Avi Publishing, Westport, CT.

Kulwich, R., Struglia, L. and Pearson, P.B. (1953) The effect of coprophagy on the excretion of B vitamins by the rabbit. J. Nutr. 49:639-645.

Matsui, T., Murakami, Y., Yano, H., et al. (1999) Phytate and phosphorus movements in the digestive tract of horses. Equine Vet. J. Suppl. 30:505-7.

Schryver, H.F., Hintz, H.F., Craig, P.H., Hougue, D.E. and Lowe, J.E. (1972) Site of phosphorus absorption from the intestine of the horse. J. Nutr. 102: 143-148.

Stevens, C.E., and Hume, I.D. (1998) Contributions of Microbes in Vertebrate Gastrointestinal Tract to Production and Conservation of Nutrients. Physiological Reviews, 78(2):393-427.


What is a pA(2) value? I saw this article http://www.ncbi.nlm.nih.gov/pubmed/16710314 and it mentioned pA(2) values and I had no idea what they were. What are they? What do they mean?

If possible it'd be just dandy if you could cite some journal articles/books/other reliable sources for me to dig up.

Digging around a bit, I found a few resources:

Design and models for estimating antagonist potency (pA2, Kd and IC50) following the detection of antagonism observed in the presence of intrinsic activity.

and PHARMACODINAMIC on page 30, describes pA2 as:

  indicates affinity of antagonist for receptors

(as Alan Boyd just commented on)


Conjugation in bacteria I was studying about conjugation in bacteria, I have a doubt. In conjugation F- cell transforms into F+ cell when there is a formation of sex pilli in between the two. The doubt is if the F- cells convert into F+ cells how can F- cells form again...?

If all the F- cells convert into F+ can we expect F- cells to form again?

Within a bacterial cell exists circular chromosomes, and plasmids. During cellular division, chromosomes are always conserved - passed to both daughter cells.

As you are aware, plasmids can be passed between cells by a form of horizontal gene transfer called conjugation - whereby plasmid DNA is replicated, and passed through a sex-pilli into an adjacent cell.

When a cell divides in to two daughter cells, it is possible that one cell will not receive a plasmid. Thus, the result is one F+ daughter cell, and one F- daughter cell.


What really is color and how do we perceive it? How do our brains actually transform the information that the cones in our eyes  receive into the different colors that we can see and imagine?

Despite its simplicity, this question demands a so complex answer that we can start by saying:

We still don't know.

Because you are talking about the colour as a sensation, as something that I feel and that I (literally) see. And here is the problem: as such, the "colour" is not a physical reality.

Some people may disagree here, but colour is not a physical property of any material. Light is a physical property. The wavelength, the energy, the frequency of light are all physical properties. Even the crazy quantum nature of the photon with its restless existence is a physical property. But not colour. Colours are creations of my mind, my nervous system, my idiosyncratic consciousness.

For instance, It's simply impossible to know if the red that I see in my mind is the same red that you see in your mind. The fact that we both call it "red" or the fact that we both agree that the colour of the blood is the same colour of the wine doesn't help at all: this is a problem of qualia:

http://plato.stanford.edu/entries/qualia/

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

And the same goes for all other conscious experiences derived from the exteroceptors, such as "taste" and "sound". What I feel is particular and nothing can guarantee that another person feels the same, even if the stimuli are the same and the nervous impulse to the CNS are the same.

To finish, I'd like to propose a thought experiment, for you to understand the subjective nature of the colour:

We tend to imagine that the world is the way we see it (as primates, we value the vision very much). But we have only 3 different cones, giving us roughly 1 million (100$^3$) different colours. Reptiles, as the birds, have 4 different cones, and some of those reptiles, as pigeons, have 5 different cones, giving them the ability to "see" 10 billion colours (100$^5$). This is hypothetical, of course, to really perceive all these colours the animal needs a huge brain cortex, but let's suppose that they see (perceive) all these 10 billion colours.

Now try to imagine these 10 billion colours, you, who are an organism that only perceives 1 million colours. It's impossible. And it's impossible for a talking pigeon to explain to you how he/she sees the world, how all these 10 billion colours are, the same way that it's impossible for you to explain to an animal with achromatic vision what is green, purple, orange, cyan, magenta etc...

This is what we call qualia.

But, as someone that loves cognitive ethology and science in general, I don't think that this is something beyond the realm of sciences, something impossible to know... this is a problem that can be scientifically addressed and, with the ingenuity of the neuroscientists and other biologists, we can someday understand the "redness" nature of the red we see.


Why in some cells is GTP made in citric acid cycle and in some ATP? In many  animals GTP is produced in citric acid cycle. While in  plants,bacteria and some animals ATP is produced. Why is this so ? What is the advantage ?

This step is catalyzed by succinyl-CoA synthase which has two different isoforms- one which produces GTP while the other produced ATP.
It seems from this study that predominantly anabolic tissues prefer the GTP-producing form whereas the predominantly catabolic tissues use the ATP-producing from.
In the same paper they discuss that GTP is important for protein synthesis and it is also involved in production of phospho-enolpyruvate by PEP-carboxykinase in mitochondria; therefore playing an important role in anabolic processes.


Why don’t humans have eyes at the back of their heads? How does evolution rule out the possibility of humans or others fragile herbivores from having 2 pairs of eyes, one at the front and the other at the back of their heads? Why didn’t that ever happen?

Vertebrates have ears which sense 360 degrees for a range of many meters, and they have social eyes, where they group many eyes and ears into one social group, it's easier to listen and live in groups, than grow eyes in the back of the head.

2 eyes exists in nearly all bilateral animals, arthropods, flatworms, sea-slugs, crabs, crickets, squids, flies. Arthropods have compound eyes and it would be easier for them to have 4 eyes, and only spiders and horseshoe crabs have more than 2.

It would be easier for a vertebrates to develop 4 nostrils and ears than 4 eyes because they are simpler than the orbs of the eye.

Same reason as 5 fingers has been the optimal numbers for all vertebrates since early lizards. in short, it's very easy to lose extra organs and to modify old ones, but it's very difficult to evolve new organs, and to relocate ones around the nerves and veins... centrally connected organs travel around the body and the circulation moves in front of them, i.e. if you did get 4 eyes and two of them moved to the back and sides, the nerves for your face expressions that are next to your ear would have to go in front, around, and through the moving eye pathways.

To simplify, we stopped evolving our symmetrical archetypes when we were related to starfish, ammonites and ediacaran fauna, and the fastest most versatile animals all had 2 sided symmetries, with entirely symmetrical nervous systems, and forwards moving at that point in time, using binocular compound vision, which did have 180, and that binocular compound vision afterwards became our 2 eyes. We share the kingdom Animalia with starfish, our common ancestor experimented with shape during the Ediacaran era.

To understand the difficulty of adding new eyes later, you should learn why nearly all vertebrates have 5 fingers, except some frogs which have 4. it

google: why do animals all have two eyes?


Source of hydrogen in reduction of oxygen in electron transport? What's the source of hydrogen in the reduction of oxygen to water in metabolism?

Is this implying that half the hydrogen comes from NADH and the other half from lone protons?

The equation you've shown is similar to other cellular respiration equations that I've seen, in that, it is trying to simplify a pretty complex process.

My guess is that you're doing first year cell biology like I am, so you probably know that there is a difference between the pH of the mitochondrial matrix (7.8 - making it alkaline) and the inter membrane space (roughly that of the cytosol - usually about 7). The lower the pH of a solution, the greater the concentration of H+. My point is that the solutions on either side of the inner mitochondrial membrane both have a concentration of H+.

So even though, when NADH is oxidised, it loses a H+ to solution, thereby contributing to the pH of the mitochondrial matrix, what is the likelihood that that particular H+ will be the H+ that is part of the molecule that takes the electrons at the end of the electron transport chain? I think low.

Indirectly, NADH does contribute H+ to the overall pH of the mitochondrial matrix but it doesn't directly give the H+ to "half an oxygen gas molecule".

Check the video below which is from the publisher of the textbook my course uses.

http://www.garlandscience.com/garlandscience_resources/resource_detail.jsf?landing=student&resource_id=9780815344544_CH14_QTM02


What are the survival limitations of alcohol? This question was inspired by watching one of the Pirates of the Caribbean movies; particularly where Jack Sparrow allegedly survives on a desert island by finding an unlimited supply of rum. I've heard alcoholic drinks dehydrate you more than hydrate you, so this seems like an unsustainable strategy.

My question is threefold.

How long can a human survive by drinking hard liquor (40%
alcohol by volume) for their sole water intake (ignoring food)?
If it's unsustainable, what will finally take you down?
If the hard-liquor approach isn't viable, what % alcohol can
keep you hydrated (beer, wine, etc.)?

Related:
1. Question on dehydration studies
2. Question on what dehydrates

I commented above that it will depend heavily on at what pace you drink your rum, but in short, no, no you cannot.  If you do it quickly, you'll die of alcohol poisoning, and if you drink it slowly, you'll probably die of dehydration[1].

io9 summed up some research a few years ago, the majority of which is largely bunk.  One study (ncbi, free pdf) however, from 1996, claimed to find that:

  These results suggest that alcohol has a negligible diuretic effect
  when consumed in dilute solution after a moderate level of
  hypohydration induced by exercise in the heat. There appears to be no
  difference in recovery from dehydration whether the rehydration
  beverage is alcohol free or contains up to 2% alcohol, but drinks
  containing 4% alcohol tend to delay the recovery process.

So stick to (American) beer.

Sidenote: In Belgium, they divide their (truly excellent) beer into two categories: special, which are stronger and often bottled, and thirst-quenching, which have a lower alcohol content and are often had with lunch.

[1]: Citation: Personal experience and the story of Johnny Tarr.


How did mitochondria make energy long ago? I've learned that mitochondria is thought to have been eaten by a larger cell, resulting the mitochondria to be part of a bigger cell. Well, here's my Q. If you look at how mitochondria works, you find that in order to initiate the TCA cycle, you need to have pyruvate acid.

Then does this mean that when mitochondria was all by itself, there were pyruvate acid around it? I mean, isn't pyruvate acid a complex molecule, therefore, cannot be abundant??? How could this be?

Furthermore, if cell A swallowed a mitochondria, then that cell A should provide mitochondria with NADH and pyruvate acid. How could this be? Did ancient cells produce NADH and pyruvate??

You are asking a very interesting question.

As you correctly mention, the substrates of mitochondrial metabolism (TCA or Krebs Cycle) are pyruvate and NADH, and, through oxidative reactions, ATP is produced. Indeed, it seems unrealistic that when the "mitochondria" were by themselves there was pyruvate and NADH in the environment. Let's take a step back.

In the 1970s, Dr. Lynn Margulis proposed the extracellular origin of mitochondria. What does this mean? Margulis suggested that, due to the bacteria-like characteristics of mitochondria (e.g. circular DNA), it is plausible that the first mitochondrion was in fact a bacterial cell that had been introduced into another cell by endocytosis. Therefore, we cannot really describe mitochondria as having been "by themselves", since originally they were (most likely) bacteria. (I am emphasizing this because in your statement it seems like perhaps there is some misunderstanding with this point.)

Where were we? Ah, yes, so we have a bacterium (pre-mitochondrion) inside another (host) bacterium. Consider that the combination of one bacterium inside another works and, voilà!, we have symbiosis and, more precisely, endosymbiosis. This means that the two bacteria collaborate to survive, they benefit from interacting with each other (symbiosis) and one of them is inside another (endo-).

But, of course, the combination is not optimal: the two bacteria have common steps in their metabolism and this is a waste of energy. And evolution does not like that. Evolution encourages organisms to minimize their energy expenditure through natural selection: those organisms that manage to make the most out of their energy supplies will survive and thrive. This means that the pairs of endosymbiont bacteria that manage to use less energy to carry out the same actions will be positively selected for.

Indeed, what this possibly lead to was the host bacterium keeping its basic glucose metabolism (glycolysis), and the "inside"-bacterium exclusively keeping its TCA metabolism, effectively becoming a mitochondrion. Hence, the current arrangement of glycolysis in the cytosol and respiration in the mitochondria.

In short, it is important to look at the bigger picture: were there ever really "free" mitochondria? No, according to Margulis' Endosymbiosis Theory there mitochondria-precursors, which were bacteria. Once these bacteria were introduced into the cytoplasm of another cell, their metabolism degenerated and was reduced to the minimum necessary. This is a success story: the mitochondria are evolved bacteria that have managed to survive and thrive, and have made themselves fundamental for survival of many lifeforms, including humans.

I hope this is a useful answer to your question. Feel free to ask for clarifications in case I did not describe something well enough :)


Why can't Turner Syndrome occur in males? In Turner Syndrome, one X chromosome is missing, meaning that the resulting egg or sperm has 22 chromosomes (without pair) and the 23rd chromosome is missing.  If this develops in an egg, and a normal sperm carrying a Y chromosome fertilizes that egg, then due to presence of a Y chromosome, can a male with Turner Syndrome develop?

Because it is not viable to not have any X chromosome (non-peer reviewed reference).

The X chromosome is much bigger than the Y chromosome and carry a lot of essential genes (see here). A zygote just does not appear to be viable without X chromosome.


C. elegans are either male or hermaphrodites, but why aren't there any females? From my understanding C. elegans are mainly hermaphrodites but are occasionally males to increase genetic variation. Why is it that random females aren't born instead to achieve he same goal (genetic diversity)?

The evolution of self-fertile hermaphrodites is thought to be a specialization that occurred several times in the nematoda. For example, most of small, free-living soil nematode species related to C. elegans are male/female. C. briggsae, which last shared a common ancestor 80 myr ago is also male/hermaphrodite, but I believe their ancestor is thought to have been male/female.
At the developmental level, the first germ cells to mature in the somatic gonad develop as sperm and then the Germline switches over to make oocytes.


The relationship between the shape of the bacterial DNA and the blocking of replication machinery I was reading a course about tolemers when I arrived to this phrase :

  [...] The ends of a linear DNA molecule cannot be replicated by the cellular replication machinery (which may be one reason why bacterial DNA molecules are circular).

I want to know what is the relationship between the circular shape of the bacterial DNA and the blocking of replication machinery ?

This has been covered elsewhere (I highly recommend this page ) but it basically has to do with the priming of the strands and the fact that all polymerases work from the 5' prime to the the 3'. I made a quick schematic to illustrate (the explanation is below):

The priming is done with RNA during DNA replication in the cell, unlike PCR where you use DNA oligo's to prime. This RNA-DNA is called the Ozakazi fragments. After replication RNAse H will remove these primers leaving only DNA's and gaps. In the middle of the sequence the gaps can be filled in by the normal repair machinery but at the ends there is no 3' terminus to fill in the gaps. That is where the telomerase comes in and fill these gaps with a fixed sequence (also based on an RNA template but that is going into details).
If you have a circular chromosome there is always a 3' to complete the gap.


DNA and gene activation As far as the genetic content of each cell is concerned I have read to my satisfaction that all cells of a person's body except the red blood cells (with no nucleus and so no genetic message) and the gametes ( with just half the genetic copy or 23 of the 46 chromosomes) have the same DNA copy and so all the 60,000-80,000 estimated genes. The only difference is that which genes are active and which are dormant. For example the gene for insulin would be present in all cells but would be active and functional only in the cells of pancreas assigned the function of insulin production.

My question is:-

  What is the factor or process or molecule or information that
  tells a cell or helps it to activate the genes necessary for its own
  growth and more importantly its designated function?

Your question refers to differential gene expression and methods of Eukaryotic gene regulation. This is a very broad question for there are a lot of methods to control gene expression. They can function as transcription control, mRNA processing control, translational control, post-translational control and so on in eukaryotes. In prokaryotes, the methods include the operon model etc, which is much simpler than eukaryotes and multicellualr organisms but still quite complicated when studied in its entirety. Here and Here are few places where you can study differential gene expression. As an introductory text,  chapter 19 of Life:The science of Biology by Purves, Sadava, Orions and Heller(the link is to a supplementary-material site and not to the book itself), Otherwise, to elucidate all mechanisms here would become too long and in any case uncomprehensive.


Which cells will pass cancer to offspring? Each of these types below contains a DNA mutation. Which type(s) will affect the children of the individual whose cell it is.

Red blood cell
T cell
Skin (epithelial) cell
Neuron from the brain
Sperm cell
Cell from lining of the uterus
Placenta cell
Stem cell

My attempt: I think it's only a sperm cell, because that is the only cell to get passed on.  Is this right?

Red blood cell

Will probably not. You inherit blood type, but not actual erythrocytes (though the mother's erythrocytes do interact with a fetus).

T cell

Will probably not. However, while in the uterus and for the first few weeks outside the uterus the Mother's immune system is effectively the newborn's immune system. While the mother doesn't pass on any myeloid progenitor cells, a disease affecting a leukocyte might also be passed on to the child (HIV).

Skin (epithelial) cell

Will not. You inherit many traits to do with skin (melanocyte activity resulting in melanin concentrations, for instance), but no skin cells are involved in the creation of the fetus.

Neuron from the brain

Will not.  Neurons are the last time of cell I'd expect to vertically pass on a mutation, not only because their environment is usually tightly controlled (Schwann Cells, Blood-Brain Barrier, etc.), but also because the fetus will develop the beginnings of its nervous system very early on and I'm not aware of the mother's CNS or PNS interacting with the fetus in any significant way.

Sperm cell

Can certainly pass on a mutation as long as the mutation is part of the sperm's DNA. Though the particular gene the mutation exists on may be inactivated, it would still be passed on to the offspring and potential future generations.

Cell from lining of the uterus

I'm not positive on this one. The fertilized egg cell must implant itself in the lining of the uterus, and the landing location eventually becomes the umbilical cord. I suppose it's possible, particularly if the mutation occurs closer to the child's end - like the obliterated artery.

Placenta cell

Probably not, though like Cell from lining of the uterus I'm not super positive on this one. Given that the placenta is detached from both the mother and child soon after birth, a mutation in a placental cell that hasn't metasticized won't affect either. However, there may be interactions I'm not aware of.

Stem cell

"Stem cell" is a little vague. The body has many specific types of stem cells, and the fertilized egg itself basically turns into all of the stem cells the developing fetus will ever have. If it's referring to the daughter cells of a fertilized egg, then only the child will have the cancer, as the genetic inheritance is unidirectional (the mother's genome is not modified to resemble the child's in any way).

If someone has better knowledge on the interaction between the fetus and the uterus/mother or can come up with some references, listen to them. It's been a while since I've studied development.


Why are childhood cancers less frequent than infant or adult? According to data provided by Cancer Research UK, the lowest rate of cancer incidence by age occurs between 5 and 15 years.  Infants have a higher rate, and the odds of an adult developing cancer increase over time, especially during old age; until the odds plateau around age 85.

I understand that an accumulation of DNA damage over time increases likelihood of cancer with age.  But what explains the almost flatline rate of cancer amongst those aged 5-15?  Surely it makes more sense for the rate of cancer to increase uniformly every year from infancy?

There are 2 main causes of cancer: "born defective" (heritable or genetic problems producing a large predisposition to cancer) and "accumulated damage" (random mutations accumulated over life).

Due to how the UK health system rations treatment (and the recent stories about Charlie Gard being prevented from traveling to the U.S. or Vatican for treatment), it's likely that the government there often "deprioritizes" (complete guess, no idea if they actually do that) infants with severe heritable/genetic problems causing near-immediate cancer. Obviously this means that those cases never live to the 05-09 age bracket.

Cancer deaths peak at 65 rather than 90 or 100 on similar statistical grounds, although late-in-life cancers are almost always due to accumulated mutations  rather than being born defective. Cancer deaths drop off after age 79 because of the relatively large die-offs in the previous few age brackets, in addition to deaths from old age and related conditions.

If there was infinite funding for health treatment and enough hospitals to match, the graph might instead match your expectations as the public would do everything to maximize survival. This means that some of the 00-04 bracket would survive to later age brackets, with the largest cause of death in those cancers being failed treatment.


what snake is that in northern italy About 75 cm long. Thin tail. Camping site near Grado, Italy, northern Adriatic sea.
It climbed a tree in the rough bark and i followed it to take these photos.

It looks like a whip snake, either a Balkan whip snake or a green whip snake. They are both present in the very north of Italy, close to Slovenia. They both vary in color, but the coloration of this one seems to be more similar to the Balkan whip snake.

See also this discussion.


More proteins from diet when common cold and flu? My coach says that I need to eat 1.2 - 1.5 grams of proteins per kilogram when I have a common cold and flu.
I normally eat one gram of proteins per kilogram, while double it when doing my exercise training.

He explained that the reason why you need to get more good proteins when you are sick is that the body is building antibodies by the adaptive immune system and later for innate immunity.

I think he can be right based only on my own experiences getting better from common cold with low protein diet - it just takes a lot of time, while under high protein diet, you get better faster.
I also think his explanation makes complete sense to me, since antibodies and antigens are proteins.

Why do you need more proteins when you are sick?

Your body needs more energy when you are ill to facilitate the recovery process which includes the production of white blood cells to help fight the infection. This shouldn't be limited to proteins though, carbs are also very important as they are provide high amounts of energy. Basically just making sure you eat a varied and balanced diet is more important when you are ill to make sure your body receives the nutrients it needs to fight infection and heal itself. As it is having to work harder when you are ill it makes sense to eat more high energy foods. Micronutrients are also very important!

  Minerals such as selenium and zinc work to keep the immune system strong. These minerals are found in protein rich foods such as beans, nuts, meat, and poultry. — Source

Although if your diet is varied you should be getting plenty of these anyway, without needing to take supplements.


Why do we still have genetic disorders that show anticipation? Anticipation whereby symptoms of genetic disorders occur earlier and with more severity as it is passed from one generation to the next.

So wouldn't these inherited diseases over a few hundred generations affect offspring before they can reproduce and thus shouldn't these diseases like Huntington's disease no longer be with us today?

Or are most of these genetic diseases generated through sporadic mutations at a high enough rate to persist?

I can think of 3 explanations (not mutually exclusive) for the maintenance of important genetic disorders that prevent the sick carrier to reproduce.

Following what you said, the frequency of a given allele in a population is influenced by selection, drift, migration and mutation. Some disease present at low frequency can typically spontaneously de novo appear in a population. This is typically the case of cancer and trisomy 21 where new mutations (mutation in the broad sense) likely explain a big part of why such disease do not disappear through time.
Many genetic disease are carried out by recessive alleles. In consequence, only homozygotes for the recessive allele express the disease and the disease can persist through drift. Note the interesting case of hemophilia and Malaria resistant where the heterozygote actually has higher fitness than any homozygote (heterozygote advantage), particularly in regions where there is a high prevalence of malaria. In this case, the disease is not washed out of the population not only due to drift but also due positive selection on the heterozygotes.
Many so-called genetic disease actually have an important environmental component. For the Huntington's disease, the carrier of the autosomal dominant mutation does not necessarily express the disease. From wikipedia:

  The disease is caused by an autosomal dominant mutation in either of an individual's two copies of a gene called Huntingtin, which means any child of an affected person typically has a 50% chance of inheriting the disease.

As a result the Huntington's disease can still segregate thanks to drift in the healthy heterozygotes.


Ways to identify/distinguish individual coyotes? Are there any methods to distinguish individual coyotes from a distance (with a binocular or telephoto lens)? Are there marks or patterns we could be looking for?

Similarly, if I have seen a coyote at the same location multiple times, what should I look for to see if it has been the same coyote?

I've been searching about it and only found ways to distinguish individual wolves.

Thanks!

The Wikipedia entry for subspecies of coyotes has a very useful chart here (click [show]) that gives a description, range, and other information for each of the 19 subspecies of coyotes. Since I presume you are from the California area, I would focus on the descriptions of coyote subspecies that could exist around your area, such as the San Pedro Martir coyote, which has "reddish summer fur and a short, broad skull" to differentiate among the various coyotes you many encounter. Generally, the coyotes differ in color, teeth, tail size, fur, ears, and other such factors. As for determining if you've seen a coyote already, I suppose there's no real way of knowing unless there is a unique marker on the coyote's fur or appendages that differentiates itself from the others; however, examining the coyote's scats and comparing them may be a viable option for this, but that would require you to examine close to the coyotes rather than from afar.


In cancer, why do cells duplicate themselves? In regards to cancer why do cells replicate themselves? If it's a mutation, what kind of mutation would this be classified as?

This article covers some of the key issues of cancer in layman's terms.
Essential, cancer is caused by multiple mutations in key regulatory genes which function in maintaining the cell cycle. This provokes uncontrollably rapid cell division, with only furthers the problem with genetic mutation. Here are some quotes from the article to strengthen your understanding in cancer cell mutations.

Image source

The cells become progressively more abnormal as more genes become damaged. Often, the genes that are in control of DNA repair become damaged themselves, rendering the cells even more susceptible to ever-increasing levels of genetic mayhem.
[...] Most cancers are thought to arise from a single mutant precursor cell. As that cell divides, the resulting 'daughter' cells may acquire different mutations and different behaviors over a period of time. Those cells that gain an advantage in division or resistance to cell death will tend to take over the population. In this way, the tumor cells are able to gain a wide range of capabilities that are not normally seen in the healthy version of the cell type represented.
[...] Mutations in key regulatory genes (tumor suppressors and proto-oncogenes) alter the behavior of cells and can potentially lead to the unregulated growth seen in cancer.