Why don't we see life form again and over again? If life formed on earth by natural laws, why can't we observe the formation of life from matter today? Is it because this is a rare phenomenon? It seems just after formation of earth life formed on earth and around 2-3 billion years has passed. It must be enough time for life to form several times from scratch.

The first life was probably so fragile and simple we would likely not even recognise it if it did appear. We don't know exactly how, or where, life first appeared but nearly all theories suggest simple collections of enzymes in protected environments that slowly gather the mechanisms needed for free-living life over time.

This works in the ancient world because there is no competition so even the simplest and most inefficient replicator is able to reproduce, spread, and advance. Today, any new life would have to compete with existing life which has had billions of years to evolve into highly efficient forms. A new abiogenesis event would simply pass unnoticed, a brief flicker quickly snuffed out by modern life.


Is this an asian hornet My mother found a hornet at home (in northern France) that is probably building a nest. Is that an asian hornet? If yes, how can I exterminate them?

This is not a hornet, this a wasp. See the yellow dots on the thorax ? They are typical of the Vespula genus. So is the yellow and black stripe pattern on the abdomen. Those wasps are smaller than hornets (1-2 cm for wasps, 3-4 cm for hornets). Picture from Wikipedia:

There are two common Vespula species in France  (V. vulgaris and V. germanica), but to identify yours, we would need a better view of the head and abdomen.

On the image below, you can compare it to the two hornet species you can find in France (source). The first one is a bee, the second one is a wasp (Vespula), the third one is the invasive "Asian hornet" (Vespa velutina) and the fourth one is the native "European hornet" (Vespa crabro).

So no extermination needed ;) You can find more information (in French) on how to recognize these species on the Natural History Museum website.

Sources:

Le Rucher des Plaisirs - French beekeeper website
Natural History Museum - hornet and wasp identification in France
Same source in English
Wikipedia page


Can the excessive consumption of mineral water lead to kidney stones or other health issues? I heard that drinking too much mineral (bottled) water could lead to problems such as kidney stones because of the high amount of minerals in it. Is it true? If so, what is considered to be excessive?

I suffer from calcium oxalate stones.  My doctor pointed me to this study:

http://www.ncbi.nlm.nih.gov/pubmed/9096270

tl;dr;  For calcium oxalate, drinking Mineral Water high in Calcium and Magnesium may reduce the risk of forming stones.


genetic difference subpopulations vs movement rate Someone told me that if a geneticist finds no significant difference between 2 subpopulations that have temporal spatial overlap it might be that they are still almost closed (no connection). Is this right?

Can I deduce anything about the individual exchange rate between populations and the genetic similarity/difference? For instance, one would need 5% of individuals to switch populations to keep them almost genetically identical. Does this differ between species (let's say fish and mammals)?

Thanks.

ps: any references to this would be great

[..] if a geneticist finds no significant difference between 2 subpopulations that have temporal spatial overlap

This isn't clear. Significance difference between what? What statistical hypothesis are you testing for which one would found no signicant difference (accepted the null hypothesis). Are you maybe thinking about a t-test between testing difference between the average phenotypic traits?

  it might be that they are still almost closed (no connection). Is this right?

Do you mean no gene flow (aka. no migration)?

  Can I deduce anything about the individual exchange rate between populations and the genetic similarity/difference?

"Individual exchange rate" is typically "called migration" or "gene flow".

At some extend, yes you can. But the question is really broad and will be hard to answer in the general sense. I will just provide a very common methodology here.

You can compute $F_{ST}$, a statistic of population divergence. A very good paper explaining the math of $F_{ST}$ is Nei (1973). I recommend computing $F_{ST}$ following Weir and Cockerham (1984). Then, if you can assume a finite island model (equal migration rate $m$ between any two population) and a constant and known population size $N$, then

$$F_{St} = \frac{1}{1 + 4N(m+\mu) \frac{d}{d-1}}$$

, where $d$ is the number of demes (number of islands)This equation can be found at many places. Slatkin (1995) is a very good paper but note that its final solution differs a little bit from the one I presented (by a square term) for reasons explained in Charlesworth (1998). You can solve for $m$ and plug the observed $F_{ST}$ and $N$. Note that depending on the markers used, $\mu$ will be negligible in comparison to $m$.

You might want to have a look at the very related post How could one calculate the gene flow between two populations?


Can growth rate be used as an indicator of fitness in fish populations? I would like to calculate selection gradients in order to gain insight into the strength and type of selection influencing my study population.

(see here for review. http://jgking.web.unc.edu/files/2012/06/Kingsolveretal.AmNat_.Mar2001.pdf )

(see here for what I would like too do in the end. http://onlinelibrary.wiley.com/doi/10.1111/evo.12077/epdf).

For this I need an indication of fitness.

My question is this:

Does it make sense to use growth rates (in mm. per year or other) as a "proxy" for fitness?

Thanks in advance for your time

Welcome to Biology.SE!

Possible confusion

When talking about growth rate as a proxy for fitness, most authors think of population growth rate (whether in terms of the Malthusian parameter or the net reproductive rate). Such methods are typically used for unicellular that have very short generation time. You seem to be referring to the individual growth rate.

Possible proxies for fitness

There are a number of different proxies for fitness one can use.

growth rate
Some phenotypic trait correlated with fitness such as:

seed production
body size
etc..

Competitive abilities
Experimental evolution

How to chose a proxy

The proxy you want to use depends:

The accuracy you need
The organism you are working with
The a priori knowledge on the biology of the organism of interest.

For example, if you have little knowledge of what phenotypic trait could be correlated with fitness and if the organism of interest have a very short generation time, then growth rate might be good (and accurate) proxy to use indeed.

Ressource

You should probably read some papers that have used a method of potential interest before doing it yourself.

At page 1232 of Kawecki and Ebert 2002, there are a few paragraphs reviewing the different proxies and their usage. They cite key papers you might want to have a look at.

Proxy for fitness in fishes

I know little about fish biology in general but I doubt there is such thing as a generalization of whether "individual growth rate" is a good proxy or not. As you don't specify what species of fish you are working on, I don't think it is possible to answer this question accurately.

You should look at previous work done on the species (or related species) you are working on in order to figure out what would be a good proxy.

Issue in your post

I think it is clear from above that you should indicate what species you are working on.
The paper you link should come with more explanation. You say a paper is a review but a review about what?
You cannot say "I would like to do something like them" and link a paper. You should describe with you own word what you are trying to achieve.


Which species of bee or wasp are in this photo? Please tell me what do you think :)
The photo is from Santander, Colombia. I didn’t take any closeups photos , but these were little bees, like 5 x 1 mm. The tube didn’t seem man-made, it was indoors and the owner of the house said that they are stingless, since no one has been stung.

Looks like the family Halictidae to me. Known as a sweat bee. Maybe Lasioglossum zephyrus?


Blood testing for chlamydia I am working with the bacterium Chlamydia trachomatis.

The main test for this species is the naat test, which is based on amplification. But I would like to know how the bacteria affects the blood composition, and if there is a method of diagnosing it from the blood.

Blood antibody tests for Chlamydia trachomatis can be done, but they are far less reliable than amplification:

  According to our results, serologic testing for Chlamydia can exclude active infection of the lower genital tract with a high reliability (> or = 95%). However, detection of C. trachomatis can only be reliably achieved by nucleic acid amplification assays.

Low correlation of serology with detection of Chlamydia trachomatis by ligase chain reaction and antigen EIA


Will a completely removed cat whisker grow back? I just accidentally pulled out, while playing, my cat's whisker entirely, follicle and all. I feel terrible as I know she is a kitten and whiskers are rooted deep in a place rich in nerves. I'm wondering if the whisker will grow back and if it will cause a lot of pain as it regrows.

The short answer is that yes, they will grow back. Cats do regularly shed their whiskers and grow them back in time (reference). The thing is that if damage has been done to the root of the whisker, it may grow back in an irregular manner (reference). Wish for the best and by now I think the whisker should be back just fine.


Effect of extremely hard water on marine life? When researching water quality standards, I found that a minimum and maximum was set for water hardness. Several sources also state that water can in fact be too hard. The question is how does hard water harm marine life? I understand that it is required to reduce the toxicity of Hydrogen ions and other trace metals, but cannot find anything concerning the effect of water that is too hard.

Hard water helps in direct and indirect ways.

Indirectly, hard water plays an important role in regulation of pH. Respiration and other physiological activities release substances into water that change the water pH and the ions that cause hardness act as buffers and help maintain pH.

Directly, they determine the ease with which osmoregulation occurs. The harder the water, the lesser the influx of water. So the fishes act like an open system and are influenced by the surrounding water.

There are very few fish who absolutely need soft water to survive.
Since your pH and hardness are pretty low, it allows you to raise multiple fish from South America. You could do tetras, dwarf cichlids and New World cichlids, Plecos as well.

Potentially discus and altum angelfish as well if you're up to the huge challenge.

However, livebearers will not tolerate this type of water. That goes the same for African cichlids.

Otherwise hard water is completely fine for marine life and other aquatic species.

Link

Link

Hope this information helped!

-Sartoaster


Has a new functional structure ever been observed arising spontaneously? Have we ever observed a new functional biological structure arising spontaneously such as a new functional organ (sensory or otherwise. such as tracing some creature in the past few hundred years which had no electroreception organ and now has evolved this organ)

Or has what we observed been limited to changes in existing structures.

(Lenski's E. coli bacteria is not what i am looking for since it is a change in an existing metabolic system (not a new functional structure) and furthermore e-coli already had some ability to use citrate as an energy source )

Looking for a completely new functional organ (such as a new sensory organ) that we have actually observed - not deduced from fossil record.

Also not looking for something trivial such as a new/modified enzyme or protein molecule but rather a new organ in a species at least the size of an insect.

It seems like you are attempting to frame this as a question about current evolutionary theory. However, current evolutionary theory doesn't expect anything as complex as an organ to arise spontaneously without any precursors. You suggest a new claw in an insect would be something "spontaneous" enough for you. This again shows that your question and the answer you are looking for are not related to evolutionary theory. The insect organs you are talking about are all modified appendages. This includes claws, mandibles, antennae, legs, fangs. These appendages all share a common genetic and developmental framework that has been slightly modified over long periods of time to give raise to the variety of insect appendages that we see today.

The idea that evolutionary theory supports the spontaneous creation of organs is a willful ignorance of evolutionary theory. The molecular mechanisms that generate novelty (e.g. genome duplication, gene duplication, de novo genes, mutation, gene regulation) for natural selection to work on are relatively well understood. Since we have an understanding of how novelty is created it is known that spontaneous organ generation has never happened or is expected to happen under evolutionary theory.

Here is link to the University of California, Berkeley's webpage designed to teach the public about evolution.


Can genes change as we age? Let's say you're a 23-year-old man who impregnates a woman. Will your genes be the same if you were to impregnate another woman at age 35? Will your genes in those 12 years have changed/mutated/become smarter?

Yes, there are some differences between the gametes that a parent produces at different ages!

Mutations in the germline during mitosis

Every time a cell replicates some mutations may occur (even through mitosis). Of course, any mutation that occurs in cells are located in your hand or in your brain, for example, will not be transmitted to the offsprings. Only mutations occurring in the germline (cells in the testis and in the ovaries whose descendent or themselves go through meiosis) are possibly passed to the offsprings. Interestingly, because of the developmental pathways of sperm cells and ovules, sperm cells go through a lot more mitosis than ovules do, resulting in more mutations in the sperms than in the ovules. Therefore, if you look at a mutation in an individual and assuming you know that the mutation occurred during the lifetime of the parents, then you are more likely that the mutation comes from the father than from the mother.

As reviewed by Cochran and Harpending (2013), mothers transmit on average a number x of new mutations to their offspring. This number x is independent of the age of the Mother. Fathers, however, transmit a number of new mutations to their offsprings that is very much dependent on the age of the father for developmental reasons.

Of course, as it has been pointed out there are various environmental factors that may increase or diminish the mutation rate (such as the mutagens (Tobacco, X-ray, ..))

Note on the process of adaptation

It is important to know that a vast majority of mutations are deleterious (impact negatively the reproductive success and survival of the individual carrying it). If we assume that no selection occurs between the cells of the germline, then no adaptation is possible. And in average sperm cells of an old guy should have lower fitness than the sperm cells of the same guy when he was younger. This process is referred to as mutation accumulation (mutation accumulation is not a concept that is specific to somatic lines mutations). However, one may argue the opposite! One might think that the cells that carry the new mutations (the mutation that occurred during the lifetime of the man) may be selected for or counter-selected. In such a case, the few beneficial mutations might be enough to make our cell lineages more fit with age. Whether the fitness of cells increase or decrease through our lifetime is dependent on the effective population size, the mutation rate and distribution of mutational effects. One can calculate the critical parameters yielding to one (mutation accumulation and fitness decrease) or the other (fitness increase through age) thanks to the mutational meltdown literature.

It is important to note however that what increase the fitness of a cell might decrease the fitness of its carrier. Knowing the joint distribution of mutational effect for both the carrier and the cells should allow us to calculate if reproducing late in life allows transmitting better genes than reproducing early in life. Intuitively, I would expect that reproducing early in life would allow a parent to transmit better genes.

Epigenetics

We have to talk about epigenetics also. Epigenetics refers to all the modification that occur "around" or "on" the DNA but which are not the modification of the sequence of nucleotides. It is possible that the transmission of epigenetic modification is dependent on the age of the parents. But I have never heard of any case where this happens.


What do the haploinsufficiency scores in the clinVar database represent? I understand that haploinsufficiency occurs when one of the two copies of a gene is mutated to the point of being unusable, and the single copy remaining is unable to cope with the cell's demands for a given peptide, resulting in a phenotypic deficiency.

In the clinVar database, there is a "haploinsufficiency score" (example here) which seems to range from 0 to 3 (though that is anecdotal only; based on the genes that I've looked at).  I assume it refers to how phenotypic or how deficient the cell is.  However, I fail to find a place where this is clearly outlined...

Am I correct in this assumption, and if so, what does a score of 3 (for example) represent?

Okay, I finally found an official source outlining what the dosage sensitivity scores represent.
0 represents no evidence of dosage sensitivity: clinical interpretation is that dosage differences is "likely benign."
1 represents little evidence of dosage sensitivity: This can be marked if only secondary evidence shows dosage sensitivity; clinical interpretation is that dosage sensitivity is "uncertain."
2 represents "Emerging evidence," meaning that the evidence suggests fairly strongly that the gene is dosage sensitive, but that there is insufficient evidence to prove it.  The clinical interpretation is that dosage sensitivity is "Uncertain, likely pathogenic."
3 represents "Sufficient evidence," meaning that the evidence is sufficient to prove that the gene is dosage sensitive.  Clinical interpretation is "Pathogenic."

Source:

Riggs ER et al., Towards an evidence-based process for the clinical interpretation of copy number variation. Clin Genet. 81(5): 403–412.


Can any organisms see non-electromagnetic radiation? Some examples would be cosmic rays, neutron radiation, alpha radiation, beta radiation, muon radiation, and antimatter radiation.

Some related questions: How is non-electromagnetic radiation detected, and would it ever be evolutionarily beneficial?

Some fungi have radiotropism; they grow toward radiation sources. Melanin-expressing (melanotic) fungi migrate toward radioactive sources, which  enhance their growth. According to this paper.

These Melanotic fungi inhabit some of the most extreme habitats on earth such as the damaged nuclear reactor at Chernobyl and the highlands of Antarctica, both of which are high-radiation environments.
Radiotropism was triggered primarily by gamma radiation, but it is possible that both alpha and beta radiation could be  “ sensed ” by the fungi as well.

It seems like these melanotic fungi can detect gamma and beta or alpha that they can use as energy source.


Tea that makes everything taste like dirt My highschool biology teacher once gave us (her class) a tea which made everything taste like dirt. I remember that chocolate candies, spicy hot sauce, and salty crackers all tasted the same after drinking the tea. The effect only lasted a minute or two. It's been a long time, and I can't remember the name of this tea - can anyone identify it?

(I am not certain if this question is appropriate for this SE, please let me know if it is not.)

This sounds like gymnemic acid, which can be isolated from the leaves of Gymnema sylvestre. It’s an “anti-sweet” compound, which wouldn’t necessarily make everything taste like dirt but might do so for you particularly. When I had it, it made my tongue slightly numb and candy tasted like nothing rather than sweetness, so it may not be what you’re looking for.

Lactisole (from coffee beans) is another option, but I haven’t tried that one personally so I’m not sure what its taste effects are like.


How are antibodies specific for a disease detected in the blood if everybody produces a different antibody for the same antigen? To break the title down into parts:

There exist serology tests that detect the amount of an antibody (Ab)
against a specific pathogen/antigen.
Every human produces their own Ab for a specific antigen by
(relatively) random combination of different gene segments in their B
cells, until one that recognizes the pathogen is found and produced
in massive amounts.
One portion of every Ab is constant, whereas the portion that
recognizes the antigen is variable. Even for antibodies (in different
humans) that recognize the same antigen, albeit to a lesser degree.

What exactly does an antibody titer/serology test detect in the blood so that it can accurately measure the amount of antibodies against a specific antigen? I am assuming they use antibodies against the antigen-binding/variable portion of an antibody. But if the variable region differs from person to person, how can a universal antibody (to be used in serology tests) against it be generated?

Is the variable region not that variable, so that any lab-generated antibody against any functional antibody against a virus works well enough for an accurate measurement of antibodies against that virus? But even so the concept sounds hard to believe since even a single antigen can have multiple epitopes, and one person might have an Ab for epitope 1 of antigen X, while the other would have an Ab for epitope 2 of antigen X. And they would still be immune to the same virus, while a universal Ab titer test for the virus would be unable to detect antibodies from one of them.

Do they perhaps employ multiple lab-generated antibodies against most of the possible variations of human-generated antibodies in the tests?

Specific antibodies are typically detected using ELISA.

The way you make a test for an antibody to a particular pathogen is not by using secondary antibodies to the specific part of the target antibody, but by using the antigen.

Different kits work differently, but the general idea is that you have antigen stuck to a surface, you put the sample on that surface. If there are antibodies to the antigen, they stick to it. Then you wash everything away and add a tagged antibody that binds to generic human antibodies.

See also https://www.sciencemag.org/news/2020/03/new-blood-tests-antibodies-could-show-true-scale-coronavirus-pandemic


An example for N50? Why do we need it? I'm trying to understand N50 on the wikipedia. But I was unable to get a sense of the definition:

  Given a set of contigs, each with its own length, the N50 length is
  defined as the length for which the collection of all contigs of that
  length or longer contains at least half of the sum of the lengths of
  all contigs, and for which the collection of all contigs of that
  length or shorter also contains at least half of the sum of the
  lengths of all contigs.

Is there a simple example that illustrates this definition? Furthermore, why do we need this statistic? What does it really tell me? Do we want a higher or less value?

Contig or scaffold N50 is a weighted median statistic such that 50% of the entire assembly is contained in contigs or scaffolds equal to or larger than this value.

Mathematically:

  Given a set of sequences of varying lengths, the N50 length is defined
  as the length N for which 50% of all bases in the sequences are in a
  sequence of length L < N. This can be found mathematically as follows:
  Take a list L of positive integers. Create another list L' , which is
  identical to L, except that every element n in L has been replaced
  with n copies of itself. Then the median of L' is the N50 of L. For
  example: If L = {2, 2, 2, 3, 3, 4, 8, 8}, then L' consists of six 2's,
  six 3's, four 4's, and sixteen 8's; the N50 of L is the median of L' ,
  which is 6.

In simple words:

  scaffold N50 is the median contig size of your genomic assembly. It's
  a metric that you can use to evaluate the quality of your assembly,
  since an overly small N50 suggests that you were unable to generate
  many contigs of biologically meaningful size (i.e. you probably have a
  lot of bogus little contigs in your assembly). You can increase your
  N50 by eliminating sequences which are bound to cause you problems,
  e.g. short repetitive stretches.

  note that this metric only applies when doing de novo assembly. If you
  are aligning to a reference (i.e. for variant discovery applications)
  this metric doesn't apply

For a sample workout on an arbitrary small dataset:
http://www.r-bloggers.com/calculating-an-n50-from-velvet-output/

This answer was compiled from multiple sources:

http://www.researchgate.net/post/What_is_N50_Scaffold_in_Genome_sequencing_Technique
http://seqanswers.com/forums/showthread.php?t=2332
https://www.broad.harvard.edu/crd/wiki/index.php/N50


What are microRNA, siRNA and antisense RNA? From what I understand, microRNA binds to proteins which can cut certain mRNA strands do that this protein is not synthesised. This seems like gene silencing to me, however I have also come across the term siRNA and antisense RNA...

Would be grateful if someone could explain what these are and how they work, and perhaps how they can be applied to treating diseases... Thank you in advance :)

MicroRNA (miRNA) are gene-regulatory RNAs that are loaded onto the RNA-induced silencing complex (RISC) and interact with partially-complementary targets on mRNA to suppress protein expression.  The miRNA is originally double-stranded and composed of strands about 21 nucleotides long; on loading onto RISC, one strand is degraded and the other, the "guide" strand, is held on the surface of RISC where it can interact with mRNA. The targets recognized by the guide strand are most commonly on the 3'-untranslated region (UTR) of an RNA.  Binding can suppress assembly of an initiation complex on the 5' cap of an mRNA because the mRNA is bound into a circular shape at the initiation of translation, bringing the 3'-UTR and 5'-UTR close together.

If the RISC loads an RNA than then finds a perfectly complementary target, RISC cleaves the target RNA using the activity of one of the protein components of RISC called Argonaute.  This property is exploited experimentally by manufacturing small interfering RNAs (siRNA) intentionally targeted to particular target sequences.  Once loaded into RISC these siRNA might recognize and cleave their perfectly complementary target sequence within an mRNA (though there is a significant failure rate, so several sequences are often tried).  The siRNA will also have miRNA-like effects on some partially-complementary targets on various mRNAs, leading to the observation that a single siRNA sequence can modulate expression of hundreds of off-target genes.

Antisense is a nucleic acid strand (or nucleic acid analog) that is complementary to an mRNA sequence.  Antisense occurs naturally and can trigger RNA degradation by the action of the enzyme RNase H.  Originally natural antisense RNA was tried as a method for silencing a gene, but the poor stability of RNA in cells led to development of nucleic acid analogs that are more nuclease resistant and still activate RNase H (such as phosphorothioate RNA) and other nucleic acid analogs that bind to RNA and sterically inhibit processes without activating RNase H (such as 2'-O-methyl phosphorothioate RNA, Morpholino oligos, locked nucleic acids, or peptide nucleic acids).  These latter RNase-H independent oligos do not trigger degradation of mRNA but they can be used like molecular masking tape to block translation, alter splicing of pre-mRNA, inhibit activity of miRNA, block ribozyme activity, and interfere with various other processes that require some other factor to bind to a particular sequence on an RNA molecule.


Why do stars disappear when I look at them? I've noticed that when I'm out at night stars seem to vanish when I focus on them. I assume the reason is physiological and not astronomic. Why does this happen? I would expect that things would be more clear when I focus on them.

When there is little light, the color-detecting cone cells are not sensitive enough, and all vision is done by rod cells. Cone cells are concentrated in the center of the eye, whereas rod cells are very rare in the center (image source):

When you focus on the star, the light is projected close to the center of the retina, where it will hit few rod cells. Thus the star appears to vanish.


Do mammals develop tolerance to anticholinergics? I know that first generation H1 antagonists, commonly known as antihistamines have anticholinergic effects. Their sedative side effects go away due to tolerance, but as for their anticholinergic side effects well that's something that is unknown to me at least. You might say use second generation H1 antagonists, but for this application the antiemetic effects that are unique to H1 antagonists that cross the BBB (i.e., first generation H1 antagonists) are desired.

The tolerance to antihistamines is an ongoing debate in the community. Although there were early studies citing that tolerance to therapeutic effects of antihistamines could occur, more recent data, especially studies involving nonsedating antihistamines, indicate that tolerance to the therapeutic effects of these drugs does not occur.

Overall, it seems like the mechanism driving the sedation vs. the therapeutic effects are two separate down stream effects of regulating the inflammatory response. Neuronal tolerance and synaptic transformation is a fairly fluid and ongoing process, whereas the inflammatory response is much more robust. Meaning, the neuronal response is, theoretically, more able to adapt to chronic use of the anihistmaine while still giving the therapeutic effect. This hypothesis is supported by data, but yet to be confirmed, thus creating polarization on the topic.

Also see, Goodman and Gillman Pharmacological Principles of Therapeutics


Enhancer elements in prokaryotic DNA? I know that in terms of post-translational modifications of genes, prokaryotes and eukaryotes differ highly because of the lack of introns in prokaryotic DNA.
With this said, do prokaryotic DNA sequences contain enhancer elements other than the UAS(upstream activating sequence)?

In addition, are enhancer elements like promoter-proximal elements and enhancer elements encoded directly within the DNA? Or are they proteins that attach themselves to the strand of DNA in order to enhance transcription?

do prokaryotic DNA sequences contain enhancer elements

Yes: https://www.ncbi.nlm.nih.gov/pubmed/1776167

  other than the UAS(upstream activating sequence)

The Gal4/UAS system is borrowed from yeast, a eukaryote https://en.wikipedia.org/wiki/GAL4/UAS_system

  In addition, are enhancer elements like promoter-proximal elements and enhancer elements encoded directly within the DNA?

Yes. Enhancers are usually considered to be encoded directly within the DNA; e.g.: see the following recently published historic perspective on the discovery of enhancers by its discoverer, Walter Schaffner : https://www.ncbi.nlm.nih.gov/pubmed/25719310

Sidenote: Enhancers have originally been discovered in a virus, and thus neither in prokaryotes nor eukaryotes

  Or are they proteins that attach themselves to the strand of DNA in order to enhance transcription?

Enhances (often / ~always) exert their function though proteins. https://en.wikipedia.org/wiki/Enhancer_(genetics) Note that this doesn't necessarily affect the definition of enhancers.


What studies are there showing the effectiveness of any substance on canine hypertension? Searching on http://www.ncbi.nlm.nih.gov I could only find the article titled as "Telmisartan Treatment of Refractory Proteinuria in a Dog".

Check out this consensus statement (PMID 17552466):

J Vet Intern Med. 2007 May-Jun;21(3):542-58.
Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats.
Brown S1, Atkins C, Bagley R, Carr A, Cowgill L, Davidson M, Egner B, Elliott J, Henik R, Labato M, Littman M, Polzin D, Ross L, Snyder P, Stepien R; American College of Veterinary Internal Medicine.

It includes 185 references, at least a dozen of which are related to your question. Also, if you look to the right of the article on PubMed, there are links to other relevant articles.

FYI: I located this article using search string

(canine hypertension) NOT pulmonary Filters: Review

There are quite a few others. (Canine pulmonary hypertension is apparently a popular research topic, so I found it useful to exclude those.)


Nature versus nurture regarding aggression in specific dog breeds A week ago I was bitten in my face by a dog that originally came from an asylum. That dog is half Rottweiler. Some people claim that the history of the dog is probably different from what the asylum thinks or says, whereas other people claim that Rottweilers or male Rottweilers are unreliable. But let's not focus on this single occurrence and ask the wider question:

Is there scientific evidence to indicate that there are certain breeds that produce significant numbers of dogs that are inherently and unreliably aggressive, or is such aggression usually the consequence of how their owners raised them?

It seems that there are some important differences in dog aggression depending on the dog breed (towards strangers, owners, and other dogs):

That being said, it seems that a significant proportion of a dog's behavior can be due to its environment (training, etc), according to a study, this 'nurture' component might explain up to 80% in the variation in aggression (which should be considered when interpreting the other study I cite).


Can bacteria be reservoirs for animal viruses? When people talk about reservoirs, they usually talk about bats, dogs, deer, etc. All animals. But can bacteria be reservoirs for animal viruses? Any examples?

I know that bacterial viruses can at least infect bacteria (bacteriophage). But can animal viruses also hide in bacteria for extended periods and come out at "will" by commandeering bacterial machinery?

I know that bacteria have different polymerases and ribosomes than animals, but is this at least a theoretical possibility?

The Answer is No

There are no examples of animal viruses infecting bacteria or incorporating themselves into bacterial genomes. Nor is it a theoretical possibility, given our knowledge of bacteria, eukaryotes, eukaryotic viruses and bacteriophages.

Why is it not a possibility?

As the questioner admits, the replication, transcription and translational systems of eukaryotes and prokaryotes are quite different. None of the known viral genomes could replicate and their genes be expressed in cells of the other kingdom. Why, the questioner may ask, could not a virus evolve to have signals recognized in both types of cell — at least in theory. Perhaps it could, but there is another factor to be considered, and this is the question of how viruses interact with the cells they infect. This is relevant to how other species can harbour human viruses and why there would be nothing driving a virus to acquire the means to replicated and be expressed in both system.

Receptors for Viruses on Host Cells

The point the question fails to take into account is that entry of both eukaryotic and bacterial viruses is a specific process involving interaction between protein or carbohydrate components of the virus and those in the membrane of the host cell. The host components are called virus receptors, and generally differ for different viruses. There are many reviews of this topic in the literature, so I cite a couple of examples freely available on the internet: Grove and Marsh on animal viruses and Rakhuba et al. on bacteriophages.

Viruses evolve to exploit one particular host species, and tend to be specific to that species because, although there may be a functionally similar protein in other species, differences in amino acids in the proteins (or sugars in carbohydrates) preclude recognition. When viruses cross the species barrier, this is due to mutations that allow recognition of the receptor protein in another species. If the change still permits recognition of the receptor in the original species then even if the virus is eliminated from the second (e.g. human species) it will still be present in the original species. Subsequent contact between humans and the species can therefore lead to a reappearance of the virus in humans.

This is how the original species acts as a reservoir. There is no question of a virus ‘hiding’ in bats by some sort of evolutionary pressure to allow it to return later to humans. Understanding this you will see that:

The differences between the membranes of bacteria and humans are so great that there is little likelihood of an animal virus finding a receptor on a bacterial cell.
Even if it managed to do so, it would not be able to replicate in the bacterium.
There is no evolutionary pressure that would select for the series of mutations that could convey the ability for such replication.

Footnote: ‘Dormant’ Viruses

There is another quite different phenomenon in which certain bacterial or animal viruses ‘hide’ within the species they normally cause a lytic infection. This involves incorporation in the genome and later release. In bacteriophages it is called lysogeny and in animal viruses examples include retroviruses and herpes viruses. This has no relevance to the question.


What specific membrane adaptations do cells have for saline-rich environs? Are the cells of marine animals and flora equipped with special ion exchange pumps to mitigate the effects of a saline-rich environment?

Or have the cell's membranes adapted through structural changes to counter the osmotic forces?

This 1969 Steensland paper seems to suggest that the membranes of halophiles are stabilized by sodium ions and they rapidly denature at lower-salt conditions (2.2 vs. 4.3 M).  The protein composition of the membrane was generally acidic, stabilized by all the Na+.

As far as what the role of the halophile membrane is in sheltering the cell from the high ionic strength solution seems left unsaid.


Supercomputer and undergraduates Is it common for an undergraduate to run their thesis (evolutionary genomics) in a supercomputer? In my country, few supercomputers exist, but I'm not sure how it is for bachelors in the US or Europe. I am writing my application to graduate school abroad and I want to know if it is a remarkable point I can use as hook to begin my statement.

IMO irrespective of country and level (undergrad/Masters), if you can run a job on a High Performance Computing cluster or a supercomputer, you should mention that on your resume. And sure, you can use that in your statement, especially given the fact that not many have access to it, you had the rare opportunity and made full use of it.

In my experience, I haven't seen many undergrads here in the US that can run a job on a HPC - not without prior computing experience!

All the best to you!


Identification of a caterpillar My daughter has become one with nature somehow and came across an odd looking caterpillar. The odds of finding one never found before is great,  however I'm unable to find what kind it is. It's head is bright red.

From Eastern North Carolina, USA.

Would anyone be able to point me in the right direction?
Thanks!!!

This is a tussock moth caterpillar in the Lymantriidae family.

The image is not clear enough for a definitive ID, but it appears you have some species in the genus Orgyia.

Likely, this is a white-marked tussock moth caterpillar (Orgyia leucostigma).

From Auburn University:

  The full-grown larva (Photo 2) is around 35 mm long. The head and shield on the segment behind the head are red. There are two long black pencils of hairs on the first segment of the thorax that project forward. A single black hair “pencil” arises from the eighth abdominal segment and projects upward and rearward. The back is mostly black and the sides yellow, cream, or grayish. There is an erect brushlike tuft of white or yellowish hairs on each of the first four abdominal segments, and a conspicuous red dot on segments six and seven.

Range: Entire eastern U.S. and west to Minnesota and Texas. [source].


Have there been multiple aboriginal species of dogs? In "Variation under Domestication", Darwin writes that:

  I may here state, that, looking to the domestic dogs of the whole world, I have, after a laborious collection of all known facts, come to the conclusion that several wild species of Canidae have been tamed, and that their blood, in some cases mingled together, flows in the veins of our domestic breeds.

From this, I understand that several species of dogs evolved independently and half-civilised man tamed them later on, but I want to confirm this. Does Darwin argue that there have been multiple species of beings that resemble the shape of what we now call "dogs", or that there has been one meta-species of aboriginal dogs, which branched off into several wild varieties?

That's one of — quite a few, we have to say — the mistakes Darwin made in his edition from 1859 (I have to confess that this is the only edition I've read, and I reckon this is the only edition anyone should read). This mistake is even more contrasting if you realize that he failed to apply the very same reasoning he had made just a few pages earlier, when discussing variation in pigeons: he explained that, even if counterintuitive, all different pigeons with all different features descend from the same wild species. Then, when he talks about dogs a few pages later, he incomprehensibly makes the same mistake he had just accused his readers of commiting.

Darwin is not the only one: Lorenz made the same unfounded claim, namely that the domestic dog would have two different origins, one from Canis lupus and another one from Canis latrans. We have to agree that Lorenz was way more bold than Darwin when it comes to making unfounded claims.

The fact is that, today, we're pretty sure (the scientific and statistical meaning of sure is being used here) that all domestic dogs (Canis lupus), from the chihuahua to the german shepherd, descend from a population of wolves (also Canis lupus) from east Asia.

Here is a Nature paper from Peter Savolainen, one of the best researchers on this subject: Wang, G., Zhai, W., Yang, H. et al. Out of southern East Asia: the natural history of domestic dogs across the world. Cell Res 26, 21–33 (2016) doi:10.1038/cr.2015.147


Linkage Disequilibrium in GWAS I see a lot of studies on GWAS not filter out for linkage disequilibrium or even make the slightest mention of it. Why is this the case? I would imagine that you want to keep SNPs that are only in linkage equilibrium to promote independence (and besides, without it an additive model makes no sense)

One possible reason to not filter for linkage disequilibrium is to produce peaks/hits with multiple SNPs, thereby clearly indicating a region of a causal genotype. For example, in the manhattan plot below, each point represents a SNP, the higher it is in the plot the more it relates to the phenotype.  We see that in each of the peaks multiple points are significant due to linkage disequilibrium.  If instead we had pre-filtered all of these points out then a peak has a greater choice of representing some type of error in data collection, since there is some probability that there is some error in each SNP, but not much chance of the error occurring in all the SNPs of one peak.

I am unclear why not pruning for linkage equilibrium would prevent an additive, or any model from working.  After all a GWAS is just a series of regressions between the genotypes of one SNP and one phenotype.  In this single SNP frame of reference the LD does not affect the calculation of the betas.  Zooming out, all of the significant SNPs should group together because of the LD, thereby indicating only a few regions and not causing an increase in the false error rate.


RNA polymerase and DNA helicase Is DNA helicase or RNA polymerase responsible for breaking the hydrogen bond between the 2 strands during transcription for eukaryotic cells? My textbook (WJEC Biology for AS level) says it is DNA helicase that breaks the hydrogen bonds while RNA polymerase catalyses the formation of bonds between RNA nucleotides.

  The enzyme DNA helicase breaks the hydrogen bonds between the bases in a specific region of the DNA molecule. This causes the two strands to separate and unwind, exposing nucleotide bases. The enzyme RNA polymerase binds to the template strand of DNA at the beginning of the sequence to be copied.

However, when I searched online, for example on https://en.wikiversity.org/wiki/Effect_of_hydrogen_bond_on_RNA

  Transcription can be explained easily in 4 or 5 simple steps, each moving like a wave along the DNA. RNA polymerase unwinds/"unzips" the DNA by breaking the hydrogen bonds between complementary nucleotides. RNA nucleotides are paired with complementary DNA bases. RNA sugar-phosphate backbone forms with assistance from RNA polymerase.

Then do RNA polymerase break hydrogen bonds? If RNA polymerase can break hydrogen bonds between strands then what is the role of DNA helicase in the transcription process?

Disclaimer

As I have pointed out in my comment, it is not clear whether the sources mentioned relate to eukaryotes or prokaryotes, assuming they are correct. I am a translation man, rather than a transcription man, and so am answering this from the 2002 edition of Berg et al. ‘Biochemistry’, as I happen to have a copy of my own (a freebie from when I was still teaching) and this edition is freely available online. List members with more expertise in this area are encouraged to post comments to correct any errors in my answer or supply updates.

Answer

in neither prokaryotes nor eukaryotes is the DNA helicase that operates during DNA replication involved in transcription although other proteins necessary for transcription have DNA helicase activity.
In prokaryotes it appears that the RNA polymerase holoenzyme (made up of just four subunits) is responsible for unwinding about 17 base-pairs of template DNA. Quoting from Section 28.1.3:

  Each bound polymerase molecule unwinds a 17-bp segment of DNA, which corresponds to 1.6 turns of B-DNA helix

There may be some ambiguity caused by the description of how this value was determined experimentally as it involved addition of topoisomerase II. However it is clear from discussion elsewhere that this is an enzyme of DNA replication and is not involved in transcription.
In eukaryotes transcription is much more complex, involving separate polymerases for different classes of RNA product and a variety of auxiliary transcription factors in the case of RNA polymerase II, which transcribes mRNA. According to Section 28.2.4:

  The TATA box of DNA binds to the concave surface of TBP [the TATA-box-binding protein]. This binding induces large conformational changes in the bound DNA. The double helix is substantially unwound to widen its minor groove, enabling it to make extensive contact with the antiparallel β strands on the concave side of TBP.

So the initial recognition of the TATA box causes some unwinding. However the major player appears to be transcription factor TFIIF:

  an ATP-dependent helicase that initially separates the DNA duplex for the polymerase


Availability of a database containing the proteins of Vibrio cholerae and their corresponding gene sequences I wanted a list of all the proteins (amino acid sequences) and their corresponding gene sequences of Vibrio cholerae. I tried to search in patric, but the number of amino acid sequences and gene sequences do not match, as they have provided the whole genome. I need to know if there is a database where all the proteins of Vibrio cholerae and their corresponding gene sequences can be obtained in a single file or in a couple of files. Copy pasting 4000-5000 genome and protein sequences individually from the internet seems cumbersome to me.

You want to go to PATRIC > Data > Download Tool.

From the Taxonomy tree, find Vibrio cholerae, choose Type of annotation as either PATRIC/RefSeq or both, choose the type of file you want (gbk or faa) and download from there.


Does a bird nest out of its breeding range? I have a book by the Audubon Society on building bird houses and for each bird they show a breeding, wintering and all year range.

Do the birds only breed in their breeding range, or in both breeding and all-year range?

For example, the northern flicker is shown as breeding in Canada, but its all-year range is in the United States. So, am I wasting my time building a bird house for a northern flicker in the United States which is south of the breeding range, but inside the all-year range?

An all-year range for a bird species is obviously a range where a population exists year round, and since birds generally breed each year, there will be individuals of the species breeding within this range.  Precisely speaking, this is part of the breeding range of the species, but maps of bird ranges commonly call this range the all-year range, and will reserve the term "breeding range" for that part of the range map where birds breed but are not present during part of the year.  This is helpful since it communicates which times of the year the birds can be expected to be present.

Because in temperate zones summer is the time when breeding most always occurs, maps commonly show the summer-only breeding range in a warm color such as red. For migratory species, a range where they spend the winter but do not remain during the breeding season is usually shown in a cool color such as blue.  Typically such maps will show the year-round range in a combination of these two colors, e.g. purple.  (Some maps also show a migratory range, where birds transit but do not stay for long periods, in some other color.)


Definition of "Effective population size" Could you explain to me, what is the meaning of "Effective population size ($N_e$)"?

I would appreciate an example as well.

Short answer: The effective population size of a population is the corresponding population size of a idealized (fisherian) population that would function in the same way with respect to genetic drift and inbreeding as the focal population under interest.

Long answer, below.

Definitions:

Heterogenity: the probability that two randomly sampled alleles in the population are identical (identical by descent).

Census Population Size: The census population size ($N$) is the number of individuals in the population.

Fisherian population

A fisherian population is an idealized population of size $N$, where all individuals mate at random, there is no selection, there is no population structure, there is no mutation and generations are non-overlapping. There probably are no perfectly fisherian populations in nature!

Genetic drift causes a decrease in heterogeneity. As the genetic drift is a function of the population size (see this post) this decrease of heterogeneity is a function of the population size. The heterogeneity at time $t$ is:

$$ H_t = H_{0}\left( 1-\frac{1}{2N} \right)^t$$

, where $H_0$ is the heterogeneity at $t=0$. You can verify by yourself that as $t$ increase , $H_t$ decreases. Also, as $N$ decreases, $H_t$ decreases. In other words, the longer you observe, the more heterogeneity gets lost and the smaller is the population, the higher is the loss of heterogeneity.

Effective Population Size

Let Pop_A be a real population. The effective population size ($Ne$) of Pop_A is the size of an idealized fisherian population that would have the same loss of heterogeneity than Pop_A.

You can read the above sentence twice to make sure you understand it. It basically is the definition of the concept of effective population size.

In other words: Let $N$ be the population size of Pop_A. If Pop_A is a perfect fisherian population, then its loss of heterozygosity through time is given by:

$$ H_t = H_{0}\left( 1-\frac{1}{2N} \right)^t$$

If Pop_A is not a perfect fisherian population, then it's decrease in heterozygosity is greater than the one given by the above formula. The decrease in heterozygosity of Pop_A corresponds to the decrease of heterozygosity of an idealize fisherian population of a different size. This size is called the effective population size $Ne$. So, we can rewrite the loss of heterogosity through time of Pop_A as:

$$ H_t = H_{0}\left( 1-\frac{1}{2Ne} \right)^t$$

(Note $N$ has been replaced by $Ne$)

, where $Ne$ is the effective population size of Pop_A.

Usually $Ne < N$, meaning that a real population undergoes more genetic drift than does a fisherian population of the same census size. There are many reasons that may yield a real population to have a higher drift than it would be expected with the same census size but respecting the assumptions of the fisherian population. Below I discuss three reasons:

Examples

Unequal sex-ratio

Think as a first example of a population where the sex-ratio is extremely biased to the point of having one male for 99 females. In such population, half of the alleles of a given locus at the next generation will come directly from the father. In such situations, the genetic drift is much higher than what would be expected from a fisherian population of size 100. Therefore $Ne<N=100$. To calculate $Ne$ when the sex-ratio in unequal you can use this formula:

$$Ne=\frac{4N_mN_f}{N_m+N_f}$$

, where $N_m$ and $N_f$ are the census populatino size of males and females respectively. You can verify that when $N_f = N_m$, then $N_f + N_m = N = Ne$.

Variation in population size through time

If your population size varies throughout a given time (a year for example) and that at time $t=3$ (a given period of the year) the census population size is given by $N_i$, then the effective population size is:

$$Ne = \frac{1}{\frac{1}{t}\sum_{i=1}^t\frac{1}{N_i}}$$

This is particularly relevant for insects for example which population size varies a lot between seasons.

Selection

Think now of a population where there is a great variance in fitness (there is selection). In such population, maybe all offspring will be produced by only a tenth of the current population. As a result the effective population is ten times smaller than the census population size.

You can probably find all these informations from wikipedia: http://en.wikipedia.org/wiki/Effective_population_size

Let me know if the concept of the effective population makes more sense to you now.


How are babies born without a brain? In the United States, anencephaly occurs in about 1 out of every 10,000 births. There are several forms of this condition, wherein the forebrain is absent. The forebrain is host to most of the higher functional areas in the mammalian brain. In the most extreme case of anencephaly, the so called holo-form, only the brain stem remains.

In MacLean's model of the brain, the term brain stem is used interchangeably with the term reptilian brain, to designate the most primitive parts of the central nervous system. Many are taught this model.

  An anencephalic newborn (warning: graphic content)
  ("An anencephalic newborn", wikimedia, author: Almazi, license: public domain, DOR 27/09/2012)

From my layman's perspective I can't help but notice a reptilian likeness of the anencephalic newborn. Whilst it goes without saying that correlation doesn't equal causation, I would like to know what is known so far about the cause of this condition to yield this particular morphology (as seen in the picture)?

Perhaps someone (eventually) has even some evodevo insight to share as well?

Know your databases! This is just the query fit for OMIM.

http://omim.org/entry/206500

  Anencephaly is considered an extreme form of neural tube defect
  (182940), which has been associated with variation in several genes.
  The entity described here is believed to show autosomal recessive
  inheritance.

The genes are those associated with neural tube effects, i.e., VANGL1, T, CCL1, and FUZ. See also folate-sensitive neural tube defects.

http://omim.org/entry/182940

The folate evidence was so convincing that the US/Canada in the 1990s introduced folate supplementation in all bread, flour, and cereal products. Today, US/Canada have a lower incidence of NTD (neural tube defects) than Europe, where folate supplementation is completely left to one's choice (and if women actually care they take it too late).


Bootstrapping (symmetry breaking) in evolution Many fascinating phenomena in nature show different behaviours on the micro and the macro level. Here I am especially referring to phenomena that are symmetric on the micro and asymmetric on the macro level. Let me give an examples from physics:

  Arrow of time: Physical processes at the micro level are
  completely time-symmetric, if you reversed time, all laws would remain
  the same. Yet on a macro level they are not time-symmetric, we have an
  obvious direction (flow) of time.

It seems to me that we have a similar situation with evolution:

On the micro level it is really only about adaption (and not about improvement): You put some beings into an environment and they adapt, you change this environment and they adapt. No improvement, just blind "back and forth".

Yet looking at the whole tree of life on the macro level we have a different picture, we see all kinds of emergent phenomena:

explosion in diversity
emergence of complex interconnected ecosystems with completely new dynamics of their own
true innovations in functionality (sensors, actuators, information processing etc.)
and finally of course higher order functions like abstract intelligence (and  even qualia)

To make the difference more concrete I will give a gedankenexperiment of two planet simulators. In both cases you accelerate time so that one hour translates into one billion years. Both simulators function differently in a subtle way but you don't know how. You throw some simple sims onto both planets and let the evolution simulation run. You don't switch your computer off and go to bed, the next morning you decelerate time and take a look:

Planet 1: The simple sims quickly adapted to the environment as expected (but they stayed simple because evolution is not about improvement but about adaption).
Planet 2: Some strange looking sims wish you a good morning and want to discuss the technicalities of the Riemann hypothesis with you.

My question
What are the minimal conditions that have to be met to get this kind of bootstrapping (symmetry breaking from micro to macro level) started. And what is going on at the core of this transition from micro to macro.

Edit
My specific point is about the symmetry breaking process in the sense of system dynamics. To give an example of a possible answer it could be something like Parrondo's paradox, a fascinating phenomenon from game theory where you combine two symmetric (losing) processes to get a (winning) asymmetric process. More can be found here: Parrondo's paradox.

I found a paper which gives four conditions that have to be met:

Condition 1: A rule should be enforced that individuals
must meet some minimal criterion (MC) before they
can reproduce, and that criterion must be nontrivial
Condition 2: The evolution of new individuals should
create novel opportunities for satisfying the MC
Condition 3: Decisions about how and where individuals
interact with the world should be made by the individuals
themselves
Condition 4: The potential size and complexity of
the individuals’ phenotypes should be (in principle) unbounded

Source: Soros, Stanley (2014): Identifying Necessary Conditions for Open-Ended Evolution through the Artificial Life World of Chromaria

Chromaria is "an experimental platform that allows the exploration of evolutionary theories in an intuitive and visually engaging way" from EPLEX, the Evolutionary Complexity Research Group at the University of Central Florida (UCF)


Why do we get sleeply after we eat? After we have eaten, we feel cold and sleepy. I think it's because the maximum blood supply is transferred towards the digestive system so that digestion is done, and therefore the brain to does not get adequate blood supply. Am i right about this?

Also, why do they suggest to take a short walk after dinner especially?

After we have eaten... the maximum blood supply is transferred towards the digestive system so that digestion is done, and therefore the brain to does not get adequate blood supply. Am I right about this?

This is a very, very common myth, but it is a myth. Because blood flow and oxygen delivery to the brain is critical for survival, cerebral circulation is one of the most tightly regulated systems in the body. Blood is not shunted from the brain to the gut for digestion.

  In a normal physiological state, total blood flow to the brain is remarkably constant due in part to the prominent contribution of large arteries to vascular resistance.

Eating, sleeping, walking, etc. are all normal physiological states. If we had blood shunted away from our brains after eating, we'd literally collapse after every meal.

  In normotensive adults, cerebral blood flow is maintained at ~50 mL per 100 g of brain tissue per minute, provided CPP is in the range of ~60 to 160 mmHg.

As eating alone doesn't normally cause our blood pressure to rise or fall, cerebral perfusion is constant regardless of what is or isn't in our digestive systems.

Blood flow to the gastrointestinal system (or GI tract) is also regulated, but the flow varies widely:

  Estimates of blood flow (in ml /min × 100 g) to the quiescent gastrointestinal tract of dogs and cats range from 15 to 100 for the stomach, 35–120 for the small intestine, and 10–74 for the colon. Somewhat lower values for resting blood flow to the stomach, small intestine, and colon have been reported for man.

So, the basic answer is that, yes, blood flow to the gastrointestinal tract varies, but blood is not shunted from the brain in favor of the GI tract.

So why do we get sleepy after a meal?

Sleepiness after a meal is caused by the level of peptides in your brain called orexins (aka hypocretins).

In 1998, two groups of researchers simultaneously discovered 2 small neuropeptide hormones that regulate, among other things, wakefulness and feeding behavior.

One group discovered them while searching for molecules that could bind to "orphan" receptors, that is, a brain receptor with an unknown "binding" molecule (called a ligand). They found that the prohormone prepro-orexin was found in a very small area of the hypothalamus which had been implicated in the regulation of feeding behavior and energy homeostasis; this suggested the possibility that the neuropeptides might be involved in the regulation of food intake. When administered into free-feeding rats' brains, one of these peptides (orexin A/hypocretin 1) stimulated food consumption in a dose-dependent manner (with attention to light and dark periods, i.e. the circadian rhythm), with a lower dose increasing rat feeding about 2-fold, and the higher dose inducing a 3+-fold increase in feeding compared to rats injected with a solution without the peptide (the other stimulated feeding to a lesser degree). The effect persisted for 4 hours. Furthermore, fasting rats produced more than twice as much orexins as rats feeding freely. For this reason, the molecules were names "orexins", after the Greek word orexis, which means "appetite". They speculated that the orexin-secreting neurons might somehow be modulated by glucose.

At the same time, another group of researchers using a completely different approach found that the same group of hypothalamic neurons were stimulated by a peptide hormone similar in composition to the gut hormone secretin. They identified the same prohormone and its two peptides, naming them hypocretins for "hypothalamus" and "secretin". They found that at least one of the peptides had a neuroexcitatory activity in specific areas of the brain (they mapped effects in the hypothalamic neurons, the posterior hypothalamus, the septal nuclei in the basal forebrain, the preoptic area, the paraventricular nucleus of the thalamus, the central gray, the locus coeruleus, the colliculi, the laterodorsal tegmental nucleus, and the nucleus of the solitary tract) suggesting that the peptides acted within the central nervous system as homeostatic regulators with a role in nutritional homeostasis.

Scientists have not decided on whether to call them orexins or hypocretins yet, so both are used. They are found in all vertebrates.

Mammalian orexin A sequences thus far identified (human, rat, mouse, pig, dog, sheep, and cow) are all identical, whereas the sequences of orexin B show some differences among species. From Orexin/Hypocretin: A Neuropeptide at the Interface of Sleep, Energy Homeostasis, and Reward System, Natsuko Tsujino and Takeshi Sakurai

In 1999, a group of scientists found that narcolepsy (a sleep disorder characterized by extreme daytime sleepiness) was caused by a lack of a hypocretin/orexin receptor 2 gene in certain dogs, therefore establishing that they play a very important part in the regulation of wakefulness.*

Since then, an enormous body of work has shown that orexins/hypocretins (O/H from here on in) are involved in the regulation of a wide range of behaviors, including wakefulness and vigilance (needed to find food), systems that regulate emotion and reward (including drug-seeking behavior when stressed and eating for pleasure - "consumption beyond homeostatic needs" - leading to obesity), and more.

What does eating have to do with sleepiness?

Several studies report that the firing rates of O/H neurons are influenced by serum glucose, triglycerides and amino acids.

In English: You are awake (O/H is being secreted by O/H neurons in your hypothalamus). You eat. Your serum glucose rises. The elevated glucose causes depolarization of inhibitory neurons that hyperpolarize O/H neurons decreasing the amount of O/H. released. Result: wakefulness decreases.

Control of Cerebral Blood Flow
The Gastrointestinal Circulation.
Comparing these two papers - the first and second references - is a wonderful example of the completely different methods used by scientists to investigate unknowns and up with the same basic conclusion.
Orexins and orexin receptors: a family of hypothalamic neuropeptides and G protein-coupled receptors that regulate feeding behavior, Cell 92 (4): 573–85
The hypocretins: Hypothalamus-specific peptides with neuroexcitatory activity Proc. Natl. Acad. Sci. U.S.A. 95 (1): 322–7
The Sleep Disorder Canine Narcolepsy Is Caused by a Mutation in the Hypocretin (Orexin) Receptor 2 Gene
The role of orexin in motivated behaviours A Nature Neuroscience Review
The role of orexin-A in food motivation, reward-based feeding behavior and food-induced neuronal activation in rats
*Human narcolepsy - caused by a destruction of O/H neurons - also is associated with metabolic abnormalities, including increased frequency of non-insulin-dependent diabetes mellitus and increased body mass index.
Hypothalamic Orexin Neurons Regulate Arousal According to Energy Balance in Mice
Orexin/Hypocretin: A Neuropeptide at the Interface of Sleep, Energy Homeostasis, and Reward System


Relation between OD with different microbial growth Equal volumes of cell suspensions of Escherichia coli, Saccharomyces cerevisiae, Streptococcus lactis and Mycoplasma pneumoniae, all have the same OD600nm = 0.50. Which cell suspension would have the minimum and maximum number of cells, respectively?

Difficult to say with the information you have given. Here is a paper on the subject if you are interested. The relationship between OD and cell count depends on morphology and size, which in turn depend on culture condition, strain, etc...


Why would a venus fly traps mouth that's still "chewing" die? A venus fly trap produces leaves that act like traps for insects. A trapped insect is digested over several days. The trap then opens again to catch another insect.

These traps regularly die off. They turn black. They are replaced with new ones. I'm not sure why that happens. As far as I know this is a swamp plant, which makes it unlikely that the traps die off due to being in contact with water. I read that a trap can only be reused 7 times. So I guess the traps are replaced by the plant in some interval.

As the dead traps start to rot in the pot, I pick them up from time to time and throw them away. Recently, during that process, I found this:

and it made me wonder why this mouth would die off. It looks like it caught something. As the mouth is still closed, I think the digestion process is not finished yet. But why would the plant give up this valuable resource?

Is it because the trap could not close entirely? There are signs of rot on the insect, but I don't know if that happened after or during the digestion process. Would rotten prey be a problem chemically? A human can dissolve quite a few things in its stomach, so I guess this could work similarly.

What are the reasons for the traps to die off in general?

There are many things that could affect the rotting of your venus fly trap while digesting including: size of the bug, age of the trap, and temperature.

Sometimes a venus fly trap will turn black and fall off while it's digesting a bug when the trap is very old. As the trap ages, the digestive juices are recycled and as a result form a weaker mixture which slows the digestion process.

The bug it was digesting was also probably very large or had a hard shell inhibiting the trap from properly closing. This allowed bacteria and mold into the trap to digest the insect also proliferating the rotting of the fly trap itself in the process.

Temperature also has an effect on the trap's digestion where higher temperatures speeds up the enzymatic process of digestion. However, this is probably not a factor in your case.

It's not so much that your venus fly trap decided to give up on the valuable resource, it was either too old to properly digest the bug or it couldn't close properly because the bug was too large that bacteria infested the bug and the trap speeding up the process of the trap falling off the plant.

For more detailed explanation see: http://science.howstuffworks.com/life/botany/venus-flytrap4.htm


Can species back-evolve? One of the tenets of Darwin's theory is the survival of the fittest, ie adaptation of features that allow a species to adapt better to its surrounding environment. I am wondering that given the right conditions, is there a possibility of a more "complex" species, say humans, back-evolving into a less "complex" species, say a dog? Is there anything in Darwin's theory or some experimental proof that excludes such a possibility?

EDIT (4/19/12): Thanks for all the responses! I definitely agree with the fact that we are no more complex than dogs or Drosophila, hence the quotes surrounding complex in the question. I learnt a lot from the answers and don't think there is any one answer that is the best, but read together, they drive home the point. Thanks all!

Complexity is a lure. Evolution isn't defined by complexity, but by adaptation to one's environment, as you mentioned.

Evolution is an ongoing, non-deterministic process. There's not one definite evolutionary "path" that brings a unicellular to a modern human being. Nor is there a predictable evolutionary path that brings a dog into becoming a human. You also have to acknowledge that, because evolution is ongoing, the dog of yesterday is not the dog of tomorrow. That applies to all the living.

Is it possible that given the right amount of time and the ideal environment the modern human could evolve into the modern dog?

Yes, it is possible.

Is it probable? No.

The chances are that if humanity were to find itself in such an exotic environment - to which dogs are 100% adapted, but humans 0%, which just shows how unprobable such an environment is - it would become extinct before it has a chance to adapt, much like a lot of other species have done.


Why use two stop UGA codons instead of one in the spike protein mRNA for the BioNTech/Pfizer SARS-CoV-2 vaccine? Unlike the SARS-CoV-2 virus, the BioNTech/Pfizer SARS-CoV-2 vaccine has two stop UGA codons  at the end of the Spike protein:
          V   L   K   G   V   K   L   H   Y   T   s
Virus:   GUG CUC AAA GGA GUC AAA UUA CAU UAC ACA UAA
Vaccine: GUG CUG AAG GGC GUG AAA CUG CAC UAC ACA UGA UGA
          V   L   K   G   V   K   L   H   Y   T   s   s
               !   !   !   !     ! !   !          !

What is the motivation behind using two stop UGA codons instead of one in the BioNTech/Pfizer SARS-CoV-2 vaccine?

The two stop codons are obviously to prevent read-through of the termination codon.  Why this should be necessary is not clear to me, but the following may be relevant:

The synthetic mRNA differs from the natural mRNA in a particular respect that is easier to explain with reference to the transcript map of the virus, below.

The two ORFs 1a and 1b are translated directly from the virus RNA as polyproteins, which are subsequently cleaved, but the proteins at the 3′ side of the viral RNA are transcribed into a series of nested mRNAs, each starting from a different 5′ position immediately preceeding the gene that will be translated. These mRNAs also retain RNA corresponding to the remaining genes (coloured grey, and not translated because of the monocistronic translation of eukaryotic mRNA) and the common 3′ polyA tail. The synthetic mRNA for the spike protein (S) lacks the RNA for the non-translated genes, and has the polyA tail near to the stop codon. Hence the secondary structure near the stop codon in the synthetic mRNA may well differ from that in the natural mRNA and possibly influence the likelihood of readthrough.

The stop codons used in this artificial mRNA are not UGA but 1-Me-ΨGA, as U is replaced by 1-Me-Ψ (1-methyl-pseudouridine*) in they synthetic mRNA to prevent degradation. As the anticodon is recognized by a termination factor — not a tRNA anticodon — the interaction with 1-Me-ΨGA may possibly be poorer than for UGA.

Footnote
*The structural relationship between uridine, pseudouridine and 1-methyl-pseudouridine is shown below. The NH and CO involved in base-pairing are similar in each case.
The sequence is generally written with Ψ, rather than 1-Me-Ψ, for compactness.


What is this Peacock-like creature? In the below picture I believe  bird in the foreground is a female. The one that opens the wings is the male.

It looks like male Great Argus (Argusianus argus) displaying to a female. The circular markings on the male pheasant's secondaries are pretty distinct. The specific epithet argus refers to a hundred-eyed giant from Greek mythology.


Is there a kind of 'rule' which decides whether the male of female is bigger? In human race usually males are larger than females, and probably is this for all primates. But some animals there are the females bigger, but what determines whether the male or female should be bigger. Is this just random with no logical system as evolution can be or are there some marks which indicates that it is better that the female should be bigger?

In short, there is not a rule of thumb whether a given species will have bigger males or females. In some cases females are larger (often insects, invertebrates or fish), in other cases males are larger (often mammals and birds) but even these generalizations have exceptions (Ralls (1976)).

When a males and females of a species have morphological differences other than differences in reproductive organs, this is called sexual dimorphism. These dimorphisms can be thought of as adaptations which have evolved due to a specific evolutionary pressure.

In males, larger sizes can evolve from sexual selection on males in competition with other males for mates. Simplified, the bigger males are better competitors. In females however, larger sizes can evolve from a number of different pressures, but rarely due to competition for mates. More common pressures resulting in larger females are rearing success, competition for resources other than mates.

Whether males or females of a species are bigger is certainly not random, but rather a precise outcome of numerous trade-offs and benefits of being bigger.


PCR products with no band in gel I am a PhD student and stuck with the no band in the gel  results.

I am using the following

1 microliter  Primer R (20mM)
1 microliter  Primer f (20mM)
1 microliter  dNTP  (10mM)
1 microliter  DNA Template ( 448 ng)
1 microliter TAQ polymerase
5 microliter Buffer (10x)  added MgCl2  by 1:1
30 microliter PCR grade water

Program:

95 for 4 minute
95 for 45 sec
55-65 for 1.20 minute
72 for 1 minute
Gradient 35 cycle
72  for 4 minutes

Gel:

110 volt, 200 mPA for 30 - 45 minute

I get PCR products as in the images. There are no bands  while there are intense bands at the bottom and some of the wells.

My question is,  is that at the bottom products??
what can be done to make them real? If not then why there are differences between the two lane of wells. Each 12 well are representing a one type of DNA template (I used three different organisms DNA).

Use control primers targeting something which for sure gives a product. If you have none, ask your colleagues or take some out of literature. Make sure your product is small enough to be amplified in the time given and check for the correct band with a restriction enzyme.


Ethidium bromide and mutagenesis on cloning When performing a DNA cloning, sometimes PCR amplicon is run in agarose and it is detected by ethidium bromide marking under UV light. After that, gel is sliced, DNA extracted from gel....... until eventually you have your transgenic organism. The thing is that when doing so, you use the very same DNA sample that was "contaminated" by ethidium bromide, so does this DNA you are using for transformation contain ethidium bromide? if so, how can it affect in numbers to mutation risk?

Purified DNA contains negligible amounts of ethidium bromide. PCR and gel clean-up kits remove it quite well. There is, though, a risk of mutation from the fact that you're visualizing the gel in UV light with ethidium bromide. The risk of mutation from UV is minimized by exposing the gel as little as possible, and by using "preparative" transilluminators that come with a low-light setting for cloning purposes. If you work well and quickly, the chance of mutagenesis isn't higher than the chance of a polymerase incorporating the wrong nucleotide.


Cell differentiation by non-identical copies There are in principle two ways that two cells with the same mother cell can differentiate/specialize/diverge:

Because they are not perfect identical copies (= different internal influencing factors). I explictly don't mean "non-identical on the DNA level", but on the level of other cellular components!
Because they are exposed to different external influencing factors (chemical, mechanical).

Can it be said, which of these two reasons of cell differentiation is the more common, frequent, resp. "important"? Or does it completely depend on the (type of mother) cell and some general circumstances?

If internal factors (= non-identical copies) are an important source of differentiation, I have two (optional) questions:

How does the mother cell manage to cleave into two non-identical copies in a rather fine-tuned and determinstic way? Or is any kind of asymmetry enough?
Which is the first cell (starting with the zygote) that cleaves into two non-indentical cells, different enough to give rise to differentiation? (From this answer I believe to have learned that this might happen already after 1-4 divisions.)

I found a partial answer to my and this question at Quora:

What regulates initial cell differentiation?

Ian Driver says:

  In many organisms the initial cell has mRNA (or protein) partitioned
  in one half of the zygote.  One daughter cell inherits most of the
  mRNA or protein and goes on to activate or repress genes in that cell,
  but not in the other.  This has been visualized and well studied in C.
  elegans: Asymmetric cell division and axis formation in the
  embryo.


Difference in reptile inner ear and otosclerosis In reptiles, the sound is conducted from the tympanic membrane to the inner ear by a single bone.

In the disease otosclerosis the stapes of humans become fused to the other middle ear bones( or to the oval window ). This disease leads to the loss of hearing.

My question is - From what seems like superficial resemblance between otosclerosis and having one bone in reptiles, what is the difference between the two that leads to loss of hearing in one case but not in another ?

Good question. To understand it perfectly, you'll need a good reference to a text on detailed explanation of sound conduction by the ear ossicles in reptiles and humans. I couldn't find anything better than these here and here.

But these are partly inadequate in addressing your questions and are a bit involved in the physics used.
But, if we leave the physical details aside below is the possible reason as to why a single bone in case of reptile conducts just fine but in humans fails to conduct.
 The reptile ear has evolved such that it uses a single bone for conduction, while the human ear is functioning with three transmitting ossicles (the only example i could think of). This is similar to the working of a watch. You can create a time-keeping device by using a combination of three gears (old play watches) or a combination of a large number of gears (my Timex Retrogade). Both have the same function, but if we fuse several gears in the second case to equal the number in the first (hypothetically only), it will obviously stop working. In our analogy, the ear has evolved such that the sound is optimally transmitted due to several effects like, resonance, impedance, transformation and simple amplification along the ossicles, and all these functions depend very specifically on the shape and orientation of the various conducting elements of the system. And therefore, even a slight disfigurement might severely impair the conduction of sound. Therefore, had the human ear system evolved to work with one ossicle, it would have evaded osteosclerosis by being able to conduct with one ossicle also.


If a DNA letter is one of A,T,C and G, and there are 3 billion base pairs, why don't we say that there are 6 billion letters in the genome? A DNA letter is either one of A,T,C or G. Human genome is supposed to have 3 billion base pairs coming from each parent. But these are pairs - a combination of A-T or C-G. So, doesn't that make the total number of DNA letters from a single parent, equal to 6 billion ?

If a DNA letter is one of A,T,C and G, and there are 3 billion base
  pairs, why don't we say that there are 6 billion letters in the genome?

It is a convention, and stating the actual number of bases would not add any information, but would actually lead to more confusion. It's like saying

  I have six pairs of socks

vs.

  I have twelve socks.

It means bascially the same, but now one could assume that these twelve socks are not from actual pairs (e.g. twelve left socks). The same goes for DNA. Saying we have pairs of bases emphasizes the redundancy of the DNA double strand.


How do you convert mtDNA sequences in FASTA to FSTAT format? I've got control region sequence data from a population of shark and I'm looking to convert this from FASTA to FSTAT in order to calculated the effective population size of females. The software I want to use only accepts FSTAT or Genepop files.

Is it possible to convert FASTA to FSTAT or even Genepop?

Check out PGDSpider. The inputs and outputs table indicates that it supports conversion between FASTA and FSTAT formats, among many others.


Easy Hardy Weinberg Equilibrium Hi
My friend and I get 2 different answers to this question. I would like to know how to calculate the value of q. My friend says that 500/1500=q because there are 500 recessive alleles in the population and there are 1500 alleles in total. I say that p2= 500/1500 and P is the square root of that value and  q+p=1 but we both get different answers.  Please let me know which way is correct. Thank you guys in advance

P=(250 × 2 + 500)/1500 = 0.66
Q=500/1500 = 0.33
Your friend was right, you miscalculated P because forgot to add the alleles coming from the heterozygotes.


How to know if your breathing is normal? Is it possible for a device to measure how much air we breathe in and out over the entire day and at what rate? I think if we have access to this data we can compare it across people.

What you are looking for is a spirometer. There are different types of spirometers serving different purposes like the Incentive spirometer and the peak flow meter. I would suggest that you go through the wikipedia page on it to get more info.


If a gene altered causes cancer and creates a protein for cancer can the new protein be isolated in some way? In the above title question, can the protein thats altered not be isolated (to separate out from other proteins) somehow?  Is there nothing that can bind to the specific cancer proteins that will not bind to other proteins?

From how I read your question, you're wondering if there is some technology to somehow isolate oncogenic proteins inside the cell so they don't do harm, is that correct?

The answer is somewhat complicated, as it depends on the protein. First, though, you need to understand that cancer is a very complex disease, and cancer is not caused by a single mutation alone. The "multiple-hit" or Knudson hypothesis essentially states that a cell progresses from a normal cell to a cancerous one, accumulating multiple mutations along the way. In pretty much all cases, at least two specific mutations are needed - the constitutive activation of a proto-oncogene, a group of proteins responsible for cell growth and proliferation, and the deletion or inactivation of one or more tumor suppressor genes, which are used to keep growth and proliferation under control. This way, you have a tumor driver (often this is a single protein, like a growth factor receptor) "driving" the oncogenic process, with no "brake" or regulation.

As I said, mutations in tumor suppressor genes generally result in loss-of-function changes, or complete deletion/inactivation of the gene altogether, so "isolating" these proteins in the cell wouldn't do much good. The focus of many tumor therapies is to down-regulate, inhibit, destroy, or otherwise remove the function of the protein that is driving the uncontrolled growth and proliferation of cells, forming tumors and metastases. If we're lucky, the tumor driver is an extracellular domain-containing protein (like a cell-surface receptor) that can be identified and targeted from outside the cell. Once this has occurred, scientists and doctors can use specially-derived monoclonal antibodies to target and kill the cells containing these proteins:

Monoclonal antibodies for cancer. ADEPT, antibody directed enzyme prodrug therapy; ADCC, antibody dependent cell-mediated cytotoxicity; CDC, complement dependent cytotoxicity; MAb, monoclonal antibody; scFv, single-chain variable fragment.

From WikiMedia Commons, released into the public domain.

There are a number of ways the cancer cells can be killed, from delivery of radiation or other cytotoxic compounds, to attracting killer cells from the immune system, to activating the complement system. However, all of these depend on the surface presence of biomarkers for the cancerous cells, so as to avoid non-specific killing or off-target effects.

The reason so much focus is put on killing the cancerous cells instead of trying to isolate the "bad guys" inside the cells is that by the time the cell has become cancerous, it already has accumulated so many mutations that a) the cell isn't really worth saving, and b) it would take an extraordinary amount of effort to corral all the mutated proteins together, and leave whatever unaffected or "wild-type" proteins were left to do their jobs.

You may recall that each gene we have (except for some on the X and Y chromosomes) is present in duplicate, one copy from our mother and one from our father. The initial mutations that begin the progression to the fully cancerous state may at first only affect one of those two copies of the gene, leaving a working version around for a while. However, as oncogenesis progresses, and more and more regulatory proteins are inactivated, chromosomal damage grows, and frequently the surviving "normal" copy is either mutated itself or completely destroyed. Once this occurs, even if you could isolate the misbehaving proteins, there would be no good proteins left to do the jobs of the cell. Therefore, killing is really the only option.

I hope I've covered what you were interested in. Please let me know if you don't understand any of it, or you can always ask a new question.


Why are some vegetables/fruits seasonal? How does the mango tree perceive the summer season, so tree starts producing the fruits?

Every tree requires sunlight to grow but what limits the production of fruits to a certain season?

For example: Mango only grows in summer season, whereas banana grows in all seasons.

Many plants start flowering (and subsequent seed / fruit production) based on light, temperature, and / or humidity changes, which tell them summer is near. That is when they need to grow fruit. Surely, there are plants trying to look for sunlight, pollinators, good conditions for seedlings, in the winter, but they are specially adapted, and thrive in their niche only through some season sensing similar to the summer-flowering plants.
At the Equator there isn't much difference between seasons and days, and there  should be no need for such mechanism. Bananas are suited to the Equator, meaning banana trees don't know what seasons are.
Plants in temperate climates care about seasons a lot. We put them in greenhouses and we play with their light, in order to force off-season flowering. Tomatoes are kept in the greenhouse not because we don't like them shivering outside, but because we want to fool their temperature-sensing organs that summer is here.
At the Tropics there is an important difference in the amount of rain water and a smaller change in day duration. Mangoes are more suited to the Tropics, meaning they care about seasons. People who grow mangoes in greenhouses try to fool them by adjusting humidity, but I couldn't find any evidence that it is humidity rather than day length.


conversion from cpm/mg to mg I 've an essay about wheat sprout extract, there's a graph about protein content in first 4 day of wheat sprout. so under the graph there's this text

  Phosporylation by endogenous kinases of the macromolecules contained
  in 1 g of the aqueous wheat sprouts extract. Results are expressed as
  cpm/mg of protein±SEM at 4 different days of germination. 0 are
  unsprouted seeds

so my problem is to know how many mg (milligrams?) is content for 1 g of protein
in few words I need how many mg of protein is content in 1g of products, a conversion from cpm/mg to mg ... is possible?

cpm = counts per minute

E. Cpm to fmol/mg:  Enter the specific radioactivity as cpm/fmol, the number of cpm counted, and the protein content of the sample in mg. The result is the number of binding sites in fmol/mg protein.

here is a guide of conversions.

The measure is a relative measure, and it can't be very precise as a discrete measure without knowing the precise measurement conditions, i.e. is it mixed every 5 minutes or every 1 minute, is it dissolved in 1 liter or 100ml? CPM denotes the reactivity and not the weight. You are more likely to get a Mol/L rating associated with a CPM, and two vials with the same CPM rating can have different Mol/L and Mg/L depending on their reactivity.

So, if your paper gives you a comparative measurement, and if it gives you a specific measurement at some stage you should be able to multiply it and figure out the numbers for the various days.


Why do people say that smallpox has been eradicated? I keep reading things like “smallpox has been eradicated” or “there are only two samples of the virus left in existence in a lab somewhere”, but couldn’t there be a bunch of smallpox viruses in an alleyway where some infected person sneezed years ago? Is there some reason the virus can’t exist without a human host?

The viruses that caused smallpox (Variola major and Variola minor) are generally not stable in the environment (<24 hours as an aerosol), though they may persist for more than a decade within scabs Reviewed: Sinclair et. al., 2008 OSHA.

UV light is an excellent disinfectant, so typically any virus exposed to sunlight will lose rapidly infectiousness.

You may also find this answer to a related question of interest:
https://biology.stackexchange.com/a/59165/46609


Do any cells change in size or mass as mammals grow? That is to say, are there cells that, between infancy and adulthood, get larger?  Or is all growth done entirely via cell division?  I'm wondering if it is safe to assume that the approximate number of cells per unit mass in a mammal will remain fairly constant throughout its lifespan.

I'm wondering if it is safe to assume that the approximate number of cells per unit mass in a mammal will remain fairly constant throughout its lifespan.

Not exactly.  When a tissue is put under stress, it can respond in four main ways:

Hypertrophy - individual cells get larger.  E.g. stressed muscle cells get bigger.
Atrophy - invidivual cells get smaller.  E.g. naturally in the thymus during development.
Hyperplasia - increased cell division to produce more cells.  E.g. mammary gland cells in pregnancy
Metaplasia - one type of specialised cell is replaced with another, usually more durable one, E.g. columnar epithelium in the respiratory tract of a smoker being replaced with squamous epithelium.

The first three responses to stress can change both cell size (auxetic response) and number (multiplicative response), meaning you can't really say that cells per unit mass stays constant throughout life.

Muscle tissue grows predominantly by hypertrophy, meaning that the muscle gains during puberty are likely to be more as a result of cells getting larger than the development of new ones.

Both auxetic and multiplicative growth occurs as the body develops.  In addition to this, accretionary growth also occurs - where connective tissues such as bone and cartilage increase in size.


Cockroach-like insect identification (India) I just saw an insect in my room, and I have never seen anything like it ever before. I captured a photo, please see if you can identify it. It has got quite unique colours on its exodermis and it has 2 pairs of wings ( I was not able to get a picture of them) which are very similar in structure and position to those of a cockroach. In addition to that, it is able to fly, albeit for short distances.

I live in Kolkata, India and the length of the insect is approx. 6-8 cm.

It's a longhorn beetle (Cerambycidae).
Most likely, it's a Red-spotted longhorn beetle (Batocera rufomaculata), also known as a mango tree borer, mango stem-borer and tropical fig borer.
See this SE question pertaining to the same insect.

From Biolib:

Country check-list: China, India, Israel, Jordan, Laos, Lebanon, Madagascar, Malaysia, Mauritius, Myanmar, Pakistan, Puerto Rico, Sri Lanka, Syria, Thailand, Virgin Islands  [Might Not be complete]
Food: Ficus carica L. (Fig), Carica papaya L. (Papaya), Mangifera indica L. (Mango), Shorea robusta Gaertner f. (Sal Tree)

It might also be B. parryi, which, similar to B. rufomaculata, is common in SE Asia (but which is absent from Western Asia or Africa where B. rufomaculata is also found). Since you live in India, both are possible. I will look for a key to determine how to differentiate the 2 species.
Meanwhile, here is a list  of related species in the Lamiinae subfamily for further reference.
Also, a great resource (including keys) for wood boring beetles of the world!


What's the difference between a simple and 1-foliolate (unifoliolate) leaf? How is a 1-foliolate leaf (e.g., Hardenbergia) different from a simple leaf?

Short answer:

Look for a pulvinus at the leaf-stalk/leaf-lamina junction.

Long Answer:

So from a strictly anatomical identification standpoint, this can be a bit confusing.

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):

  Simple: Undivided, as a leaf blade which is not separated into leaflets.

Where:

  Leaflet: A division of a compound leaf

and

  Compound Leaf: A leaf separated  into two or more distinct leaflets.

So the definition of a compound leaf is to have "two or more distinct" leaflets.

But wait...

From plantnet:

  one-foliolate (1-foliolate, unifoliolate): a compound leaf reduced to a single leaflet, usually recognized by the articulated or jointed ‘petiole’, which is in fact a petiole plus a petiolule.

So what gives?

Perhaps this is due to a deficiency in terminology, as discussed (and corrected) by Jiménez-Saa 2011.

But, again Harris & Harris (2001) hint toward how this might arise [emphasis mine]:

  Unifoliolate: a leaf theoretically compound, though only expressing as a single leaflet and appearing simple.

So there is still a fundamental difference between the two.

Structurally, we can see the difference at the basal joint of the foliar structure:

  Simple or unifoliolate: The leaf is undivided...with (unifoliolate) or without (simple) an articulation between the leaf lamina and leaf stalk. [source]

Put differently:

  Unifoliolate leaf is usually recognized from a simple leaf by the presence of a distinct joint or a pulvinus at the lamina-petiole junction, which is in fact a petiole plus a petiolule.

Note: Pulvinus = a distinct enlargement/swelling at the base of (sometimes at the apex of) a petiole or of a petiolule.

Note: a discussion about the developmental evolution of unifoliolate characteristics in Cercis canadensis is discussed here.