Why do genes with closely related functions often reside on different chromosomes? Why do genes with closely related products are so often positioned on different chromosomes?

To illustrate what I mean, here is an example from immunology:

the invariant region of MHC is on chromosome 5
the variant region of MHC is on chromosome 6
β2-microglobulin is on chromosome 15

These three gene products associate into a single protein-complex to present antigens. Why are these genes situated on different chromosomes? Wouldn't it make more sense to keep them associated into a localized region onto a single chromosome so that their transcription can be jointly regulated?

It is just an example; I get the impression that many multiprotein complexes are formed with products from different chromosomes.

The thing we must remember is that during evolution, there occurs many events that may result in genomic reshuffling.

Considering your example of MHC, when we look into the evolution of the complexes

  The classical human MHC contains 224 genes, .... Antibody and T cell mediated immune responses against invading pathogens are initiated through MHC class I and class II molecules. These main components are not only missing from invertebrates, but are also not present in primitive jawless fish, such as hagfish and lamprey. MHC class I and II molecules do, however, exist in all jawed vertebrates, including the cartilaginous fish.

Now that tells us something in itself. If you observe the universal evolutionary tree, we can conclude that the hagfish and lamprey are most ancestral, especially compared to telostii. This is crucial when speaking in terms of evolution, as

  this demonstrates that the separation of the MHC class I and class II loci is characteristic of teleost fish, which represent half of all vertebrates. Since the genes of the immune system were present in the common ancestor of tetrapods and teleosts, the differences in their genomic organisation may be the result of lineage-specific chromosomal events such as duplications, inversions, deletions and translocations.

You can read more about the MHCs here:

Sambrook, Jennifer G., Felipe Figueroa, and Stephan Beck. "A genome-wide survey of Major Histocompatibility Complex (MHC) genes and their paralogues in zebrafish." BMC genomics 6.1 (2005): 152.

And thats usually the reason for the major changes you see. Often other changes occur, due to transposons, which cause pseudogenes to form and/or neofunctionaliation to occur. You can read about them here:

Feschotte, Cédric, and Ellen J. Pritham. "DNA transposons and the evolution of eukaryotic genomes." Annual review of genetics 41 (2007): 331.

I am fairly certain, that this applies practically to majority of the genes, that are not linked strongly genetically (http://learn.genetics.utah.edu/content/pigeons/geneticlinkage/).


What is background signal in a Western blot? I have done a western blot and I want to remove the background signal when doing densitometry analysis of my protein bands of interest. I have read some articles online such as this one regarding high background in western blots. I have learnt that there are many factors that can contribute to high background in a western blot. However, I am still not sure what exactly is defined as background. Does it refer to non-specific antibody binding on the membrane, or can it also refer to regions on the membrane where there is no binding to any protein?
Any insights are appreciated.

In this context (and many others), the terms "background signal" and "noise" can almost be used interchangeably, if that helps.
Generally speaking, noise or background refers to any signal that isn't coming from the thing you're trying to detect (typically in reference to how that signal might interfere or be confused with your "true" signal). So non-specific binding could qualify as background, but it can also refer to regions of the membrane that shouldn't have any protein binding (with any number of causes). One exception I can think of in practice is if you have a specific non-target band that consistently shows up, that might technically fit the definition (sensu stricto) of "noise", but a molecular biologist will more likely refer to it as a "technical artifact" rather than "background".
That said, there are still a number of different kinds of "noise" or "background" that may show up on western blots, and the article you referenced does a pretty good job of describing them, but it could benefit from including some images. Here's a similar guide with more images and links to other Western troubleshooting guides. Hope it helps.


What is the opposite of a mutation (the regular state)? What is the term, if there is one, to describe the natural state of a gene? The one single word to describe it, just like mutation is the one single word do describe a deviation from that state.

A mutation can be both the act of changing the genetic material (the process) or the changed genetic material itself (the result of the process). You're using the second meaning. See What is the definition of a mutation? for more info.

That being said, the opposite of a mutant allele is a wild type allele.

According to Pierce in his book "Genetics: A Conceptual Approach" (2012):

  The normal allele for a character is called the wild type because it is the allele most often found in the wild. (emphasis mine)

The same way, the opposite of a mutant phenotype is a wild type phenotype.

Besides that, you can sometimes find "wild" alone, without "type": wild allele, wild phenotype etc...

Source: Pierce, B. (2012). Genetics. New York, NY: W.H. Freeman.


What are the functions and differences between axons and dendrites? My textbook doesn't do a very good job of pointing out what the differences between the two are. It basically mentions axons only in the same breath as the synapse (that synapses are the endings/tips of axons).

This reference is a bit basic, but lists the functions and differences between axons and dendrites.  Specifically, dendrites receive signals from other neurons, to the cell body; whereas, axons take signals away from the cell body (essentially 'input-output').  A diagram of the parts and the processes is below:

(Image source with additional information)

This Youtube tutorial is a nice visual description of both, and how they function within a neuron.


Identification of caterpillar in Texas I found this caterpillar eating my parsley, around Austin, TX.

It looks very monarch-ish, but apparently monarchs don't eat parsley.  Plus it has knobs on its back.

But it also does not look like the Eastern Swallowtail since there is almost no hint of green in its color.

Hoping that this turns into some type of pretty butterfly I am letting it run amok on the parsley for the moment.

Any ideas?

It is the caterpillar of Papilio polyxenes.

  The pupae may be green or brown, but not depending on surroundings or the background on which they have pupated. The color of the chrysalis is determined by a local genetic balance that ensures the majority of pupae will blend in.[10] A section of the green pupae will turn a much darker green at the very end of the pupae stage. This color change occurs a few hours to a full day before hatching.[10] Unusually, this butterfly's chrysalis is girdled with a loop, with its feet attached to the silk pad, which helps the butterfly to unfold its very large wings when crawling out.[11]

Here is a photo of black swallowtail caterpillars at different life stages:

Here is a link to a post, which describes all the stages your caterpillar will eventualy go through.


Strictly from a biological perspective, what is the functional expectation of a human being Just like the title says: Strictly from a biological perspective, what is the functional expectation of a human being.

No religious or philosophy-based answers will be accepted, we are talking biology not religion or philosophy.

Answers involving excessive psychology will be frowned upon unless found to be exceedingly insightful. (The brain is a biological entity)

If you are considering claiming this to be too broad or unanswerable consider the hypothetical question "what are the functional expectations of human feet" which can be answered fairly easily by a child with no formal training in biology. In my actual question I simply ask about the feet and the other parts attached to them.

Edit: Originally this question was titled "Strictly from a biological perspective, what is the purpose of a human existence." To clarify the question i have changed it to "Strictly from a biological perspective, what is the functional expectation of a human being."

Despite the concerns raised with the use of the word "purpose" the question was serving its purpose with the answers I am seeing.  I did have  some reservations about the word "purpose" as well, but I thought I would try it and see what others thought.

So if a human stomach has the overall functional expectation of mechanically and chemically breaking down and digesting food, what would be the overall functional expectation of a human as a whole? I am looking for not so much of psychologically specific functional expectations and more of physical functional expectations.

For instance a house cat's functional expectations are generally considered to be sleeping, eating, reproducing, socializing, hunting, etc.

I will start with a quote from François Jacob, a French geneticist:

  The sole ambition of a bacterium is to make two bacteria.

The same reasoning can be extended to all life on Earth, including humans.

There is no purpose to human existence, in the same way that there is no purpose for life at all. Life is there because it can. It works, chemically, physically and thermodynamically, given the physical conditions present on Earth.

Biology does not give any moral reason for our existence. It only describes what is there. Using experimental techniques we can infer the purpose of the human feet. All we need to do is to remove the feet of a human subject and see what happens. The subject will be unable to walk, and therefore we will be able to infer that the feet's purpose is to enable locomotion. In biological research, we usually remove or silence genes or proteins from an organism to infer their purpose. We then observe the phenotype. Most of the time however, such an experiment does not give any information on the purpose of the gene because its function is not obvious enough to be observed.

In the same vein, one could remove humans from the Earth and see what happens. If something changes for the worse on Earth, then we would be able to infer that our purpose was to prevent such event from happening. Obviously, such an experiment is impossible to perform, therefore we will never know what is our purpose, neither will we know whether we actually have a purpose.


Why is the manchineel tree so poisonous? The machineel tree is incredibly toxic to humans. What advantage could Hippomane mancinella have for being so poisonous? It's name even apparently translates to “little apple that makes horses mad”.

Is it an incidental toxin, or an evolutionary hangover from a previous predator, or is it still actively predated by a species with high immunity?

I ask because this seems somewhat paradoxical; the tree has fruit, yet is toxic to animals.

According to http://www.atlasobscura.com/articles/whatever-you-do-do-not-eat-touch-or-even-inhale-the-air-around-the-manchineel-tree, it evolved to be poisonous to discourage animals from digging into it. Here's one possible way that could have happened. It was once only a tiny speck more poisonous than other trees by random fluctuations in toxicity. By natural selection, animals evolved to prefer it less. They were more likely to dislike the taste of the more poisonous manchineel trees, which in turn caused it to evolve to be more poisonous. Maybe it was such an advantage to get more energy by eating some of it that some species evolved to be more resistant to the poison so that they could eat some of it. That caused the manchineel tree to evolve to be even more poisonous to discourage animals from eating it. It was an evolutionary disadvantage for the apples to be poisonous. That was just an accidental result of the rest of the tree being so poisonous. Indeed, they did evolve to be much less poisonous than the sap for that reason. Animals evolved to dislike the taste of the apples because they're poisonous. The less poisonous ones were more likely to get eaten and have their seeds spread. Since they couldn't evolve to be nonpoisonous, they instead evolved to taste like there's nothing wrong with them so that they could get eaten. Since iguanas did evolve to be immune to the poison apples, there wasn't much of an advantage in them evolving to be even less poisonous.


What is the definition for vitamins? I have found the following definition on Wikipedia:

  An organic chemical compound (or related set of compounds) is called a
  vitamin when the organism cannot synthesize the compound in sufficient
  quantities, and it must be obtained through the diet;

That doesn't seem to exclude essential amino acids and essential fatty acids though, and those are also organic chemical compounds that by definition can't be synthesized in sufficient amounts.

So is the definition incomplete?

Generally speaking, bulk essential nutrients (e.g. amino acids, fatty acids) are used stoichiometrically to form macro cellular structures and are 'baked in' to the structures or compounds they are used to make. Once those structures are destined for degradation, sometimes the bulk essential nutrients can be recovered and reused in the synthesis of other structures or compounds, but catabolic elimination from the organism is always an option that yields useful energy.

Vitamins, on the other hand, are usually used catalytically. Vitamins are not 'baked into' the compounds they help make or process; vitamins transiently participate in the reactions required to make or regulate a compound or structure, but don't ultimately get 'used up' by that process.

Ultimately, vitamins don't have a bulk energetic value to a cell. For instance, once vitamin E (α-tocopherol) is oxidized, its only fate is to be excreted as waste. Fatty acids and amino acids, once destined for degradation, have their remaining chemical energy extracted prior to excretion of their downstream waste products.

It is philosophically interesting to remark on the diversity of bulk biomolecular building blocks that are still necessary for some organisms to obtain from their environment. Not all of them get called vitamins.


Why does agrose gel runs horizontally, and SDS-PAGE gel runs vertically? It seems in electrophoresis, agrose gel always runs horizontally, and SDS-PAGE gel always runs vertically, why?

When you stand general agarose gel vertically, the gel is slippery coming out from the bottom; although, some run vertically.

To polymerize acrylamide, it is good idea to avoid air because oxygen inhibits polymerization of acrylamide. You would get an air tight condition, pouring acrylamide between glass plates, but how could you run gel made between glass plates. When you set such gel plates horizontally, how do you load samples? Then, it is easier to set gel plates vertically.


How harmful is aluminium? I have been taught in school that aluminium is harmful for brain.
Thus sour meals should not be cooked in aluminium pots and it is unhealthy to add lemon juice to tea while there is teabag in the cup, as acid facilitates aluminium release.

The only safe limit for aluminium intake I know is FDA pediatric limit for parenteral sources (5 μg/kg bw/day). I know no research the limit is based on, but I have read an abstract of a paper claiming it was impossible to comply with the regulation in patients weighting less than 50 kg.

Nowadays aluminium ions are present in several vaccines, which are considered safe to be injected intramuscularly in infants despite despite being  nowhere near the FDA limit.

I'm quite confused how strict should I be in avoidance of aluminium intake (especially dietetary intake - which I expect to be far less effective than parenteral).

[EDIT]

It seems aluminium is also a component of some antacids which are used to treat heartburn.
Does it mean aluminium consumption is safe at general, or it is just considered to be less harmful than acid indigestion (there are some side effects  mentioned - but nothing about accumulation in the brain)?

Here is a link to the Public Health Statement for Aluminum produced by the Centers for Disease Control and Prevention (CDC) in the United States.  There is much more information on the web page but the following are some of the more pertinent points to your question.

Potential Health Effects

Workers

  Workers who breathe large amounts of aluminum dusts can
  have lung problems, such as coughing or changes that show up in chest
  X-rays. The use of breathing masks and controls on the levels of dust
  in factories have largely eliminated this problem.

  Some workers who breathe aluminum-containing dusts or aluminum fumes
  have decreased performance in some tests that measure functions of the
  nervous system.

Humans

  Oral exposure to aluminum is usually not harmful. Some studies
  show that people exposed to high levels of aluminum may develop
  Alzheimer’s disease, but other studies have not found this to be true.
  We do not know for certain that aluminum causes Alzheimer’s disease.

  Some people who have kidney disease store a lot of aluminum in their
  bodies. The kidney disease causes less aluminum to be removed from the
  body in the urine. Sometimes, these people developed bone or brain
  diseases that doctors think were caused by the excess aluminum.

  Although aluminum-containing over the counter oral products are
  considered safe in healthy individuals at recommended doses, some
  adverse effects have been observed following long-term use in some
  individuals.

Some regulation and recommendations:

Drinking water

  The EPA has recommended a Secondary Maximum Contaminant Level (SMCL)
  of 0.05–0.2 mg/L for aluminum in drinking water. The SMCL is not based
  on levels that will affect humans or animals. It is based on taste,
  smell, or color.

Consumer products

  The FDA has determined that aluminum used as food additives and
  medicinals such as antacids are generally safe.

  FDA set a limit for bottled water of 0.2 mg/L.

Workplace air

  OSHA set a legal limit of 15 mg/m3 (total dust) and 5 mg/m3
  (respirable fraction) aluminum in dusts averaged over an 8 hour work
  day.


At what saltiness will water simply pass through us? If water has a low salt content, it hydrates us. When water has too high salt concentration, like sea water, it drains water out of us instead when we drink it. At what salt concentration would water leave us completely unaffected?

"Unaffected" is impossible. If you meant homeostasis, where fluid ingested = fluid excreted, well that happens all the time, and all "output" is not through urine. Sweat, respiration, fluid in feces, etc. are fluid loss. The body constantly needs water. Fluid regulation is a highly complex system managed by the body through a variety of osmotic gradients in the body and hormones which is not driven solely on the osmolarity of the fluid ingested. Under no circumstances would fluid ingested pass through the stomach, small and large intestine, and colon without absorption. Once absorbed from the GI tract to the bloodstream, our kidneys regulate fluid balance. For more reading, reference the renin–angiotensin–aldosterone system.


What does FETCO2(end-tidal fraction CO2 concentration) represent? What is end-tidal fractional CO2 concentration? I have searched online and found little actually explaining what this measurement is. Thanks again.

I'm not sure if you're asking about the procedure or the underlying concepts of CO2 concentration or how a capnometer works.  But in brief, it is measured at the end of an exhaled breath, which is least 'contaminated' by inhaled but unused air from the conduction zone (trachea, etc.).  The measurement is done by looking at the blockage of light from an infrared light to a sensor by the CO2 - exactly the same mechanism by which global warming works.  And the way it's reported is, in this case, as a fraction from 0 to 1.  It could be reported as a percentage by multiplying by 100, or as a partial pressure by multiplying by the total atmospheric pressure (often 760 torr at sea level).


What does differential consumption mean? I have not been able to find any definition of differential consumption online. What does it mean in this quotation?

  Vertebrates can influence natural fire regimes in several ways. First, herbivores limit fuel quantity by consuming and recy- cling plant matter that would otherwise accumulate as litter, and by reducing the density of vegetation [3]. Second, differential consumption of plant growth forms can enforce changes in the composition of vegetation and thereby alter the type and arrangement of fuel. Third, herbivory can gen- erate large-scale habitat heterogeneity, as a result of variation in herbivore activity in response to factors such as terrain and water availability [3,11], and this can mean that zones of low and high flammability are interspersed in arrangements that could impede the spread of landscape fires. Finally, herbivores and other animals may alter the abiotic environment in ways that affect flammability: by forming trails, dust-baths or leks, large animals create lines or patches of bare ground that can act as fire breaks, while some species forage by turning over or digging through the litter layer and surface soils, and in the process bury fine fuels and thus reduce fuel loads. In the sections below, we explore the evidence supporting these effects of herbivores on fuel and fire regimes, in the past and present.

Johnson, Christopher N., et al. “Can Trophic Rewilding Reduce the Impact of Fire in a More Flammable World?” Philosophical Transactions of the Royal Society B: Biological Sciences, vol. 373, no. 1761, Dec. 2018, doi:10.1098/rstb.2017.0443

Second, differential consumption of plant growth forms can enforce changes in the composition of vegetation and thereby alter the type and arrangement of fuel.

This sentence means that herbivores eat more of certain plant growth forms than others. "Differential consumption" just means "different consumption." This can be important in the context of fire risk because herbivores will tend to not eat certain types of plant biomass, such as full-grown trees, but will eat new growth, grasses, etc (therefore the total amount of fuel by type is different).


Are synaptic boutons always located on axons? I am learning about the protein Synaptophysin and I have read that it is an integral membrane protein localised to synaptic vesicles. I have also read that it is a specific and sensitive marker for synaptic terminals. On this site, I have read that synaptic terminals are the presynaptic endings and on Wikipedia that the presynaptic axon terminal is also known as the synaptic bouton. From what I have read online it seems to me that synaptic boutons are located only on axons.
However, I have found out about dendrodendritic synapses which are connections between the dendrites of two different neurons. Can the presynaptic ending of a dendrodendritic synapse be referred to as a synaptic bouton or are synaptic boutons only located on axons? Any insights are appreciated.

Axonal boutons are named as such due to their shape. Dendro-dendritic synapses do not resemble this shape and are never referred to as boutons. It does not appear that synaptophysin is expressed on dendrites (Fletcher et al. 1991), but I am unaware of a study that targeted dendro-dendritic synapses specifically.

References
Fletcher, TL, P Cameron, P De Camilli, and G Banker. ‘The Distribution of Synapsin I and Synaptophysin in Hippocampal Neurons Developing in Culture’. The Journal of Neuroscience 11, no. 6 (1 June 1991): 1617. https://doi.org/10.1523/JNEUROSCI.11-06-01617.1991.


What is the appropriate blender speed to maximize nutrition and digestion of fruits and vegetables? Blender companies state that a blender for smoothies should have speeds of at least 30000 rpm. They argue that only at 30000 rpm are cells of fruits and vegetables sheared enough to maximize nutrition and ease of digestion.

Would blending at lower speeds, such as 20000 rpm, be sufficient?

I'm guessing that what they mean by 'maximize nutrition' for digestion is that they are assuming that the cells are broken open.  This would make the co-factors we call vitamins, protein and sugars freely available to the digestive system and more easily absorbed.

I think it is a marketing literature claim, though the blender may have some valid advantages... details below.

Stainless steel waring blenders used to be typical pieces of lab equipment which could be used to homogenize tissue to extract proteins or DNA from tissue.  These blenders would typically run from 10k-30k rpm.  The web search for 'cell lysis blender' gives lots of examples of prepping DNA from plants at these speeds, but they don't complain for speeds towards the lower end of the range.  A reputable looking example in my short search: This paper for tomato fruit cell wall preparations doesn't even give a speed the blender might have run at.

Cell lysis in the literature is not precise - the cell toughness, the strength of the tissue around it and other such factors all come into play.  Putting woody stems into your blender and those cells won't really get opened up at all.  Also in the cell literature cell lysis buffers may have detergents or other chemicals (the reference above is done in 50% ethanol) to weaken the cell walls.  Not exactly what you'd want to use if you were making a health drink.

In experiments they have to contend with oxidation that happens when the cells are broken open with all the air whipping through the mixture.  This is one reason you don't see blenders in labs to much anymore - hydraulic presses, sonicators, and bead beaters have taken their place - they have less aeration in the mixture and also deliver more power so that they can break open yeast and bacteria, which blenders really can't.

So there will be some vegetables where the cell walls won't break open and all the nutrients won't be so easily accessible.  It must help to be running at the top end of the range, but there will always be some vegetables which won't be broken open.  For most things like bananas and apples it sounds like you'll get similar benefit with other blenders too.  Just have to think about how much more are you paying for that extra 10k of rpm I guess.

Is there a benefit to breaking open the cells and letting all the nutrients (as well as cell waste) break out into solution?  It might give you a quick pulse of nutrition when you drink, but I'm pretty sure all the cells of a piece of fruit or vegetable will be pretty much broken down and extracted by the end.  On the other hand, it sounds like it will save the digestive system some work...  So there's that question too.


Are tergo-sternal muscles of cockroach involved in blood circulation? Tergosternal muscles help in the blood circulation in a cockroach as well as in movement of the wings for flying. I came across a question that claims that these muscles are used in blood circulation as well. I can't seem to see a relation between blood circulation and these muscles.

It is not the tergo sternal muscles that are involved in blood circulation in cockroaches. Tergo sternal muscles help in breathing. It is the Alary muscles that help in blood circulation. The alary muscles are associated with all the thireen chambers of cockroach's heart on either side of it. The alternate contraction and relaxation of these muscles help to pump the blood.

Sources which support my answer:

Tergo sternal muscles are involved in respiration, Look into the book "A Dictionary of Entomology" pg 4, link
Alary muscles help in blood circulation, link


Problem with joining the gene of interest into the open plasmid when their lengths are not the same Before the recombinant plasmid is obtained in recombinant DNA, the gene of interest is inserted into a linearized plasmid by DNA ligase.

What happens if the length of the gene of interest is not the same as that of the gap in the open plasmid? (e.g. far longer) Can the gene still be connected with the gap or are other processes needed before the recombinant plasmid can be put back into the bacteria?

From your question I suspect that you are thinking of DNA as being a very rigid molecule — it isn't.

Double stranded DNA is reasonably flexible and a useful mental model would be to think of this as being like tying the ends of two pieces of thin wire together to make a circle.

Double stranded DNA can make a closed circles smaller than 250 bp long1,2 and I don't think there is any known upper limit — for example there is a known circular bacterial chromosome 14,782,125 bp in length3.

A typical plasmid can accommodate inserts of any size up to total size of around 50 kb, but plasmids that are more than 20 kb are very difficult to work with and may require special transformation techniques.

References:
1: Thibault, Thomas et al. “Production of DNA minicircles less than 250 base pairs through a novel concentrated DNA circularization assay enabling minicircle design with NF-κB inhibition activity.” Nucleic acids research vol. 45,5 (2017): e26. doi:10.1093/nar/gkw1034
2: Shore, David, Jorg Langowski, and Robert L. Baldwin. "DNA flexibility studied by covalent closure of short fragments into circles." Proceedings of the National Academy of Sciences 78.8 (1981): 4833-4837
3: Land, Miriam et al. “Insights from 20 years of bacterial genome sequencing.” Functional & integrative genomics vol. 15,2 (2015): 141-61. doi:10.1007/s10142-015-0433-4


What is this insect? Possible assassin bug? or kissing bug? I saw this bug (around 2 cm) in the front of the balcony door inside the room.

I googled and found two same insects- Assassin bug and Kissing bug. Could they hide their eggs inside the room? Should I be worried?
I live in Vienna, Austria
Thanks in advance
Update: I found this bug here https://www.massaudubon.org/learn/nature-wildlife/insects-arachnids/western-conifer-seed-bugs
The bug that I saw looks like a Western Conifer Seed Bugs! Do you agree?

Yes, it does seem to be a Western Conifer Seed Bug (Leptoglossus occidentalis). Not a hazard to people.
Photos from Italian language wikipedia.

This ref below suggests it may be looking for somewhere indoors to wait out the winter. It lays eggs on conifer leaves.
http://www.zin.ru/animalia/coleoptera/pdf/steyrer_perny_2008_new_insect_species_in_austria.pdf
"Two New Insect Species in Austria: One Established, the Other One Not (Yet)" by
Gottfried Steyrer and Berhard Perny,
Forstschutz Aktuell, num 44, 2008


Can anyone identify this grey spotted insect -- is it a tree bug species? This insect was found in Pune, India near a Bauhinia variegata (orchid tree). I think it's a bug. What species is it?

This is one of the last instars of a bug nymph from the genus Erthesina (Family : Pentatomidae). There are two common species, but according to David Rider, the only species in India is  Erthesina acuminata (Source here, also for the image).

You can recognize it from other bug nymphs by its grayish colour and the distinctive orange patterns on its back. Also, the base of the last antennal segment (where it turns from grey to black) should be orange, but we cannot see it on the picture.

These bugs are phytophagous, and quite generalist. They are phloem-feeding insects that feed from leaves, stems and fruits of various species of trees.

Fore more proper classification and identification of Indian bugs, you can look at:

Ahmad, I., Memon, N., & Kamaluddin, S. (2004). A Revision of Hayline Stink Bug Genus Erthesina Spinola (Hemiptera: Pentatomidae: Pentatominae) and Their Clasdistics. Pak. J. Zool, 36, 285Ğ293.
Salini, S., & Viraktamath, C. A. (2015). Genera of Pentatomidae (Hemiptera: Pentatomoidea) from south India—an illustrated key to genera and checklist of species. Zootaxa, 3924(1), 1-76.


List of dinosaurs synonyms Is there a comprehensive list of dinosaurs synonyms with indications of which name is now considered correct? Something like "there's no brontosaurus, there's only Apatosaurus", "there's no Anatotitan, there's only Edmontosaurus" and so on.

Encyclopedia of Life includes information on synonyms (see link for Apatosaurus) - not a list but searchable and often with references and background info. After a quick google search I also found this list from dinosaurcentral.com, but I don't know how credible and updated it is and it seems to lack references.


Metapopulation structure - book recommendations What book would you recommend me to study:

the dynamics of metapopulations,
the structure of metapopulations,
the evolution in structured metapopulations?

I am not looking for an introduction but for a book that offers good and extensive mathematical formulations.

Probably the best source to start would be Ilkka Hanksi's work, you can find a full list here: http://www.helsinki.fi/science/metapop/People/IlkkaPub2.htm.  The seminal work would be "Ecology, Genetics and Evolution of Metapopulations"  It gives a strong mathematical treatment


Does Remdesivir cause bone marrow suppression? According to Wikipedia, Remdesivir is a prodrug of GS-441524 which is a nucleoside analog.
I know that nucleotides are the building blocks of both DNA and RNA, meaning nucleotide analogues that prevent the creation of viral RNA can also prevent the creation of normal cell DNA, meaning they can cause problems in dividing cells. This is also reflected in the nucleotide analogue article of Wikipedia:

They are not specific to viral DNA and also affect mitochondrial DNA. Because of this, they have side effects such as bone marrow suppression.

So does Remdesivir cause bone marrow suppression?
If not please explain why.

From Off-Target In Vitro Profiling Demonstrates that Remdesivir Is a Highly Selective Antiviral Agent:

Overall, the cellular and biochemical assays demonstrated a low potential for RDV to elicit off-target toxicity, including mitochondria-specific toxicity, consistent with the reported clinical safety profile.

This isn't a very complete answer, but the wikipedia article doesn't go into detail or link references explaining the mechanism by which nucleoside analogues suppress bone marrow function. So I can't say if the assay results in my link rule out a suppression effect by remdesivir


How can I extract ligand with neighboring protein atoms from PDB with complex? I'm not familiar with biology and coming from Data Science field, so please excuse me for the lack of knowledge. What I want is to create 3D voxel representation of ligand atoms with neighboring part of the protein (looks like it is called pocket) from PDB file which contains complex.
For example, let it be 10gs from RCSB (https://files.rcsb.org/download/10GS.pdb). For other example, it can be 4xit or 4wkc.
What I planned, was identify both protein and ligand atoms, compute the geometric center of the ligand, and then calculate proximity for each atom and fill some 3D surrounding cube.
When I open PDB for this complex (10gs) I see what I understand as two possible binding sites for ligand VWW, and another two - for MES:
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE VWW A 210
REMARK 800
REMARK 800 SITE_IDENTIFIER: AC2
REMARK 800 EVIDENCE_CODE: SOFTWARE
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE VWW B 210
REMARK 800
REMARK 800 SITE_IDENTIFIER: AC3
REMARK 800 EVIDENCE_CODE: SOFTWARE
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE MES A 211
REMARK 800
REMARK 800 SITE_IDENTIFIER: AC4
REMARK 800 EVIDENCE_CODE: SOFTWARE
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE MES B 211

How can I proceed from this point? Does this PDB contain atoms for ligand VWW, properly oriented, and how can I identify them along with neighboring ones of target protein?
Or my formulation of the problem is totally wrong?

You might find RCSB's Guide to Understanding PDB Data and the PDB file format documentation useful. I'll go over some of the information present in PDB files that seems relevant for you, using your example of 10GS.
Ligands are specified in the heterogen section:
HET    VWW  A 210      33
HET    MES  A 211      12
HET    VWW  B 210      33
HET    MES  B 211      12
HETNAM     VWW L-GAMMA-GLUTAMYL-S-BENZYL-N-[(S)-CARBOXY(PHENYL)
HETNAM   2 VWW  METHYL]-L-CYSTEINAMIDE
HETNAM     MES 2-(N-MORPHOLINO)-ETHANESULFONIC ACID
FORMUL   3  VWW    2(C23 H27 N3 O6 S)
FORMUL   4  MES    2(C6 H13 N O4 S)

These records tell you the identity of the ligands that are bound to the protein (VWW and MES), how many are bound (4 in total), the chemical name (in the HETNAM record) and chemical formula (FORMUL record). The HET record also gives the number of associated HETATM records (33 for VWW and 12 for MES). Here are the first five HETATM records for VWW of chain A:
HETATM 3265  N   VWW A 210      15.088  10.798  23.547  1.00 14.90           N
HETATM 3266  CA  VWW A 210      15.010   9.987  24.792  1.00 20.92           C
HETATM 3267  C   VWW A 210      16.115   8.924  24.830  1.00 21.55           C
HETATM 3268  O   VWW A 210      16.520   8.515  25.940  1.00 17.16           O
HETATM 3269  CB  VWW A 210      13.635   9.327  24.908  1.00 14.23           C

Each HETATM record corresponds to an atom in the ligand and gives the chemical coordinates for each on the X, Y and Z axes. For example, the first record specifies a nitrogen atom at coordinates (15.088, 10.798, 23.547).
The connectivity (ie covalent bonding) between atoms in a ligand is specified in CONECT records. Here are the first five from the PDB file:
CONECT 3265 3266
CONECT 3266 3265 3267 3269
CONECT 3267 3266 3268 3273
CONECT 3268 3267
CONECT 3269 3266 3270

This tells you that atom 3265 (the first nitrogen in the HETATM records above) is bonded to atom 3266 (a carbon). Atom 3266 is bonded to atoms 3265, 3267, 3269. Et cetera...
The atoms of the protein are specified in ATOM records. Like the HETATM record, these records give some identifying information (atom serial number and type, residue name and number, etc) as well as the coordinates in 3D space. For your purposes, it sounds like you can just loop through the atoms of the protein and find the ones which are within some threshold distance of an atom in a ligand (or the geometric centre of the ligand). However, this PDB file does already contain some information about the binding sites for these 4 ligands in the SITE records (here are the first four corresponding to site AC1):
SITE     1 AC1 15 TYR A   7  PHE A   8  ARG A  13  TRP A  38
SITE     2 AC1 15 LYS A  44  GLY A  50  GLN A  51  LEU A  52
SITE     3 AC1 15 PRO A  53  GLN A  64  SER A  65  TYR A 108
SITE     4 AC1 15 HOH A 229  HOH A 303  ASP B  98

The SITE records also have corresponding REMARK 800 records (which are given in the question). For example, site AC1 is described as BINDING SITE FOR RESIDUE VWW A 210 as identified by SOFTWARE. So in this case, these SITE records are a list of residues that make up the binding site of their respective ligands.
You may want to be somewhat wary of these SITE records because (1) as far as I know they are not mandatory records in a PDB file and therefore may not always exist, and (2) it is not entirely clear how they are generated. In this case they are software generated... but which software... or what algorithm? I have previously looked through the SITE record of a binding site in a protein I am very familiar with and noted some conspicuous absences from the list of residues, so take that for what it's worth.


Is there such thing as "half-life" of dopamine? If a dopamine is released at T=0 and binds to receptor D2, what determines the time when the concentration of this neurotransmitter bound to the receptor reaches half of the original concentration? In other words, when will the effect of neurotransmitter on the intercell signalling fall in half?

Is there any time estimate of how quickly the brain thinks that neurotransmitter has "fulfilled its purpose" and is to be re-uptaken? Or is this process completely random?

Thank you for your input!

Dopamine (DA) secreted by neurons is selectively reuptaken by the dopamine transporter (DAT), present on nerve terminals.

(source: inist.fr)

Image source: Plasma membrane monoamine transporters: structure, regulation and function - Torres et al. - Nat Rev Neurosci., 2003

DAT acts as a symporter, using the Na+ and Cl- gradients to generate the energy required to transport DA back in the cytosol.

The mechanism of reuptake has been investigated in vitro allowing the description of a model for DA reuptake by DAT.

In particular, from the abstract of this paper:
A multisubstrate mechanism of striatal dopamine uptake and its inhibition by cocaine. - McElvain and Schenk, Biochem Pharmacol., 1992

  Dopamine uptake was found to be first order in dopamine with a Vmax of 582 pmol/sec/g wet weight and a Km of 1.2 μM. The results of experiments in which choline and isethionate were substituted for Na+ and Cl−, respectively, suggested that the uptake process is second order in Na+ and first order in Cl−. Multisubstrate analyses of the initial velocities of uptake over the concentration range of 0.025 to 1.5 μM dopamine suggested that the mechanism of binding of dopamine to the uptake carrier is a partially random, sequential mechanism where dopamine or Na+ binds first with the uptake carrier and Cl− binds last.

A transport scheme is reported in:
Dopamine Neuronal Transport Kinetics and Effects of Amphetamine

  Scheme 1 is a kinetic scheme for a simple carrier adapted from that of Stein (1986) for the DAT. The subscripts o and i represent the outside and inside, respectively, of a DA neuron. Scheme 2 describes a possible mechanism for
  the cotransport of another species. All symbols are as in scheme 1 except that A corresponds to amphetamine.

From the text

  This scheme describes transport as a series of steps: the competition between binding and dissociation of the substrate to the transporter on the  extracellular side, a similar process on the cytoplasmic side, and an equilibrium between the unoccupied transporter facing toward the extracellular or cytoplasmic side. The driving force for inward transport arises from the cotransport of Na1 and Cl2 as well as the membrane potential difference
  (Stein, 1986; Sonders et al., 1997). Biochemical (Krueger, 1990) and electrophysiological (Sonders et al.,1997) studies have established that DA transport is accompanied by transport of at least two Na1 ions and one Cl2 ion and that DA transport can be bidirectional in isolated preparations.


Arabidopsis thaliana RCSB active site gene mutant I'm looking for an Arabidopsis thaliana gene listed in RCSB with a clear mode of function and active site. In addition it needs to have an obvious phenotype when knocked out like severely retarded growth, lethal or near lethal. The gene also has to be exclusive to plants so RNA polymerase wouldn't work.
I found this paper in plant physiology but I'm having trouble finding those genes with an obvious active site.
Thank you very much

I can tell you generally how to go about it.

Go to table S2 from the paper and download the spreadsheet.  You can search RCSB for each gene symbol. There are 2400 individual genes and there are probably over 1000 alias genes, so that's a lot of searching.  You can do this en masse by using a python script and a library like BioPython, or you can put each symbol into the search box at RCSB.org and see if a structure comes up.

You can and should look over that table for phenotypes you think you can actually work with.  Many of the phenotypes in the paper might require a microscope or a good deal of experience with arabidopsis.  E.g. "Embryo defective; Preglobular / Globular" what does that mean?  You can also write the authors for advice but they might be too busy to get back to you.

Cutting down your search like this before you do it would be very helpful.  The number of genes with both an accessible phenotype and a structure will probably be a relatively small list (50?).

Relatively few arabidopsis protein structures are solved, so you will have to do homology modeling - aligning any protein structure sequence(s) you find with the A. thaliana sequence, and deciding where the active site or disruptive mutation would be in the plant gene.

Example: CHY1(CoA Ester Hydrolase) must be solved - searching for "CoA Ester Hydrolase" at rcsb I find a three structures.  the human structure 2DQZ has a lot of annotation associated with it.  This class of enzymes has been studied for a while, so the active site probably has been studied.  A pubmed search should give a lead on where the active site research has been done.  using BLAST to align the structures to the arabidopsis gene or to all other CoA Ester Hydrolases would be an important step to take too.

Hope this helps.


Is it possible to sort droplets inside an oil phase with a FACS In a nutshell, is it possible to FACS a sample that is in oil rather than in a buffer (water based solution)?
I would greatly appreciate any help with this.
Thank you

It's possible that there's some specialized modified machine that can do it, but conventional flow cytometry machines can't do it. This article suggests one possible approach:

  Unfortunately, FACS instruments are incompatible with nonaqueous suspensions, so to sort a water-in-oil emulsion, it is necessary to carry out a further emulsification to produce a water-in-oil-in-water double emulsion. The resulting sample, now dispersed in an aqueous phase, is amenable to FACS sorting.

--One in a Million: Flow Cytometric Sorting of Single Cell-Lysate Assays in Monodisperse Picolitre Double Emulsion Droplets for Directed Evolution

There are also microfluidics machines that might be able to do it, but I think you'd have to build your own rather than being able to buy a solution (which would be expensive in any case, I think).


How to manage fat-gluten oxidation in celiac disease? Assume you have been in non-gluten diet 20 years.
You built mass 8 mass with substances containing gluten (endogenous gluten stored in fat).
Then, celiac disease is diagnosed.
You have been 3 months in gluten free diet.
After mass period, you go to fat burning period.
The challenge starts: endogenous gluten stored in fat.
It is painful if too intensive training program.
Even little amount of gluten causes enteropathy.

What are the protectant methods for burning fat containing gluten?

How can you prove that there are no gluten-derived peptides that accumulate somewhere?
Since the cellular receptors for gluten have been identified, I think this may be over-complicating things. - Ryan's answer

I have not found any good solution for this, since I do not understand the pathophysiology enough well.

Toxic factors related to celiac disease

gliadin
...

How is endogenous gluten released from fat?

Gluten is a protein. The textbook answer is that protein is not stored in fat cells.

Proteins are hydrolyzed into amino acids through digestion; some amino acids are ketogenic, and can contribute carbon towards fat biosynthesis. So some of the carbon that originates in gluten may be incorporated into a fatty acid. But the carbon has no 'memory' of its previous role in a gluten molecule, and could not act as gluten when the fat is subsequently oxidized.

One can imagine an undigested gluten molecule (or its peptide fragments) binding to the exterior of a fat cell, but there's no mechanism for it to get incorporated into fat as an intact protein.


How does the value of K determine number of local optima in NK model? BACKGROUND

The NK model of fitness landscape considers N states which can interact with K other states. For example N is the total number of genes in a haploid genome and K is the number of other genes that each gene may interact with.

In this article Kaufman says:

  The fully connected NK model yields a completely random fitness
  landscape. For K = N - 1, the fitness contribution of each site
  depends on all of the other sites in the sequence and therefore
  altering any site from one to the other value, 0-1, alters the fitness
  contribution of each site to a new random value. Thus the fitness of
  any 1-mutant neighboring sequence is completely random with respect to
  the initial sequence. The landscape is fully random. As was shown in
  Kauffman & Levin (1987), Weinberger (1988), and Macken & Pereison
  (1989), such random landscapes have very many local optima, on
  average, 2N/(N +1).

I did not read the references mentioned in the text but I read the related section in Kaufman's book: Origins of Order: Self-Organization and Selection in Evolution.

In the book he says that the fitness of a genotype can be ordered and given ranks; the probability that a genotype is fitter than its neighbours (local optima) is same as its probability of ranking higher than its N neighbours. So this probability:

$$P_m=\frac{1}{N+1}$$

and if each gene can have only two states lets say on or off then the expected number of optima with respect to one-mutants (i.e. the difference between a gene and its neighbour is just one mutation) would be:

$$M_1=\frac{2^N}{N+1}$$

What I don't understand is the role of K in this expression. This reason should be valid for any number of K (See the quote above). Even in the book this explanation is given in the case where K is maximum i.e. N-1. I can understand that K can affect the ruggedness of the landscape but can anyone explain how K affects the number of optima? (or are they just two separate statements written together, which is confusing me)

Let's take the opposite extreme, $K=0$, so that each site has an independent effect on fitness. Without loss of generality, we can say that at each locus $n$, the $1$ allele confers an advantage $s_n$ over the $0$ allele. Then there is just one local optimum, the global optimum, at $\vec{1}$, so $M_1=1$ (and $P_m=2^{-N}$).

The key difference is that in the $K=0$ case each fitness comparison of a focal genotype with a neighbor is independent of the rest: the fact that mutating the first gene decreases fitness, for instance, doesn't make it any more likely that mutating the second gene will decrease fitness. For any $K$, it is necessarily true that the focal genotype has a probability $1/(N+1)$ of being fitter than all of a set of $N$ other randomly chosen genotypes, but we're interested in comparing it to its neighbors, which are not a random selection, and are only equivalent to a random selection when $K=N-1$.


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

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


Is new idea equivalent to forming new synaptic connection? We get new ideas quite frequently hence I am curious that is getting new idea equvant to formation of new synaptic connections? I am aware of neural plasticity but somehow doubt that it happens quite rapid.
Since that idea was missing before one creates it makes me believe that the structure of synaptic connection was not present earlier and once the new idea was formed then the structure to simulate/produce that idea was created.
If that's the case that that's lots of neurons being connected/disconnected in few seconds which don't seem physically possible.

There is a lot of debate over what "thoughts" are in terms of consciousness, and this has been referred to as the "hard problem". However, it seems pretty clear that in some form patterns of brain activity are the "stuff" that underlies a thought/idea: if you change patterns of brain activity, you change the thought.
Therefore, I would describe a "new" idea as a "new pattern of brain activity" rather than connections. While the exact timescale of a "pattern" should be is unclear, perhaps a few hundred milliseconds is a good guess (see for example Luczak et al 2015, and the recent paper by Davis et al 2020). Brain activity is constantly shifting, of course, so really every moment experienced is a new thought of some sort.
There are too many studies to name all of them that show that some consistent pattern of brain activity is associated with some thought. The review by Harris, 2005 is a favorite of mine, but there are many levels of analysis to approach these questions. You might find some more compelling work among the studies of the biological basis of perception.
One particularly elegant paper is Liu et al, 2012. They used some molecular tricks to identify neurons in a rodent brain that are activated during a fearful context, and they cause long-term expression of a protein in those specific cells that they then use to reactivate those same cells at a later time. Reactivating those cells causes the fear behavior to return, effectively triggering the same ideas.
Connections between cells can also change pretty rapidly, but this would be better described as memory rather than an initial thought or idea. This can involve de novo creation of synapses, but more often is studied as a change in synaptic strength. Weak synapses can be strengthened with certain input patterns, and we call this long-term potentiation. The idea of connections between neurons as the stuff of memory goes back some 100 years to Ramón y Cajal.

Davis, Z. W., Muller, L., Martinez-Trujillo, J., Sejnowski, T., & Reynolds, J. H. (2020). Spontaneous travelling cortical waves gate perception in behaving primates. Nature, 1-5.
Harris, K. D. (2005). Neural signatures of cell assembly organization. Nature Reviews Neuroscience, 6(5), 399-407.
Liu, X., Ramirez, S., Pang, P. T., Puryear, C. B., Govindarajan, A., Deisseroth, K., & Tonegawa, S. (2012). Optogenetic stimulation of a hippocampal engram activates fear memory recall. Nature, 484(7394), 381-385.
Luczak, A., McNaughton, B. L., & Harris, K. D. (2015). Packet-based communication in the cortex. Nature Reviews Neuroscience, 16(12), 745-755.


Distribution of genotypes after adverse selection I am doing some research into Mendelian genetics and came across this phrase called adverse selection.

I found a few questions but I am unsure of the calculations. For example given a distribution

  [0.36 0.48 0.16]

it is stated that 25% of individuals with Aa(middle) genotype dies. The distribution changes to

  [0.4091 0.4091 0.1818].

I initially thought to just take off 25% of the middle becoming 0.36 and equally distributing the 0.12 change to the other two geneotypes. Can someone explain how they did this computation.

If you distribute the 0.12 equally to the two other genotypes you change the relative frequencies. You have to withdraw 0.12 to 0.48 and then set the three frequencies so that they sum up to 1. Therefore, the correct calculation is the following:

If we set $fAA = 0.36$, $fAa = 0.48$ and $faa = 0.16$ and then simulate the death of 25% of the Aa individuals, the same variables at the next time step (without reproduction) will be...

$$faa = \frac{0.16}{0.36 + 0.36 + 0.16} ≈ 0.1818$$

$$fAa = \frac{0.36}{0.36 + 0.36 + 0.16} ≈ 0.4091$$

$$fAA = \frac{0.36}{0.36 + 0.36 + 0.16} ≈ 0.4091$$


Biological siblings possible with <9 months age difference? I'm currently in the middle of writing a story, and one of the story elements threw up a question for me. In this story, there are two siblings, who are only one or two months apart in age. As they grow older, they start to question how this age difference is even possible. How could their mother have had another child after just a month of giving birth to the first child? They suspect that they're not related and don't actually have the same mother, and it turns out that it's true.

I want to know if that suspicion is justified. I began to think of ways two siblings can be less than the usual nine months apart in age and yet still be related to each other. One idea I had was of twins, one of whom is born earlier, while the other had to stay inside the womb for another month for whatever medical reason.

Basically, my question is: can you have siblings (with the same mother and father), who are less than nine months apart in age? And if yes, how?

What do you mean by siblings?

If by siblings, you accept cases of individuals having the same father but not the same mother, then of course, it is possible! Below, I will assume you are referring to full siblings (eventually twins).

Age gap between twins

According to the huffingtonpost, there is a case of two twins that were born 87 days apart. On average, the age gap between two twins is rather of the order of 15 minutes (Rayburn et al., 1984).

Cousins that "look like" full sibs

Imagine family A has a pair of homozygotic twin daughters. Family B has a pair of homozygotic twin sons. If the sons of family B mate with the daughters of family A, then the offspring will be cousins but will have a relatedness of two full siblings.

One can of course extend this kind of crazy scenario to any number of generations apart.

Superfetation

I discovered the concept of superfetation in @froimovi's answer. From wikipedia

  Superfetation (also spelled superfoetation and superfœtation – see fetus) is the simultaneous occurrence of more than one stage of developing offspring in the same animal. It is not believed that it occurs naturally in humans. There have been 10 reported cases of possible superfetation in humans.

As @1006a rightly pointed, the two babies might well be delivered during the same labour though. If they are delivered during the same labour, then they will have the same age counting from birth but different age counting from the time of fertilization.

Uterus didelphys

See @Bakuriu's answer!

Human intervention

Other alternatives would require some human intervention. For example, fertilization could have happened in vitro and the eggs were implanted in two different wombs. One womb could be a surrogate mother and the other one could be either another surrogate mother or the woman who actually donated the ovules.

Plenty of cloning techniques could yield two full siblings to be less than two months apart. Also, techniques of ex utero pregnancy could be used (although I am not sure we have the technology ready for that). Note that human cloning is illegal in many countries.


Difficulty in finding protein inhibition drugs I was reading an article on a recent identification of a PARP-14 protein in cancer cells that is responsible for production of additional glucose which keeps cancer cells from dying, and that a PARP-14 inhibiting drug is still a long way from becoming reality.

Would like to ask any medical researchers/anyone with adequate knowledge, what is the difficulty in producing drugs that inhibit production by a certain protein? Isn't it about analyzing the chemical makeup and structure of the protein and finding ways to neutralize it? As how other types of drugs are made? Please give some specific examples regarding this topic. Your help is much appreciated.

Drug production is very long, tedious and costly process. It generally takes more than 10 years to make entirely new drug. It has various iterative aspects. take a look at following cartoon showing various steps in drug design ( Taken from Anderson 2003 )

Now coming to your questions,

  what is the difficulty in producing drugs that inhibit production by a certain protein?

First of all you need to know other effects of that protein which might be essential for normal cell function. For example, there are many genes overexpression patterns which have correlated with cancer. This suggest excess quantity of these proteins/factors leads to cancer. Now one would like to block these proteins with inhibitors. However if you block these proteins, they might also affect regular cellular function. For example, SHC1 overexpression is correlated with breast cancer. However that protein is very important in apoptosis regulation, EGFR pathway, Oxidative stress and many more functions. Now if you inhibit this protein, your normal cells will also get damaged.

  Isn't it about analyzing the chemical makeup and structure of the protein and finding ways to neutralize it

It is not that simple, for this you need inhibitor which can specifically either bind (it can be competition also) specifically with given protein. Most of the time there are other problems like , there might be other proteins with that structure which can affect other protein's function. There will be other important problems like

Delivery of inhibitor
Specificity (Inhibitor need to act only on target cells)
Sensitivity (Inhibitor need to be sensitive enough to get full response in low concentration)
Side effects (There might be side effects of this inhibitor which should be minimized)
Cell resistance (Many times cell becomes resistant to inhibitor)

Above mentioned points are actually major issues in all cancer treatments like Chemotherapy  , Radiation therapy, Immunotherapy , Hormone therapy etc.


Does TSH and Growth hormone have any role in menstruation? Actually, I came across this on a mcq (multiple choice question) exam:

Name the hormone which has no role in menstruation:

A. LH

B. FSH

C. GH

D. TSH

(only 1 correct option)

Both FSH and LH have direct roles in the menstrual cycle, they're responsible for the follicular phase and ovulation, respectively. Menstruation takes place due to the decreased levels of progesterone. Does GH and TSH have any role in the process? If so what is that role?

TSH has an effect slightly similar to that of FSH and LH. This is found to be problematic in thyroid diorders. For example, in hypothyroidism the TSH overflow causes children to become fertile at an earlier stage, compared to the norm [1].

[1] Ann N Y Acad Sci. 1997 Jun 17;816:280-4. PMID: 9238278. http://www.ncbi.nlm.nih.gov/pubmed/9238278


What is the definition of "Natural Selection"? Natural selection is the differential survival and reproduction of individuals due to differences in phenotype.

Natural selection, a process that results in the adaptation of an organism to its environment by means of selectively reproducing changes in its genotype or genetic constitution.

Natural selection, then, can be defined as the differential reproduction of alternative hereditary variants, determined by the fact that some variants increase the likelihood that the organisms having them will survive and reproduce more successfully than will organisms carrying alternative variants.

Darwin's definition of natural selection his book "On The Origin Of Species By Means Of Natural Selection or the Preservation Of Favoured Races In The Struggle For Life" is:

  The preservation of favorable variations and the rejection of injurious variations

In Evolution 101, natural selection is not defined, but rather the concept "evolution by natural section" is characterized as the outcome of variation, differential reproduction and Heredity, and a clarifying example is provided.

Clearly, the wording in each of the above is different!

I searched Biology StackExchange for any explicit statement of the definition of natural selection, I couldn't manage to find one. There are some discussions about whether it is a tautology or not, but even in those discussions, the definition of natural selection was not quoted.

I tried to search tags "natural selection" and "definitions" of biology StackExchange, and yet I didn't see any particular wording mentioned as the official definition of natural selection.

Actually, the tag [natural selection] mentions this definition in the tag information itself:

Natural Selection is a mechanism of evolution that leads to non-random spread of genes due to the effect that genes have on reproductive success

Natural selection is the process by which heritable traits that make it more likely for an organism to survive and successfully reproduce become more common in a population over successive generations.

Is there an official definition of natural selection that is adopted by biologists nowadays? and what is that definition exactly?

[EDIT] It came to my awareness that this question might be a possible duplicate of the following question: "How is Selection best defined", and indeed in the answers provided to that question the topic of definition of natural selection has been addressed.

I didn't know of this posting. I simply surfed for "natural selection", and not just for "selection", and I didn't notice it. But indeed what's presented in the answers does cover the question present here.

However there is some difference in the question itself from that present here. Here I wanted to know of what I thought would be an official definition, and I was asking in particular about "natural selection", while in the referred question, the question is more general, it's about what qualifies "any" force (apparently he means related to biology and especially evolution) to be labeled as "selection", including artificial selection, sexual selection, etc.., so it's a wider topic, at least as far as terminology is concerned.

Here in this question I've quoted the main results that one would see upon surfing the web for "definition of natural selection", and I wanted to know which one would be the official or as @Remi.b had put it, the most commonly used or referred to in biological research.

I still think, that for precision purposes, exact wordings are important, and such an extremely important concept like "natural selection", it would have been expected that it had an agreeable, kind of, official definition, by some convention or the alike.

Anyhow, I think, whether this question is a duplicate or not, can be better assessed by experts in evolution field present in this website, like those who provided answers, and others.

Thanks.

Official definition

  Is there an official definition of natural selection that is adopted by biologists nowadays? and what is that definition exactly?

I don't think there is such a concept as an "official definition" of any concept in science. There are common definitions though.

The definitions you cite

Let's go through your three definitions

  Natural selection is the differential survival and reproduction of individuals due to differences in phenotype.

This definition lacks the idea that this fitness differential must be caused, in part at least, by genetic variation.

  Natural selection, a process that results in the adaptation of an organism to its environment by means of selectively reproducing changes in its genotype or genetic constitution.

Part of the phrasing is about the consequence of the process rather than the process itself. The part that describes the process itself is "selectively reproducing changes in its genotype, or genetic constitution", which is a rather unusual phrasing and I would argue is slightly vague.

Note that while most authors refer to natural selection as the fitness differential, it is not impossible to refer to natural selection as the resulting change in allele frequency. I have never seen cases where this semantic difference matters though.

  Natural selection, then, can be defined as the differential reproduction of alternative hereditary variants, determined by the fact that some variants increase the likelihood that the organisms having them will survive and reproduce more successfully than will organisms carrying alternative variants.

I have never encountered the expression "alternative hereditary variants". I think the author made it up. It sounds like the author tried to avoid the term "allele" by replacing it with "alternative hereditary variants". The author also seems to have tried to avoid the term "fitness" by replacing it with "likelihood that the organisms having them will survive and reproduce more successfully".

But overall the definition sounds correct to me. There is an important difference between the first and the third definition is that in the first definition, it emphasizes the fact that the genetic elements that explain fitness variance are doing so via its effect on the phenotype. The third definition just ignores phenotype. As such, I would consider the first definition more complete (and more compact).

  Natural Selection is a mechanism of evolution that leads to non-random spread of genes due to the effect that genes have on reproductive success

Here, the definition is again very much based on the consequence of the process rather than the process itself. Only "due to the effect that genes have on reproductive success" refers to the actual process of natural selection.

I don't really like the term "random" here as the concept of randomness is somewhat unpleasant to define outside of a well-defined model. I don't really like the term "genes" either because selection doesn't only act on genes (but can act at any locus) and because the term "allele" would be more appropriate even if the phrasing would still remain unclear.

So in short, shame on us, the StackExchange definition is pretty bad!

  The preservation of favourable variations and the rejection of injurious variations

I shall not talk here about how different is Darwin's theory of evolution from today's theory of evolution (which is called the "modern evolutionary synthesis"). I shall not talk either whether this single short sentence is a good summary of Darwin's representation of natural selection (see @Luaan comments for more information).

This definition is short and a bit vague. One would want to think of this definition as applying to a genetic variant, without regard to the phenotype, however, Darwin did not know anything about DNA.

My favourite definitions

Lewontin's recipe

A very simple way to think of natural selection is to consider Lewontin recipe. The Lewontin recipe says that natural selection occurs whenever:

Individuals in a population vary in terms of a given trait
This trait has a non-zero (additive) heritability. See this post for a definition of heritability.
The fitness varies (not necessarily linearly) as the trait varies

Single sentence definitions

If you prefer a shorter and simpler version I would personally suggest

  Selection is the fitness differential among genotypes in the population.

This definition lacks the concept of phenotype but talking about the fact that an individual fitness is dependent on its phenotype (among other things) is, IMO, not required to mention in the definition of what natural selection is. Not that I also removed the term "natural". I don't quite like it because it leads people to think that natural and artificial selection could be fundamentally different. Same applies to sexual selection, IMO, but I shall not go down this slope now!

In a very similar post, I wrote the definition

  Selection is a fitness differential associated to a genetic variance among individuals in a population.

I also like this definition because it highlights that selection acts on populations (and not on individuals or on species).

Mathematical modelling

You might want also to consider as a definition the mathematical modelling of the process. In absence of genetic drift (assuming infinite population size), assuming a bi-allelic locus with alleles a and A, one can model (haploid) selection as

$$p_{t+1} = \frac{p_t W_a}{p_t W_a + (1-p_t) W_A}$$

, where $p_t$ is the frequency of the allele a at time $t$. $W_a$ and $W_A$ are the fitness of the genotype with alleles a and A, respectively. Of course, you can extend this model to any kind of ploidy and any number of alleles. You can also extend this model to include genetic drift (typically done via the use of diffusion equations or via branching patterns).

For more information about these mathematical modelling, please have a look at an intro book in evolutionary genetics (see here for book recommendation).


In protein-protein interactions what is the difference between a binding site and an interface? I see binding site and interface used almost interchangeably in the literature, but I'm not sure if it is exactly the same thing or not - what is the difference?

A protein-protein interaction (PPI) binding site is a type of interface. If it has been established that the interface is a PPI binding site, then the terms can from that point forward be used interchangeably. But the word "interface" is very generic and does not have any specific scientific meaning so the nature of the interface must be defined or else the term is fairly meaningless.


What is a good list of unsolved protein structures? I'm trying to get a list of unique soluble structured proteins that don't have a solved structure. That is, they aren't the usual membrane proteins or some derivative of another protein.

Things that I've been able to think of are low producing transcription factors and novel fusion proteins.

There are some funded projects and analyses available just for this purpose.

Structural genomics or high throughput structure projects take all available peptide sequences group them into families and make sure sequence families pointing to most likely novel folds were available.

Here are the status and target list for the joint center for structural genomics. This list is filtered by species as well as by project status.

Their analysis is availble for us to browse through.  http://www1.jcsg.org/prod/newscripts/psca/help/document.cgi

Sorry this isn't so thorough.  Nature also hosts Target Track, which allows several high throughput structure centers to coordinate their efforts.  Each might have resources which could do your work for you.


Catalytic Triad of Serine Proteases Is serine considered an acid in the catalytic triad involved in the mechanism of action of serine proteases? It is donating a proton to His but I am not sure if this really qualifies as an acid?

It depends how you define an acid. For what it‘s worth, the chemical definition Google presents when I search is “a molecule or other species which can donate a proton or accept an electron pair in reactions”. On that basis the serine residue in the catalytic triad is acting as a weakly ionizing acid.

Of course in aqueous solution a free serine hydroxyl group is not acidic, but one of the important features of enzyme catalysis is that amino acid residues are operating in a different environment that can enhance their activity. One factor is the proximity of other residues. Another is the effective dielectric constant can be different in the hydrophobic interior of a protein which can exclude water molecules.


Can molecular genetics make a boolean variable from a continuous variable? In the same kind of idea than this question. Gene expression are regulated through complex interactions. The concentration of enhancers and repressors is an important aspect that dictate the level of expression of a given gene. These concentrations can take different value on a continuous scale.

Imagine a case where fitness is maximized when a given gene produce n proteins per minute if the concentration of a given protein is greater than x. If the concentration of the protein was to be lower than x, then the gene should not be expressed (0 proteins per minute are produced). In such case, it would be great if a bunch of reactants were to be able to simulate a "switch function" that would switch from "NO EXPRESSION" to "EXPRESSION" at x.

It seems to me that such switch function should be very complicated to evolve. I would suspect that all chemical reactions, including the binding of enhancer to promoter region should follow the law of Michaelis-Menten and the Michaelis-Menten function is not at all switch function. So, I have been thinking about cooperative binding. Hill's equation describes a function that is effectively a switch function given that the hill coefficient is high enough. However, seeking a bit in the literature, it's seems that the Hill coefficient never really overpass 3 (or 5 for extreme estimates). A Hill coefficient of within this range gives a logistic function but still looks quite suboptimal compared to what a perfect switch function could do.

Are there switch functions in molecular genetics that could translate a concentration into a TRUE/FALSE signal?
How well do they simulate the perfect switch function?
Are they based on cooperative binding or on some other mechanism?

References for estimate of Hill coefficients:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1435008/pdf/biophysj00200-0109.pdf
http://onlinelibrary.wiley.com/doi/10.1046/j.1537-2995.1983.23283172857.x/abstract
http://www.pnas.org/content/93/19/10078.short
http://www.ncbi.nlm.nih.gov/pubmed/8816754
http://www.fasebj.org/content/11/11/835.short
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2816740/

Positive feedbacks can be one alternative. Positive feedbacks exhibit bistability and can therefore adopt one of the two stable states depending on the initial condition. A famous example of a positive feedback switch would be that between cI and Cro in λ-phage, which repress each other. Positive feedbacks also display hysteresis: if the state of the system is dependent on an inducing ligand X such that system attains state S2 at high levels of the ligand, then to switch from S2 to S1 the concentration of X would have to be reduced below the level that was required for the S1 to S2 switch; and vice-versa. In other words, the system tries to remain in its current state.

If the transcription factors that constitute the genetic positive feedback have a co-operative behaviour then you can expect a steep switching curve.

For details see this review.


How does temperature affect photosynthesis? I am doing a lab for biology and my teacher required me to do this virtual lab. However, it does not make sense when seeing the results of the lab. In 30 second trials, it shows that there are 16 bubbles at 10C, 6 bubbles at 25C and 19 at 40C. This should not happen as 25C is near the optimal temperature (at least in respiration) but it shows the opposite.

Is the site wrong or am I wrong?

Site link: http://www.kscience.co.uk/animations/photolab.htm

Constants: 50 Light intensity, full disolved co2, white light color.

Your experiment should look something like this: The effect of temperature on photosynthetic rate of Elodea (pondweed). I assume you used Elodea canadensis for your test. Maybe the plant is already a bit "exhausted" - try to take a different branch. Or maybe it needs more time to get used to the new temperature.


Do people need nitrogen from air for health? Can people breath totally nitrogen-free atmosphere for a long time? I know, nitrogen is essential for life, and in big quantities, but maybe people can take it entirely from food, from proteins, etc?

Do people need nitrogen from air for health?

No. This is well established!

Can people breath totally nitrogen-free atmosphere for a long time?

Yes. Also well established!

I know, nitrogen is essential for life, and in big quantities, but
maybe people can take it entirely from food, from proteins, etc?

As expounded on in the comments by AliceD, nitrogen gas (N2) is entirely taken in by humans from their diet, since atmospheric N2 is pretty inert. It is also not necessary for gas exchange to take place in the lungs.
Some extra questions as an addendum:

Can one substitute N2 in atmospheric air with another gas, and sustain human life?

Yes. All side effects would be attributable to the effects of the substituting gas (e.g. it may be heavier or lighter or equally or more reactive than N2).

Can 100% O2 sustain human life?

No, and such a case has never been recorded. Oxygen toxicity following hyperoxia is very dangerous. Ironically, too much oxygen damages lung tissue and epithelial membranes via oxidation and render the lungs unable to exchange gases correctly; and so death by suffocation follows in such extreme cases such as with 100% O2.


What causes muscle spasms? What causes muscle spasms with muscles that are not in the heart  ? Could it be some sort of stimulus overload that causes a massive contraction?

According to wikipedia and MedlinePlus muscle cramps can be caused by muscle overuse or injury or dehydration and lack of minerals (eg. potassium or calcium). In this wikipedia page you can read about the mechanism of muscle contraction. I'd emphasize and quote the most important parts here:

  ATP binds to myosin, allowing it to release actin and be in the weak binding state (a lack of ATP makes this step impossible, resulting in the rigor state characteristic of rigor mortis). The myosin then hydrolyzes the ATP and uses the energy to move into the "cocked back" conformation. In general, evidence (predicted and in vivo) indicates that each skeletal muscle myosin head moves 10–12 nm each power stroke, however there is also evidence (in vitro) of variations (smaller and larger) that appear specific to the myosin isoform.
  Steps 9 and 10 repeat as long as ATP is available and calcium is freely bound within the thin filaments.

As you can see ATP is essential in the release of myosin from actin. In case of muscle overuse and dehydration ATP is depleted from the muscle cells and may cause the muscle to cramp.

Also according to this site it is said that repetitive firing of motor units with high frequency is associated with muscle cramps, although tehe origin of this is yet not clear. It can be either from the central nervous system or the peripherial.


Is it easier to burn a calorie of fat or a calorie of a carbohydrate? Say someone eats 100 calories of chocolate vs. 100 calories of carrots. Something tells me that eating the chocolate will lead to you generating more fat. Will it? Is it harder to burn the calories that you consumed from the chocolate?

It isn't burning of the calorie you should consider as once digested different calories are stored in the same manner, it is actually the digestion itself.

Proteins are by far the most energy requiring foods to digest such that around 20% of the calories in proteins are used in extracting them. In comparison carbohydrates are much easier at around 5-10% whilst fats are even easier to digest.

But think of it in simple terms, chewing a vegetable and digesting it down and the relatively sheer quantity of mass you need to make it calorifically the same value as chocolate means that yes 100 calories isn't 100 calories.

All then in terms of real life application, our bodies respond to how much we eat. If we eat a large volume of low calorie food we will eat less calories in total. This also plays an important role.

Source: http://www.ncbi.nlm.nih.gov/pubmed/20613890


Why does the olive tree produce a bitter tasting fruit? What is the survival value for the olive tree to produce a bitter tasting fruit, even when it is ripened?

I realize some fruits and berries are species specific, i.e., meant for specific animals to eat and disperse the seed widely. Is this the case of the olive?

You guessed it correctly: seed dispersal by zoochory, specially when the animal eats the fruit to spread the seeds (endozoochory), is an intimate relationship between the plant and the animal: the fruit has to be attractive to that specific animal, not attractive to you or me.

And, as you also seem to know, the same fruit will taste differently for different species. We could explain that using the concep of qualia (see my answer here), but the case here is even simpler: different species may have different receptors and different sensory perceptions (not sensations, I actually mean perception) for the same fruit. The most famous case is that one involving birds and chilli peppers, which don't taste hot to them (birds lack capsaicin receptors).

All that being said, olive (Olea europeae) fruits attract birds, which are their main dispersal agent (REY et al., 1997; Spennemann and Allen, 2000).

According to Spennemann and Allen, 2000:

  Worldwide, olives have proved to be a successful invader of disturbed lands, with birds as the principal seed vectors.

So, we can hypothesise that olives don't taste as bitter to birds... or, that birds do like a bitter taste. It really doesn't matter: what's important is that the fruit is eaten and the seed is dispersed.

A male blackcap (Sylvia) eating an olive. Source

Sources:

REY, P., GUTIERREZ, J., ALCANTARA, J. and VALERA, F. (1997). Fruit size in wild olives: implications for avian seed dispersal. Functional Ecology, 11(5), pp.611-618.
Spennemann, D. and Allen, L. (2000). The Avian Dispersal of Olives Olea europaea: Implications for Australia. Emu - Austral Ornithology, 100(4), pp.264-273.


How is Na concentration re-established after action potential I understand that the repolarization is because some K+ chanels are opened with the action potential. But whats happens with the sodium chemical gradient that is needed for a new action potential? Are there further Na-K pumps in the axon membrane?

Yes, there are Na-K pumps all over.

However, it is important to recognize that ion concentrations change very little during action potentials. The change in membrane potential is due to changes in ion conductances, very few ions actually flow. It is still necessary to maintain concentration gradients over many many action potentials, but the change in concentrations during the course of a single action potential is negligible.


Hormonal terms Somatotrophin or somatotropin? Are Somatotropin and Somatotrophin hormones the same? It's confusing because when you type in Somatotrophin in google, it says, "a growth hormone secreted by the anterior pituitary gland.", but there's no Wikipedia about it. But when you type in Somatotropin, there's whole Wikipedia for this stating that it's a growth hormone. I am 100 % sure that there is a difference between these two terms: tropin and trophin because Wikipedia itself says not to be confused with these terms and has articles separately for these two terms. So, Can anyone help me be clear about these two terms?

Yes

They are the same thing, and both are old-fashioned terms for what is now termed specifically growth hormone (i.e. not generically as in "a growth hormone"). It is clear from the Wikipedia entry for growth hormone that this is equivalent to somatotropin.

I could not find a specific scientific reference that states that the two are the same, but I present a line of reasoning based on a search for mention of the terms in books using the Google ngram.

The initial similarity in the curves in the left-hand frame reflects, I think the competing use of the terms when the hormone activity was first discovered. Eventually somatotropin won, although the use of growth hormone is much more common now (right-hand frame).

If you look at the books cited by the ngram in which somatotrophin is used, you will find that many are in the field of animal science, especially dairy science in relation to the lactogenic effect of the hormone. Years ago I worked in this area, and remember that growth hormone had such lactogenic effects.  Presumably somatotrophin stuck in this area, whereas somatotropin was more generally used, especially in human endocrinology.

General Dictionaries and possible reasons for variation

I am hesitant to quote non-scientific dictionaries on scientific topics, but in this case it is probably justified, and it also addresses the difference in meaning of ‘tropin’ and ‘trophin’, referred to in the question.

The Merriam-Webster online definition of somatotrophin redirects to:

  somatotropin
  variants: or less commonly somatotrophin

Chambers on-line only has somatotrophin, But my own 1994 printed edition has:

  somatotropin or somatotrophin a polypeptide growth hormone

My Chambers Dictionary iPhone app also has both.

And Saunders Comprehensive Veterinary Dictionary, 3rd ed. (2007), according to a citation in the Free Medical Dictionary, has:

  somatotropin, somatotrophin
  growth hormone

If you check the meanings of the two suffixes in Merriam-Webster:

  -trophic
  of, relating to, or characterized by (such) nutrition

Whereas

  -tropic
  1 : turning, changing, or tending to turn or change in a (specified) manner or in response to a (specified) stimulus
  2 : attracted to or acting upon (something specified)

It seems probable, therefore, that the original form was somatotrophin, but, either by confusion with the second definition of -tropic or a North American chemical aversion to ‘ph’ (as in sulphur/sulfur), somatotropin became dominant, except in the field of animal science. Perhaps that is why the Oxford Dictionary, both online and in my printed edition of 1991, ignores somatotropin completely. However you would have difficulty ordering somatotrophin from the chemical supplier, Sigma-Aldrich/Merck, whereas somatotropin is available.


What does "thermodynamic equilibrium" mean for an enzyme-substrate complex? From Fersht, Enzyme Structure and Mechanism p. 87:

  The Michaelis-Menten mechanism assumes that the enzyme-substrate
  complex is in thermodynamic equilibrium with free enzyme and
  substrate.

In my understanding what this means is that the (E-, S- and ES-concentration dependent) rates of association and dissociation have equated.
So we're kind of in this situation:

where "product" would be referring to [ES] and "reactant" to [E] and [S]. Does that make sense?

Thermodynamic equilibrium means that:

Rate of forward reaction = Rate of backward reaction

In this case:

$E + S\xrightleftharpoons[k2]{k1} ES\\ \ \\
 \ \\ \\ at\ equilibrium:\\ \  \ \\ \ k1.[E][S] \tiny{\ (forward\ rate)}\normalsize=  k2.[ES] \tiny\ (backward\ rate)
$

This was the initial assumption in the Michaelis-Menten model.

Later on this was improvised by assuming pseudo-steady state of ES complex. This means that $[ES]$ does not change over time, which is both as a result of its production by the reversible reaction:  $E + S \leftrightharpoons\ ES$ and consumption by the irreversible reaction $\ ES\ \xrightarrow{k3} E+P$

that is:

$k1[E][S]\tiny\ (production)\normalsize=(k2+k3)[ES]\tiny\ (consumption)$


How long does Lentivirus take to express in vivo mouse neurons? Does anyone know how long it takes for a standard Lentivirus vector to express its genes (under a strong promoter such as CAG, CB7, etc.), after injection into the brain of a mouse?

By hearsay I think it's 2 weeks for full expression, is that true?

This depends a lot on what you are expressing (such as how stable it is), and where you need it (soma vs dendrites vs axons, and whether it is trafficked actively in the cell).

For optogenetic constructs, our lab has typically seen near-peak expression around 3 weeks, though expression may be suitable earlier, and toxic later.


It is possible for person with AIDS be negative for HIV antibodies? I'm just curious as there was a bit controversy around this topic. It is possible for person with AIDS be negative for HIV antibodies?

As of 1989, the CDC reported that 5% of all U.S. AIDS patients who had been tested for HIV to that time were HIV-negative. No figures have been reported by the CDC since 1989.

If so, how it's possible?

See:

Unexplained CD4+ T-Lymphocyte Depletion in Persons Without Evident HIV Infection -- United States at Centers for Disease Control and Prevention

Usually an antibody test against HIV is positive three month after the infection. Before this time a test can only be done with molecular biology methods as PCR. However, it is possible, that patients which have definitely been tested in an early phase using molecular biology methods and which afterwards receive a antiretroviral therapy (ART) that these patients do not develop high serum levels of antibodies, as the virus titer in the blood is not high enough for a sufficient reaction and thus stay undetected by the tests. This has been improved, so that the kits are supposed to have a higher sensitivity now. See these papers for more details:

Seroreversion in subjects receiving antiretroviral therapy during
acute/early HIV infection.
The effects of early antiretroviral therapy and its discontinuation
on the HIV-specific antibody response.

I haven't found any papers on the decline of HIV-antibodies in AIDS (which is the late stage of the disease), but if they do, this is probably due to the effects of the infection on the immune system.

Low counts in CD4 positive T cells (which are usually associated with an HIV infection) can also occur with other diseases. See these papers (especially the first, as this is a review which contains a lot of further references):

Idiopathic CD4 Lymphocytopenia: Spectrum of opportunistic infections,
malignancies, and autoimmune diseases.
Decreased CD4 and increased CD8 counts with T cell activation is
associated with chronic helminth infection.
Acquired immunodeficiency without evidence of HIV infection: national
retrospective survey.


Why is coffee a stimulant? The effects of coffee as a stimulant are quite well-known. What are the mechanisms by which coffee helps prevent sleepiness? I have heard of the presence of caffeine, but what does it actually do inside our body?

Drowsiness is caused by the chemical adenosine binding to a nerve cell's adenosine receptor. A compound that binds and elicits a response, in this case a slow down of nerve activity, is called an agonist.

Caffeine is also capable of binding to the adenosine receptor. However, it does not elicit a response and no drowsiness is experienced. This type of compound, binds with no response, is called an antagonist.

When caffeine is in your system it blocks the nerve cell from "seeing" any adenosine, causing the cell to increase activity. This increase of neural activity is interpreted by the brain as an emergency resulting in the release of adrenaline, the "fight of flight" hormone.

Caffeine stops you from being drowsy, speeds up your nerve activity, and gives you an adrenaline rush. All of these interfere with sleep.


How did the nucleus of eukaryotic cells evolve? What is/are the most popular theory/theories on how the nucleus evolved?
I know mitochondria came from alpha-proteobacteria, chloroplasts from cyanobacteria and that eukaryotes evolved directly from archaea, but what about the nucleus?

I hope these papers by Wilson and Dawson (2011) and Devos et al. (2014) will help you.

In summary these two review provide evidence for the following statements:

The nuclear pore complex is well conserved with some regions of divergence.
The nuclear lamina appears quite variable between major supergroups.
Centrosomes are ancient structures but exhibit a complex evolutionary history.
There is evidence for prokaryotic ancestors of some nuclear components.
Analysis of divergent organisms is essential to fully understand nuclear biology and its origins.


Evolution in 37 years, is it possible? I am confused, can evolution ( speciation ) really occur in such a short time ?

  In 1971, biologists moved five adult pairs of Italian wall lizards from their home island of Pod Kopiste, in the South Adriatic Sea, to the neighboring island of Pod Mrcaru. Now, an international team of researchers has shown that introducing these small, green-backed lizards, Podarcis sicula, to a new environment caused them to undergo rapid and large-scale evolutionary changes."

Here is a short video featuring the scientist.

Two related articles:

http://www.sciencedaily.com/releases/2008/04/080417112433.htm
http://news.nationalgeographic.com/news/2008/04/080421-lizard-evolution.html

Edit: I asked a similar question previously about two people having 44 chromosomes and their possibility of creating a new species. You might like to read/answer that as well:

Can two humans with 44 chromosomes produce viable offspring?

I am confused, can evolution ( speciation ) really occur in such a short time?

Well, Evolution and Speciation are not the same. Evolution is the adaptation of an existing species to an environment over generations. Speciation is the development of a new species, and the definition of "species" can vary depending on who you talk to - but a very commonly accepted one is that two individuals cannot produce fertile offspring.

However, the answer is still Yes. Evolution can occur in as little as two generations because that's all the time it takes for a change in the DNA to be exhibited in the newest generation. For instance, Lactase Persistence - which allows the bearers to ingest dairy products without digestive stress into adulthood - has evolved at least twice in humans in separate groups. Both are the result of either one or two point mutations (single changes in a Nucleotide within the DNA). The result is that at one point in time for each appearance of lactase persistence, a child was born that could drink milk into adulthood while their parents and cousins could not.

That is evolution; the child was better adapted to the resources available, and because lactase persistence either...

Provided a significant advantage over their kin in the environment (which is likely, as being able to digest milk in an agrarian society opens up a new source of energy)...

or

Didn't hinder the child's ability to grow and produce fertile offspring of their own...

...it has persisted in the populations where it initially evolved.

Speciation is a little trickier, but that's because there isn't a known qualitative way to differentiate species at the genetic level quite yet. It could be a few key gene changes, it could be a whole genome difference of 10%, or a million other factors. Practically speaking, though, Speciation is simply the result of accumulated genome changes that at some point prevent the members of one group from producing fertile offspring with their ancestral group.

Because we simply don't know how much of or where the genome has to change, it's certainly possible that speciation could occur in the same time period as it takes to evolve: Two generations.

Since I'm doubting the wall lizards have a generational time of >37 years (don't mistake it for lifespan, humans can reproduce in our teens - even if we live into our 80's), it's definitely possible that the wall lizards could evolve (and potentially speciate) in such a short amount of time.

With organisms that have a very, very short generational time - like E. coli or other bacteria - you can observe the Evolution of populations in days or hours.