an umbrella term for homeolog and ohnolog? Is there a word that refer to homologous chromosomes within a polyploid species? If I have AABB species, what is A to B?

The words "homeolog" and "ohnolog" are reserved for the cases if the homologous chromosomes have diverged via speciation or whole genome duplication event. But what if we just don't know?

I hesitate to use word "homologous chromosomes" since they do not for a choromosome pair anymore, they are homologous in sense of an recent common chromosome ancestor.

Unfortunately, there is no such term. Look at Glover et al. 2016 for a proposal how to unify the ploidy related homology terms, none of the words describes exactly what I searched for, so I at least compiled the relevant vocabulary

homoeolog/homeolog - homologous chromosomal sets in an organism diverged in isolated populations/subspecies and broght back by a hybridization event; note that the two spellings with exactly the same meaning are possible
ohnolog - homologous chromosomal sets originated from a whole-genome duplication (WGD) event; however usually this is used for ancient WGD events (like the R1 and R2 at the base of vertebrates, or the WGD at the base of bony fishes). It is not really possible to distinguish between WGD and hybridization in these ancient cases and therefome ohnologs perhaps suit "unknown" category better.
homologous chromosomes - chromosomes that pair during meiosis (does not strictly correspond to the homology in the context of molecular evolution)
homologous sequences/homologs - any sequences that have a common ancestor (as used in molecular evolution; but does not have to be on a genome-scale or within a genome; tandem duplicates or orthologs in two species are also homologous sequences)

2020 update:
I asked when I was writing this paper. I needed the term to describe the heterozygosity structure of some polyploids and I ended up calling them homolog (A <-> A' divergence) and homoeolog heterozygosity (AA' <-> BB' divergence) or composite when I was unable to set them apart (the majority of cases in fact).


What's the maximum pressure inside a bombardier beetle? This question got me wondering about the pressure inside a bombardier beetle.

Lots of articles mention pressure, but don't specify the amount of it:

  One study records the velocity of the spray to be within a range of 325 to a stunning 1950 cm/s.
  [...]
  Once the muscles around the reservoir squeeze the first amount of
  reactants through the valve into the reaction chamber, the resulting
  explosion causes the pressure to rise rapidly in the reaction chamber,
  forcing shut the one-way valve. The products of the reaction then exit
  the chamber with a pop and a puff, and the pressure inside the
  reaction chamber lowers again, falling below the pressure of the
  collection reservoir, which is still being squeezed by the reservoir
  muscles.

Calculating from the spray characteristics is beyond me.

According to this study, model data shows a maximum pressure of 110 kPa, that's 16 psi and only 1.086 atm:

  The three-phase process involved in the beetles explosive secretory
  discharge (ESD) process. The inlet size is shown as a proportion of
  the inlet radius. During the first phase of refill and heating (blue),
  only the inlet valve is open. During the second phase (red), the
  chamber is closed. Finally, the third phase (marked by an arrow) is
  the exhaust phase, when only the outlet valve is open. This phase is
  significantly shorter than the first two phases. This cycle then
  repeats with phase 1 starting at approximately 5.1 and again at 7.8
  ms.


Regarding different nucleotides on a DNA strand I am not a biologist therefore, it might seem as an elementary question. I retrieved rodent sequences from UTR database:

http://utrdb.ba.itb.cnr.it

And I know there are supposed to be four nucleotides namely: A,G,C, and T. However, on this database I get sequences that have 'n' nucleotide in several locations, 'm' and 'k' as well. What does these letters mean? I haven't been able to find anything regarding it. Does it mean these positions in UTR are undefined or they are some 'intermediate' nucleotides if there are any?

These are IUPAC codes for so-called "degenerate" or ambiguous bases, alternatives to the usual A, T, C, and G nucleotides (for DNA). The N code represents any base, while M and K map to A or C, and G or T, respectively.


What is meant by bionomics of a vector? What is supposed to fall under the title Bionomics (The study of an organism and its relation to its environment; ecology.)?

Suppose we are dealing with a vector, Anopheles sp. are the following going to be included in its bionomics:

Life cycle
Interaction with parasite (Plasmodium sp.)
Mode of transmission of parasite by this vector
Control
Diseases caused ?

Bionomics is indeed the 'thorough' study of living organisms and their relationship with the environment/ niche they thrive in.

Aim of Bionomics is mainly to decipher the driving factors for an organism to prefer a given niche. Given this key goal, it is apparent that one needs to focus on all aspects of an organism's life cycle and community dynamics.

So the answer to your question would be: Yes, one will need to focus on all the five points pertaining to Anopheles sp. (the 5th point i.e diseases caused) will more be an information resulting out of the study of its interactions with other living/ non-living forms), than a specific focal point for Bionomics.

References:

A good article on Bionomics

An amazing and detailed report on Bionomics of Entomophagous Coleoptera

Other references:

The dominant Anopheles vectors of human malaria in Africa, Europe and the Middle East: occurrence data, distribution maps and bionomic précis. Sinka et al., 2010

Description and Bionomics of Anopheles (Cellia) ovengensis (Diptera: Culicidae), a New Malaria Vector Species of the Anopheles nili Group from South Cameroon. Awono-ambene et al., 2004


Co dominance, breeding and genes Let's say we are talking about a complex being with many variations.
Let's take coat colour as an example and pretend we have a creature with codominant genes to do with coat colour (for example BR (B for black and R for red, assuming they're both dominant and visible).
We now breed said animal to a co dominant coat type of a different variation (for example, YW (Y for yellow and W for white, assuming again that they're both dominant).

Assuming all 4 dominant genes are as dominant as each other (so red isn't going to appear over yellow, for example)
What comes out of said breeding?

I am not sure I understood your question. I will try to rewrite your question below with my own words and you will let me know if I udnerstood your question correctly.

Description of the genetic of interest

There is only one locus for coat color. Individuals are diploid. At this locus, there exists 4 alleles in the population. B, R, Y and W. BR individuals are both black and red (as B and R are codominant). Another individual is YW and its phenotype is yellow and white (as W and Y are codominant)

Question

What phenotype do BY, BW, RY and RW have?

Answer

There is no way to know! Relationships between alleles, say Y and B in determining a given phenotype cannot be extrapolated from relationship B and Y have with other alleles. A relationship between two alleles in determining a phenotype is specific to a pair of alleles.

It is for example theoretically possible that A is dominant over B and B is dominant over C and C is dominant over A.

In your case, as you only have codominant relationship, it is tempting to expect that BY would be both black and yellow but there is really no way to be sure of that from the "Description of the genetic of interest"

EDIT

You have now changed your post. I don't really understand the new question either. You seem to imply that two alleles may be both dominant. This is impossible. They can be co-dominant.

I think your issue is that you are trying to associate a property of relationship between alleles as a property of an allele itself. Keep in mind, that saying that an allele is dominant only makes sense in a particular context that is in relationship to another allele who will therefore necessarily be recessive.


How are blood vessels affected by UV and infrared radiation? The lining of the blood vessel as an interface and boundary layer is of existential necessity to the life-support of mammals.

My question is:
How are major blood vessels and the blood vessel lining affected by sun-irradiation in humans, when exposed through equal or less than a millimeter of skin in total (including subcutaneous fatty tissue)?

Information regarding infrared exposure is welcome too.

Source: http://www.dermatology.ucsf.edu/skincancer/General/prevention/UV_Radiation.aspx

Thanks.

UV rays cause damage is by thinning the walls of surface blood vessels, leading to bruising, bleeding, and the appearance of blood vessels through the skin. Longwave UV radiation (UV-A) accounts for up to 95% of the UV radiation that reaches the earth's surface. Although UV-A is less intense than UV-B, it is more prevalent and can penetrate deeper into the skin layers, affecting the connective tissue and blood vessels, which results in premature aging - Photoaging.

At the same time UVB – is even more dangerous than UVA radiation and also causes skin damage and skin cancer. It affects the surface skin layer. The skin responds by releasing chemicals that dilate blood vessels. This causes fluid leakage and inflammation – better known as sunburn.

I am not quite sure what chemicals are generated by UV radiations beneath the skin surface. I guess it might be excess free radicals which accumulate and cause damage to blood vessels since they are delicate. There is one theory which talks about damages to skin due to Free Radical theory of aging

To give an example how UV radiation affects the blood vessel here:

  In actinic purpura, UV radiation damages the structural collagen that supports the walls of the skin's tiny blood vessels. Particularly in older people, this collagen damage makes blood vessels more fragile and more likely to rupture following a slight impact.

Below figure to give an idea of how strong UV radiations are:


Can cognitive enhancement from exercise be replicated/replaced through prolonged standing? Can cognitive enhancement from exercise be replicated/replaced through prolonged standing?

Like, will BDNF be released from prolonged standing.  I would prefer to use a standing desk than exercise (due to wanting to save time).

Short Answer

Probably not.

Slightly longer answer

This fairly recent review shows little positive effect of standing desks and mixed results of treadmill desks for cognitive outcomes (note: this is a summary of 23 full studies). Only treadmill desks were actually studied for cognitive performance, and even those showed no effects.

There were some positive physiological outcomes for both standing and treadmill desks, but much more consistent with the treadmill desks. The treadmill desks seemed good for weight loss, though, especially in obese participants.

All in all, it doesn't seem like a mere standing desk is known to give direct cognitive benefits, though the existing studies are all fairly small. It probably won't hurt, although standing for long periods can be problematic, too.

None of these studies compared the effects of the standing desks to the effects of exercise.

References:

MacEwen, B. T., MacDonald, D. J., & Burr, J. F. (2015). A systematic review of standing and treadmill desks in the workplace. Preventive medicine, 70, 50-58.

There are studies, however, like this one:

Mehta, R. K., Shortz, A. E., & Benden, M. E. (2015). Standing up for learning: A pilot investigation on the neurocognitive benefits of stand-biased school desks. International journal of environmental research and public health, 13(1), 59.

...that purport cognitive benefits of standing desks. However, it is important to note that one of the authors has patents on standing desks that are licensed by companies that produce them, including some of the desks used in the study.


If the flu vaccine is the exact same as last year, would it still offer protection this year? I understand why the flu shot changes and that's why we get an annual vaccine; however, if the vaccine is the same as last year, wouldn't people theoretically still have the same antibodies this year? Do antibodies disappear after a year?

If one flu strain wouldn't change between the years (meaning there wouldn't be any new mutations in it) and the same strain would circulate again in the following year, the "old" vaccination would protect people. This is the same as with other viruses which do not change, once you reached a protection (usually one basic immunization and one booster), this protects for a long time (see measles vaccination as an example here).

There are surprisingly little articles available on how long the immune response after a vaccination lasts. There is a difference between the livettenuated influenza vaccine (LAIV) and the inactivated influenza virus (IIV), with the former giving a less good protection (see reference 1).
Data for the LAIV suggests that there is protection for at least one year after the vaccination (see reference 2).

However, there is evidence that the immunity against the flu after an infection against this specific strain might last life-long, as a paper demonstrated on survivors of the 1918 flu epidemic (see reference 3).

Having the flu against being vaccinated against it is a complete different thing (higher exposure, probably more antigens), but the question is if the immune response against vaccinations may also for a longer time.
The problem with the flu vaccination are:

The strain circulating in a year is changing.
The stains are mutating, making them different from the virus used for vaccine production. Depending on how different these mutations make the circulating strain, it can render the vaccine more or less useless. This is something what happened this flu season.
The flu vaccine is prepared from different flu strains to cover a broader range. In a tri-valent vaccine these are typically 2 Influenza A and one Influenza B virus strains, in tetra-valent vaccines 2 A and 2 B strains. The composition is based on a prediction (from epidimiologic data) which strains are likely to circulate in the next season and is done early in the year for the following season (production takes time, etc.).

Because of these problems, researchers are working on a universal flu vaccine; which is based on virus parts which do not change and should protect against all virus strains. Then only the basic vaccination would be necessary as with other vaccinations.

With all these limitations, it is still advisable to get a flu vaccination, as it is a pretty severe infection.

When not challenged (i.e. upon infections) antibodies are cleared from the blood within a few weeks, but there are low amounts produced (which are enough for detection). The immunologic memory is maintained by memory B cells which can ramp up production of the highly specific antibodies in a very short time - this is the reason for the protection by immunizations.

References:

Modest Waning of Influenza Vaccine Efficacy and Antibody Titers
During the 2007-2008 Influenza Season.
Longevity of B-cell and T-cell responses after live attenuated
influenza vaccination in children.
Neutralizing antibodies derived from the B cells of 1918 influenza
pandemic survivors


How are the images of both eyes combined to form one image? When you see an object by one eye, ex.right eye, you see it from the right direction and the opposite if you see it by your left eye, but when you open both eyes, the image appears somehow centric in between.

  How does the brain combine both images to form the final image?

The visual system contain several stages in which the information from both eyes is progressively mixed and analyzed, starting in the lateral geniculate nucleus.

Even if you feel seeing just one merged object with both eyes, your brain is using both images to calculate the 3D position of that object.

One fun fact: The image that you feel centric, it is actually bias towards one of your eyes, the called "dominant eye". You can check what is yours by a simple experiment


Why do herring have fine bones Most fish have largish bones which support the core muscles.  Around the abdomen, they act as a sort of framework protecting the organs.  With herring, the bones are really fine: almost thread like and there are lots of them: more than on any other fish I've eaten.  I would like to know why herring have such fine bones.

Most likely to assist in maintaining neutral buoyancy. Many fish have reduced weight of heavy structures (evolutionary wise)like bone to assist in maintaining nuetral buoyancy. The swimbladder struggles to maintain  buoyancy near the surface for some herring

https://www.researchgate.net/publication/231918276_The_herring_swimbladder_Loss_and_gain_of_gas/amp


In plasmid-based transient transfection of mesenchymal stem cells, do I have to select for transfected cells and verify GOI expression via a reporter? I am transiently transfecting mesenchymal stem cells with a mammalian plasmid-based expression vector that does not contain any mammalian selection marker and also the gene of interest will be cloned into the plasmid without co-expression of any reporter fusion gene.
I would like to know if selection or expression testing is good practice and mainstream in plasmid-based transient transfection of mammalian cells.
As you know, in bacterial transformation selection against non-transformed bacterial cells is mandatory so that transformed bacterial cells could be enriched for. I wonder whether this is also mandatory in plasmid-based transient transfection of mammalian cells. If not, then  would not non-transfected cells outgrow transfected ones and affect downstream cell-based functional assays? Also, do I have to measure transfection efficiency beforehand? Also, how long can a mammalian cell retain a plasmid without a mammalian selection marker? Thank you.

No and Yes, respectively.
No, you don't need to select for and generally you can't unless you use something like FACS to sort and capture cells expressing your marker/GOI.
Transient transfections are generally not selected for, if they are it is to make a more stable line, and either requires integration of the marker site into the genome (most common) or in some cases use of a plasmid and cell system that supports propagation of the plasmid.
With transient transfection it is normally a good idea, at least for the first few times, if not every time, to confirm that the plasmid is expressing as you expect. You can do this by immunological methods, most commonly western blotting (WB) or immunocytochemistry (ICC). ICC will give you a percentage transfection, which can be useful in assessing how well you would expect an overall population to respond to a stimulus and how well you can see that effect - what if only 10% of your cells transfected compared to 50% or 90%, but it can't tell you how much protein is being expressed. ICC can also tell you how cytotoxic your transfection is - commonly used methods like the Lipofectamine family of reagents are often in the 20-50% cell-death range. WB on the other hand gives you how strong your expression is - how much protein is there, but it can't tell you how many cells were transfected or how much cell-death there is.
In theory at least FACS can do both number and strength, but it would require calibration of your antibody by both western and ICC.
You can also look at RNA expressed off the plasmid, but this may not bear a direct relationship to how much protein is produced.


Directed evolution: Point mutation vs Insertion-Deletion vs Shuffling When attempting enzyme function improvement via Directed Evolution I can see three different strategies to generating variation for the gene sequence:

Point mutations
Insertion / Deletions
Shuffling

Is there a systematic difference between how successful each of these approaches are likely to be for a particular gene or in general? Does one choose one over the other approaches in any specific project based on any characteristics / goal differences?

A related question: On a methodological front, I know one can use error prone PCR to get #1 i.e. point mutations.

What are similar techniques for #2 & #3? i.e. How does one execute gene shuffling or Insertion / Deletions in practice?

In general, point mutations are introduced in the proteins of interest during directed evolution. These can be specific mutations in the active site of an enzyme if you would like to change its specificity towards a new substrate, for example. The point mutations can be introduced with primers when you amplify your gene of interest. However, if you don't know specifically what changes to make, then yes, a way to generate mutations is by error prone PCR or by Quick change PCR. If you'd like to see if a certain amino acid change abolishes activity/stability/etc, you would do Alanine scanning (https://en.wikipedia.org/wiki/Alanine_scanning).

I haven't heard much about introducing deletions or insertions for directed evolution. First of all, they have to be in-frame, so that the overall coding sequence does not change. People are usually introducing epitope tags on the N- or C-terminus for two reasons: 1) to purify the proteins; 2) to increase its solubility. But in general, the introduction of deletion will lead to unpredictable changes to the 3D structure of the protein of interest.

The DNA shuffling is very often used for directed evolution. Here is a figure from a Nature paper [1] describing DNA shuffling. The way it is usually performed is by using sequence homologs of the protein of interest. The different fragments can be obtained by PCR-amplification and introducing short overlaps with the neighboring fragments. The fragments can be then assembled by various methods, including Gibson assembly and homologous yeast recombination.  The advantage of DNA shuffling over introducing single mutations is that you have to screen fewer mutants and the activity/stability of the protein could be improved several hundred fold more.

DNA shuffling figure from [1]

Interestingly, a DNA shuffling using a method called SCHEMA [2] was developed in Chris Voigt lab. Shortly, SHEMA is a computational algorithm used to identify the fragments of proteins, or schemas, that can be recombined without disturbing the integrity of the three dimensional structure. It is based on the 3D structure (of one of the parents) and an alignment of the parental sequences. It calculates the interactions between residues and determines the number of interactions that are disrupted in the creation of a hybrid protein. A window of residues w is defined and the number of internal interactions within this window is counted. The window is slid and the schema profile is created. For example. in the figure below, the number of interactions that are broken in the possible chimeras are 0 on the right chimera and 3 on the left chimera. The right chimera will be used in the screening.

SHEMA method from [2]


Can other animals see black differently? I am not sure if this is the right place for this question, but this is a debate that has been going on between two colleagues for days and I need a resolution because it's driving me crazy. So any help would be appreciated.

It is a common philosophical argument that it is impossible for one person to know if another person is at the same place on the colour wheel (e.g. how I see blue and how you see blue could be different, and we will never know). By that reasoning, it is possible that some species see colours differently to us. However, black and white are not the colour wheel because they are not colours. So essentially, the question is, could another species that "sees" by sensing light with their eyes as humans do ever see an "absence of light" as a colour OTHER than black.

I am not quite sure what these two imbeciles are debating, but I believe they are arguing as follows:

Party 1: Black and white are shades not colours, and therefore, even if another species saw colours differently, they would always see black as black, white as white, and all shades of grey relative as usual to the colours they see.
Party 2: Black is only inserted into our vision by our brain to resolve the "problem" of not receiving any light. So, therefore, it is equally possible that another species could deal with this problem" differently, and they will see something other than black.

Yes, animals can see 'black' differently, in terms of different shades, similar to what you stated about humans perceiving different hues of 'blue'. It is all relative to the cones in the eye of the referenced animal. Animals that see in black-and-white see several different hues of both, black and white. Animals that depend on color to judge the ripeness of a food also see in several different hues of black. For example, a parrot differentiating between seeds that humans may perceive as both being 'black'. Here is a color chart showing the colors that bees can perceive in juxtaposition to humans; it indicates high differentiation between hues of black, as opposed to humans' low differentiation.


What kind of bee can dig through stone? My house (in Israel) has a concrete structure, with a decorative veneer of Jerusalem Stone at least an inch thick. Yesterday I came out to discover a little hole in the wall - and a pair of bees coming in and out of it! (See video)

This wall is no more than 5-6 years old, and I have never drilled anything there; they're not reusing a human-made hole. I must conclude that the bees somehow dug that hole.

Is that possible? What kind of bee could do this?

Update: As interesting as these bees are I didn't want them living in my wall, so I filled up the hole with a silicone-type glue. A few hours later, they had dug through that, too.

Here's a paper in Current Biology1 on the discovery of a species of bee (Anthophora pueblo) in Utah (US) that burrows through sandstone. Pretty cool!

Sandstone is harder than limestone, so I suppose it could be possible for this type of bee to get through your wall material, though Utah is a long flight from Israel.

Perhaps you have discovered a related species of Anthophora local to where you live (perhaps this one?), except that it is unclear if the bee in your picture has the same large mandibles that would help it dig through stone:

  As sandstone is harder than other substrates bees excavate (e.g., sand or soil), higher energy and time costs are expected. Mandible wear is consistently seen in older females, a consequence of excavation that likely limits their further use.

Unless you have a lot of similarly-sized and -shaped holes in your wall material, with large-mandible-d bees coming and going, it seems reasonable to infer that this hole came from something else and that these particular bees are just reusing it.

1. Orr, M.C., Griswold, T., Pitts, J.P. and Parker, F.D., 2016. A new bee species that excavates sandstone nests. Current Biology, 26(17), pp.R792-R793.


Why do some animals try to imitate other animals? There is a tendency of some animals (including people!) to be "copy-cats" and try to imitate members of their own, and sometimes other, species.

The most obvious example is a parrot copying human speech. Humans also try to copy the speech of their parents when they are little. "ma-ma, da-da"

The less obvious examples, I'm not even really sure are occurring. Like when a gorilla at the zoo assumes the same posture as a person sitting on just the other side of the glass. Like my cat, who tries to chew on bones similar to the two dogs we have.

I'm sure there are more/better examples I'm not aware of.

What is it that creates this behavior? Is it something that was learned, or is it some natural tendency? Is there such a thing as behaviors that are "encoded in the dna"?

Mimicry, in biology, phenomenon characterized by the superficial resemblance of two or more organisms that are not closely related taxonomically. This resemblance confers an advantage—such as protection from predation—upon one or both organisms through some form of “information flow” that passes between the organisms and the animate agent of selection.

This link describes different types of animal mimicry

  The two step mechanism of mimicry evolution states that,

  1) Mutations at genes of major effect first allow a phenotypic leap
  achieving an approximate resemblance to a particular model.

  2) Once these mutations have increased in the population, resemblance can be enhanced through the gradual selection of epistatic
  modifiers.

Considering the case of butterflies, the working of two step mechanism evolved through different types of natural selection process. Experiments show that birds associate certain patterns in the butterfly wings to identify the specie and generalize those features, but a small deviation from the exact pattern is neglected. The increased resemblance is advantageous to species having imperfect mimics. So the species which displays/perform imperfect mimics can some how fall under the list of rejection and manages to survive, thereby passing genes to next generation.

  "Largesse of the Genome", an idea put forward by J.R.G.Turner states that, it is believed that the modification of a trait can be achieved by so many different genes that some of them will inevitably happen to be linked.Amoung the many possible combinations of the loci, selection could simply sieve out the ones that involve linked genes.

  Encyclopedia of Insects by Vincent H. Resh, Ring T. Cardé

Although the exact mechanisms of mimicry is still a questionable area, experiments are giving hopes regarding the two step mechanism and more over natural selection is the predominant factor which makes a mimicry successful.

This link describes insect mimicry and two step mechanism in detail.

  References

  A Dictionary of Birds

  Encyclopedia of Evolution

  Rapidly Evolving Genes and Genetic Systems


Lytic Viruses -- Cell lysis? So in the video my instructor sent on viruses, he said that for lytic viruses, new viruses manufactured by the host cell could get out of the cell in one of two ways.

The new viruses would leave by exocytosis.
or,
The cell would be "ruptured" and the new viruses would "erupt out of the cell".

In the rupturing option, is the cell destroyed? The way he phrased it as well as his tone of voice brought to mind an image of the cell bursting and the viruses spilling out....but the diagram showed a little gap in the cell membrane, and the viruses leaving from that one exit point.

Which is more accurate?

Thanks!

evamvid

Yes, ruptured here means that the host cell is destroyed. The virus "hijacks" the cell anyway and uses its protein production machinery to make as much virus particles and its transcription enzymes to makes as many viral genomes as possible. If the ressources of the cell are exhausted, it get destroyed and the viruses are set free.

See this image (from the Wikipedia article on the lytic process). It actually doesn't matter, if the virus infects the cell from the outside or if it comes from the genome.

Adsorption of the virus to the cell.
Injection of its genetic material into the cell.
Production of new viruses (hull and genome).
Rupture of the cell and release of the viruses.


What is this rather large insect in northwestern USA? As you can see from the ants in the first picture, this insect is peculiarly large - over an inch long. I thought it was dead in the first picture, but it started moving around the next day. A couple of days later I found it again, dead. I have two dead specimens and other pictures if desired.

I think I've seen a shedded exoskeleton of one on a forest trail and another dead one from months earlier.

What species is it?

Location: Oregon, USA.

This is a Jerusalem cricket, an insect from the Genus Stenopelmatus.

Here is an image of Stenopelmatus fuscus for comparison:


Prevalent large (>=90kDa) maintenance protein/loading control I was wondering if anyone had recommendations for good, large (hopefully 100kDa+), control proteins that would be present in most mammalian cells.  I'm working mostly with tissue samples from humans and mice, and airway epithelium in particular if that matters.  So far the best I've thought of is HSP90, but that is far from ideal for a number of reasons.  My target proteins are between 125 and 210 kDa.  To improve resolution, we've run pretty much everything under 90kDa off the gel.

That removes the old standbys like actin or GAPDH.  I understand that the protein levels could vary between cell types for a good loading control target.  Bonus points if you know a good antibody clone to it.

Vinculin!  I love our grad-students, I can't believe I didn't think of it last night.

Also, awesome chart, even if it's from a company.


A theoretical ethical dilemma For all those who keep in touch with advancements in field of biology iPSCs ought not to be a foreign term. iPSCs are now being used to make organ models to be able to study diseases and how drugs will affect them without needing any living host. I expect this organ modelling to become more and more advanced in future and soon all complete organs to be made using this technology. However should making a complete living brain ever be allowed for studying diseases as we are mostly our brain, so maybe while using such living brains we are making conscious systems on which we are experimenting?

I agree that iPSCs will continue to be developed and will probably be used to make brains at some point in the future. Whilst it's obviously not possible right now, feasibility isn't the issue here. A lot of my answer will be somewhat opinion based as a result of the nature of such an ethical question.

As to the ethics of experimenting on such living brains, It's undeniably a tricky question - and, as with all ethical dilemmas, suffers from the inherent variability of ethics and morals (you will struggle to find two people with exactly identical ideas about right and wrong, and from a purely logical and scientific perspective there's no reason to believe that moral objectives exist at all).

An interesting phrase that you use in your question is "we are mostly our brain". I suppose it depends on what characteristics you're looking at: a brain alone would be incapable of surviving and by mass the brain only accounts for around 2% of the human body. we are mostly water; simple, lifeless and unconscious.

Therefore we are evidently ranging into territory of consciousness, and by "we" you are referring to our seemingly conscious 'mind' as conjured by the complexities of the brain. As for this, I think perhaps the philosophy stack exchange is the place to go...

Ultimately it depends on whether we look at a brain as simply a collection of atoms which form molecules, cells, tissues and then organs or as something more - this is the whole idea of emergence (for example, an individual ant is unconscious and negligible, but many thousands of ants communicating using chemicals and simple commands forms a highly complex and adaptable ant colony - the ant colony is greater than the sum of its parts). if the former is true, then there should be no difference in manufacturing a brain and experimenting on it to making muscle tissue and performing experiments on that (or even creating a crystal from chemicals and using that for experiments). If we look at the brain as something greater than the simple sum of its parts - as a living, conscious being - then I suppose we'd need to go through the proper channels that we have now when dealing with something that's alive.

From here an infinite variety of problems crop up: would the brain be given the full rights of a human, or treated more like animal test subjects? Would consent from the brain be required? Could a brain even be conscious if unattached to the rest of a body? Would killing the brain be murder as it would be with a human?

So far I've just been stating issues: my personal opinion is that we ought to find a balance somewhere between treating the potentially conscious brain as merely an impressively complex collection of lifeless components and giving it the full rights of a human being. where that line should be drawn? I don't really know. Personally, I'd rather test drugs and treatments on a mere brain than on a fully formed and functional human being, but someone else might not agree.

These questions are always difficult, and science can't really give any reasonable answers (scientists can't even agree on what makes something alive, let alone conscious). there is an entire field called bioethics devoted to things like this.
my advice would be to ask this on the philosophy stack exchange as you will get some interesting answers there.


Consistency of consciouness So I was wondering if consciousness is continous and I found out it might not be the case. But in that case it begs a question, what if in every frame of consciousness my old me dies and new is reborn or rather there is nothing as consciousness but its just a reaction?

What I mean is if I clone a person, the clone would think its the original and we would be unable to determinate it either (if by clone i mean literall copy on the atomic level and with exclusion of any effect of quantum mechanics). If we would annihilate original and put clone into its place noone would be able to tell and to him it would look like everything is continous and nothing happened.

So can it be just illusion in our minds that we are continous sentient beings because we have access to our memory which tells us its like that, same as a clone but as the perception lost focus we die - frame stops to exists?

Can someone clarify this to me or point me to some interesting literature/article on this topic?

You trespass upon a question as old as antiquity: what properties constitute consciousness? The best means to respond to the question concerns a metaphysical answer and an answer in modern biology

We can perhaps divide consciousness into two categories: contiguous thought from past experience and identity and secondly, self-awareness.

The reputed example of the Sorites problem of Theseus' Ship describes how the physical entity of Theseus' ship, during his various battles and broils, loses certain components of his ship: his braces or mast, in example. They are replaced with exact replicates until the time that every component of the ship has been supplanted by a replaced component. Is it the same ship? It is dependent on your definition of identity.

Leibniz's Law of Identity whether in humans, ships or spaghetti monsters, states that objects x and y hold the same identity if and only if they share all the same predicates - qualities or attributes. If this be of functionality, the ship completes the same function and comprises the same components, albeit of different origin - thus, the ship has the same identity. This is important regarding your question whether your 'old [you] dies'. Over time, your cells undergo mitosis and eventually apoptosis. Hence, although your parts are in constant flux, the predicates between your old self and latter self are constant. Ideologically however, there is no set identity!

If you read David Hume's literature, you will observe the notion that one is only the composition of impressions (sensory reception) and thus there exists no identity.

Your question regarding clones is a challenge for biology. Behaviourism is an approach in biology concerning the interpretation of behaviour as a response to a stimulus. Furthermore, humans express complex instinctive behaviours in response to various stimuli. If there exists no 'mental substance' distinct from the body, then it seems plausible to consider human consciousness merely an extension of an advanced instinctive epiphenomenon: self-awareness is a by-product to these advanced behavioural patterns. To support this position, simply recall what factors allow one to discriminate individuals whom one meets, behavioural patterns and appearance.

Finally, one could attempt to assess consciousness in regard to self-awareness by conducting the mirror assessment. If one is capable of identifying himself/herself, then it is indicative of an ability to discern one's personal existence from general matter.

This is by no means a comprehensive answer to this question yet I bid you well in your continued explorations of human consciousness.


Anti-antibodies for preventing transplant rejection Transplanted organs from the donor are attacked by antibodies from the recepient. So can't we construct anti-antibodies and destroy specifically those antibodies which are causing the rejections ? (Instead of giving immuno suppressants)

Well, I can think of some problems :

You would have to administer this for life time which is really expensive.
So, what if anti - antiantibodies were made by the body ?

Any other problems you can think of ?

Within an organism, antibodies which bind to other antibodies in the body would be eliminated during clonal selection.  They are not made by the body after that period, which is in the first few months of life.

Such antibodies would have to be introduced from the outside.  Many have been designed or engineered for biotech and as therapeutics.


What is a concussion? When I was a kid and someone got a concussion, I seem to remember people telling me that it was when your brain impacts the side of your skull, accelerating fast enough to do so despite the cerebrospinal fluid buffer.

But wikipedia doesn't mention this explicitly. Is this just one possible cause for concussions? Is it possible to generalize about them? How much don't we know?

Concussion generally refers to the set of clinical symptoms that are secondary to the head injury and are characteristic by altered state of consciousness like instant onset of transient neurologic dysfunction, lack of consciousness or temporary respiratory arrest and loss of reflexes.

Since it's connected to the head trauma by definition, there is in principium no other cause of it.

The patophysiologic mechanism of concussion is not well understood yet, it's thought it results from two main sources:

the acceleration of brain causes increase of pressure
the impact of brain on the hard shell causes deformation and sheer stress in brain tissue (probably stronger cause of cytologic changes discussed later on)

These two mechanisms might lead to changes in the tissue structure and also trigger cytologic changes in the astrocytes and neurons such as:

  Astrocytes respond to a focal mechanical stimulation by propagating intercellular waves through their network. Mechanically stimulated astrocyte networks show changes in the cytoskeleton, organelle function, and biochemical cascades over time.

The changes in neurons detected in vitro include microstructural changes, direct membrane permeability change and change in the receptor abundance, structure of subunits and

  Early evidence showed that these physical insults can affect the properties of important synaptic glutamate receptors that can regulate neurotransmission and plasticity in networks. Moreover, inhibitory synaptic receptor functions can be altered with a physical force, showing that the balance of excitation/inhibition coupling is important to consider when assessing the effects of these physical forces. Perhaps equally important is the alteration in the receptor composition and intracellular signaling that occurs after a microinjury.

Microinjury is also linked to triggering of cell death pathways in brain cells.

The importance of these mechanisms are not yet clearly understood though and there probably are many more playing their role.

Sources:

Overview study
Robbins and Cotran pathologic basis of disease


What winged insect is in this photo? Is it Axymyia furcata? Posting on behalf of a neighbor who asked:

  Can anyone identify this insect? It's about 3/8" long. There are, it seems, hundreds flitting low over our lawn. There were none 2 days ago.

This is the Northern California Bay Area Peninsula.

Great pictures.  First, fly or wasp?

In the second picture, under the head you don't see jaws of a wasp, but do see a bit of a tongue-like organ, like a fly.  Further down, you can see that there are only 2 wings.  Just below where the left wing meets the thorax, you can see what looks like a tiny wing or paddle.  That's a haltere, a reduced wing that vibrates to provide stability, like a gyroscope.  Flys have halteres.  Finally, in the first picture at the very end of the abdomen are 2 points.  That ain't a stinger, it's an ovipositor.  It's a fly, female, and from the size of the abdomen, gravid.

The closest I've gotten to identifying this one is Axymyia furcata http://bugguide.net/node/view/1216479.  Everything matches, as well as we can see from a photo, except the coloration.  Also, A furcata is associated with streams and is found in the north-east and north-central US, while, your bug was found on a lawn in CA.  For more information about A. furcata than you need, there is a master's thesis available:  http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1882&context=etd.

I've looked at hundreds of fly pics to find the one I linked to above.  That's the only fly I found that matches the shape of yours.  Maybe it's a different fly within that genus, maybe it's just a color variation.

Their maggots live in rotten wood and decaying plant material, and the adults are mostly interested in more maggots, so this isn't a pest, just a neighbor.

Edit: furicata --> furcata, oops.


Does vitamin C decrease after reacting with oxygen free radicals? From the research that I have done, I know that antioxidants such as vitamin c donate electrons to oxygen free radicals and effectively neutralize them. They themselves do not become free radicals as they are stable in both forms.

So, would it be correct to say that after the vitamin C is oxidized(giving electrons to free radicals) so much that it can no longer give any more electrons(not sure what the actual limit is):

What happens to vitamin C (does it get broken down and therefore
decrease)
Is it any useful in destroying free radicals?

Correct, vitamin C (ascorbate) acts by donating 1 electron to a free radical (reducing them to a stable compound with paired electrons), and is thereby itself oxidized to semidehydroascorbate. This is actually a radical itself, but can be reduced back to ascorbate by thioredoxin reductase or cytochromes, using NADH or NADPH as the reducing agent. A pathway diagram with references is found here.

So to answer (1), ascorbate is continuously recycled after neutralizing free radicals, and is therefore not consumed to any large extent. Therefore, vitamin C is only needed in the diet to replenish the small fraction that is lost from the body (about 1--3% per day; see this book).

And yes, vitamin C is very important in defense against free radicals; it is considered the major water-soluble antioxidant in humans.


Recombination Data Set So I was looking over some genetics question and came across this data set.
In Fruit fly Drosophila melanogaster, there is a dominant gene b+ for grey body color and another dominant gene c+ for normal wings. The recessive alleles (b,c) of these two genes result in black body color and curved wings respectively

The question was asking about the calculation of the recombination frequency. To me Ada's data set makes sense as the parental type offspring numbers are higher than the recombinant offspring. However, Donald's data set doesn't. Is there any way a recombinant offspring could be in a higher proportion than the parental type offspring?

b+/c+
b/c
b+/c
b/c+

Ada
~0.39
~0.42
~0.08
~0.1

Donald
~0.09
~0.09
~0.4
~0.41

The other chromosome beeing b/c (I assume each one got an heterozygote fly and than they did a testcross)
There are a two possibilities for an heterozygote fly:
(b+/c+, b/c), (b+/c, b/c+)
If there was no genetic linkage we would except 0.25 for each fly group, but we didn't which means that fly groups with a higher probability are showing the original parental chromosomes phenotyping.
Since they didn't get the same results (by far) I assume (there are statistical tests for this) each scientist got a differently genetic fly
Donald got (b+/c+, b/c) since in his experiment the predominant flies are those showing a dominant phenotype and recessive phenotype and Ada got the mixed fly.
With this in mind we can see that the recombination frequency is 0.18 or 18cM
Yes, the recombinant can appear more than the parental (for example, if the parental is lethal or by pure chance) but in this case I belive it is simply a different organization on the chromosomes


Why do we have the tibia and fibula (a 2nd bone) in the lower leg? Does fibula participate in rotational movement of ankle or not (just like the radius in forearm)? If not, what is the purpose of that bone?

It does function in the rotation and stabilization of the foot, but that is not why we have it, even species in which it serves no function still have it. A bone does not necessarily have to have a purpose in an organism, instead it can have on in its ancestors.

We have this arrangement becasue we inherited the basic limb bone arrangement from our fishy ancestors. Basically all tetrapods share the same pattern of bones in their limbs, one bone, two bones, many small bones, followed by several groups of long thing bones. this goes for front and hind limbs.

tetrapod evolution


How best to count bees entering and leaving a hive to measure hive activity? This is my first question here, so I apologize for all mistakes I could have possibly made.

I'm a high school student in East-Central Europe and I need to complete some research for a biology contest (asking for advice is accepted, so I'm not cheating). My task is to analyze the influence of certain environmental factors (temperature etc., it's not that important for my question) on the activity of bees. The method is pretty simple: once a week I record the entrance to the bee hive (I do it on four hives), play it in slow-mo (It's impossible to count them properly without doing so) and simply count the number of bees entering or leaving.

Problem is, I don't know how long the observation should take. I play it in like X1/8, you need to play it twice (entering/leaving), so it takes a lot of time to gather one piece of information for a certain day. Till now I've been doing it for one minute - and there seems to be some kind of pattern to their activity analyzed that way. Yet, I'm not sure if it's actually eligible. I can't do the observation for hours - I still need to learn and have other duties.

So, what should I do? Could anyone give me some advice? Is one minute (several, like 6 times a day per hive) legitimate enough?

Thank you in advance.

One thing that's certain is that the activity of bees varies according to time of day, so more important than how long you record for is probably at what time you record. If you always record at the same time of day, this should allow a reasonable comparison between results of different days. For example, recording from time 14:30 to 14:35 every day could be fine. You could then record conditions at this time each day (temperature, weather, etc.) along with this.

As for the exact length of your recordings: Of course, the longer they are, the better. More samples usually increases reliability and representativeness of your results. However, more importantly you want a practically useful time as well. This really depends on the actual number of bees entering into the hive within different time frames, as well as the baseline variability between days irrespective of the conditions you are investigating. I don't know anything about either of these :)

You want the number of entrances in your recording to be at a level where you will notice if there is a meaningful difference between days, and the only way of going about this is usually to start with a guess and then change if you notice that you can't really make sense of your results.


Why did Trilobites evolve armor? The Trilobite is probably one of the most successful created which evolved in the cambrian explosion.

Though many sources stated the Opabinia has been hunting for Trilobites, this has yet been proven wrong.

Due to my research I haven't found much more animals in the Cambrian age that grow larger than Trilobites or Opabinias - so I do wonder why did Trilobites evolve such a powerful full-body armor when they're have been no clear natural enemies.

Your link that says "proven wrong" includes a hypothesis that Opabinia could have eaten trilobites during their molt, simply that it would not be able to eat through their armor (all the better reason to have armor).

The best evidence we are likely to have that trilobites had predators is that they have defenses; the fossil record is incomplete, and just because trilobites are well-preserved does not mean their predators must be. Unless other evidence surfaces for an alternative explanation, the simplest reason for why trilobites evolved armor is that trilobites with armor were protected from something and therefore selected for.

Injuries seen in fossil trilobites are similar to injuries from failed predation of modern related species (see for example Bicknell et al., 2018) and seem to be widely reported (Bicknell et al. 2018 cite a variety of other sources).

Bicknell, R. D., Pates, S., & Botton, M. L. (2018). Abnormal xiphosurids, with possible application to Cambrian trilobites. Palaeontologia Electronica, 21(2), 1-17.


Examples of intracellular parasites of medical or economic importance? What are examples of intracellular parasites of medical or economic importance? I have read that Xanthomonas oryzae is an intracellular parasite in rice that produces proteins able to cause changes in the gene regulation of the rice cells in order to feed off the sugars produced by the rice cells.

I would like to know of other examples of intracellular parasites of medical or economic importance that would be potentially (even if not tested) able to interact with the host's genome in a similar manner.

As Armatus pointed out above, all viruses are obligately intracellular, and their medical and economic importance cannot be overstated.

Many bacterial species live intracellularly. The arthropod specific Wolbachia has a wide variety of consequences for its host, including alteration of reproduction and sex ratios, induction of reproductive isolation possibly driving speciation, and conferring protection from some viral infections.

Eukaryotes can be intracellular parasites as well: Malaria is a well-known example. Toxoplasma gondii is another intracellular parasite that uses cats as a primary host, but can use other warm-blooded animals (such as humans, rats, and birds) as intermediate hosts. T. gondii infection has been shown to induce behavioral changes in rats, causing an attraction to cats (thereby increasing the chance that the parasite will infect the cat and sexually reproduce). There is also some evidence that T. gondii infection in humans causes behavioral and psychological changes such as decreased reaction times, and links to depression and suicide.


Is it safe to autoclave seawater agar? For an experiment I'm going to prepare an artificial seawater agar. Before use, I have to sterilize the medium of course. I imagine, that autoclaving will cause the salts in the seawater to precipitate. Can I re-suspend them afterwards, or will it irreversibly change the composition of my medium? Should I use a different sterilization method altogether, e.g. filter sterilization?

I see no reason why it would precipitate chemically. Besides, you need to dissolve the agar via heat. Hence, auclaving is fine.

If you do not believe me these protocol allow for autoclaving of seawater agar 15min cycle 121 degrees:
1. https://www.dsmz.de/microorganisms/medium/pdf/DSMZ_Medium246.pdf
2. http://himedialabs.com/TD/M592.pdf


Why do boys sweat more than girls during exercise? I noticed that boys sweat more than girls in the PE class performing same physical activity. Is there any other specific reason except muscle mass?

Your assumption seems to be true that Males sweat more than Females, but, not necessarily because of muscle mass.  The jury is still out as to the reasons.  However, in a 2010 study, it was concluded that…

  … training improved the sweating response, and a sex difference was
  observed in the degree of improvement in the sweating response due to
  physical training. This sex difference became more pronounced with
  increasing exercise intensity. A sex difference was observed in the
  control of sweating rate to an increase in exercise intensity, i.e.
  the maximal activated sweat gland responses of untrained females
  required a higher body temperature or work intensity than the other
  groups.

So, there does seem to be something different in the way males and females sweat.  Recent research suggests

  that when we're under heat stress from high temperatures or an intense
  workout -- regardless of what shape we're in or how much body fat we
  have -- women consistently sweat less than men but tend to have a
  higher skin temperature.

(http://health.howstuffworks.com/wellness/men/sweating-odor/men-sweat-more-than-women.htm)

In a nutshell, the cause(s) for the differences in how men and women sweat is still unknown.  Some think it may have to do with body composition.  While others think more research is required to determine

  how efficiently we use the sweat we produce, but also to our capacity
  for making sweat, hormonal fluctuations, sex hormone differences and
  how our bodies regulate water as possible reasons why men sweat more
  than women.


Amount of Heterozygosity How many loci in the human genome are heterozygous? How about other species?

EDIT:
I was wondering, considering for example the whole world population, how many of the human genes actually have two or more different alleles, or, vice versa, which genes everybody shares because there are no different versions of them. Since this seems not to be clear, I don't consider a mutation in a single individual an allele, maybe take 1% occurrence amongst all individuals as a start? I'm no biologist though...

By loci I mean whatever you think makes sense. Again, I don't mean single bases, preferably something like the classic idea of a gene. But I'm happy for whatever you can tell me.

If you want an actual number, well, it depends (of course).  First off, what is your definition of loci?  That term is broad, and can be construed to mean everything from large, megabase-length genes to every individual base.

That being said, it turns out there are some serious runs of homozygosity (ROH, meaning long regions of the genome that are homozygous) in human populations.  This of course will vary widely from population to population, and amongst outbred individuals.  This paper has some AMAZING figures that are worth checking out but are a little more involved.  Here is a table from this paper which is likewise quite excellent; also, check out figure 3.

EDIT

Your new/edited question is actually very difficult to answer.  For an extreme example, look at the Human leukocyte antigen; some have hundreds or thousands of alleles, but if you were homozygous for each it would be bad (disease susceptibility) but you'd be fine otherwise.

Again, it depends on what you consider an allele or locus.  Most studies look at single base changes (SNPs) because they are 1. easy and 2. useful.  It turns out that there are a lot of these single changes.  The Human HapMap project is hard at work on this and recently published a data set with 3.1 million of these SNPs, among 270 individuals from different populations, roughly one every kilobase.  In a similar vein, the 1000 genomes project recently published an enormous catalog of variation from almost 1,110 individuals in 14 populations.  Both projects focused on major variants.

The best answer I can give you from these studies is that, within a given population, any two DNA strands are around 80% identical, of which around 0.5% is by direct relation (table 5.  Those numbers vary hugely between populations, with Yoruba Nigerians being the most diverse, followed by Utah Whites and then Han Chinese and Tokyo Japanese.  This is just an average across the entire genome, as purported functional differences are comparably rare, with over 85% of protein-altering changes being very rare (<0.5% frequency).

In summary, almost every single site we know of has more than one version somewhere.  Most traits are very complex and are affected by many genes, so even similar appearances can come from very different genetics.  Individuals tend to be highly heterozygous, even if populations on a whole have limited heterozygosity.  A single pair of siblings mating can produce massive defects, showing just how necessary our heterozygosity is.  We each have dozens of large, lethal mutations (deletions, mostly) that don't usually matter thanks to heterozygosity.


Why can early embryos survive freezing? According to this

Blastocyst & Embryo Freezing in IVF

  Embryos can be frozen at the pronuclear stage (one cell), or at any stage after that up to and including the blastocyst stage (5-7 days after fertilization).

Given that freezing normally destroys mammalian cells1 why can early stage embryos survive being frozen?

Reference:
1: Shier, W. T. (1988). Studies on the mechanisms of mammalian cell killing by a freeze-thaw cycle: conditions that prevent cell killing using nucleated freezing. Cryobiology, 25(2), 110-120.

The reason why cells (and tissues) die during freezing is that ice crystals rupture the cell membranes1,2, so to me it seems the question is actually why early embryos can survive this process.

The answer depends on the technique used, but it comes down to size.  Small tissues (or cells) have a large surface area to volume ratio.

In techniques that use cryoprotectants (compounds that suppress ice crystal formation), the small size allows efficient replacement of water by cryoprotectant prior to freezing (and the reverse after thawing) so that the cells don't have time to die1,2.

In flash freezing (vitrification), the small size allows the entire tissue to be frozen instantaneously, which also suppresses ice crystal formation1,2.

This Scientific American article is very relevant as well.

References:
 1: Konc, J., Kanyó, K., Kriston, R., Somoskői, B., & Cseh, S. (2014). Cryopreservation of embryos and oocytes in human assisted reproduction. BioMed research international, 2014.

2: Loutradi, K. E., Kolibianakis, E. M., Venetis, C. A., Papanikolaou, E. G., Pados, G., Bontis, I., & Tarlatzis, B. C. (2008). Cryopreservation of human embryos by vitrification or slow freezing: a systematic review and meta-analysis. Fertility and sterility, 90(1), 186-193.


In vitro virus assembly Are researchers able to assemble viruses in vitro?

For example, I imagine that a phage display library may be generated by throwing in a test tube the capsid proteins (or what have you) along with relevant DNA that will self assemble. Has this been done? If so, is it a technique readily applicable to a broad range of viruses?

Yes, and a quick search for viral in-vitro assembly will turn up tons of results. — it's a little more complicated than that! — but it's not usually done as such, which I will explain.  Basically, there are four things you might want to do:

You want to make large amounts of virus and study it. If so, then all you need to do is infect your cell culture with your virus and let it replicate.  Some are obviously easier than others — from my own experience, HIV is pretty easy but Hepatitis C is a real PITA — but that's essentially it.  This obviously presumes you already have some virus stock on hand for infection.  You could also transfect the culture with full-length viral plasmids, which leads me to...
You want to study some specific aspect of the virus.  That's cool!  Most people aren't just concocting virus.  Generally, for viruses that humans can get, it's generally recommended/heavily encouraged to only use what you need for safety reasons.  So, for example, you might transfect the one protein you think is important to see what it does by itself.  After that, you might transfect the cell culture with the full virus, but with one important gene knocked-out.  I used to make single-round HIV by using a plasmid for full-length HIV without a functioning envelope gene and another plasmid for VSV envelope; new HIV particles would be made infectious because of the VSV gene but after infecting they no longer had that gene anymore.  Basically, a limited version of the virus, which leads me to...
You want to make virus-like particles.  These are one of the better-named things in science and are just what they sound like — particles that look a lot like virus, but aren't.  Generally, they're empty shells.  We can use these for all sorts of things, from vaccine studies to other genes and diseases.  Techniques can vary, but generally it's similar to the above.
You want to introduce some other gene to a cell culture system, using a virus backbone for transduction; think "I want to fix these cells... permanently."  Generally, these viruses are usually based on adenovirus or lentivirus (aka HIV) because they will insert their genes into the cell's genome, so the gene will persist.

Item 4 is probably closest to what you specifically meant.  Here's a free review on the use and safety of retroviral vectors in humans, and here's a nifty one in fish.  As for which viruses it's applicable to, well, that varies a lot by virus, host, culture system, and so on.


List of species recently found of economic value Is there a website or organization cataloging lists of biological species to have been recently found of great economic value? For example, a plant that wasn't of economic relevance a while ago but has been found recently to be important, due to advances in breeding varieties and more crops being planted. The same for species that were already important but have turned to be even more important in the last few years.

I can only answer for plants. The short answer is no, there is no central source of information of that kind.

You are basically asking about the sub-classifications economic botany and ethnobotany, which cover the economy and human uses of plants respectively. Neither field is particularly fast-paced, so you could simply keep up to date with the latest issues of journals like Economic Botany or Ethnobotany.

One key area of development for new valuable crops is in crop wild relatives, but there is no particular publication you should watch for that. Keep an eye on the Crop Trust as they will shortly be releasing, in collaboration with us (the Millennium Seed Bank) some reports and data about this.

If I wanted to keep up to date with all those things over time, I would set up some saved search alerts on Google Scholar for key search terms like 'emerging crop', 'new crop', 'crop wild relative', etc. Just perform a search on Scholar and then click the envelope button to the right of the search field to create a recurring search alert.

One other potential source of information would be to check FAOSTAT each year. You can examine global and local data about area under cultivation, yield, investment, commodity value, etc. of most crops. If something new were to emerge as a big player, it would appear on there.


How close genetically is the most human-like chimpanzee to the most chimp-like human? I understand that:

Chimpanzees are the closest species to humans genetically. Only 1%-6% of their genes are different.
Within any species there is genetic diversity, i.e. no two individuals have the same exact DNA sequence.
This variability applies to humans and chimps.
Thus, there exists a pair consisting of a human and a chimp that will have the smallest number of different (edit: genes) DNA base-pairs within the two populations. One can say that the pair forms an "inter-species genetic gap".

Question: What is the smallest estimated inter-species genetic gap between humans and chimpanzees?

Edit: I changed the last point to base-pairs instead of genes. Most of the comments seem to suggest the population genetic variabilities are much, much smaller than the genetic distance between the populations. Visually, that looks something like this:

Is this a fairly accurate picture of the human-chimp genetic distance?

You may be interested in this 2005 Nature paper from the Chimpanzee Sequencing and Analysis Consortium: Initial sequence of the chimpanzee genome and comparison with the human genome. It breaks down the most common categories of genetic variation:

  Single-nucleotide substitutions occur at a mean rate of 1.23% between copies of the human and chimpanzee genome, with 1.06% or less corresponding to fixed divergence between the species.

So if we accept their analysis, ~1% (it says "or less", but elsewhere in the paper they estimate a lower bound of ~0.96%) of the genome difference consists of fixed single-nucleotide differences between species.

  Small insertions and deletions: On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies.

So another ~3% comes from small insertions and deletions, which gives around a ~4% fixed divergence between populations. This rough estimate of the fixed genetic distance between humans and chimpanzees is probably a reasonable estimate of the distance between the nearest human-chimpanzee pair.

If you also want to know how far apart the two furthest humans are, as @Remi.b mentioned, the populations we've sequenced don't span the whole diversity of our species, but it is likely much smaller. You could look at some of the HapMap or Human Genome Diversity Project papers. For reference, when Watson's genome was sequenced, they reported around 0.1% of the sequence to be different from the reference genome, but that isn't a particularly diverse comparison.

You may also be interested in this paper comparing the human, chimpanzee, and bonobo genomes: http://www.nature.com/nature/journal/v486/n7404/full/nature11128.html.


Does our DNA change during our lives? As far as I know, DNA is the construction protocol of all organisms on Earth.

Does it change when influenced by time and environment (physical laws)?

As parents with schizophrenia are more likely to have children with schizophrenia and an individual with no genetic predisposition for schizophrenia can suffer from such a condition because of drug abuse or environmental influence, does this prove that human DNA is changing during our lifespan?

To quickly answer your question, yes DNA changes over the life time of many organisms including humans.  You have a whole host of mechanisms in your body that try to prevent your DNA from changing, but they are not perfect.

A good example of this is DNA degradation due to aging.  When discussing aging in biology, we use the technical term senescence.  Of interest here is the shortening of telomeres due to mistakes made in your cells as they continue to divide (copying the DNA to each new daughter cell).

In a grown adult, there's not some master well of DNA somewhere such that if you change it there it will immediately change the DNA throughout your body.  Most of the cells in your body have DNA in them (red blood cells are just one example of cells that don't have DNA in the traditional sense). Most of these cells can and will divide over time (mitosis) to produce new cells with copies of that DNA.  However, there are also plenty of cells that don't divide often or at all in healthy adults.  If one is concerned about schizophrenia, it would be important to note that many neurons in the CNS are in this group of static cells.

Considering environmental effects, there are plenty of things that can change your DNA. Radiation, gamma and x-rays in particular, do a great job of disrupting, degrading, and occasionally mutating DNA.  The class of chemicals and physical agents that can change DNA are called mutagens.  This shares a root with the verb mutate, which is when something is acting on genetic material to cause it change.

You will note that I said genetic material, and not DNA.  Without getting too far into the debate of what is "alive," DNA is most certainly not the only "construction protocol" for earthly organisms.  RNA is one common alternative, but there are weirder ones that are hard to describe like prions.


Number of Chromatids in G1 I know that in G1, the number of chromosomes is 23 pairs, so 46.

I assumed there were 46 chromatids too.

Why is the number of chromatids in G1 actually 0, not 46?

Thanks.

These terms are quite similar and, for many, confusing:

Chromatin
Chromosome
Chromatid

But they are not synonyms. According to Molecular Cell Biology, Lodish, 4th ed:

  Chromatin: Complex of DNA, histones, and nonhistone proteins from which eukaryotic chromosomes are formed.

Which brings us to:

  Chromosome: In eukaryotes, the structural unit of the genetic material consisting of a single, linear double-stranded DNA molecule and associated proteins.

So, you can think of chromatin as the building material of chromosomes.

But chromatid has a very different definition:

  Chromatid: One copy of a duplicated chromosome, formed during the S phase of the cell cycle, that is still joined at the centromere to the other copy; also called sister chromatid.

So, one should not use the term chromatid as synonym of chromosome. Chromatid is the name of each copy of the chromosome after the S (synthesis) phase. According to that terminology, there is no chromatid before the duplication.

I have to confess that I personally don't follow that terminology: I like to say to my students that, before S phase, each chromosome has 1 chromatid and, after the S phase, each chromosome has 2 chromatids. Even this not being the most correct terminology, it has some advantages: it makes the student understand that the number of chromosomes doesn't double after the S phase.

Source:

Lodish, H. (2002). Molecular cell biology. 4th ed. New York, N.Y.: Freeman


Polymerase Chain Reaction Questions First question is about why we use primers in PCR. It requires two reasons. I know only one reason though. It is so that DNA polymerase can attach to primer and make a copy of nucleotide from there. But i don't know what is the other reason.
Another question is about why the primer bonds to 3' end of the DNA you want to copy. and explained why. I really have no clue for this one. Plzz help.

We use primers in PCR because we are mimicing natural processes. DNA polymerase cannot act without primers. It needs primers to start it's work. Binding of molecules happen by chance, so the more there are of your primer, the more likely it is that it would bind to any given string of complementary DNA. DNA replication occurs in the five prime to three prime direction because phosphate doesn't allow the reverse reaction.


What is the name of this spikes insect? Location is South India.

Behavior: It is not moving.

Month: May,

Place: No people come. (Actually species chooses the place on my next door, where neighbors left 2 months ago)

The Creature is "Debris-carrying Lacewing.".

(Source)


Where can I find FDist2 executable? I am trying to download the program FDist2 (Beaumont and Nichols 1996) for Mac but for some reason it appears that all the links I find are broken.

It appears that the program Lositan is an faster implementation of FDist2 but in my understanding Lositan works only through a GUI and not via the command line (and given the number of analyses I want to perform I need to be able to run this algorithm from the command line).

The link that ddiez has mentioned, has a download link for a zip file (fidist2). The zip file contains windows executables and C-codes. Just compile the C-codes in your terminal.

This is from the readme:

  The .exe files are pc binaries, which is only what most people want. I
  include the source file in case anyone wants to play with them. In
  this case compilation is e.g.:

gcc -o fdist2 -O fdist2.c -lm
gcc -o cplot -O cplot.c as100.c as99.c -lm
gcc -o datacal -O datacal.c -lm

Actually in the readme, the first compile command says fdist.c (no such file) instead of fdist2.c. I corrected that here.

Your system should have gcc. I tried compiling in my system (linux) and it works. It should work in Mac too.


How are the wings of birds, pterosaurs and bats related to each other? Homologous organs are organs which have same arrangements of bones, blood vessels and muscles with different functions, and analogous organs are those which have different arrangements of bones but serve same function.

I want to know whether the wings of birds, pterosaurs and bats are analogous or homologous organs. My book says that their wings serve same function and have similar structure but they evolved independently. It confuses me because this seems like a blend of both homologous and analogous organs to me. So which is it?

Here is a discussion of homology and analogy that clearly presents bat and bird wings as an example of analogous organs:

http://amrita.olabs.edu.in/?sub=79&brch=16&sim=132&cnt=1

You are right however that bat, bird and pterosaur wings are homologous in a sense, as they have similar underlying structure and a common evolutionary origin - the front limbs of tetrapods.

One could perhaps say that bat, bird and pterosaur wings are homologous organs as front limbs, but analogous organs as wings.

This page has pictures of the skeletal structure of each:

http://www.ucmp.berkeley.edu/vertebrates/flight/converge.html

As you can see, they are similar front limbs - made of a common set of bones and muscles. But those bones have been arranged into wings in different ways: Pterosaurs have a lengthened pinky finger maintaining a flap of skin that makes up the wing; bats have three lengthened fingers with a flap of skin around them; and birds have small, fused finger bones with the surface of the wing being made up of feathers.

And it is in fact the case that as far as their evolutionary history goes, bat, pterosaur and bird front limbs have a common origin in the front limbs of tetrapods, but have separate independent origins in terms of how those front limbs evolved into wings. Or put another way, the common ancestory of bats, birds and pterosaurs had front limbs, but those front limbs weren't wings.

Compare with the "wings" of flying fish, which does have a common origin with that of birds/bats/pterosaurs: both developed from the pectoral fins of their bony fish common ancestor. Obviously they became wings independently, and they also have a very different evolutionary origin as "limbs". On the other hand when you look at the wings of insects, there is no common origin between those and the wings of vertebrates at all. The common ancestor of insects and vertebrates had no limbs at all, not even bones or an exoskeleton. Both lineages developed limbs and hard support structures independently, and then adapted some of the structures they had for flight.

Interestingly it seems a book recently came out on the flight of bats, birds, pterosaurs and insects: On the Wing: Insects, Pterosaurs, Birds, Bats and the Evolution of Animal Flight by David E. Alexander. It could be an interesting read to anyone interested in the question. Here are some reviews of the book:

http://www.bioone.org/doi/pdf/10.1642/AUK-15-210.1

https://academic.oup.com/icb/article/56/5/1044/2420642

ETA: If you want to bend your mind a bit around the question of homologous vs analogous organs (or homology vis homoplasy), look at these two questions from the sidebar:

The pectoral fins of a whale and a shark. Are they analogous organs?

How large is the range of 'same origin' when determining whether two organs are analogous or homologous?

Which ask similar questions you did, but of the fins of whales vs the fins of sharks. And that's a funny one isn't it! Because where in the pterodactyl example we have a common ancestor who had front limbs but didn't have wings, in that case the common ancestor of whales and sharks did have pectoral ("chest-level") fins, that the fins of whales and sharks descend from! So, homologous? But the fins of whales spent so much of their evolutionary history not being fins at all that it does make one want to say the homology is at the "front limb thingy" level not the "fin" level. I mean, as far as evolutionary distance goes, the wings of flying fish and of bats are actually more closely related to each other than the fins of whales and of sharks are!!! (the evolutionary history there goes: jawed fish (Eugnathostomata) -> cartilaginous fish (Chondrichthyes; led to sharks) and bony fish (Osteichthyes; led to flying fish, bats and whales).

99% of the "shark-fin-like" appearance of whale fins developed long, long after their split from the shark lineage; and I don't know what the front fins of the jawed fish common ancestor was like but it's possible it looked different from whale/shark fins too, so the some of the "whale-fin-like" appearance of shark fins may also have developed independently after the split.


Why do women live longer than men? According to Wikipedia and many other sources, women live substancially longer than men (over 5 years in the U.S.).

Men can reproduce for much longer than women.  So longer living men would have the most offspring, while the longevity of the women would be more or less irrelevant in reproducing.  These offspring would be the product, on average, of men and women where the men are older than the women.

So why do women live longer than men?  Am I misinformed, or what don't I get?

The best explanation I have come across so far is that male sex hormones have an adverse affect on longevity.

The effect may simply be that a high testosterone level suppresses the immune response against a variety of infections.

There was a recent study about korean eunuchs from a few hundred years back, that found that "The average lifespan of eunuchs was 70.0 ± 1.76 years, which was 14.4–19.1 years longer than the lifespan of non-castrated men of similar socio-economic status."

That's a pretty hefty difference and a strong argument for testosterone as risk factor for an earlier death. This would also vibe well with reports about increased risk of cardio-vascular death in steroid users.


Electrophoretic mobility of isozymes If isozymes are seperated using electrophoresis, which of the following will be the principle of separation ?

A.charge density

B.molecular weight

C.polarity of molecule

I think it should be B.

(B) is incorrect. I think the answer is (C) but to my mind those other two options are badly worded.

Here is an explanation.

The classic example of isozymes is the case of lactate dehydrogenase.

As you will see if you visit the Wikipedia page the enzyme is a tetramer, and there are two subunit types, the muscle or M type and the heart or H type. Consequently there are 5 isozymes, ranging from M4 to H4 with all possible combinations in between. Different tissues express these two subunit types to different degrees and so are characterised by a different pattern of isozymes.

The M type is encoded by the LDHA gene and the H type by the LDHB gene. I obtained the sequences of the two proteins and analysed them:

LDHA: 332 amino acids; 36.7 kD; pI=8.45

LDHB: 334 amino acids; 36.6 kD; pI=5.93

You can see from this that the ability to separate these isozymes depends upon charge and not molecular weight. That big difference in pI (isoelectric point) means that at neutral pH the LDHA protein will carry a net positive charge while the LDHB protein will be negatively charged. Consequently each tetramer will have a unique overall charge. You can find some details and an image of an electrophoresis result here.

In general, protein electrophoresis is much more sensitive to charge differences than it is to molecular mass except in the special case of SDS-PAGE when the large amount of negatively-charged detergent that binds to the proteins masks their intrinsic charge differences.

Another classic example of this is the ability to separate haemoglobin S in sickle cell patients from haemoglobin A in normal blood. In this case the only difference between the two molecules is a single Glu>Val substitution in two of the monomers in each tetramer.


Why Poisson Process for neural firing? I am new to the world of neuroscience and I would like to understand how come every paper in neuroscience that I read uses a Poisson process to model neural firing. Do I just have a biased sample of the papers I chose to read, or is it a biological fact that neural firing must follow a Poisson process? Why can't it follow, say, binomial, since it either spikes or it doesn't in a given time period. Also, where can I read more about how such a biological phenomena was discovered?

A small correction: I do appreciate the explanation on the difference between the two distributions but I am a statistician who is trying to understand my neuroscience colleagues and communication is key in statistics. I am just trying to comprehend why everyone in the field is using Poisson as opposed to using Binomial even when the bin size you decided on is sufficiently small. In other words, why would you not use Binomial, the bin size is so small that your data is only 0's and 1's (i.e. the spike happened or did not happen within this bin). Is it because Poisson counts discrete occurrences in a continuous domain? What discipline-specific papers would you recommend to read that justify/discuss/explain the continuous domain on neural spiking?

You can read about the differences between a binomial and poisson distribution at this other question on Math.SE.

First, since spikes are discrete events, it makes most sense to use a probability distribution that is discrete. A Poisson process is a process where an event occurs randomly with no "memory" for how long it has been since the last event. A Poisson distribution is the number of events if you integrate draws above some threshold from an infinitesimally small uniform distribution. Therefore, the Poisson distribution is the distribution you choose if occurrences of an event are only dictated by an underlying rate parameter - this turns out to be a reasonable, if ultimately false, assumption for neurons.

There is definitely no biological fact that neurons must follow a Poisson distribution - in fact, no neuron can be truly Poisson because, if nothing else, the refractory period makes it impossible. Rather, Poisson behavior is sort of the simplest behavior you would expect from neurons in a system where they are firing occasionally due to random noise - sort of a "null hypothesis." For many modeling approaches, this is close enough, and it allows the modeler to avoid making more nuanced assumptions. It turns out to be a decent assumption when you look at individual cells, but if you look at populations the activity deviates a lot from Poisson.

Note that the Poisson distribution is often only valid for spontaneous data; it is possible to use a nonstationary Poisson distribution to model responses to some external stimulus, but the results are likely to deviate more from experimentally derived data.


After how many generations descendant is not more related to ancestor, than to a random individual in an ancestral population? Descendant of n generation has on average 1/2n DNA of ancestor. (For example children have 1/2 DNA of parents and 1/4 DNA of Grandparents, After 10 Generation 1/1024 DNA and after 100 Generations 1/2100 DNA).

Is there a point (value of n) when descendant is no more related to ancestor and is similarly related to random individual from an ancestral population.

There is an interesting way to look at this question. By definition, two individuals are related only if they have a common ancestor. (If you mean something else by it, please correct me. For completeness, I include the trivial case in this: that is, I regard you as one of your own ancestors.) So your question can be inverted: it is really asking after how many generations everyone in the ancestral population is your ancestor?

As indicated in the comments, the answer will depend on the specifics of the population structure, including its size. But a first stab can be taken in this way: you had 2 ancestors one generation back, 4 two generations back, ..., $2^n$ (not necessarily distinct) $n$ generations back. So you certainly cannot be descended from everyone in the ancestral population if less than $\log_2 N$ generations have passed. ($N$ = population size, which for simplicity I assume to be stable.) In a freely mixing population under the very simplest assumptions, you will eventually decay exponentially towards complete coverage with a half-time of one generation.

This is complicated by the fact that some lineages die out completely. For instance, some of the individuals in the ancestral population didn't have any children. Some had children, but no grandchildren, etc. Obviously none of them were your ancestors, so you will never be related to them (except through previous common ancestors), no matter how much time passes. In fact, as time passes, more lineages tend to die out. So, if you look back very far, you'll find that the entire current population has only a very small numbers of ancestors in the distant past. This is called coalescence, and is what people are talking about when they speak of "mitochondrial Eve", for instance.

So, in summary, it's complicated. It takes only a fairly small number of generations ($O(\log_2 N)$) before you're potentially related to most of the ancestral population. But over longer times ($O(N)$ generations) your relationship to the ancestral population actually goes down.


Artificial Adrenalin I was watching Sherlock Holmes - A Game of Shadows yesterday. I saw that he had developed a serum that causes a  person to react like he has been injected with adrenalin.

Watsons's dog fainted, I think, and the moment Holmes injected the dog with this serum, it jumped up and ran away.

So my question is: Is it possible to extract adrenalin, or was it a steroid?

Yes, it is possible to extract adrenaline from the adrenal glands.  This was done in 1901, a patent was filed, and it was marketed under the name Adrenalin.  It is also known as epinephrine.  It is synthesized nowadays for most uses.


Why do obese people heal more slowly? I recall an obese patient who was referred to a transplant clinic as his stitch wounds hadn't healed after a year. While there's a myriad of side effects caused by immunosuppressive medication after transplants, the usual healing process for patients that underwent the same procedure is around one to two months1.
It's not an isolated example, as patients with very high BMIs can be considered ineligible for transplantation because of the post-surgical complications that follow, namely, delayed wound healing and increased chance of infection. It does not seem to be dependent on diabetes or merely low metabolism rates caused by a sedentary lifestyle (some of the patients perform well in exercise tests and monitor and control their blood glucose levels) and as such, BMI tends to remain the only (imperfect?) factor.
Why does a large percentage of body fat or a high BMI delay or impair healing?
It seems counter-intuitive to me because, as I understand it, the two major parts of the healing process involve 1) a great range of proteins for the creation of new vessels, tissue etc., and 2) The energy needed for the different processes, such as the mitosis of the cells. If blood glucose levels are close to normal and there isn't much of an insulin resistance, then surely it's not a problem of availability for either of the parts to play their role?
Clarification: I restrict the scope of the examples to transplant surgical procedures as what I state is more likely to be factually correct due to  personal experience. I would expect wounds other surgical operations to follow the same patterns, but I could be wrong.

[1]: That is an extreme case, especially considering the possibility of effects of diabetes, obesity and steroids compounding. However, there's a general trend.

It's well known that obese patients have slower wound healing, but the specific cause isn't known; most likely there are multiple causes acting together.

  The correlation between obesity and deficient wound healing has long been established. ... Substantial evidence exists demonstrating that obesity is associated with a number of postoperative complications. Specifically in relation to wound healing, explanations include inherent anatomic features of adipose tissue, vascular insufficiencies, cellular and composition modifications, oxidative stress, alterations in immune mediators, and nutritional deficiencies.

--Obesity and Surgical Wound Healing: A Current Review  (This is an open-access article that nicely summarizes the open questions)

  Obesity has been shown in a number of studies to impair wound healing, and chronic nonhealing wounds in obesity and diabetes are a major cause of limb amputations in the United States. ... Recent evidence indicates that aberrant wound site inflammation may be an underlying cause for delayed healing. Obesity, diabetes, and other conditions such as stress and aging can result in a chronic low-level inflammatory state, thereby potentially affecting wound healing negatively.

--Exercise, Obesity, and Cutaneous Wound Healing: Evidence from Rodent and Human Studies (Also open-access, a little more recent but less wide-ranging)


How is deviated nasal septum related to cold I have a deviated  nasal septum and I always suffer from  common cold I was just wondering how a deviated nasal septum can be the cause for chronic common cold

Nasal septum deviation is a condition where the cartilage which divides the nasal cavity into two nasal passages isn't centrally aligned, making one of the nostrils smaller and thus obstructed. Now, in our nose we have something called mucociliary clearance and that is the mechanism getting rid of unwanted particles and pathogens that get into contact with the mucous membranes in the nose.

Studies show that in individuals with a deviated septum the nasal mucociliary clearance time is slower than in individuals whose nasal passages are symmetrical. From this information one can conclude that the particles and pathogens that you inhale are getting to spend more time inside your nasal passages, thus giving the pathogens a better chance at striving and giving you sinusitis.

By looking at the information above you could think that the connection between nasal septum deviation and chronic sinusitis is clear. This literary review however states that the correlation between a deviated nasal septum and having chronic sinusitis is still unclear.


How does hypochlorous acid inactivate viruses? I was reading how bleach was used very widely as a disinfecting agent during the 2014 West Africa ebola outbreak and am interested in the mechanisms with which hypochlorous acid inactivates viruses. Most of the studies I could find only focused on its activity against bacteria. I know viruses tend to be much more difficult to inactivate than cells as they're somewhat simpler and aren't really alive.

The other answer by @CMosychuk talks about the general aspect related to use of hypochlorous acid. I will discuss here its molecular mechanism of action.

Hypochlorous acid (HOCl) is a very powerful oxidizing agent. In aqueous solution, it dissociates into H+ and OCl- as:

$$\ce{HOCl \leftrightharpoons H^+ + OCl^-}$$

However, HOCl also destroys viruses by chlorination. It acts on anything, from lipids to nucleic acids. For example, Hawkins et al ,2002 describe in detail the effects of HOCl on nucleic acids. HOCl, by direct chlorination, leads to the formation of chloramines, and ultimately nitrogen-centered radicals. These radicals often react with each other to form dimers. Also, they have reported formation of single- as well as double-stranded breaks on application of HOCl on plasmid DNA. See this image:

These reactions render the nucleic acid useless and the virus harmless. In a similar manner, HOCl also reacts with polypeptides, ultimately leading to their fragmentation. See these images (from here):

Also, as mentioned in the other answer, application of HOCl has been shown to promote denaturation and aggregation of proteins. The linked paper also talks about HOCl's effects on other biomolecules, such as carbohydrates, but those effects would be out of scope here.