Definition of "structural underdominance"? In Stathos and Fishman (2014), the authors refer to the concept of structural underdominance. The first time they mention it is in the first paragraph of the second page (left column) and the term is followed by some kind of definition in parenthesis. It is written:

  Furthermore, artifical doubling of chromosomes in sterile plant hybrids can sometimes restore normal meiosis and fertility (Stebbins 1950), a pattern diagnostic of structural underdominance (heterozygote inferiority).

In addition to how they use the term "Structural underdominance" in this paper, the above definition is confusing to me.

Is structural underdominance a specific type of underdominance (heterozygote disadvantage)? Is it the evolutionary process by which a population is lead to diminish the average underdominance along their loci? Is it a predisposition of the genetic architecture to display underdominance when a chromosomal rearrangement occurs? In short the question is:

What is the definition of "structural underdominance"?

I understand heterozygote inferiority (also underdominance or heterozygote disadvantage) as the opposite of heterozygote advantage, that is, lower fitness of the heterozygous genotype than either homozygote (as reference, see Hedrick, 2009, p. 119). I haven't seen the term structural underdominance before. However, heterozygote disadvantage can sometimes be seen in species/subspecies hybrids and also chromosomal heterozygotes (see Hedrick, 2009, p 140), and this might be what the term structural underdominance is describing (structural as in chromosomal). This can then lead to unbalanced gametes with low viability, which means low fitness compared to homozygotes. The quote you have included also talks about plant hybrids, which makes this explanation likely, and it also makes sense since they mention artifical doubling as a solution. If I have understood the process correctly, chromosomal doubling should lead to better pairing of chromosomes and lower risk of unbalanced chromosome translocations.

Also note that Hedrick labels heterozygote disadvantage as an unstable equilibrium (p. 140ff), but I haven't looked more closely at the dynamics behind this.


What molecules does amylase enzyme work on? I know that in the human body cellulose cannot be broken down by enzymes; however, I am confused as to which molecules amylase enzymes during fermentation.

I also looked at https://en.wikipedia.org/wiki/Amylase where it says that "All amylases are glycoside hydrolases and act on α-1,4-glycosidic bonds." so now I am confused.

Does amylase work to break down starch into glucose exclusively?

If not...
Does amylase enzyme break down corn cob extract which contains xylans, cellulose, lignin and some sugar for fermentation?
Does amylase enzyme break down corn stem which contains cellulose, hemicellulose and lignin for fermentation?

Your incomprehension is due to the fact that both starch and cellulose are polysaccharides.

As it is said in the wiki page. Amylase is active only on alpha linkage like starch or glycogen. If you want to break beta linkage like in cellulose you need a cellulase enzyme, which humans do not have.


Can cell division be stopped during prophase? There are three known checkpoints which ensure proper division of the cell.

  These are: the G1 checkpoint, also known as the restriction or start checkpoint or (Major Checkpoint); the G2/M checkpoint; and the metaphase checkpoint, also known as the spindle checkpoint.

I wanted to know that is there any way cell division can be stopped during prophase(once it has started).

I'm unaware of such stop occurring at a mitotic prophase, but if your definition of "cell division" includes meiosis, the answer is yes: in several species, the oocyte stops at the first prophase (prophase I), in a resting phase called "dictyotene": https://en.m.wikipedia.org/wiki/Dictyate


Why is the number of PCR cycles limited? I've been told that the maximum number of cycles in PCR is between 20 and 30.

Is this true, and what are the reasons for this limitation?

I would draw the line beyond 35, but thats a bit cosmetic.
The reasons are manyfold:

due to the exponential fashion of the amplification (ideally)
reagents are used up at some point
reagents degrade, this is especially true for the dNTPs
the activity of the enzyme, despite being heat-stable is declining
over time
beyond 35 cycles the exponential curve is flattening out (reasons see
above)
if you run the PCR for too long, you will get more and more
side-products (mostly primer dimers, but mis-aligned primers can also
make problems), this is more a problem for real-time PCR than for ones run on a gel

If you need a higher sensitivity with more cycles, you can use the technique called "nested PCR". There you do a first round with a primer pair specific for the region of interest and then do a second round with primers which are located slightly to the inside of the amplified DNA. This is done to avoid the amplification of unwanted contaminations. Since you do some 50-70 rounds of PCR amplification in total, this method is extremely sensitive (also to contaminations). See the image from the Wikipedia article for details:


Do any terrestrial herbivores use auditory crypsis for predator avoidance? Some terrestrial predators "stalk" their prey: they sneak up on it slowly, maintaining a low profile, while keeping as close to silent as possible.  This makes sense from an evolutionary perspective: silent predators catch more prey.

However, the prey near where I live are hopelessly noisy.  Deer will freeze if they suspect the presence of a predator, then bolt when they see one for sure.  Squirrels and other small mammals run around at top speed all the time - you can hear them dozens of feet away, rustling the dead leaves around.  Hedgehogs just wander, making a similar noise.  It seems like the only "stealth" option they have, as far as sound is concerned, is to remain still.

Are there any examples of terrestrial herbivores evolving to move more quietly in order to avoid predation? I'm not looking for a comprehensive list, but rather simply individual examples.

Does soundproofing count?

Most predators locate prey using visual or olfactory cues; the only predators I can think of that use auditory cues are nocturnal ones - owls and bats. Bats, of course, use echolocation, so even completely silent prey are still detectable. It has been suggested that the soft, fur-like body coverings of some owlet moths (Noctuidae) and tiger moths (within the Arctiinae) help hide them from echolocating predators by passively absorbing sound, although subsequent studies have suggested that they may instead be mimicking the acoustic signature of unpalatable prey.

(public domain image: source)

I have a suspicion this isn't what you meant by 'land-dwelling herbivore', but insects are people too...

Edit: just discovered this paper from May that provides evidence supporting the hypothesis that the twisted tails of luna moths (Actias luna) disrupt tracking by echolocating bats.

Image owned by Shawn Hanrahan, licensed under CC BY-SA 2.5


What species is this? We found this on a beach in the Bay of Lannion, Brittany, France. What is it? About 6 cm long.

It is  the skeleton of Sea Urchin or sea hedgehog.

There are a lot of species (nearly 1000), so it is very difficult to identify just in five minutes, but in general you can start from knowing the Subclass Perischoechinoidea.


Hardy-Weinberg Equilibrium: To compute probability of finding two siblings (random mating) I've been working a little with M. G. Bulmer's Principles of Statistics (Dover, 1979) and cannot see how to properly compute half of one question. This should be a basic probability computation, but I am not getting the same answer as the book's suggestion.

Here is the question (Chapter 2, Problem 2.4): If the three genotypes (i.e., AA, Aa, aa) are all distinguishable, find the probabilities that a) a pair of siblings and b) a pair of unrelated individuals will appear the same when p=q=.5.

The book offers .59 for a) and .38 for b). I can get b correctly, but I don't understand how to properly compute part a).

This does not seem like a complicated exercise!

Are you sure it is 0.59 because I am getting 0.5625 for part (a) and this is how I computed.

To check genetic similarity of siblings we first have to pick up mating pairs. Six mating pairs possible with following offspring probabilities (choice of first mate x choice of second mate x same offspring genotype freq).

AA x AA : will always give same type of offspring: prob = 0.25x0.25x1
aa x aa : will always give same type of offspring: prob = 0.25x0.25x1
AA x aa : will always give same type of offspring: prob = 0.25x0.25x1
Aa x Aa : will give Aa in half the number of times: prob = 0.5x0.5x0.5
Aa x AA : will give two types of similar offsprings, half the number of times - AA and Aa: prob = 0.5x0.25x0.5x2
Aa x aa : will give two types of similar offsprings, half the number of times - aa and Aa: prob = 0.5x0.25x0.5x2

Total probability = 3x(0.5x0.5x0.5) + 3x(0.25x0.25) = 0.375+0.1875 = 0.5625

Assumptions:

Population is infinite
Population in equilibrium


How did the human brain evolve? A common question posed is, "how did the eye evolve?", because the eye is so complex.  However, this has been answered rather clearly and there are several examples around the world of animals in which the eye has evolved independently.

The human brain, however, only seems to have evolved once in the history of life on Earth - a brain which is capable of advanced speech, predicting the future given information on the past, producing art, imagining advanced abstract concepts such as algebra, creating advanced tools, etc.

How, then, could the human brain have evolved?  What stimulus was there for progressive Homo individuals to have brains that were slightly more advanced than the previous one's?  I've heard Richard Dawkins summarize it as "big brains are sexy", but that's a comment made in hindsight (and not even shared by all members of the human species today!)  At the time, why would a human female choose a male with a slightly larger brain, so slightly larger that the increased intelligence probably wouldn't be noticeable?  Or why would such an individual have an evolutionary advantage?

New work suggests a prominent role for genes in the SRGAP2 family, as explained here. Data suggest a mechanism where incomplete duplication - most likely at SRGAP2C - created a novel gene function some 2–3 mya, which is a time corresponding to the transition from Australopithecus to Homo and the beginning of neocortex expansion. Further, in the mouse neocortex, Srgap2 promotes spine maturation and limits spine density, supporting sustained radial migration and leading to the emergence of human-specific features.


Is there any evidence of increased life expectancy for animal species? Life expectancy for human has significantly increased during the last century or so. We all know that there are many reasons that are not linked with "evolution", but I am wondering if such change in life expectancy has been observed "naturally" (not counting animals in zoos or domestic ones). Does evolution favor long lasting individuals?

As far evolution is concerned, there is no benefit whatsoever in having long lived individuals. Evolution only "cares" about individuals while they are capable of reproducing. Survival past the maximum age of reproduction is irrelevant from the evolutionary point of view since it does not make you any better at reproducing, and therefore your genes will not be selected for.

This is highlighted by the various species that die to give birth to or feed their young. One of my favorite examples is the giant pacific octopus (Enteroctopus dofleini) whose females lay their eggs and then die, leaving their body to feed the emerging young.

Now, a mutation that makes an individual both longer lived and capable of reproducing at a greater age could well be selected for. It just always needs to be combined with the ability to reproduce. By itself, dying older will confer no selective advantage unless it is combined with producing more offspring.


Can you identify this insect for me? Does anyone know what this is? I have lived in this area of northern Utah, USA for over 30 years and played with insects, snakes and spiders growing up here. However, until this week, I have never seen this insect before, nor anyone else we have asked. Suddenly they are all over our porch, patio, trampoline and house. This one is about the size of a lady bug, but we have seen some about double that size.

At first we thought it might be a beetle, but their shells are not bifurcated. Looking underneath, they have a long thin tube that they fold into their body that appears to be their mouths. We thought a weird tick, but they only have 6 legs. Can't seem to find anything similar online either.

Does anyone know, what it is?

Definitely a nymph of some species of true bug (order Hemiptera), most likely in the suborder Heteroptera (i.e., the shield bugs, stink bugs, assassin bugs, etc.) and family Pentatomidae.

For example, see these photos of nymphs of similar species:

 From L->R: Podisus maculiventris, Troilus luridus, Glaucias amyoti, Cosmopepla lintneriana, Carpocoris purpureipennis, Murgantia histrionica

Using yet another species, Piezodorus lituratus, as an example, you can see how a Pentatomidae nymph typically develops to maturity:

 Source

As to your species...

This site lists Cosmopepla lintneriana, Chinavia hilaris, Podisus placidus, Chlorochroa rossiana, and Sehirus cinctus as species of Pentatomidae that live in Utah. None of their nymphs looks quite right, though your specimen reminds me most of a stripe-less Podisus. That might be a good jumping off place for further digging...

As you can see, there are many species with similar nymphs, and various instars within species even have fairly great variation.

I can't find a great match yet, but I can keep looking. I'll update if I find one.


Alfred Jost's rabbit experiment: how did he actually do it? I was watching a Crash Course on Biology YouTube video by Hank Green: Great Glands - Your Endocrine System.  Hank humorously describes a sex determination experiment by Alfred Jost as follows (beginning at time 9.17 in the video):

So, he, ah, very carefully... very, very carefully (and this is a little disturbing) removed bunny embryos from their mother, and then, also very carefully, removed the part that would become the ovaries or the testes from the bunny embryos.  And then, also very carefully, he put the embryos back in the momma rabbit.
What Jost found, after the bunnies were born, was that the ones that he performed the surgery on turned out to be girls.  So, in the absence of gonads, and therefore hormones that specifically instructed the development of testes and the growth of a pee-pee and a deep bunny voice, he discovered that the default setting for mammalian embryos is "make it female".

Q: How did Alfred Jost actually perform this experiment?
Essentially I'm after a less superficial description of how Jost implemented this experiment in practice.
I did a bit of Googling; what I found was consistent with Hank's description, but still omits a description of how Jost excised rabbit embryo gonads (instead just asserting that he did it).

Check out Fig. 7 in the document at http://ipubli-inserm.inist.fr/bitstream/handle/10608/4343/MS_1991_3_263.pdf . The caption says: "Castration of a 23 day fetus. [Mother's] womb is open, the rear end of the fetus is pulled out, a flank incision is performed, and the testicle, located on the mesonephros, is exposed, then cut. After bilateral testicular removal, the fetus is re-placed in the womb. [..] For ease of explanation, an older fetus is in fact shown."


Is there anyway from which we can measure the viscosity of honey using a refractometer? Is it possible to use a refractometer to measure the viscosity of honey because as we know, a refractometer is used to measure moisture and therefore water influences the viscosity of honey so is there a way that we can use to measure the viscosity of honey that way or using any other method apart from time since time has a high percentage of uncertainty?

Theoretically, if refractive index and viscosity are both simply functions of moisture content, you should be able to use one to approximate the other using an empirical standard curve. However, based on this paper, it looks like the relationship between moisture content and viscosity at 25C can vary quite a bit between different types of honey, expecially down below ~18% moisture. So I'd be pretty hesitant to rely on refractive index for acurate viscosity measurements unless you first rigerously validate your methodolgy against empirical viscosity measurements.


How can I detect which antibody is produced by the B cell? In the primary immune response, IgM is produced (in addition to IgD ). In the secondary immune response, various types of antibodies are produced.
So how do I detect which antibody a B cell is producing at a particlular time?

The major antibody in the second exposure is IgG and in the first exposure it is IgM. IgG and IgM would be produced by Plasma Cells, which are effector B-Cells activated by Cytokines.
If you want to see which antibodies (not just antibody types) are produced by the B-Cell, I would suggest transforming a GFP gene into a Naive B cell and using a Restriction Endonuclease and DNA Ligase to insert the GFP gene to the 5'-end of the Constant (C) region of the Antibody producing gene. Then, you could see which Antibodies are produced by B-cells since the Antibodies would fluoresce.
Note: I am currently in high school so I don't have much experience with Immunology, so there might be a few things wrong about my answer. However, I tried my best to answer the question. Hope this helps!!


How can haired mammals synthesize vitamin D? The human body can synthesize vitamin D in the skin from cholesterol, when sun exposure is adequate. But how can haired mammals do it? Do not they need it?

According to "Melanocyte biology and skin pigmentation" (Yin and Fisher, 2007), the exposed parts of mammal bodies, such as their noses have melanocytes that can be locations of vitamin D production.

According to this Wikipedia article, the secretions in woolly animals also produce vitamin D.

This is further explored in "Vitamin D(3) synthesis in the entire skin surface of dairy cows despite hair coverage." (Hymoller and Jensen, 2010), where they found that cows synthesise vitamin D all over their body, where they dispute an idea that vitamin D is manufactured in the fur secretions, and ingested via grooming.


Mutations/deletions with CRISPR I need to stop some protein from being active and searching for some universal way to do so. In mammalians.

With CRISPR it is possible to knock-out the entire gene. But it's a little complicate (need two gRNA for eg.). There are also another reasons, so I need to do this with only one gRNA.

So I am thinking about inserting some mutation.

My question: Is there way to make some mutation that will prevent creation of functional protein, with high efficiently - with one gRNA. And without need to know the active site of protein.

For example, frame-shift or mutation around start codon? Is it possible? If so, how can I do this? To where I need to send the gRNA?

Thanks.

You can do with a single gRNA. All that CRISPR-Cas, ZFN or TALEN systems do is to introduce a double strand break at a specific site. The DNA gets repaired via two mechanisms — non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ is error prone and it may introduce indels that can compromise with gene function (frameshifts etc). While HR can be used to integrate a transgene or repair a mutation, NHEJ can be used to create mutations.

I haven't really knocked out a gene using CRISPR-Cas but it is good to target the initial part of the ORF. There will be many other factors too that will determine what site should be chosen for targeting and an important factor would be the uniqueness of the target sequence. See this site for guidelines on selecting a good target sequence.

You would have to do rigorous screening nonetheless; the advantage of insertional knock out is that screening can much be easier (for e.g. by inserting GFP or puromycin-resistance gene).

You can have a look at this paper and the supplemental information; they have targeted 18080 genes with a CRISPR-Cas library.


Why is the ebola virus so intense now? So i'm looking into the ebola crisis and it seems the death toll is really getting crazy.  I understand that it's a cytomegalovirus and that it basically overwhelms the immune system due to it's size and virulence but why is it so bad now?  What has changed about it?

The folks at the Dallas hospital were said to have 'broken protocol' but to me it seems the virus may be more infectious this time around.  Has it changed?  Mutated?

The answer here lies in epidemiology and the pathogenic nature of the virus. Humans infected with Ebola have a range of recovery rates of 5-75%, meaning that most of those infected will not survive infection. Given the combination of preparedness factors at first recognizing a true outbreak in Ebola and viral load which had already been spread by the point healthcare workers have organized an efficient response, it is not surprising that some outbreaks are worse than others. I think attempting to correlate the virulence to the type, size with the extent of the viral spread is not pertinent, but rather, as you mentioned breaking "protocol" can have more deleterious effect than simply explaining it by a mutation.

That is not to say that this strain of Ebola is not different from those detected in other outbreaks--in fact it is likely to be quite different and accumulated several mutations.


Can animals speak like humans? I know some animals don't have the required vocals. But, I do think that some like parrots, etc may have the capability to produce speech and talk just as we do.
My question is that if an animal is trained from birth, spending all the time around only humans, in the initial years of growth when their brains are much into learning everything, can they learn to talk just as we do?

It depends on what is understood by speaking.
Anatomy  If by speaking one means producing sounds similar to those produced by humans, than the ability to speak is largely determined by the anatomy of the speech organs - whether they can produce the same type of sound as human does. There are very few animals capable of this (I will find the reference), and this notably excludes some rather close human relatives, such as the great apes.
Neurology  Language is a more complex phenomenon than speaking. The most notable difference between the animal and the human communication is that the former typically uses a set of signals with hard-coded meanings, whereas the humans can construct an infinite number of phrases coveying complex meaning. The study of language from this angle has been traditionally carried out by linguists and computer scientists rather than biologists, under the general name of universal grammar (but may also appear under such terms as transformational grammar, generative grammar, etc. ) However, these studies have a direct biological implication that humans possess a genetically coded set of rules for sentence/phrase structure, which is independent on their native language. This clearly requires certain degree of neural development, which the language-less animals do not necessarily possess.
Psychology  Finally, language requires significant psychological development - even in humans. Feral children often fail to acquire language competences. Similarly, the extensive studies on small chidlren in care homes (starting from the works by Anna Freud and Melanie Klein from more than a hundred years ago) demoinstrated that children deprieved of normal human contact have significantly diminished speaking abilities. Getting back to the OP - one can therefore question whether an animal could concievably be exposed to normal human environment to facilitae development of linguistic ability similar to that of a human.
See here and here for more background.


Are wild cats the same species as house cats? I thought that the definition of species is "can interbreed"

From Wikipedia:

  The wildcat (Felis silvestris) is a small cat found throughout most of
  Africa, Europe, and southwest and central Asia into India, China, and
  Mongolia. Because of its wide range, it is classed by the IUCN as
  Least Concern. However, crossbreeding with housecats is extensive and
  has occurred throughout almost the entirety of the species' range.[2]

So why does it have a different name than the house cat?

From Species at Wikipedia:

  A species is often defined as a group of organisms capable of interbreeding and producing fertile offspring. While in many cases this definition is adequate, the difficulty of defining species is known as the species problem.

While I understand that sometimes problems arise, what makes biologist mark the wild cat as a distinct species from the house cat? If they are genetically different, how different?

Donkeys can breed with horses. The result is sterile. Tigers can breed with lions with lots of complication. Wildcat seems to interbreed with housecat without problem whatsoever. Or does it? That's actually the essence of the question.

There are many definitions of species - look at the wikipedia page for an overview (this is a large and tricky subject). Some hybridization is not uncommon between "proper" species (often in narrow contact zones), also with fully or partially fertile hybrids. Definitions of species in these cases often comes down to genetic similarity/dissimilarity of populations. Even though hybridization is taking place it usually does so at very low rates, so the gene pools stay relatively distinct. The biological species concept (which is what you are referring to) is also problematic when it comes to e.g. ring species.

As for wild cats and domestic cats, my feeling is that modern evidence (e.g. molecular studies and phylogenies) places domesticated cats firmly as a subspecies of wild cats (Driscoll et al. 2007, 2009), with the domesticated cat as Felis silvestris catus. In the study by Driscoll et al. (2009), domesticated cats fall in the same mtDNA clade as F. silvestris lybica. However, domesticated cats were traditionally described as a separate species (by Linnaeus), and this has stuck and some still label them as separate species (as does Mammal Species of the World). I can imagine that some who argue for species status now might use a mixture of ecological, phenetic, and biological species definitions.

From Driscoll et al. (2009):

  In contrast, the world's domestic cats carried genotypes that differentiated them from all local wildcats except those from the Near East. Domestic cats show no reduction in genetic diversity compared with the wild subspecies (37), thus giving no indication for a founding genetic bottleneck. Multiple genetic analyses produced concordant results, in each case tracing the maternal origins of cat domestication to at least 5 wildcat lines (A through E, Fig. 2B) originating in the Near East. The domestic cat is referred to as a sixth subspecies, F. silvestris catus, although it is clear that domestic cats derive very recently from F. silvestris lybica (37).

   ... the vast majority of sampled domestic cats fall into the same mtDNA clade, which also includes F. silvestris lybica...

There is also evidence that hybridization can help adaptation by facilitating gene transfer (even though hybrid fertility/viability might be low), so you might want to check out e.g. results from the Heliconius Genome Consortium (2012).


Does the effect of light on melatonin release adapts to light level over long periods of time? Or do you go to bed with low levels of melatonin when you stay behind a computer screen all day?

This paper, for example, shows that indeed, melatonin is suppressed more in the light after a week of dim light exposure compared to after a week of bright light exposure.

However, the authors note that although the result was statistically significant, the effects were fairly small compared to the overall variability in the data.


Alternatives to CFU plating for measuring number of viable cells? I am hoping to measure growth rates of a bacterial culture in several growth conditions. I am concerned that these growth conditions may cause cell death, which would lead to a decreased correspondence between optical density and number of live cells, so I want to independently measure the number of live cells. I understand that plating serial dilutions of a culture and counting the number of colonies to calculate the Colony Forming Units (CFU) per mL is the gold standard for measuring the number of viable cells. However, I have seven different conditions I want to test in parallel, and making 3+ plates for each condition (to do serial dilutions) and taking measurements at several points in the growth curve leads to a lot of plates. In general this method seems more labor intensive than what I need. I am mostly doing this as a sanity check, so it seems like a lot of work just for a sanity check.

My question is: are there any alternative methods to CFU plating for measuring cell viability, given that I am doing a lot of experiments in parallel? I don't have access to a FACS machine, so cell sorting won't work. I have read this question on measuring live cells in algae. I'm not sure that a hemocytometer is the right alternative for my particular high-throughput application (though you could convince me otherwise). The best answer to this question would compare from experience the precision, accuracy, sensitivity, and ease of use of this alternative method with CFU plating.

Thanks!

I've only used it for mammalian work, but the Cedex HiRes Analyzer from Roche is pretty sweet. From their docs you can analyze particles from 1-90 μm in size (the cells I work with are about 20 μm), and there are a ton of configuration options depending on your needs. As long as your cells can be stained with Trypan Blue (it's been a long time since I've done bacterial work, pardon my ignorance) to look at viability, then this machine should work quite well. When set to Maximum (i.e., the analysis takes as long as possible), I get results in less than 4 minutes per sample - and this includes about a minute for the sample to settle in the flow cell. If you lower the sensitivity, you can get results faster.

Basically the way it works is you take 300 μl of your liquid culture (diluted if you think the concentration is too high), and add it to a sample cup. Put all your cups in the tray, fill out the sample info and analysis options in the MultiRun screen, and hit Start. The machine includes all the reagents onboard, so it mixes the Trypan Blue with your samples, then injects the proper amount into a flow cell. The sample is allowed to settle, then a high-resolution image is taken of the entire length of the flow cell. Then, depending on your sensitivity settings, a certain number of frames are taken from the full-length image and analyzed. An average count is then generated based on all the images, and your final numbers are spit out. You can then print or save a report of the cell counts and viability.

The software comes with some analysis tools as well, so if you keep multiple cultures going over time with different growth conditions, you can aggregate the data for each one and generate graphs of cell counts, viability, cell size, etc. - there are at least 10 or 20 parameters to choose from. All the image analysis options are configurable, so if you look at the results and think the machine is picking too many dead cells, or not enough, you can change the parameters to your liking, and save the options as a custom analysis type.

One option I like that would beat the pants off CFU-based counting (besides the drastically-reduced time) is the fact that the machine can detect aggregation of the cells. One issue with CFUs is that it's hard sometimes to know that a certain colony really arose from just one parent cell - if you let the colonies grow long enough you may be able to tell based on size, but it's a tough call. Since the Cedex is looking at the cells themselves, it doesn't matter if they're aggregated or not, as they'll all get counted (assuming the aggregation particle doesn't contain a huge amount of cells, like 50+, that can't be resolved by the software due to occlusion of the image).

I don't know how much these guys cost, so depending on your budget you may not be in the market for one, but if you're going to be doing a lot of counting then one of these is invaluable. I'm sure other companies make similar instruments, but I haven't used them, so I don't know how they compare to the HiRes. I do know that the person at my company that was responsible for buying the HiRes is very good about researching possible alternatives, so this one is probably as close to the top of the line as we could find, for the needs that we have.

Good luck with your counting!


Is autoclaving sucrose solution necessary? I use 10% sucrose solution to feed lab mosquitoes. Until now, I mix sucrose in autoclaved water and use it directly for feeding mosquitoes. Is it necessary to autoclave the sucrose solution itself before use?

I wouldn't autoclave this solution - sucrose will partly break down into glucose and fructose. A portion of the sugars will also caramellize and color the solution yellow to brown.

If you need the solution to be sterile, I would filter sterilize it, although this can be hard because of the higher viscosity of the sugar solution. If you haven't seen any negative effects of preparing the solution fresh with autoclaved water, I don't think there is any need to change your protocol.


Action potential and sodium channels In this video on electro tonic potential, the tutor says that when the potassium channels open the potential drops from +40mV to -80mV, where the sodium channels have already closed at +40mV.

Now in that case,
wouldn't the sodium channels that usually open at -55mV open up again when the potential is on its way reaching -80mV from +40mV, thereby making changes in all the potential differences that are occurring normally(according to the video)?

Thanks for the help.

The key to understanding this is to digest the fact that there are two gates blocking a normal sodium channel. These gates are called the activation gate (on the extracellular side) and the inactivation gate on the intracellular side. Both of these together, or any one of these alone, if closed, can block the sodium current from entering the cell.

In the resting state, the activation gate is closed and the inactivation gate is open. There is no influx of sodium. Owing to a neurotransmitter release, there is depolarization of the plasma membrane around the channel. As soon as the potential reaches a fixed threshold value, there is a change in the conformation of the sodium channel. The voltage is sensed by a biophysical voltage sensor, a part of the channel.
At the threshold potential, both the gates respond by reversing their state. But owing to the biophysical structure, the response of the activation gate is faster than the response of the inactivation gate. What happens is that the activation gate quickly opens allowing the influx of sodium ions, generating the action potential. The inactivation gate is closing but before it closes, the activation gate has been open for some time and the action potential is already fired due to considerable depolarization.
After some time, the inactivation gate also closes completely, blocking the sodium influx. By this time, the potential is at the peak of the action potential, the potassium channels have opened, and the re-polarisation phase begins. Here the inactivation gate is closed, thouh the activation gate is still open above the threshold potential. As the potential dips below the threshold, again the gates reverse their states but they respond with different speeds. First, the activation gate closes while the inactivation gate is still closed, and then the inactivation gate opens. In this way, during repolarisation, no sodium influx occurs since atleast one of the two gates is always closed.

I hope I answered your questions. Here are further links to understand this in greater detail.

Wikipedia
Mechanism of sodium channel inactivation
Basics of Voltage-Gated ion channels in Neuroscience
Mechanism of Voltage gated Channels in general(Detailed)

A more technical and biophysically accurate version of the diagram.


Would it be possible/plausible for a type of spider to fly by weaving web between it's legs to create bat-like wings? I've been thinking about this lately.  Would it be possible for a type of spider to gain the ability to fly freely by weaving its web between it's legs and creating wings much like those of a bat?

Is there anything like that in nature currently?
Is it plausible at all?

It takes more than wings to fly, just look at the poor penguins. The first problem is that simply weaving webs between a spider's legs would probably not generate enough lift to keep her airborne. Flying creatures have a specific body plan that allows them to fly, if you just add a couple of wings to a hippopotamus it won't be able to fly.

On top of that, the spider would not have the necessary muscles to enable it to flap these wings even if they were capable of producing sufficient lift.

While it is theoretically possible (I stress theoretically) for a spider species to adapt over time (long long time) into a flying form, then it would no longer be a spider. So, in answer to your question, no, it is not possible.


Difference between micro RNA and short-interfering RNA and CRISPR Cas 9 system? I read this article https://www.quantamagazine.org/20150206-crispr-dna-editor-bacteria/ and am slightly puzzled as to why the CRISPR/Cas 9 system is seen as being so revolutionary. It seems like the very same thing that micro RNA and short interfering RNA does- cleaves synthesised mRNA strands by attaching to the complementary part of the mmRNA strand, and the restrictive enzymes combine to this RNA and cleave it. I don't see how the CRISPR system is any different or better...

Thank you in advance :)

EDIT: Also, does anyone know whether Cas 9 cuts both DNA strands at the same place, or whether it leaves 'sticky ends'? Thank you.

The CRISPR Cas 9 system is used to introduce insertion or deletion in a genomic sequence not mRNA.

https://www.addgene.org/CRISPR/guide/


What are the sources of molecular hydrogen in human breath? In the BBC News article CES 2019: Tech preview of the expo's hottest new gadgets there is a new product that one can use to measure the hydrogen in ones breath, and this is supposed to have some connection to diet:

By contrast, FoodMarble's Aire measures the hydrogen in your breath and combines this with a log of what you have eaten, to warn you of foods you should avoid and possible substitutions.
Aire is designed to discover which foods are being passed to the large intestine without being fully digested

There also exist air quality monitor chips that measure both TVOC (total volatile organic compounds) and "eCO2", where "eCO2" is really a measurement of H2 in the air, and via some electronic algorithm uses it to calculate the expected rate that people are exhaling CO2.
Question: Both of these are examples of interpreting the presence of molecular hydrogen as having some indication that we are alive, breathing and eating. Here I would like to understand the sources of hydrogen in human breath, and how that hydrogen makes it from source to breath.
potentially related: Where does molecular hydrogen in the atmosphere come from?

Hydrogen in breath arises from normal intestinal bacteria, mainly in the colon, which break down (ferment) the undigested nutrients that have passed through the small intestine. Hydrogen is absorbed from the intestine into the blood and exhaled via the lungs.

Conditions in which intestinal bacteria produce hydrogen:

Normal digestion in which soluble dietary fiber is not digested in the small intestine. Examples of soluble fiber: beta-glucan (in oats and barley), pectin (in apples) fructo-oligosaccharides (in red onions), raffinose (in beans), etc.
Lactose intolerance in which lactose remains undigested due to lack of the enzyme lactase (gas is produced mainly after ingesting milk)
Fructose malabsorption in which fructose absorption is reduced due to lack of a certain molecule in the intestinal lining (gas is produced after eating foods high in fructose: apples, pears, honey, agave, etc.)
Sucrose intolerance due to lack of the enzyme that digests sucrose
Small intestinal bacterial overgrowth (SIBO) due to various malabsorptive conditions

Hydrogen breath test is an established method for diagnosing various intestinal disorders. It includes drinking a solution high in certain substance (lactose, fructose..., depending on which disorder is expected) and measuring hydrogen in the exhaled air.

To properly interpret the results of a hydrogen test you need to consider the time in which hydrogen appears in breath after ingestion of a certain substance.

Food Marble provides a relatively thin explanation of their breath test. The question is if this test can distinguish between the hydrogen produced during normal digestion of the soluble fiber and hydrogen produced in the mentioned intestinal disorders.

Business Insider made a review of FoodMarble in which they mention some other reviews...In summary: it's not proven reliable, yet.


A source for leaf architecture of different plant species/genus? I'm currently working on extracting some features of the leaf architecture based on their images (like L:W ratio, laminar shape, ...). I use the Manual of Leaf Architecture as the reference. It is really great in mathematically describing the features and how to calculate them.

But, the problem is I am not able to find a source (a book, or a data set) to have this architecture of different leaves (plants). For example, whether the Acer genus has leaves with a certain (or a range of) L:W ratio or the laminar shape for this species is mainly ovate,....

Does anybody know any source of this kind?

Quantitative descriptions of leaf shape used as diagnostics are hard to come by. There are numerous qualitative descriptions (lyrate, cordate, acicular, etc.), and I think this fits within the example you give that "the laminar shape for this species is mainly ovate." But actual quantitative ranges as you mention (e.g., that the L:W ratio of Acer lies within a certain range) are much more difficult to come by. Also, there are ways of quantifying leaves using all the shape variance present in their outlines, and I describe some of these methods below. By using quantitative methods such as these, you can avoid the trap of a subjective criteria that arbitrarily distinguishes leaf morphs by a particular feature. Plus, you won't be biased by using a particular shape attribute, as you will be measuring the entirety of shape. Use of these various methods though depends on the species you are studying.

Oreotrephes I think is on track saying that, if possible, you should build your own diagnostic criteria for whatever system you are working in. You mentioned certain "ranges" that can diagnose a species ... this is a critical question. Measuring intra-genotype/individual variance in shape for your system is critical. Which leaf to measure for a species? ... i.e., shoot position, developmental age of the leaf, if working with compound leaves, the placement of the leaflet along the proximal distal axis of the leaf, what about heteroblasty (changes in leaf form at different nodes), leaves from lateral vs. main branches, environmental effects on leaves (e.g. sun vs. shade leaves)?

For tomato, I measure shape quantitatively using Elliptical Fourier Descriptors, which reduces the shape of an object to a series approximation and explains variance with a Principal Component Analysis. I use the resulting Principal Component values of leaves as a trait and explain shape quantitatively that way. A very useful program to perform Elliptical Fourier Descriptors is described in Iwata & Ukai 2002 and can be downloaded here. In Chitwood et al 2012, I describe how to perform shape analysis on tomato leaves, separating components of shape based on genotype (e.g., by species), by position in the leaf series (heteroblasty), the ontogentic age of the leaf, and placement of leaflets along the proximal-distal axis.

Other easy ways to measure shape: Circularity, solidity, L:W ratio (or aspect ratio) as you mentioned. All very easy to measure in ImageJ!

You mentioned Acer leaves, which piqued my interest because I study differences in the shape of grape leaves. But like grape, many Acer leaves are palmately lobed. If every one of your samples has certain features (e.g. 5 lobes and 5 sinuses as in Acer, including petiolar sinus) then you can perform a landmark analysis using a Generalized Procrustes Analysis (The "Shapes" package in R is useful for this analysis).

Using global methods to describe shape, that is, methods to quantify the totality of shape variance, are critical to distinguish leaves. It may very well be that two leaves are so similar from different species that they are not statistically separable by shape! Be creative in the ways you measure shape, and if need be, create your own system for doing so!

 Chitwood DHD, Headland LRL, Kumar RR, Peng JJ, Maloof JNJ, Sinha NRN. 2012. The developmental trajectory of leaflet morphology in wild tomato species. Annu Rev Plant Physiol 158: 1230–1240.
 Iwata H, Ukai Y. 2002. SHAPE: a computer program package for quantitative evaluation of biological shapes based on elliptic Fourier descriptors. Journal of Heredity 93: 384–385.


Why do doctors do chemo or transplantation for cancers that don't respond well to these treatments? From the UpToDate article on multiple myeloma:

  In most people, chemotherapy partially controls multiple myeloma;
  rarely, chemotherapy leads to complete remission.

Also:

  Transplantation, when successful, prolongs survival, leads to a
  remission, and, infrequently, cures multiple myeloma. However,
  transplantation has several limitations. The high-dose chemotherapy
  given before transplantation usually fails to kill all of the plasma
  cells, allowing the condition to relapse after transplantation. Such
  treatment also puts the patient at risk for serious infections and
  bleeding, which can be fatal.

UpToDate is used by 700,000+ physicians worldwide; it's not alternative medicine. Thus, if even mainstream medicine recognizes the relative ineffectiveness of chemo and transplantation for multiple myeloma, why do they do it?

To long for a comment: Its more an ethical thing I would say.
I do research which is connected to melanoma - a cancer which is notoriously treatment resistant, once it started moving. Until very recently there was only one chemotherapeuticum which has pretty low (around 20%) response rates. It was usually tried anyway because its possible that the patients belong to this 20% which respond. If not, treatment was usually not prolonged.

I think its something similiar here. The other problem for chemotherapy is that it is cytotoxic (until we got the small molecule inhibitors which are tested and used today) and the problem is to kill the cancer cells (all when possible) while you leave the rest of the body as unaffected as possible. To get this balance is hard (people tend to react differently to chemotherapy). The other problem is that cancers are not homogenous. So its possible that 99.9% of the cells present respond to chemotherapy and get killed, while a few acquired an additional mutation, which gives them an advantage. The conditions of chemotherapy are very selective.


Do pyrosomes reproduce by ways other than cloning? I know that Pyrosomes are large colonies of floating tube-like animals that live in the sea, particularly in the tropics. They are just like any type of free floaters

I know  that pyrosomes can reproduce by cloning, but are there any other ways that they can reproduce?

Indeed pyrosomes use a very interesting form of reproduction. They actually use both sexual and asexual form of reproduction each time they reproduce. Pyrosomes, which are colonial tunicates, produce both egg and sperm. In each pyrosome of a colony, a single egg is fertilized and develops into a 4-staged animal. This form leaves the parent body and starts forming its own colony. It does so using the process called budding, which rapidly develops a new colony of pyrosomes. You can see here, here or here for more information.

source (in french though ;)


Why are humans and almost every species on earth symmetrical? I admit I'm not very learned on the subject of evolution, I just started researching it for myself about a week ago. One of the things that I don't understand is why humans and almost every other animal/bug/fish etc. on earth has a symmetrical body. What advantage does this have for the survival of the fittest? It must be quite important, since it re-occurs so frequently and early in the evolutionary family tree.

[If we are talking about animals, there is a number of types of body symmetry: asymmetry, radial, bilateral, spiral, rotational, glide and metameric symmetries. Bilateral and radial are the two basic types, which served as main classificatory character for animal mega-systematics in the past.]

It's assumed that body symmetry is associated with general environmental gradients.

Animals with (elements of) radial symmetry have one dorso-ventral axis which echos only one environmental gradient: substrate/water column, depth etc. Besides this polarity, resources/signals/danger may come from any direction. Imagine a Hydra polyp with its foot attached to a waterweed and its tentacles surrounding the mouth on the opposite end and expecting the victim to come from any side.

Body of bilateral animals possesses the same dorso-ventral axis and yet another polarity, orthogonal to it: the anterior-posterior axis. This axis is conjugated with the gradient created by locomotion: the anterior margin of the body is likely to encounter something new first. This principle lies in the basis of cephalization: most bilaterial animals have more or less shaped "head".

Evolutionary changes in body symmetry are thus thought to be associated with changes in life-style, e.g.:

there is a hypothesis that cnidarians were originally bilateral (and many of them still show some degree bilaterality), but lost it after becoming sedentary.
non-walkers echinoderms originated from fully bilateral animals and later acquired their famed pentameric radial symmetry (were they originally fully sedentary like modern stalked sea lilies?). This symmetry, however was again distorted towards secondary bilaterality (not matching the original plane of symmetry) in endobenthic forms: sand dollars and some holothurians.
worms like nematodes or priapulids are dwellers of viscous media, similar in all directions: dorso-ventral gradient of environment in this case is absent or weak. Though the original bilateral symmetry is very clear in their body plans, signs of radial symmetry prevail in some organ systems, including the general vermiform appearance. Thus, nematodes combine triradial (head sensilla, pharynx), biradial (musculature) and bilateral (nervous system, genitalia, tail) symmetries.


How does the immune system recognize pathogens? There are useful and pathogenic bacteria in our body. How does the immune system differentiate between them?

Pathogens will often have non-peptide antigens, peptide antigens, and pathogen-associated molecular patterns that are recognized by innate and adaptive immunity mechanisms. Useful bacteria are not differentiated, and often sit beyond the grasp of our immune system, or have mechanisms to escape an immune response. When contacted they do, however, produce an immune response and due to their location, this often involves mucosal immunity:

This portion of the immune system varies greatly in response to the systemic immune response because it is constantly stimulated, and in a way trained, by the presence of all microbes, such as gut flora. As a result, it often resolves infection quickly with low severity, and little lasting tissue damage. Keep in mind that self cells have mechanisms which desensitize them to autoreactivity with immunity. Microbes don't share these same mechanisms, but can evade or escape the immune response through their own methods. But by no means are microbes of any sort, for the average immune system, disregarded.

Unfortunately, to respond more specifically would go into textbook chapters of material so to that end I'm going to cut the explanation here, and recommend you do some research of your own.


Formation of peptide bond..? Proteins peptide bond is made by condensation process in which a molecule of water is released and according to this process it is not favorable in water systems than how peptide bond is formed by condensation in cytoplasm in the presence of water ?

The condensation is not done in water alone - the enzymatic function of the ribosome plays the essential part here. And in the active center of the ribosome where the formation of the peptide bond takes place, no water is present, only the growing peptide chain and the single amino acid (bound to the tRNA). See this schematic image from the Wikipedia:

If you make x-ray crystallography, this looks like this (from here). You can see that the tRNA with the unbound amino acid is actually inside the ribosome and protected from the outside:


Why is sex hurtful for some animals but pleasurable for others? Sex seems to be pretty hurtful for feline for example. On the other hand sex is pleasurable for humans. Why is sex pleasurable for some and not for others? How do these things evolve?

There are various selection pressures that may lead to sex being more or less harmful. I don't think there is an easy way to summarize these selection pressures other than just going through load of examples. Here is an attempt to give you some notions of why can sex be pleasurable and/or painful. Note that I do not consider myself particularly knowledgeable in this field.
Why could it be pleasurable
We tend to seek for positive experiences. If we like sex, we have more sex. If we have more sex, we are more likely to have more offspring. Hence, the trait "liking having sex" is positively correlated with "fitness".
Why could it be harmful
Dick pics
In many species, the penis has spikes and stuff and is most definitely hurting the females. Here is a Drosophila penis

And here are penises of two dragonfly species

Here is a feline penis

By the way, according to wikipedia (could not find peer reviewed paper on the subject so take this with a grain of salt), some humans still have on remnants of those barbs you can still see on many feline penises left from our ancestor. They are called hirsuties coronae glandis. Here is a perfectly healthy (but I would tend to consider quite extreme) example of hirsuties coronae glandis

Some theory
There is a lot to say here and I only want to say a few words and hopefully you will go get more information by yourself.
So why do these species evolve these fancy and scary "armed" penises. In many species, it is a small investment for a male to make a baby (just mate and the job is done) but a big investment for the female (producing the egg, eventually even parental care, ...). Because the sex-ratio is always (assuming no group selection) pushed toward 0.5 (see this post and Fisher's principle), it happens that males end up with lots of free time looking for females (see Why are female not competitive for reproduction like males? and Bateman's principle). You might also want to read about sexual conflict.
Why would such penis evolve?
The reason vary among species. Here is a non-exclusive, non-exhaustive list of reasons:

In some species (e.g. nudibranch, damselflies)The goal is to remove the sperm from an eventual previous male so as to reduce sperm competition (Cordero-Riviera, 2016).

In some species, the goal is to damage the female reproductive track so that she will not subsequently mate with other males hence reducing sperm competition ().

In some species, the male can even leave toxic products in the female (Chapman et al., 1995).

In some species, females get severly harrassed by males for mating and rape is not unusual (e.g Drosophila). Some penile barbs and spikes can be used to get the female stuck in place. To avoid that the female can escape before the sperm has been delivered ()! That being said, in some circumstance such use of spiky penis might be beneficial to the female too. This non-peer reviewed article may bring some light.

In some species, the male can pierce through the female abdomen to deliver its sperm. This is called traumatic insemination.

In a classical experiment, Rice 1996 shows that there is an arm race between males and females. Race in which males increases their negative impact on female's reproductive organs and females protect themselves from it. The paper is free, is short, easy to read and has a pretty amazing experimental design. It is worth having a look at it.
Feeding the babies via the mother
I just want to point with other examples that sex does not have to be romantic in many species. In some species, the female eats the male after sex or even while having sex. To what I have heard (; please be cautious with this information), in some mantis prey, the male does not even release his sperm before the female has cut the male's head off. Why would the male do that?
A male that let himself get eaten by the females ensures that the female has lots of energy for taking care of her babies. Hence a male may increase his fitness by sacrificing himself to his partner.


MIT's Programming Language for Cells I have read a lot about the programming language, Cello, that MIT created to program DNA; however, I cannot seem to find any sources online that shows you how to program with Cello. Are there any good sources out there with regard to this topic?

Thanks

I’m not sure that this is on topic, as you really could have found this information yourself.

You don’t quote a source for your info about this, which doesn’t help you or anyone interested in this topic. Here is a Nature News article.
If you click on the link in that article you get to the Cello site. You need to choose a name and password to gain entrance, but are not asked for any personal information. All they will have is the IP number of your computer.

The info on this site will not mean much to anyone not involved in synthetic biology.


Does Povidone-Iodine that penetrates through the skin stays in the body (cells, liver etc)? Here it says on povidone-iodine:

"Route of Elimination: Povidone-Iodine is intended for topical application and is not eliminated"
"Clearance: Povidone-Iodine is intended for topical application and is not eliminated"
"Metabolism: Povidone-Iodine is not absorbed or metabolised"

Now Povidone-Iodine is a very widespread antiseptic used directly on open wounds and there are cases of people using it as a disinfectant before and after microneedling (ie: inducing micro-injuries with a dermaroller device over the skin) which ensures penetration of the substance through the skin and blood circulation and into the body.
What happens with it once it's inside the body - even if some is excreted what happens with the rest which isn't? does it forever lingers within the body (cells, liver etc)?

Your source (DrugBank via PubChem) is describing the typical pharmacokinetic information (ADME, absorption, distribution, metabolism, excretion) on Providine-Iodine, under the assumption it is not absorbed. It's true, a thing that is not absorbed has no volume of distribution, is not metabolized, and is not eliminated.

Though Providine-Iodine is not absorbed as is, Iodine is.

From the Lexicomp drug information for prescribers:

  Absorption: Absorbed systemically as iodine; amount depends upon concentration, route of administration, characteristics of skin

Other pharmacokinetic properties are as for Iodine. It may be taken up by the thyroid. Clearance is primarily unchanged (as Iodine) by the kidney.

The absorption through the skin as iodine and elimination by the kidneys are the reasons for the prescribing precautions:

Use with caution in patients with burns (excess absorption)
Use with caution in patients with renal impairment (impaired excretion)
Use with caution in patients with thyroid disorders (taken up by the thyroid)

This case report of Iodine toxicity following prolonged povidone iodine administration is available on pubmed central. It's from the 80s, but it is still relevant and the comments section has a good overview:

  The reports of iodine absorption from topical povidoneiodine
  solution suggest that absorption is enhanced when the
  compound is applied to denuded skin, mucosal surfaces with
  high absorptive capacity or extensive areas of intact skin. The
  evidence for iodine absorption includes documented serum
  iodine concentrations and thyroid function abnormalities.


Identifying structures from anterior end of dissected prawn Note: This image might be disturbing.

I want to know what the red and the black structures (directly posterior to the red structure) are. I guess it's the heart.

I guess you got your antero-posterior axis wrong. If I am correct then anterior is right and posterior is left in your image. In that case the black structure should be the cerebral ganglion and the red should be the heart. See the image below.


Why are goosebumps so ineffective at keeping us warm? If the purpose of "goosebumps" is to keep us warm, why is it so ineffective? Or are the changes subtle, but important?

When your brain, the hypothalamic temperature centers in particular, detects that the temperature is too warm or cold, it initiates a number of controls to try and correct this.

Goosebumps appear due to piloerection. This is one of the reactions that occur when the temperature is too low.

This causes hairs to stand on end as a result of contractions in muscles attached to hair follicles called arrector pili.

This particular reflex is not actually important in human beings. However, in animals, this mechanism allows entrapment of a layer of air allowing insulation. This way, the heat loss is greatly reduced.

The other mechanisms are very adept at maintaining temperature in the human body. These include sweating, dilation (vasodilation) and constriction (vasoconstriction) of skin blood vessels and increasing and decreasing the body's heat production.

For example, when it's too hot, dilation of the skin blood vessels can increase heat transfer by up to eight times.

Source: Guyton and Hall. Medical Physiology. 11th ed. Elsevier Saunders.


What term describes insects that must eat protein to reproduce? I know there is a specific term for insects that need to consume protein to produce viable eggs, as well as a term for those insects that don't need to consume protein to produce viable eggs.

The term I was looking for was anautogeny, or an anautogenous insect. I had slightly confused the definition, with the actual definition being; 'a gravid female insect that requires a blood meal before oviposition'.


Are there any organisms that lack ATP synthase? ATP synthase is used by cells to synthesise ATP from ADP using energy from a proton gradient. Depending on which sites I look at, this is either a universal feature of living cells, or it's "almost universal", used by the vast majority of organisms.

As Superbeast points out in a comment, ATP can also be synthesised on the substrate level via the Krebs cycle. However, I would like to know if there are any organisms that only synthesise ATP this way. In other words, are there any known organisms that entirely lack the ability to produce ATP synthase, and produce ATP entirely through the Krebs cycle, or through some other mechanism not related to ATP synthase?

If there are, I would like some information about them. Are there many such species or just a few? Are they all prokaryotes or all eucaryotes, or some of each? What kind of environments do they live in?

As Superbest mentioned, substrate level phosphorylation (SLP) is alternative pathway by which ADP is phosphorylated to ATP. In SLP, phosphorylation is coupled with a highly exergonic chemical reaction. Fermentative organisms (both fully and temporally fermentative) organisms depend on SLP for ATP.

Note: fermentative $\neq$  anaerobic

Fermentation can either be a temporary situation, depending on the growth substrate (for e.g. yeast) or the only option as in the case of amitochondriate organisms like Entamoeba. You can refer this book if it is available to you. See this article too.

You can also see the wikipedia page on fermentation; it mentions the SLP steps.


Why is lower case used in front of a capitalized acronym (e.g. rDNA)? Examples: rDNA, mRNA, tRNA.

Why do we use small case for "r" in "rDNA", etc? Any particular reason?

It's just a stylistic approach because "DNA" or "RNA" is an abbreviation by itself that has become a whole noun. Those terms clearly separate the modifier from the overall DNA/RNA. It makes it easier to read. Terms like DNA and RNA are almost always known just by those acronyms, whereas something like mRNA is known both as "messenger RNA" and "'m' RNA" but almost never as "messenger ribonucleic acid."


What's the difference between physical (direct) and functional (indirect) protein interaction? I read that the Protein-Protein interactions one can consider are generally of two types, namely physical and functional, but I cannot get the difference between the two.

I was just thinking that if two proteins are linked in a Protein-Protein interaction network like the ones stored in STRING database, then they are experimentally observed or somehow predicted to physically interact through binding sites to explicitly perform a function, e.g. signal transduction. But as I am reading different sources making the separation between the two kinds of interactions I got a little bit puzzled.

Can you please help me?

As I understand it, "physical" and "functional" are just two different ways of analyzing an interaction between proteins.
Proteins can and do interact physically, meaning they can bind in specific ways and sites, and this binding can produce changes in those same proteins (like conformational changes), which alter their properties. This is the purely physical analysis of the protein interaction. The functional analysis begins when we ask the questions "What is the role that this interaction performs in the cell/organism/living system?"; "What effects do these changes in the protein are going to create in the cell/organism/living system?". Often a conformational change in a protein induced by an interaction with another activates or inactivates it. In other words, an interaction can create a conformational change that enables (activation) or disables (inactivation) the protein to catalyze a given reaction, and so the referred interaction plays an important function in regulating the protein's activity. For instance, phagocytes (cells capable of phagocytosis) have in their membranes proteins capable of physically interacting with proteins present in pathogens membranes. They physically bind to them, changing their conformation in the process. This is the physical part of the interaction, it is what happens purely physically (and can be studied more deeply). This conformational change will enable the protein to catalyze a series of reactions inside the phagocytic cell that will ultimately lead to the phagocytosis and destruction of the pathogen. This is the functional analysis of the interaction, it is understanding what is functionally achieved by the interaction, in this case enabling phagocytosis (and can be studied more deeply).


Is neurogenesis essencial for learning? So I read that our brain produces 700 new neurons in the hippocampus every day and that if we perform cognitive demanding tasks, eat omega-3 or exercise (other things?) it can produce even more neurons.

What happens with this new neurons? Say I'm learning some new skills, what role do those new neurons play in the process? Is it possible to learn without neurogenesis?

Edit: I'm interested in this topic (eg: brain, hippocampus, learning). Where can I learn about this from the basics? What classes teach this in college?

No, neurogenesis is not necessary for learning (assuming you are talking about adult neurogenesis: of course you need to generate neurons sometime in development to even have a nervous system).

Easily the most-accepted theory for learning and memory is that learning happens by changes in the strength of synapses, the connections between cells. The strengths of these connections are also often referred to as "synaptic weights." The primary mechanisms for this learning are long-term potentiation and the related spike-time dependent plasticity, as well as the guiding principle of Hebbian learning often stated as "cells that fire together, wire together."

Briefly, long-term potentiation or LTP describes the increase in post-synaptic receptors that occurs under certain conditions: this is what increases the efficacy or strength of certain synapses. One of the key conditions is that LTP tends to occur at synapses that causally contribute to making the post-synaptic cell fire.

Adult neurogenesis primarily occurs in a few localized area of the brain (Zhao et al.,
 2008). Although it is possible there is neurogenesis outside of these areas, it has not been demonstrated conclusively and is certainly not sufficient to be necessary for learning in a normal, uninjured adult brain.

Neurons born in the subventricular zone continually replace olfactory receptors, which have a relatively short lifespan, probably evolved due to their constant exposure to all sorts of potentially damaging external compounds entering the nose. These cells do have to undergo some "learning" processes to integrate into existing networks, but that isn't what you would colloquially think of as learning in general.

The best candidates for cells that actually impact learning to some degree are the new neurons born in the subgranular zone of the dentate gyrus in the hippocampus. The hippocampus is indeed an important structure for certain types of learning, but new neurons aren't necessary for this learning. Although it is still somewhat unclear what the roles are of the new neurons in the dentate gyrus, it is thought that they contribute to the primary roles of the dentate gyrus, which are to help distinguish between similar patterns of activity (Deng et al., 2010), also called "pattern separation."

Two other hypotheses are that adult neurogenesis helps to encode timing information in memories because the new neurons only participate in new memories, or that they allow for incorporation of novel stimuli once the older neurons have been conditioned and tuned only to stimuli that have been experienced before (Aimone, et al., 2013). There is evidence for all of these hypotheses but none of it is conclusive, and all may be true to some degree.

There are many different types of learning and these different types of learning can occur in different brain regions, most of which do not demonstrate any substantial adult neurogenesis. Often people think about associative learning with operant or classical conditioning. There is also episodic learning: remembering events that have happened (this is the type most closely associated with the hippocampus, where perhaps neurogenesis plays some role). There is also motor learning, and several types of learning in sensory systems like habituation or sensitization. Therefore, it is important to understand that learning isn't just one thing, and although the mechanisms can be related they are not always the same.

How to learn more: I can tell you about courses at institutions I have been affiliated with, but of course these could vary between schools. Learning and memory is usually at least part of a systems-level undergraduate neuroscience course, which is often the second of two overview courses in neuroscience. The most common time for students to take such a course would be as a second-semester junior or a second-semester first-year graduate student, because there is prerequisite knowledge in physics, chemistry, molecular biology, and physiology. There are also graduate-level courses in the molecular mechanisms of learning and memory, and theoretical neuroscience courses that cover the computational considerations of learning and memory rather than just the biological mechanisms. These types of courses might be available to a senior-level undergraduate as well.

Of course you can also read some of the review papers I have included here and follow the references they cite for original research, as well. The Aimone review is particularly readable and has some very excellent illustrations for a novice, and also extensively covers the regulation of neurogenesis by behavior and environment.

References

Aimone, J. B., Li, Y., Lee, S. W., Clemenson, G. D., Deng, W., & Gage, F. H. (2014). Regulation and function of adult neurogenesis: from genes to cognition. Physiological reviews, 94(4), 991-1026.

Deng, W., Aimone, J. B., & Gage, F. H. (2010). New neurons and new memories: how does adult hippocampal neurogenesis affect learning and memory?. Nature Reviews Neuroscience, 11(5), 339-350.

Zhao, C., Deng, W., & Gage, F. H. (2008). Mechanisms and functional implications of adult neurogenesis. Cell, 132(4), 645-660.


Caterpillar identification: Peru Could you please help me identify this caterpillar (Amazon rainforest, Peru)?
Is it a species of Megalopygidae???

It is an pink flannelmoth because there is no other insect which ressembles it

Usually pinkflannelmoths have orange coloured centers


Which bacteria takes the longest to double? Currently I am writing a lab report on the enumeration of bacteria.
E.coli takes about 30 mins to double. That is going from 1 bacteria to 2 bacteria.

I want to know which bacteria takes the longest to double? Do some bacteria take a day to double?

Thank you for the help.

There is no answer to your question

The doubling time of a bacterium is dependent on the conditions: primarily on the temperature and the availability of nutrients, but other factors can apply. Because of this, the doubling time of any particular bacterial strain cannot be considered in the abstract, thus to give a single number  we can consider the optimum doubling time for a strain instead - i.e. how fast it will double under the perfect (for it) temperature and nutritional conditions. For the E. coli strain you worked with, this is likely 37 degrees and in a rich media such as Lysogeny Broth. But for the staggeringly vast array of bacteria out there, we simply don't know what the optimum conditions are much less have actually measured growth under them. In fact, there are many bacteria which are known about, but currently uncultured so we haven't even begun to understand their growth dynamics.

So even the simplified question of longest optimal doubling time cannot be answered because we don't have the data for so, so many bacteria. The question of the maximum time between divisions is even less clear: there are bacteria that live under conditions of extreme nutritional limitation that can take thousands of years to double, and strains that can exist as spores for at least 100,000 years and maybe even tens of millions. Do we consider their doubling time to be a 100,000 years? 25 million years? Without specifying the conditions under which the doubling takes place, the question is poorly defined.


How do plasmids protect themselves against restriction enzymes? How do plasmids protect themselves from restriction enzymes released by bacteria (i.e., against bacteriophages)?

The strains that we use in the lab have defective restriction machinery.

In the case of DH5α it is mostly because of the endA1 and hsdR17 mutation. The former mutation eliminates an endonuclease that can degrade plasmids and the latter one eliminates the restriction system.

Check this.


Is it possible to consume O2 via a pill form to inhibit the need to breathe? Just wondering if it would be theoretically possible to consume oxygen via O2 pills, in the effort of being able to hold one's breath without limit.

Totally just curious.

The problem is volume and surface area for gas exchange.  The volume in a pill is puny compared to the amounts you pull in and out breathing.

But could you use something other than the lung for gas exchange?  The colon has a lot of surface area and the small intestine even more.  Maybe if you flooded your gut with an oxygenated fluid like that liquid fluorocarbon the mice breathe, or even oxygen saturated water you could get some of that out via your intestinal villi.  Dragonfly larvae do something like that, performing gas exchange with their rectums.  You would need to exchange the liquid at least as fast as you breathe, getting all the depleted liquid out and new oxygenated liquid in.

Some of those high colonic machines work like that, as I understand: fast in and fast out.  People might not notice you were holding your breath because they were distracted by the churning machine with the hose up your trouser leg.  Maybe you could pass out cards or wear a T-shirt explaining what was going on because you would still have to breathe to talk and that would ruin it.  If you do this would you please post video and link it up here?  Thanks.


Why does eating saturated fat increase blood cholesterol? I am interested in the biochemistry of diet and the way we have been advised to eat for the past forty years.

In researching an explanation for the relationship between dietary fat and blood cholesterol I came across the following: "It is clear that eating too much saturated fat increases the levels of cholesterol in the blood, especially our "bad" cholesterol which doctors refer to as LDL". This is from heartuk.org.uk.

"It is clear ..." - really?

I am mystified! I understand that dietary fat, other than very short chain fatty acids, does not immediately enter the blood stream but is transported via the lymphatic system as triglycerides packaged in protein assemblies called chylomicrons, finally entering the blood via lymph nodes under the armpits. Once in the blood the triglycerides are hydrolysed into fatty acids and transported to appropriate cells in albumin complexes.

Where does LDL feature in this transportation? And, by the way, why just saturated fats? Surely the small intestine doesn't differentiate between saturated and unsaturated fats, or does it?

In short: It may not be saturated fat by itself but high saturated/unsaturated fat ratio and high animal/plant fat ratio in the diet that increases the risk of heart disease.

A systematic review of the effect of dietary saturated and polyunsaturated fat on heart disease (NMCD Journal, 2017)

  Reducing saturated fat and replacing it with carbohydrate will not
  lower cardiovascular events or CVD mortality although it will reduce
  total mortality. Replacing saturated fat with mono- or
  poly-unsaturated fats or high-quality carbohydrate [from whole-grain
  food] will lower cardiovascular events.

Saturated Fatty Acids and Cardiovascular Disease: Replacements for Saturated Fat to Reduce Cardiovascular Risk (PubMed, 2017)

  Replacing dairy fat with carbohydrates from refined starches and added
  sugar was not associated with increased or decreased risk of coronary
  heart disease (CHD), stroke or total cardiovascular disease (CVD).
  However, replacing dairy fat with carbohydrate from whole grains
  reduced the risk of CVD, CHD and stroke. Relative to other animal
  fats, dairy was found to have less impact on CVD. When 5% of energy
  from dairy fat was replaced with animal fat from non-dairy sources,
  risk of CHD increased by 6%. However, when 5% of energy from dairy fat
  was replaced with an isocaloric amount of polyunsaturated fats, risk
  of CHD was reduced by 26% and CVD risk was reduced by 24% [41].

A basic explanation of the underlying mechanisms:

The liver produces low-density lipoproteins (LDL) and high-density lipoproteins (HDL). Lipoproteins are composed of triglycerids, phospholipids, cholesterol and proteins.

LDL caries cholesterol from the liver to the peripherial tissue, including arterial walls, where it can accumulate and cause atherosclerosis. This is why LDL is called "bad cholesterol" (even if LDL is only a carrier for cholesterol). HDL clears excessive cholesterol from the blood and carries it to the liver for disposal, so it is called "good cholesterol. (Heart.org.uk)"

High LDL levels are associated with an increased risk of coronary heart disease (Bentham Open).

One possible mechanism by which saturated fats increase (LDL) cholesterol (PLOS):

  Saturated fat is thought to increase LDL-C primarily through
  down-regulation of hepatic LDL receptor activity, leading to reduced
  clearance of LDL particles [from the blood].


User friendly phylogenetic tree editing software Background: I have Hackett 2009 (from birdtree.org) phylogenetic tree and I need to reorder it according to Prum 2015. I also work only with some species relevant to my project, not the entire tree.

I currently use Mesquite, and it is absolute purgatory. Doing any reordering in Mesquite takes insane amount of time. I'd also like to add higher taxon information to each species (like order) to help my my orientation in the data.
I understand some of Mesquite's shortcomings might be shortcomings of Nexus format. As I don't need to analyse the data myself, I can work in some better format like PhyloXML as long as it's possible to export back to Nexus format in the end.

Is there any way to do this? Some software with better visual editor (and overall better UX) or other method to do this in effective manner? I find it hard to believe that much bigger data is handled in such clumsy way.

Yes, I think that you should consider using MultiSeq which is a package of Visual Molecular Dynamics (VMD). You can use visual molecular dynamics to make phylogenetic trees based on sequence/structural/other statistical means.

If you want to check it out and see if it works for you, then install visual molecular dynamics: http://www.ks.uiuc.edu/Development/Download/download.cgi?PackageName=VMD

and try out these tutorials under Bioinformatics from the distributors:

http://www.ks.uiuc.edu/Training/Tutorials/

Note: VMD doesn't work very well in 64-bit Windows operating systems if that's what you use. To get it to work well, I suggest you install virtualbox from Oracle, and install your favorite free open-source Linux operating system into virtualbox or into your guest linux machine on your host machine.

I suggest installing your guest Linux OS on virtualbox with 1/2 the ram of your host physical computer allocated, and like 100 GB of space for when you discover that you love LINUX so much and have lots of information on there.

To full-screen your guest Linux OS, you need to install guest additions.

My favorite Linux OS is Kali Linux.

To install guest additions on Kali Linux and most linux guests on VirtualBox,
you have to do this:

But as I've discovered you have to upgrade Kali Linux to Kali Linux Rolling to get Kali Linux to fullscreen. How you do that is via this:

And you probably shouldn't do your work as user "root" the default user. You have too much power so to increase security create a new user on Kali-Linux:

If you are already using linux, then you won't have any problem with getting VMD to work. But by the way, you have to install VMD from the command terminal in linux and this is how you do it.

The instructions as for how this guy does it (and sorry he doesn't speak English) are in the README file when you download VMD.

Sorry, apparently, I don't have a high enough reputation to cite you all the links. I'm sorry that I had to remove them.


How do special NK cells get to the uterus? When an embryo is creating a placenta in the uterus, some special kinds of Natural killers cell of the mother will move and gather towards this placenta (for exmaple for growth components increasing blood of the placenta). But how do these NK cells know where to go....do they kind of 'smell' the uterus?

They are attracted via chemokines, which are molecules that NK cells sense and move towards the increased chemical gradient.


Ostium: insects circulatory system What is this? Is this a part of the tubular heart? Does it pump hymolymph? Does it have ostium?

I will alter this answer in response to the poster's comments.
Looking at:
https://genent.cals.ncsu.edu/bug-bytes/circulatory-system/
The diagram doesn't show the digestive system - so no anus.
I see that there is expected to be an ostium (hole) near the end of the heart.
Think about where in the heart the many valves are located, then look at the segments of the abdomen and work out what happens with the heart when the abdomen extends or contracts, which you can see in bees.
What is more interesting in all the diagrams is the decision about whether the heart pumps just to the head, or also through pipes to the ventral region.


Neanderthal and modern human population sizes Are there any estimates of both the modern human and Neanderthal population sizes over the last, say, 100 k years? Since "purebread" Neanderthals are extinct, their population has to hit zero; that happened sometime around 30 k years ago. We have good estimates of both the Neanderthal (zero) and modern human (millions, billions) population sizes in the recent past -- what I'm wondering is what the numbers were (roughly) when modern humans and Neanderthals came into contact. How many people were there in each group? How many interbred? Is there any reliable way to estimate those numbers given what we know today? If not, would it be possible, if we sequenced the genomes of a large number of Neanderthal fossils, to get a sense of how much variation there was in their gene pool, and use that to estimate the size of their population? Could we also look at how much of that variation survives today in the homo sapiens gene pool?

In Why Did 6 Great Ape Species Survive But Only 1 Hominid Species? the poster states that "following the eruption of the Toba volcano 70,000 years ago, there were between 1,000 and 10,000 mating pairs of Homo sapiens left." Was the Neanderthal population of a similar order at that time? Was it ever larger than the modern human population? We'll never know the exact numbers -- and the exact numbers don't really matter. I'm interested in orders of magnitude. When homo sapiens and Neanderthals interbred, did sapiens already outnumber them, or were the populations roughly equal? Were the number of Neanderthal - sapiens crosses tiny relative to both populations, or were they perhaps large relative to the smaller of the two populations?

A related question:  Of the Neanderthals living, say, 100 k years ago, what fraction have descendants who are alive today?  Is that a question we can answer either now or in the near future, after sequencing more Neanderthal genomes? According to http://www.nature.com/scitable/knowledge/library/what-happened-to-the-neanderthals-68245020

  recent research on Neanderthal nuclear DNA has found evidence for
  limited admixture: a small portion (up to ~4%) of the genomes of
  non-Africans so far examined may derive from Neanderthals, suggesting
  that interbreeding probably occurred in the Near East during the
  earliest dispersal of modern humans out of Africa, but prior to their
  arrival in Europe (Green et al. 2010). Demographic modeling of
  admixture combined with territorial expansion, however, indicates that
  this level of introgression would be produced under very low (<2%)
  interbreeding rates and strong barriers to reproduction between
  Neanderthals and modern humans, arguing against assimilation (Currat &
  Excoffier 2011). Pending the completion of the Neanderthal genome and
  ancient DNA analyses of early modern Europeans dating to the Upper
  Paleolithic, and following the recent discovery of a third possibly
  coexisting species from Denisova cave (Krause et al. 2010), it is
  premature to conclude that the currently observed level of admixture
  constitutes assimilation.

That would suggest that the fraction of Neanderthals with living descendants is very small -- most Neanderthal lineages died out. What evidence would it take to conclude the reverse -- to conclude that the Neanderthal population was very small, and was largely assimilated?

Briggs et al. 2009, using mtDNA report an estimate of 3500 females. They failed to offer any estimate of the male population size. Their estimates is much  lower than previously thought. They report two hypotheses of why their estimate is so low:

Hypothesis 1 - Low population size

H. neanderthalis population size was indeed really low. After all, they mostly had to live in harsh ice age conditions.

Hypothesis 2 - Slow decline in population size

H. neanderthalis population size were quite high at some point and their population size slowly decreased in size up to the point of being completely wiped out. Such low decline in population size may explain the low level of genetic diversity observed (yielding to an estimate of small population size) in their sample. If the decline of H. neanderthalis was sudden, then even the last survivors of the lineage would have shown quite a high level of genetic diversity. Their decline may have started about 40,000 years with the arrival of Homo sapiens in Europe but this is just a speculation. This second hypothesis is congruent with the evidence of a rather rapid rate of evolution observed in H. neanderthalis

In short, we don't really know what the population size of H. neanderthalis was but it might have been as low as 3500 females only


Why do the sick and unhealthy trees leaf out first in spring? It's spring. The time of year that trees start to leaf out. I have been watching them, and noticed an interesting pattern. The unhealthy trees of a species leafs out first. I've noticed this especially with the wild black cherries. The hollow and damaged trees and the ones in poor conditions leaf out a week ahead of the good ones. The last ones to leaf out are the strongest in the area. This is not just a casual observation, and I have kept careful track of it. What causes this?

Trees that have been dormant over the winter exist on nutrients stored in their roots during fall. When a tree has been damaged or diseased, it may not have been able to store enough nutrients before winter, or may not have enough stored to heal the damage/disease. If the damaged/diseased tree has depleted its winter root stores, it must leaf out (earlier than others of its species) and resume photosynthesis in order to have enough energy to attempt healing itself.


Safety of using industrial water for hand washing Industrial water taps are present in most biology laboratories I have been too. There are accompanied by a sign stating "do not drink". So obviously it is not a good idea to drink it.

However I could not find any information or reference concerning its safety for body use. The only indication I could find is that eye wash stations are using potable water instead of industrial water, suggesting that industrial water is not suitable for eye contact - at least.

My question: is it safe to use industrial water available in labs for hand washing, multiple times per day over the course of several years?

I am looking for a precise answer about the possible long term harm of industrial water in this context, if possible with references.

The water from taps labelled "Industrial Water, Do Not Drink" comes from the same potable water line as domestic taps. The line should be split somewhere in the building, with the industrial line containing multiple backflow inhibitors to prevent cross contamination of potable or domestic water. Based on that fact, the water should be safe for hand washing, however, should be tested in the case of objective concern.


How many possible human genotypes are there that produce distinct phenotypes? This and this Quora question ask how many unique human genotypes are possible. The answers take the combinatorial approach of raising the 4 possible base pairs to a power which is some appreciable fraction of the 3 billion base pairs in the human genome, to get absurdly large numbers like $10^\text{many millions}$. But as many of the answers point out, this is a gigantic overestimate, because the vast majority of those gene sequences wouldn't produce anything remotely resembling a human, and even among the tiny fraction that do, there are enormous numbers of sequences that produce phenotypically identical humans (after all, most mutations don't produce any detectable effect). (When I say that two genomes "produce indistinguishable phenotypes," I am holding the environment fixed and only considering the genome's contribution to the phenotype.)

It seems to me that in order to avoid counting non-human genomes or double-counting phenotypically equivalent genomes, the better approach is use genes rather than base pairs as the combinatorial building blocks. The human genome has at most 20,000 protein-coding genes, and apparently most genes have two alleles, although some have only one and others have more than two. (I'm defining an allele as an equivalence class of phenotypically indistinguishable DNA sequences that form a single viable gene. For the purpose of this calculation, we can mentally group together the two chromosomes' versions of the same gene, and increase our allele count to include any interactions between the two chromosomes' sequences.) [Edit: according to the answer below (which I find much more trustworthy than this Quora link), this is a huge underestimate for the typical number of alleles per gene, with a better estimate being ~300. Needless to say, this dramatically changes the final answer.] This would produce a maximum of $2^{20000} \approx 10^{6020}$ possible phenotypically distinguishable genomes. While this is obviously still an astronomically high number, it's an infinitesimally tiny fraction of the estimates produced in the Quora answers.

Is my reasoning correct?

Is my reasoning correct?

I can see at least five major problems in your reasoning.
Do most genes have two alleles?
The claim that most genes have two alleles is wrong. Actually, the entire top answer in the linked quora post is wrong. The person answering confounds simplified cases used to teach intro genetics class with what nature really looks like.
As about one every 100 nucleotides is a SNP (bionumbers) and given that a gene is on average about 30k sites (bionumbers), the average number of alleles is probably closer to 300 although that would be counting synonymous mutations which is a bit unfair. About 20% of substitutions are synonymous (bionumbers), which would lead to an estimate of 240 alleles per gene on average. Even if you consider that 90% of these mutations have no effect on the phenotype (which is maybe an overestimation, bionumbers), you're left with 24 alleles per gene. Of course, this is a very vague estimate but it is, I think, much better than 2.
Non-coding sequences
Also, the majority of phenotypic distinction is caused by non-coding (non - gene) sequences such as regulatory sequences. You cannot ignore them in the calculation.
According to this pie chart (not sure if we can trust this chart though), 5% of the genome is made of regulatory sequences (against 1.5% of the genome that is coding).
One genotype ≠ one phenotype
If you have in mind that one genotype = one phenotype, then it would be very wrong too. There is environmental variance, epigenetic variance and other sources of variance (e.g. developmental noise) that underly phenotypic variance (see this post to understand the sources of phenotypic variance in populations).
indels and CNV
You are only considering substitutions. There are plenty of indels and ohter CNV too.
The existence of this variation does not only complicate the question, it actually renders the question a bit undefined because if you allow the genome to take any size, then number of possibilities is necessarily infinite.
Diploidy
Your calculations assume individuals are haploids. But humans are diplontic.
Gene are not atomic
Genes are not units that cannot be split. Recombination do happen in genes and it would be wrong to take the number of variants at genes (or at any other type of sequences) as basis for your calculation
Attempt at a calculation
So, ignoring many of the problems, here is my attempt at a calculation.
There are about $1.5 \cdot 10^7$ SNPs in the human genome (bionumbers). Based on this pie chart (not sure if we can trust this chart though), I will assume that about 6.5% of them are in coding or regulatory regions and I will assume (based on that paper) that 90% of them have no fitness effect and by extension I will assume it also mean no phenotypic effect (although the actually percentage should been increased). This will result in $1.5 \cdot 10^7 \cdot 0.065 \cdot 0.1 = 97500$  SNPs of interest. It results into $2^{97500} ≈ 10^{32500}$ possible haplotypes of interest. The number of possible genotypes of interest is therefore $\left(10^{32500}\right)^2 = 10^{65000}$. I also assumed absence of epistatic interactions otherwise the number would become so fantastically closer to infinity!
Interest in the calculation
I fail to find much interest in making such calculation because it entirely depends upon the model we want to consider. There is no offense against the OP's question here (and in fact the OP shows that he understands the importance of the considered model), I just want to make sure readers understand that these calculations are based on a very arbitrary model and one cannot make any sense of the given result without understanding the model.
The calculations from the Quora post that OP linked assumes that every SNP could be polymorphic. As long as the intention behind the calculation is not clearly stated, this is a perfectly reasonable model. Here, in my attempt, I assume that the number of SNPs is fixed, but any combination of it is possible. This can or cannot be a fine assumptions. Also, the estimates of the number of SNPs are of course, estimates of the number of SNPs that are at a frequency that is not too low to be detected! So, if we were, for some reason, to consider all the SNPs (by assuming some drift-mutation equilibrium), then the result would differ quite a bit. But again, it all depends upon the specific model one wants to consider.