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Are mosquitos attracted to farts?
According to wikipedia, female mosquitos (the ones that bite) use the protein in our blood to provide nutrition for their eggs.
I was lying in bed the other day with mosquito's bothering me, and had one coming. So I thought, this will teach these no-good insects to be bothering me! But then it struck me that they might actually like it because of the protein.
Since they're after the protein in our blood, and I'd imagine that a fart is a very creamy soup of proteins indeed, maybe it won't chase them away.
So I held it in. Did I do the right thing?

Lol farts are not a creamy soup of protein. http://www.oddee.com/item_98612.aspx

"I'd imagine that a fart is a very creamy soup of proteins" you sure you're talking about fart here? ;)

I'm voting to close this question as off-topic because we are trying to maintain a scientific stack. Far fetched trivial questions on gaseous (or other rearward O.o) output do not belong here imo.

It is scientific. Just because it is an often humorized subject does NOT invalidate its scientific significance. Why the downvote?

This is a biology forum - It's only natural that such subjects will occur now and then. And what's the point of using unfamiliar terms like 'flatulence' which nobody uses or understands anyways? @AliceD

@MarcoPrins do you mean, in a way, why do we call brain as 'encephalon' even if no layman uses or understands it anyways? Anyways, I downvoted because the base of your question "I'd imagine that a fart is a very creamy soup of proteins" is wrong.

If you rewrote the question with a ton more maturity AND demonstrated that you've done some previous  research of your own (i.e., determining that farts aren't creamy protein soups),  then i  would  consider this  question  on topic. See here  for tips on  writing  good questions on our site.

I confess. I didn't really hold it in.

Apart for the fact that your question is deeply strange, I will try to reply to you.
Mosquitoes are attracted by several factors that make them able to recognize their prey; two of these are: Warm bodies and CO2.
CO2 is the product of your mitochondrial respiration, when you breath out from your lungs you expel liters of this gas.  This is how mosquitoes understand that you are alive. You are warm and you breath !
One of the devices used to kill mosquitoes is in fact a giant vacum  cleaner that warms up till 37°C and emits CO2, by burning gas.
Going forward with your question: Let's speak about farts.
Farts are not "a soup of proteins". Farts are gasses (mostly methane) and CO2 produced by bacterias during the decomposition of the food that you ingest. That is also why your excrements smells more when you don't poop for a long time. They fermented more :P.
So, since it is true that part of a fart is composed by CO2 and they produce a warm cloud around you, I would say YES, they do attract female mosquitoes. But so do you. So release your gasses, or stop to breath at all.
Hope I've replied to all your doubts.
Cheers
I didn't know we were peer-reviewed.
Here my references.
https://en.wikipedia.org/wiki/Flatulence .
https://www.amazon.com/Lehninger-Principles-Biochemistry-Fourth-Nelson/dp/0716743396   .
http://labs.russell.wisc.edu/mosquitosite/preventing-mosquito-bites/carbon-dioxide-baited-mosquito-traps/ .
A biologist.

Please add some references to your answer.


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What is the lifespan of Skeletal Muscle Cells?
I have read that skeletal muscle cells cannot multiply and are generally not created after early development. However, I have also read that they have a "lifespan" of 10-15 years. Could this lifespan actually be referring to the turnover rate of the majority of material in the cell, and that the literal lifespan of the cell (if we count all of its components, including the nucleus) would be the same as that of the owner?

This is a huge debate and I'm guessing you read the lifespan numbers in one of the papers arguing that there is a certain degree of myocyte turnover.

Thanks for the comment, it's nice to know at least some context on the question. It was getting very confusing reading articles that would make arguments with absolute certainty but not qualifying those statements with much specification!

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What is the lifespan of a human skeletal muscle cell (such as in the biceps)?
I have read that most human skeletal muscles (such as those in the biceps) cannot multiply after development (except for exceptional situations of severe damage that involve satellite cells) and that human adults generally have the same number of muscle cells as they did in their childhood or teen years. However, I have also read that skeletal muscle cells have an average lifespan of 10-15 years. If both facts are true, wouldn't that suggest that humans would lose most of their muscle cells by 10-15 years of age? If only the first fact is true, it would seem that the lifespan of skeletal muscle cells is approximately the same as the lifespan of the individual owner.

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Does human skeletal muscle fascia grow new additional collagen in response to increases in skeletal muscle size?
For example, if a human skeletal muscle is growing repeatedly due to periodic weightlifting, does the fascia eventually respond to the increasing volume by growing more quantities of collagen or other components to accommodate the growth? Or rather, does it only expand by "stretching" the existing amount of collagen without the growth of new material to accommodate the changes in muscle size (except perhaps to repair possible wear/damage that might've occurred during exercise)?


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Human and chimp genome sequencing
Can someone comment on this article which claims that biologists have been misleading the masses when they compare the genome of humans and chimps
https://yaqeeninstitute.org/daniel-haqiqatjou/can-islam-object-to-evolution/

Welcome to Biology.SE. The article is very long. I doubt anyone will be willing to read it through and comment on every single claim. Can you please try to narrow your question down to a specific claim?

As a side note, you might want to have a look at Understanding Evolution by UC Berkeley for a short easy introduction to evolutionary biology.

Please note the biologists are not so much misleading any public as most biologists don't talk much to the public anyway. Science communicator can potentially mislead the big public. Most of science communicator are journalists and not researchers.

The article makes more than a dozen different claims, so ask them individually. or create a short list of the ones you are actually concerned with. Although the overarching message of the article is "different studies using different methods come up with slightly different answers therefore they are all completely wrong"

One extreme example can help you understand the article. Human have 23 chromosomes while chimps have 24, however it is painfully easy to demonstrate human Chromosome #2 is Chimp chromosomes 2Q and 2P stuck together at the ends. This could happen in a single mutation in a single germ cell. So, is this one difference (one mutation) or ~200 million differences (the number of base pairs on both). Most scientists would argue it counts as one difference(one fusion) while the article would have you believe it must count as ~200million differences.

Well. Science is a funny thing compared to say the Koren, the Bible or any other religious text. As Scientist learn more, the narrative in Science will change. For instance, in the 1800, there were ideas that there was free following water on Mar... channels and ditches and such. In the 1960s, Mars was considered bone dry. No water ever. A desolate waste land. In the 1990s, Mar considered to have water, but only in the distant past 3 billion years ago. No water now. Then in the 2010s it is now considered to have subsurface water ice, that may occasionally turn into free flowing water under rare conditions. And worst yet, until recently... perhaps all those features of recent running water way have been caused by out gassing of CO2... Conflict over basic interpretation.
Now in that time, religion text, while silence on the matter of Mars, has not changed much if at all. Religious text has stayed the same.
So has Science been misleading the masses on Mars? Does Mars have water? Yes or No? Science keeps flip flopping.
In some ways yes, Science has been misleading the public. It has not been on target with a singular message, unlike say a religious text book, which has been delivering the same unchanging message for a thousand years or so.
So if you are looking for a consist message, well Science way not the thing for you. Science tends to tell different stories as scientist learn more, learn new techniques, re-evaluate ideas and generally fight with among themselves. The holy men Science like to review, rewrite their holy text rather often and fight. And the common man may find that dissatisfying and perhaps worrisome. If holy men keep changing the holy text, how will the common people worship? Is the Science real? Given it changes when the holy text of many world religions have not changed in centuries or even millennia.
So back to article... the percentage similarity of human to chimp genome changes as techniques improve. If you look at the actual age of the citations used in said article.. we run from papers in the 1970s, before genome sequencing was available, and the ideas of one gene-one protein was how Science thought DNA worked, and karyotyping and chromosome banding was about the only means to make large scale chromosome comparison... to papers in the  2014. Where we know DNA does more than just encodes proteins, and non DNA coding are not junk but can encode RNA with biochemical activity (gene regulation, transcription factor regulation etc). And whole human genomes can be sequenced for less than USD 1,400 when it originally cost USD 2.7 billion.
This is nearly 50 years of change and development. Going from the time before the internet and calculators were serious business machines worth thousands of dollars to a time you can have a a 1980s super computer as a wrist watch.
So yes... the message changes. Science progresses, techniques that could only be imagined by previous generations of scientist have become routine. We have learned more.. RNA isn't just a middle man between DNA and protein. One gene can give rise to many proteins.
Have the masses been mislead?
Scientist are telling the Masses information that is to the best of their knowledge. And if the current generation of scientist (2014 scientist) say the past generation (1970s scientist) had it wrong or not quite right.... If scientist right now disagree on the best matrix... is that misleading?
A science book is not as safe as a religious text. And one of the worst offenders is biology. A biology text book book from the 1980s looks very different from 2010s, even if they are from the same series. Is that misleading or is that scientific advancement?
PS: Common genes and sequence identity is not the same. There is a bit of confusion in the article. A cat and a human may share many many genes. But those shared genes may have sequence difference between them. So you can say humans and cat share 90% (made up example) of their gene (ie both cat and human have the PTEN gene) but have only 70% (made up example) sequence identity (ie there are several DNA difference between the human PTEN gene and the cat PTEN gene). It is easy to confuse the two.
Also are you only only considering gene coding DNA? Or are you also considering the non coding DNA (which until cheap genome sequencing in the 2010s was extremely difficult to capture and sequence)

Most of your answer has little to do with biology but rather philosophy of biology. And IMO, you miss the point of the paper. The paper says what many fail to understand is that what is found in scientific literature and what is reported to the lay public are sometimes worlds apart. It for example discusses the fact that such percentage of similarity are computed only on what we managed to align. There entire sequence that won't align at all. It also does not make consideration of CNV.

The author also argues that the feeling that is transmitted by this high precentage is misleading if it not presented to the public the percentage of similarity between human and cat for example which is at 90%.

I would like to point out that scientific literature being use in that article range from the 1970s to the 2014s. So obviously over the nearly 50 years of time the results of papers will be different. The techniques used to make the human chimp genome comparison changed from karyotyping/chromosome banding pattern, to cDNA comparison, to whole genome comparison. The answers will be different.

What is reported to the public will change... and if reporters look up old text books of just google a number... they will get different numbers.

I can comment.
From your article:

Is 99% human-chimp genome similarity less impressive in light of the fact that domestic cats share 90% of their genes with humans and yeast share over 30% of their genes with us, etc.? What should we make of these various quantitative comparisons? In reality, it is difficult to make sense of these percentages without a uniform metric to reference. Unfortunately, the biological sciences do not provide one.

The public has not been misled. The fact is that chimps and humans share 99% of their genes. The rest is interpretation. The rest is extrapolation. The rest is philosophy.
As a biologist, it's absolutely no surprise to me that we share a lot of our genome with cats, earthworms and even yeast. We do presumably because successful life on the planet Earth takes particular biological processes which are shared. We live in a Nitrogen-Oxygen atmosphere; we have carbon-based energy sources; we need to have similar enzymes to use oxygen and carbon, etc.
Beyond that, scientists have opinions they share. But no one is forcing you to believe a particular interpretation. I happen to believe in what makes the most sense. You can believe in what makes less sense if you prefer. Have there been misrepresentations? Absolutely, but that is often because journalists sharing the information misunderstand it. One of the most misunderstood papers I've seen is Sex Differences in Brain Gray and White Matter in Healthy Young Adults: Correlations with Cognitive Performance by Ger et al. It has been repeatedly and widely inaccurately represented in the lay press, partly (or perhaps wholly) because it is not a particularly well-written paper though the science in it is sound.
Don't assign blame for any belief to science just because you want it to say something different.


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Insect ID, found in shower, northeast USA

I want to know if this is the kind of critter that will lay eggs in the drain and then have larvae emerge from there. We had that a few years ago and it was nasty...

That is a silverfish (Order, Zygentoma). The most common species of household silverfish is Lepisma saccharina. Details can be found here. https://en.wikipedia.org/wiki/Silverfish
They are relatively harmless.

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What made this tiny honeycomb-like structure?

I found this on the ground in Maryland.  I believe the twig is from a tulip poplar tree.  The structure looks like a tiny honeycomb except that the cells are individual tubes rather than a true hexagonal honeycomb shape.  It's one layer deep and wraps completely around the branch.  I assume it was made by some tiny insect, but what?

Many insects lay eggs in tight clusters; because of the shape of the eggs (like honeycomb cells themselves), the cluster looks a bit like a honeycomb.  If you had a high quality macro shot, the eggs might be easier to identify definitively.
Newly hatched Beet Armyworms:

Wheel Bug (Arilus cristatus) Eggs:

Wheel bugs are common in eastern North America, but are confirmed to occupy areas of Mexico and Guatemala.

With wheel bug for size:

My guess is that you found a cluster of Wheel Bug eggs.

Females lay eggs at a low elevation on trees, bushes, twigs, and other objects.[5] Secreted glue serves as an adhesive which maintains the cluster formation of the eggs. - Wikipedia


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Does crossover happen between chromosomes from grandparents?
Rephrasing question: does crossover happen after sperm and egg meet each other, but before formed fetus starts to grow?
As I understand sperm and egg of human are haploid cells. That means this cells undergone meiosis and chromosomes crossover before meet each other. If so then crossover happened between a pair of chromosomes which came from parents of the parent of the fetus, not between chromosomes of mother and father of the fetus.
Am I wrong?

No, you are right.

Your question and your rephrased question aren't asking the same thing, so you may want to edit your question.
Crossover occurs during meiosis, which is a type of cell division that occurs in the generation of gametes, during which of course only the chromosomes from one of the eventual parents would be present. Meiosis doesn't occur in the fetus, except eventually in the germ line cells.

Thanks for answer. So crossover happen before sperm and egg cells meet each other, right?

@wandalen Yes: it occurs when the progenitors of those cells divide to produce gametes.


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DNA base pair heading
Does it make ANY difference to which strand of DNA double helix base pair heads? I mean, could base pair AT and base pair TA makes any difference when interpreted by biochemical mechanisms which use DNA?
Double helix has two strands, right? So does pair Adenine on the first and Thymine on the second strand make any difference with Adenine on the second and Thymine on the first?
I am a novice in biochemistry, so please excuse me my ignorance if the question is ridiculous.

Absolutely yes, is the short answer.
All genes are encoded in a  5-prime $\rightarrow$ 3-prime manner on each of the 2 DNA strands of the double helix.
Here's an example of a stretch of the genome from a bacteria that I work on in my PhD:

Each of the blue boxes is a separate gene. You can see they're able to be encoded on both strands, and run in opposite directions.
Consequently, whether a base pair is AT or TA changes the overall sequence, and would affect any gene which happens to span that base pair.

When reading the DNA during transcription, the strand that the gene resides on is called the Template (sometimes "Sense") strand.

The strand is separated by RNA polymerase enzymes, and it then uses the opposite strand of the DNA, known as the "anti-sense" strand, to create a copy of the gene sequence, but in RNA instead of DNA (and Thmidine bases are substituted for Uracil, as in the diagram).
Thus, the polymerase creates a mirror image of a mirror image, restoring the sequence of the original strand, but in it's RNA representation.
Flipping the bases round in the helix would change the sequence in the DNA molecule, and this would be propagated by the enzymes etc. which rely on it for transcription and replication.


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What is this fluffy bug?
I found this bug (actually he found me) while walking through some bushes in the city (Iași, Romania).
It is a small bug, a quarter of a fingernail, white and a fluff tail. He lays a white fluff on bushes (that is how I meet him, I brushed the bush and got the white fluff on me, when I wanted to clean it off I saw 2 moving on my shirt) and it seems they stay around it. I also found it near the plants, on a stone pavement, but I presume he got lost.

The overall shape suggests a leafhopper or planthopper of some type. I can't identify the exact species. But there are species known to produce white wax structures that might explain the fluff.

Based on the image and on the description, it could be a woolly aphid, a kind of insect that produces filaments of a waxy, cotton-like substance that gives them a fluffy appearance.
The images on Wikipedia aren't convincingly similar, but I found a better reference on abundantnature.com:


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Is diabetes (type 2) a genetic disease?
My friend's father has diabetes (who was diagnosed with diabetes long after my friend's  birth). The doctor told the friend that he has more chances of getting diabetes than a normal person and he must make lifestyle changes as he is more likely to get the disease. Does it mean that diabetes is genetic (hereditary)?

According to Wikipedia there is a genetic component to the risk of developing type 2 diabetes. The page cites this source at the US National Institutes of Health. There is also a Wikipedia page on genetic causes of Type 2 diabetes

The trouble with questions like this--"is this disease genetic?"--is that diseases are complicated phenotypes that arise from interactions with both individuals' genetic makeup and also the changes in gene expression that happen as a result of the environment of that individual over their lifetime.
To put it another way: neither nature without nurture nor nurture without nature are particularly interesting, because the first amounts to a little vial of DNA in a microcentrifuge tube and the second amounts to, uh, a whole lot of nothing.
In the case of Type II diabetes, there is both a strong environmental component--persistent obesity in humans is so likely to lead to diabetes that one of the two original mouse obesity model strains was named 'db' for diabetes--and also a genetic component that affects the likelihood of developing Type II diabetes in a number of ways. Some genetic variants may be less likely to develop obesity even under the high-fat diets that typically are used to create obese phenotypes in mice. Some variants may be more or less likely to develop insulin resistance even in the presence of high levels of adipose tissue. Both of these variations would affect your likelihood of getting Type II diabetes... depending on your environment and the level of body fat you carry, and that last one is going to be dependent on not only your genetic makeup but also your environment and (almost certainly) epigenetic influences from your parents.
With respect to Type II diabetes and actual specific genetic variations that have been identified, there's the twin study cited in another answer here, which was done in Danish twins and really just looked at whether there was a genetic component done at all. GWAS studies have, predictably, resulted in several candidate loci, all with relatively small effects on risk--which makes sense, because metabolism is a complex thing and many players are probably involved in competing roles. (I'd link more, but I'm new here--hitting up a Google Scholar search for "type ii diabetes genetic variance" nets you a whole bunch more GWAS studies talking about specific types of variation noted.)


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Which cells produce HCl produced in stomach? Don't these cells get destroyed by HCl?
Which cells produce HCl produced in the stomach? Or is HCl produced due to the translation of proteins. Don't these cells get destroyed by HCl?


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All somatic cells contain the same genome, then how does it knows that it should develop into a specific organ?
All somatic cells contain the same genome, then how it knows that it should develop into a specific organ. In https://www.youtube.com/watch?v=aeAL6xThfL8, Joe Hanson says that each cell has the same book that each has 20,000 same instructions. And each cell has bookmarks, where it finds which instructions to read.
Can you tell me where these bookmarks are stored in the cells? Is it outside the chromosomes or outside nucleus?

The answer to your question is not really know yet and there is whole scientific field dedicated to it: developmental biology. I'll try to explain the basics however:
Like you described the identity of a cell (its cell type; which organ it belongs to) is dependent on which of (actually) ~30000 human genes are activated (or read) in that cell. There are two fundamentally different ways this is done in cells:

Transcription factors:

These are proteins that bind to specific (regulatory) DNA sequences and thereby lead to the activation (or repression) of certain - usually nearby - genes. Since they are proteins, their own genes have to be activated in the first place, so we already at a 'chicken or the egg' type of problem. In principle proteins can 'survive' outside the nucleus of the cell for some time, but they are usually degraded within a few hours, so I guess the remaining factors from the mother cell are not very important (I have no idea if anyone ever checked this).
Additionally many transcription factors are not constitutively active, but are waiting for some outside (from the perspective of the cell) signal. These could be certain developmental signals, growth factors, hormones or environmental factors like nutrient availability (the list goes on ...). During embryo (& therefore organ) development not only the presence of these signals (morphogens), but also their intensity are a very important factor in determining the 'fate' of a given cell.

Epigenetics

The term epigenetics describes genetic regulation that does not happen on the sequence level. Instead the accessibility of the DNA is regulated through modifications of histones (which are part of the chromosomes) and the DNA itself. Thereby the cell can almost permanently shut down certain genes. Since epigenetics are also inherited during cell division, this regulation affects whole cell lineages and is therefore very important in regulating which cells are active in certain organs or tissues.

Do you have a citation for the number of genes?

@canadianer I had the number in my head from working with NCBI data. I just looked for references: the often cited ~20000 is for protein-coding genes only, so I guess that why so different numbers are used. I tried to get the number of annotated genes from the human genome from NCBI but couldn't find it. This older book say 30k-40k genes (scroll to 'The functions of human genes'), I didnt find a better source at NCBI right now.

Thanks. I had always heard ~20,000 genes as well, but if that is just protein coding then a higher figure makes sense.


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Control of neural systems
It turns out that my work in nonlinear dynamics directly maps to Integrate and Fire models and could even provide a new way to control them (manipulate the firing rates). However, it is unclear to me if my findings are interesting or just old news.
I am looking for literature on the intersection of control and neuroscience. Specifically I am interested in any research, theoretical, experimental or simulation-based that dwells on the control of neural systems.
I am especially interested in any work that takes a mathematical point of view on this issue and on any work that summarises the state of art in this field.
Forgive me is this seems trivial to you, but coming form complex systems theory I did my best and found nothing.

I think this is a very interesting field but I don't think your question is very well-suited to Biology.SE. You don't have any specific question, you are just asking for some literature that would effectively describe the entirety of the field of theoretical and computational neuroscience. I will say though that the fields of control theory and computational neuroscience are closely intertwined. I don't know what search terms you are using but I am surprised you aren't finding anything. Try adding "neural" to any searches you would do in your field.

It seems to me that I am a little more specific than this, I am not looking into the entirety of theoretical and computational neuroscience but merely its connections with control theory. Perhaps this is still a huge field, in that case there could be for example a textbooks worth mentioning? I deeply thank you for your input, neural is in my list along with control.

Yes, applications of nonlinear dynamics to neural control is still too broad of a field to make an answerable question.

https://scholar.google.com/scholar?hl=en&q=control+theory+neuroscience

https://scholar.google.com/scholar?q=control+theory+neural

Ok, so how should I proceed? remove the question?
Personally, I think it still has something to teach. A person in my situation would be actually benefited a little but by finding out that he has to pinpoint the question further. Please let me know the canonical course of action and I will follow it immediately.


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Spatiotemporal patterns in neural networks
It turns out that my work in nonlinear dynamics directly maps to a close variant of the Integrate and Fire model. My model produces spatiotemporal patterns that resemble foam. I have to stress that this is  the result of an exceedingly simple model of neuronal activity.
The plot below visualizes the voltage levels of a network of neurons. Yellow is high, purple is low.

I am wondering is these patterns are relevant to the computational neuroscience community. To this end, I am looking for literature describing spatiotemporal patterns in (preferably biological) neural systems.
I am especially interested in any work that  proposes metrics that characterise such patterns since this would allow for a quantitative comparison with my results.
Forgive me is this seems trivial to you, but coming form complex systems theory I did my best and found nothing.

Maybe look at the neural correlation literature? It often involves looking at statistical structures (patterns) of population codes.

I will take a look as you suggest.  The term population codes is very useful to me. Can you make your direction more precise (specific book/paper)? I know I am asking for a lot.

Unfortunately, I haven't looked at this sort of literature for a long time, but here are some thoughts with which to start.
Your question is about "spatiotemporal patterns" of neural systems. One of the first things that comes to mind is neural oscillations (e.g. alpha waves). This is essentially looking for the presence of "frequency patterns" in the neural system. This has a huge amount of literature.
Another methodology that comes to mind is the graph-theoretic approach. In essence, functional or anatomical activity is used to build a graph, which can be analyzed for patterns (i.e. special properties of the graphs of neural systems that are, say, shared across species). One paper: Complex brain networks: graph theoretical analysis of structural and functional systems by
Bullmore and Sporns.
Separately, I might think about the neural correlations literature. Essentially, this is analyzing a neural population by examining the correlation structure of its members, and looking for patterns within it (i.e. that characterize the population code of the system). Two review papers: Neural correlations, population coding, and computation by Averbeck et al
and Measuring and interpreting neural correlations by Cohen and Kohn.
For a review on population codes, see Information processing with population codes by Pouget et al.
This notion is sort of orthogonal to the notion of sparse coding in neural networks, more prevalent in sensory perception.
Sorry if this is broad, but then again I feel the question is quite broad as well. If you have more specific questions, let me know.

This is broad, just like the question is. As someone coming form a different field, this is what I wanted, general directions. Thank you.


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Why do humans not have a powerful sense of smell?
It seems like a useful ability to be able to detect many different things about, say, another organism. A lot of mammals have this ability. Why not humans? Did we evolve it out or never develop it?

Note that human smell might not be as poor as thought: http://news.rutgers.edu/research-news/human-sense-smell-it%E2%80%99s-stronger-we-think/20170508

Humans' poor sense of smell is a myth, borne of 19th century speculation rather than actual data. This is described in an excellent recent paper in Science , "Poor human olfaction is a 19th-century myth" by John P. McGann. Quoting from a recent blog post of mine,

The myth dates to the work of the pioneering and hugely influential
  anatomist and anthropologist Paul Broca, who concluded that the
  relatively small olfactory bulbs in humans and other primates enabled
  the occupancy of this space by facilities of intelligence and even
  free will: “…it is no longer the sense of smell that guides the
  animal: it’s intelligence enlightened by all the senses… This is the
  cause of the atrophy of the olfactory apparatus of primates." This
  presumed “atrophy” and poor sense of smell however, were not based on
  any actual data on primates’ sense of smell! The myth propagated and
  expanded in the 20th century, becoming dogma. Back in the 19th, even
  Freud weighed in, noting that the lack of a strong sense of smell
  contributed, in humans compared to other animals, to sexual repression
  and mental disorders.

Humans, when trained, smell quite well, and can for example follow scent trails through grassy fields. Interestingly, the number of olfactory neurons is very similar in humans and other mammals (plotted in the aforementioned post).

Your first link is broken. But, please don't just mention the link. It's better if you some words of the link so that we can have a gist of what you want to say.

@Mockingbird. Good points -- I've edited the post. About the link: I don't know why it doesn't work; I've given a partial reference, also, so it can easily be Googled.

In that case, how come hunters often complain that their prey can smell them from dozens of meters, yet you hardly ever hear of a human hunter tracking his quarry by smell?

There are several factors in human.

we are upright, which brings the nose just about as far away for scents as it can get, you want your nose as close to the ground as possible for the most efficient use scent. This is not in and of itself a deal breaker but it is an important factor which made smell less important for us.
Our large brain is competing for space with our sinuses and nasal cavity. So in turn we have lost a great deal of our nasal cavity as our brain has increased in size, some even speculate this is why we have a protruding nose becasue part of the function of that cavity is thermoregulation and air filtering and the protruding nose helps compensate. The shrinking of our face and snout has pushed this even harder. the less space you have in the nasal cavity the less space you have for olfactory receptors, which reduces the number of distinct smells you can detect.
primates in general have poorer senses of smells than other mammals , they have much better vision however, so the lose of smell was an evolutionary  trade off. So humans  were starting with a handicap to begin with.

Keep in mind humans still get a lot of information from out sense of smell, but not all of it is conscious. Nearly everything you think of as "taste" is actually smell.

The order of senses from strongest to weakest or more important to less important is basically opinion based. Some would say smell is less important, other would say hearing or some might say taste.

"The sense of smell is not powerful in humans" is absolutely false. They are very powerful as it seems and can be considered as the most powerful sense in human beings. Check this Youtube video which explains why smell is the most powerful sense in organs. What makes sense of smell most powerful is due to its spontaneous ability to trigger and revive memories and emotions. According to this site:

The sense of smell is closely linked with memory, probably more so than any of our other senses.  Those with full olfactory function
  may be able to think of smells that evoke particular memories; the
  scent of an orchard in blossom conjuring up recollections of a
  childhood picnic, for example.  This can often happen spontaneously,
  with a smell acting as a trigger in recalling a long-forgotten event
  or experience.
In addition to being the sense most closely linked to memory, smell is
  also highly emotive.  The perfume industry is built around this
  connection, with perfumers developing fragrances that seek to convey a
  vast array of emotions and feelings; from desire to power, vitality to
  relaxation.
On a more personal level, smell is extremely important when it comes
  to attraction between two people.  Research has shown that our body
  odour, produced by the genes which make up our immune system, can help
  us subconsciously choose our partners – read more here.  Kissing is
  thought by some scientists to have developed from sniffing; that first
  kiss being essentially a primal behaviour during which we smell and
  taste our partner to decide if they are a match.

Smell is closely related to association and was the first sense to get evolved.

The sense of smell was probably the first sense to evolve in a living
  creature. In many animal species, smell can play a critical role in
  finding a mate, communicating with other animals or helping them to
  survive by finding food. Clearly, though, in humans, smell does not
  carry the importance that it does in other species.

But the sense of smell is overshadowed by other senses particularly vision because it is most well develop and important sense in human beings.(here, here, here, here) but actually smell is the powerful of them all.
The weakest sense in human beings would be taste.(here, here).

This is a question relegated to evolutionary biology.  Our sense of smell is as it is because that is part of our evolution and it is what works best for us. Also consider that you used the word "powerful" The word is arbitrary when comparing the sense to other animals. The more sensitive sense of smell in dogs for example is tied to their survival

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Inheriting Modified DNA after CRISPR editing
If CRISPR is used to modify the DNA sequence to cure a disease - say MS in a woman - will the RNA guides also modify the sequence in her eggs so her children could be born without MS inherited from her.

First off, CRISPR can't be used to cure diseases in an adult human or, more generally, for any adult vertebrate at present.
As you can see in this paper, a major problem with CRISPR is it has to target specific cell types in tissues. As long as the targets are somatic and not germline, the edits made by CRISPR will not be heritable.


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same SNP rs# referenced to be found in two different genes
Two GWAS papers have referenced the same SNP (rs7442295), but one states it's found in the gene GLUT9 and the other states it's found in SCL2A9. The ncbi dbSNP says it's in SCL2A9, and I thought that the rs number was unique to each SNP, so how can it be in two different genes? I'm really new to GWAS, so it might be a really stupid question, but any advice would be great!

The NCBI dbSNP entry shows rs7442295 to be in the gene SLC2A9, not SCL2A9 stated in the original question.
As the Wikipedia article for SLC2A9 says, synonymous names for SLC2A9 include:

solute carrier family 2 (facilitated glucose transporter), member 9, GLUT9, GLUTX, UAQTL2, URATv1, solute carrier family 2 member 9

So GLUT9 and SLC2A9 refer to the same gene, and the two papers are not in conflict about the location of the rs7442295 SNP.

Both mutations have caused the same changes in serum uric acid. In other words, one of those papers is older. Those are the same genes.


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Biology experiment with algae method help
I'm planning a biology experiment I need to complete. I was planning on measuring the affect of pH on algae growth. I chose chlorella to be the test algae I use (are there any algae that would be easier to test?) and I have no idea how to measure the growth. My school does not have a spectophotometer, just basic biology and chemistry stuff. Also how can I change the pH of the water for my different samples? I'm a beginner and don't really have much experience so any help is appreciated!

For growth you could measure the mass of algae before and after the experiment. If you have a centrifuge you can pellet the cells or use a filter to remove the culture medium. Alternatively, if you have access to a hemocytometer and a microscope, you could get an accurate cell count that way.
For controlling pH, you'll need a buffer in your culture medium. You should select a buffer with a pKa close to the pH you want to test and then titrate the pH of the medium with a strong acid or base (HCl or NaOH). Make sure to check the pH before and after the experiment to be sure that it didn't change due to growth of the algae.

Maybe also mention cell counting with a haemocytometer- although these are not inexpensive.

@AlanBoyd Neither are microscopes...

A slower but easier way than pelleting in a centrifuge is pour off the water and let the algae dry out, then weigh the dried mass.
Get pH paper to check pH of each grow cup full of algae each day.
You can raise pH to around 8 with baking soda (sodium bicarbonate).
You can buy sodium carbonate (washing soda) in a hardware store.  It is cheap.  That will get your pH to 10+ which is higher than you need.

Make sure to get pure stuff, not with additives like perfume or other surfactants.
You can lower pH down to 2.5 with ascorbic acid or vitamin C.  A bottle of 100 is cheap and they crush easily.
Get a bunch of jars or old soda bottles and in each one make a bunch of solution of the pH you want.  So you will have a 2.5 stock bottle, a 3 stock bottle, a 4, a 5 on up.  Then you can top up your algae grow jars as they dry out.  Or better: pour out the old water and pour in new.  Don't pour out your algae by accident.
Last: you want this algae to grow like mad when conditions are good.  Pure water will be low on nutrients.  I recommend a dilute solution of Miracle Grow.

Maybe a teaspoon per liter.
I can envision 8 2liter soda bottles, each filled up and each with a different pH made either with washing soda or vitamin C.  Each 2L bottle has 2 tsp of miracle grow in it.
Each algae grow jar is a 12 or 20 ml drinking water bottle.  3 bottles per pH level.  Big number on each showing pH.  Put them in a row in the sun.  Change the water every 2 days.  Take a photo every day.
When you are done fish out the seaweed and dry it.

I've never worked with algae, but can you be sure that you aren't pouring out cells with the medium?

The algae will probably grow as a sticky mat.  A few lost cells will not matter.   You can hold it down with a spoon and pour out most of the water then replace.  Check this.  http://irnas.eu/bio%20lab%20symbiolab/2016/06/03/collecting-and-growing-algae   An idea: just use scummy pond water.  What grows, grows.  You will still be able to determine biomass at the end.  But you may find different organism types take over the jar at different pH which is also very cool and shows the flexibility of an ecosystem.


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How long can you store tissue on 4°C before B-cell extraction and culture?
We receive tissue regularly and extract B-cells for culturing, studying differentiation and survival with diffenet stimulation conditions. However, often the tissue arrives late afternoon and might be put in FCS at 4°C overnight before cell aextarction. I'm not sure however if such storage would impact the viability or functionality of B-cells later on during the culture.


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Wikibooks claim that it is difficult to find two texts that agree on the definition of an animal
In this entry of Wikibooks we find the claim

It is surprisingly difficult to find two texts that agree on a precise definition of an animal.

Is this true?
[I know nothing about biology, but I find this claim perplexing.]

Definition of Animal
Animal is typically defined phylogenetically (just like any other monophyletic taxon; see here for intro to phylogeny). Any lineage part of the taxon Animalia (aka metazoa) is an animal. This is the definition given by wikipedia > Animal. You can find the animals here on the tree of eukaryotes.
Issue with the claim

It is surprisingly difficult to find two texts that agree on a precise definition of an animal.

This claim is pretty clumsy in my opinion. It sure can be hard to find a set of phenotypic traits that would group all animals together but it does not mean it is hard to define 'animal'.
IMO, what they meant is

It is surprisingly difficult to find a set of phenotypic traits the are shared by all animals and by none of the living organism that is are not animal.

This claim would make more sense. It is indeed true that it is hard to make such set of phenotypic traits. There are plenty of non-animals that are heterotrophic eukaryotes (such as fungi), there is at least one animal that is (at least partially) autotroph (Elysia chlorotica), not all animals have a nervous system, etc...

Thanks! +1. I tried to edit your answer by changing "triats" to "traits", but the software told me that edits must be at least 6 characters long.


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How did giant sauropods satisfy their daily energy needs, considering their relatively small mouths?
Gigantic sauropod dinosaurs had relatively small heads (and consequently small mouths) in comparison to their overall body mass.
In the book "Dinosaur Odyssey: Fossil Threads in the Web of Life" (by Scott D. Sampson) the author says (on pp. 218-219) that

The sheer size of the biggest sauropods has long shrouded them in
  mystery. How could such gigantic animals with such small heads (at
  least compared to their body sizes) manage to consume enough food to
  sustain themselves? The mystery deepens when we look inside the
  mouths of sauropods. Cows are typical of big mammalian herbivores
  (e.g. elephants, deer, antelope, and the like) in possessing oversized
  teeth well suited for processing large amounts of fodder. Chewing
  serves not only to break food-items into bite-size chunks' it also
  grinds up the plant matter and begins the process of digestion by
  making the bits of vegetation more susceptible to chemical attack. By
  comparison, sauropods have puny teeth well suited to tearing or, at
  best, slicing, but not for grinding.

(emphasis added)
I don't remember Dr. Scott providing an explicit answer to the question "How could such gigantic animals with such small heads (at least compared to their body sizes) manage to consume enough food to sustain themselves?" but somewhere in the book he did mention that the earth's ecosystem may have been rather different back then.
However, since the book came out nearly a decade ago, I was curious on whether any other findings have been made since then.
How did sauropods manage to consume enough food to sustain themselves? Was it because of some differences in the ecosystem that are now lost?

Unlike mammals, saurischian dinosaurs don't have to chew their food. Like birds they have a gizzard to do that instead.
Look at a modern ostriches: they have a very small head because the head is only used to gather food not process it. Mammals process food in the head (chewing) so the head has to be large to support the muscles, teeth, and other apparatus for this. On the other hand, birds and sauropods use stones in the gizzard to grind up their food, so all that space is taken up in the torso instead of the head.  Ornithischian dinosaurs, which do chew, have large heads just like mammals.
Additionally since the mouth is not occupied chewing the time that would be lost chewing can be spent feeding instead. This can be a lot of time a cow spends 8 hours a day just chewing.
Source

Note several things:

Their long neck allow them access to a lot of food enabling to broswe with minimal movement and energy consumption.
The sauropods had very big and long digestive system, and they probably also used gastroliths. These allowed them to process the food without chewing it in their mouths.
I didn't relate to the question rather they were "cold blooded" or "warm blooded". If they were partially cold blooded (mesothermic) then they would need less food than a warm blooded critter of their size.
I guess the vast majority of their diurnal activity was eating... a lot.

Hope it helps.

What you say about high O2 is true for the Carboniferous. Actually through at least the Triassic and Jurassic, pO2 was below present levels. https://www.annualreviews.org/doi/10.1146/annurev.earth.31.100901.141329

Point 1 here is wrong, as @kmm says. Point 2 is speculation, based on an incorrect fact that doesn't lead to the conclusion anyway. Remove those and the remaining points would make a decent answer if any references were given; there are many references to support those points so it shouldn't be hard

I removed them.


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Does Batesian mimicry rely on constant reinforcement?
If the species being mimicked, the monarch butterfly, for instance, were to become extinct, would the species mimicking it loose all of the benefit gained by their Batesian mimicry immediately?
I realize that the Monarch may be a poor example as it is a Müllerian mimic with the Viceroy butterfly, however their ranges do not overlap everywhere. Would the extinction of the monarch reduce the ranges of Batesian mimics to that of the Viceroy?


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In this poisson distribution in olfactory receptor (OR) pseudogenes neutral mutation rate, how is the mean used?
The 2005 paper A comparison of the human and chimpanzee olfactory receptor gene repertoires describes a poisson distribution, with a mean of 0.701
From that mean, how is the gene disruption rate of 1kb per year calculated? And, how is the age 3.86 Ma for relaxation of selective constraint calculated from (0.451/0.701)·6 Mya = 3.86 Mya?
The parts of the paper,

TL;DR How is mean = 0.701 used to calculate stuff in that paper?

Do they have a typo/miscalculation? λ=0.701 is the mean number of disruptions per shared pseudogene since the last common ancestor (6 Mya). Therefore, the neutral gene disruption rate is 0.701 / 6 Ma = 1.17·10$^{-7}$ disruptions/gene/year. This value differs from the paper by a factor of 10.

They also report the mean number of CDS disruptions per human specific pseudogenes was 0.480, but then used 0.451 in the subsequent calculation. As far as I can tell (which is not very far), this is also a typo. However, this is not my field and so it is more likely that I am wrong.

Does 1.17*10^−7 disruptions/gene/year mean roughly 1 disruption per gene over 8.547 million years?

I am having a bit of trouble understanding what 1 disruption/gene/8.547Ma would mean. Is a disruption defined as anything from a single base-pair mutation, to a whole codon or similar being replaced/lost in transcription? If so, then with around 400 shared pseudogenes, and 1 base pair mutation per gene, that sounds like a lot less then 0.1kb per year since every base pair is 2 bits. Sounds more like 800 bits per 8.5 million years, which is 0.1 kb


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How do Apes get their Omega 3s in the wild given so few plant sources? Are they able to convert it to DHA?
Given so few plant sources(around 6-7) of ALA, how do Apes get ALA in the wild?
Are they able to convert it into DHA in satisfactory amounts?

I am not sure they as much as a human, at least their brain is smaller afaik. and humans need is mostly for the membrane of brain cells. Another thought that from cardiovascular perspective you can compensate the missing omega-3 with omega-9. At least I have pretty good LDL/HDL ratio and I eat mostly omega-9 from olives instead of omega-3. We don't have sea nearby...


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bacterium ability to metabolize a compound toxic to most other organisms, do not know how the bacterium takes up the compound from the environment
A new bacterium is discovered that has a unique ability to metabolize a compound toxic to most other organisms. The microbiologists researching this bacterium do not know how the bacterium takes up the compound from the environment. Design an experiment to determine whether uptake is passive or active.

Please refrain from copy-pasting your homework questions in Biology.SE, instead try researching the answer yourself to show some effort and then frame a question that helps you understand the concept.

Assume that the toxic compound is some form of liquid (water or oil soluble).
Take a sample of the bacteria and irradiate them (inactivate them permanently). Immerse the inactive bacteria in the toxic liquid for a certain amount of time.
Remove the bacteria later, "wash" them off (against a sieve designed to filter bacteria) for toxin traces that could be on the membrane or cell wall, then liquefy the bacteria and test for presence of the toxic compound. If the uptake is active, there shouldn't be any of the toxic compound in the bacterium.


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Botany inquiry about tropism
Can anyone explain the mechanism of hydrotropism and what kind of plant hormone involved?
Our teacher says that it hasn't been proven yet. I looked up many data only to find about the phenomenon of this effect.


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Identification of a caterpillar from NY
I recently camped at Harriman State Park in Southern New York, in early October.  Upon returning home, I noticed that I had a passenger with me.
The caterpillar in question is an almost translucent, pale green color with a single reddish stripe running down the center of the back.  It is approximately 1.5 inches long, with a reddish face as well.
I tried using a caterpillar identification book, but the closest one I could find also had a split tail, which this one does not.

Based on this picture, I'd say it's a Macrurocampa marthesia. I realize your specimen lacks the split tail, but I note that the "tails" of the larva of this species are longer in earlier instars. I wonder if this one is just an older caterpillar, getting ready to pupate? The image is a very good match otherwise, and this species does occur in the appropriate range.

That sounds fairly reasonable.  Doing a search for it gives me a picture that looks even more similar to mine.  The diamond shapes on the mid-back seem quite distinctive.
I wouldn't be surprised if it was an older caterpillar, it did seem quite pudgy.


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Plant growing very rapidly near my house
please see attached photos of a plant, that is growing rapidly near my house. All my friends failed to classify this plant. Can any botanist/biologist help to discover the species of this plant?
Thank you in advance!

Help us. Where do you live?

It looks like a young Empress Tree (Paulownia tomentosa)
Native to China, it is an invasive species in the USA. looks beautiful when full grown however


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Please explain this notation MW around 9 MDa
I am a computational science student and was reading about the structure of Pyruvate dehydrogenase (PDH).
link to article
The article mentions "PDH is a large complex (MW around 9 MDa) consisting of multiple copies of three enzymes."
What does MW around 9 MDa denote ?
I am not a regular student of biology but rather an engineering student so please try to provide simple explanations.

MW is Molecular Weight, or the mass of 1 mole of the protein. 9 MDa is 9 million Daltons, and 1 Dalton is 1 gram per mole. So a mole of PDH is about 9 million grams.

One Dalton = 1.66×10⁻²⁷ kg and one mole = 6.023 10²³ molecules.

The molecular weight of PDH enzyme is approximately 9$\times$10$^6$ gm/mol
The Dalton (or atomic mass unit (amu) ) is a unit of mass defined as 1/12 weight of carbon-12 atom in  ground state.
1 Da  = 1/12 m(12C)
The number of atoms in 1 mole is Avogadro's number (6.023 x 10^23) so weight of 1 carbon atom is   =   (12/ 6.023 x 10^23 ) g
This means 1Da (1 amu)  = 1/12 x (12/ 6.023 x 10^23 ) g = 1/ 6.023 x 10^23 g  which is g/mole
(1 MOLE = 6.023 x 10^23 )
=> 1 Da = 1g/mole


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If animals aren't getting tooth decay because they don't eat processed foods, could similar work for humans?
In previous question here on stackexchange biology I read that animals don't get dental caries because they aren't exposed to refined carbohydrates like sugars. My question is: in theory, could a human be completely dental caries-free if he followed the diet of not eating any processed food? :))
And also, are fruits like apple or orange 'safe' against dental caries? (since they're not 'processed' sugars?) Thank you kindly for answers.

What does "processed" sugar make bad? It comes in high concentrations and is ubiquitous, but else? It is purified (not more) from a natural source (either sugar cane or sugar beets). And natural products as pure apple juice can contain more sugar than a coke...

Chris, I'm not sure, but I in the previous question discussed here someone said that "plaque is colonised by acidogenic (acid producing) micro organisms cavities are produced in the presence of refined carbohydrates" and also "...besides wild animals are not exposed to refined carbohydrates like sugars.", hence "wild animals do not have these two diseases".
I don't really know much on this matter, that's why I'm looking for more answers.

Tooth enamel is almost entirely susceptible to acidity. So grass eating animals and fruit eaters have different issues.

I think your assumption is wrong : Our small mixed breed had to have all her teeth pulled in 2 operations a year apart. The caries were so bad it damaged her kidneys.  i have had other dogs with caries but not so severe .

There is something missing from this: what was/is the dog's diet?

Her diet was the same, i expect, as most dogs in US, dry prepared dog food. Our other dog has excellent white teeth ( same food).


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Genetic engineering for experimenting at home?
I am just wondering whether it is possible to carry out small scale genetic engineering at home, without any sophiscated tools.
Ive searched google and found this http://explorebiotech.com/the-7-important-molecular-tools-used-in-genetic-engineering/
So i am wondering whether these tools are easily acquirable and how feasible it is to be done at home maybe as a hobby.
Also my budger is probably about 200 USD so my hopes arent that high.

FYI the thermocycler in your link is almost 4,000 USD. It's a Sensoquest Labcycler model. Lab consumables like plasticware can also be quite expensive (around $2 per 6/24/96-well plate, cases often come with 50-100).

Doing genetic engineering experiments at home is generally referred to as either "biohacking" or "DIY Bio". There's a number of forums out there filled with hobbyists who are doing that sort of work in their homes and garages, and discuss how to do such things in a hobbyist environment. With those terms (and the info in the Wikipedia article), you can probably find those forums on the internet. (Suggestion: look for ones where the regulars emphasize safety and appropriate conduct - not only is it better for you, it's a sign that the regulars know what they're talking about.)
However, 200 USD might be a little small to set up a decent (and safe) "biohacking" space in your own home. Possibly a better bet is to see if you can find a local "makerspace" which has a biology component. Makerspaces are places where, for a small fee, fellow enthusiasts pool together to purchase equipment (and space) to do various projects. Most makerspaces are geared toward the computational/mechanical (e.g. building robots), but there are some out there which have biotech equipment. Your mileage may vary, though, and you're likely to have more success in finding a decent makerspace in a large city than in a small town.
A final caveat is to make sure you research your local laws to figure out what is legal in the jurisdiction you're living. Especially with laws targeting illegal drug production, there are locations where possession of basic scientific equipment by normal homeowners is criminalized. There's also regulations about waste disposal and material storage that you'll need to follow. Also, in most jurisdictions accidents/damage from home labs are penalized much more harshly than, e.g., cooking accidents. Know what's legal/illegal in your jurisdiction (and by your homeowner's insurance) before attempting to set up a home lab.

There are also dedicated 'Biohckspaces' (well, there is at least one in London)

How much would you reckon I will have to spend for decent equipments etc if there isnt any markerspaces around me.

@user35897 That depends heavily on what you want to do and how "DIY" you're willing to get. For example, you don't need a thermocycler to do PCR. All you need is three heat baths at the appropriate temperature and a lot of patience. And they don't have to be "official" heat baths - you can rig something up with heating elements and thermostats. -- That's why I suggested the dedicated forums. They have the knowledge and experience to walk you through "on the cheap" options that fit your DIY comfort levels. (Which is not something that really fits StackExchange's Q&A format.)


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Why do women go through menstruation?
I do understand that the female has to prepare for possible fertilization and make sure that the egg is of the best quality, so they try to remove aged egga from the uterine. However why cant the body just simply get rid of the egg not the uterine lining?  Maybe like reabsorb the egg or pass them out as waste? I mean its extremely energy consuming etc and it would be an evolutionary disadvantage since many other mammals dont go through menses.


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Ingestion of cellulose digesting prokaryotes?
If humans digest cellulose digesting prokaryotes,  can  we start digesting cellulose like cows?

How would we get the three additional stomach chambers, and the time to eat this stuff?


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Using Transduction to reverse Antibiotic Resistance?
Is it possible to use reverse transduction to reverse antibiotic resistance. Since antibitiotic resistance is causee by transduction of the F factor, is it possible to induce a F+ non antibiotic resistant bacteria into a region of F- resistant bacteria?

This seems very confused. Apart from anything else, The F plasmid doesn't encode an antibiotic resistance. Are you asking if it is possible to get rid of a plasmid from a bacterial strain?

@AlanBoyd Wait is it the R plasmid? Hmm I guess so... My question is whter we can make resistant bacteria transfer genes with non resistant bacteria.

https://biology.stackexchange.com/a/64618/6307

OK bacteria with an F plasmid can transfer their other plasmids (which may encode antibiotic resistance) during F-mediated conjugation. Now, starting from there, what is the question?

@AlanBoyd i think canadianer's link has already answered my question . Thanks anyway!


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What is this bug? Singapore

enter image description here

Around 1 inch in length

is this all the information you have? one inch long and lives in singapore :)

I have the pictures. What more should I include?

please take a look here https://biology.stackexchange.com/tour

does the bug live in water or on land,what type of habitat,indoors or outdoors,did you see it at night or during the day.simply any details you can provide will help us help you.

Looks like an Orthoptera species.

This is an orthopteran insect. Well known members of this insect order are grasshoppers, locusts and crickets.
You can recognize them by their

greatly developed femurs specifically adapted for jumping,
hardened forewings (called tegmina), which protect the membranous hindwings folded beneath them,
long, filamentous antennae,
two cerci (appendages at the tip of the abdomen),
chewing mouthparts (with which they chew on plant material such as leaves and stems) and
prominent compound eyes.

Orthopterans undergo incomplete metamorphosis, progressing through egg, nymph and adult stages. Nymphs closely resemble adults, but lack fully developped wings and reproductive structures. As this specimen has fully developped wings, we can conclude it must be an adult.
Moreover, I assume this specimen belongs to the suborder Caelifera as antenna are shorter than the body (as opposed to their sister taxon Ensifera which have more-than-body-long antenna).


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Do some cells have more than 2n at some part of their cell cycle?
For example, do human cells reach 4n after s phase during interphase after replication of DNA?

For example megakaryocyte in bone marrow 8n.

Been told by a colleague that nuclei in early Drosophila embryos don't always manage to keep the rate of division in line with the rate of genomic replication, resulting in some of them temporarily housing 3n or 4n.

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


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L-selectin in white blood cells
The white blood cells' function is mainly to fight off external antigens. However, another one of its traits is its ability to bind to vascular endothelial cells with the help of L-selectin. What is the purpose of this, and how does this help us？

Fighting of harmful microbes (and not antigens per se, although specific antigenic recognition is important), involves a lot of processes which require several lignad-binding molecules and ligands on the WBC surface. While the whole array of these proteins and their functions is very complex, we can take the case of a neutrophil trying to defend the body against microbes in a local wound, the so-called acute local inflammation response.
1. Adhesion to the endothelium
Here is where several selectins play a role. The simple broad idea is that in presence of microorganisms, as sensed by the local immune cells (tissue macrophages, blood cells in case of a vessel breach etc), there is an upregulation of chemokines in the local environment which causes the endothelium to increase the expression of certain adhesion molecules (ligands with receptors on WBC and vice versa) as well as other hemodynamic changes causing the neutrophil to come in close contact with these in the vicinity of the wound and bind to the endothelium. This is ften subdivided into three processes, margination, rolling and adhesion. L-selectin is one of these adhesion mediators, along with other selectins and integrins.
2. Migration through the endothelium into the tissues (diapedesis)
3. Chemotaxis towards microbes
4. Action on the microbes
Points 2,3 and 4 have their own mediators (see CD31, chemokines - AA, C5a, leukotrienes).
Reference:
Robbins and Cortran: Pathologic Basis of Disease, 9e
Other sources:
Wikipedia page


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How exactly does heterozygous sickle trait help patients survive malaria
Heterozygous sickle cell anaemia trait is known to increase the survival rate of carriers to malaria attacks. How does a recessive gene not expressed in the phenotype allow for such an advantage? Is the red blood cell of a recessive carrier structurally different from that of a non-carrier?

Sickle cell anemia is characterized by the formation of sickle shaped red blood cells rather than the usual biconcave ones. For a double recessive homozygous genotypic person, i.e. an infected person, this causes severe lack of oxygen diffusion into the RBCs because of defective haemoglobin production.
In case of a carrier, he/she carries the gene for the defective version of haemoglobin but does not show the symptoms for the disease.
The malarial agent, Plasmodium uses haemoglobin, or more specifically haem as its main nutrient source The defective sickle haemoglobin induces the expression of heme oxygenase-1 (HO-1) enzyme in hematopoietic cells (those which produce erythrocytes, for example marrow of long bones). Carbon monoxide (CO), a byproduct of heme catabolism by HO-1, prevents further accumulation of circulating free heme after the infection by Plasmodium. This decreases the pathogenicity of the organism and prevents the disease from occuring.  Moreover, sickle haemoglobin inhibits activation and/or expansion of T lymphocytes (specifically CD8+T cells), which recognize the antigens expressed by Plasmodium and hence do not attack it. This is an immunoregulatory effect that does not involve the heme oxygenase enzyme.
This leads to the carrier person having innate resistance to malaria (or at least Experimental Cerebral Malaria )
And no, the RBC itself is not structurally different. Though there might be some
sickle shaped RBCs in the blood, their number is very less. The major difference comes from the haemoglobin in the red blood cell.
Here is the original paper which explains the phenomenon in detail.


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Is it possible to use virus for genetic modification of embryos during the fetus stage
I know this probably sounds rather hypothetical and not very feasible but I would very like an answer telling why it is possible or not possible and why.
With the advancement of crispr and other dna technologies, I have been wondering whether it is possible for us to use a virus, which would easily pass through the gaps of the placenta and infect the developing fetus to alter its genomic materials for the creation of designer babies. Since Zika can alter the genome of a baby to cause deformities, is something opposite also possible, like using a similar virus to develop favourable genes in a fetus.
Also, what are the chances of the virus actually purposely acting under orders of genetic engineering to intentionally deliver the genes through transduction?
Putting all ethical and moral issues aside is such a principle feasible and if no, why not?

Zika doesn't alter the host genome at all.

Since Zika can alter the genome of a baby to cause deformities

Zika virus is incapable of altering the host genome. The exact mechanism by which Zika virus infection causes microcephaly is still unclear, but basically it depletes the neural stem cells at a point when the brain is developing, meaning brain development is more limited (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516183/).
Some viruses do alter the host genome and are candidate technologies for gene therapy
Retroviruses are RNA viruses that copy their genetic material into DNA which is then integrated into a host genome. As such, and as you note, this can potentially be exploited to deliver new genetic material into an organism's genome. I'm not sure what you meant by transduction above, but the term is 'retroviral vector-mediated gene delivery'.
Retroviruses have been trialled for gene therapy for decades. See this sad report on a 2002 trial that apparently succeeded but had unexpected side effects here. However, CRISPR is probably an easier method to use.
You wouldn't attempt to modify a fetus
Some terminology here: a fetus is what an embryo grows into; it's getting bigger and more complex. And as illustrated by Zika-related microcephaly, any messing about with fetal development can have nasty side effects. There are also more cells to modify and you're likely to end up with a 'mosaic' where some cells are genetically different to others within the same organism. If you're attempting to modify the somatic cells of one organ, you might as well do it after the baby is born; if you're attempting to modify every cell in a human (including germ line cells) you'd do it to an egg or embryo.
This study describes a successful attempt to modify embryos using CRISPR. They saw only 1 mosaic in 58 embryos.

First of all, disclaimer: We do not know the effects of every gene in the human genome. The human genome has only 1.2% of its genes that actually seem to be useful. However, the 98.8% of "junk" DNA may have uses that we don't know about. Also, many genes, such as sickle cell anemia, carry unknown benefits, such as offering resistance to malaria. Now, to answer your question...
Viruses
Viruses are probably some of the coolest things on the planet. They infect other organisms, which is a hard task to accomplish. According to Khan Academy they use two cycles.

The lytic cycle: The phage infects a bacterium, hijacks the bacterium to make lots of phages, and then kills the cell by making it explode (lyse).
The lysogenic cycle: The phage infects a bacterium and inserts its DNA into the bacterial chromosome, allowing the phage DNA (now called a prophage) to be copied and passed on along with the cell's own DNA.

Some viruses only use one type of cycle, the lytic cycle. However, you could use a virus with the lysogenic cycle to insert DNA into the target embryo, which could potentially accomplish your goal.


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Why can't amylase break down glycogen?
Amylase is an enzyme that breaks down starch in the form of amylopectin and amylose. Both amylose and amylopectin are formed by alpha glucose joined together by (1-4) and (1-6) glycosidic bonds. Glycogen is no exception, just that it has more branching. However, why is it that a google search shows that it is hydrolyzed by Glycogen Phosphorylase rather than amylase? Also, how can amylase digest both (1,6) and (1,4) glycosidic bonds?
Any help would be greatly appreciated.

At an approximation the active sites of enzymes can be considered as having two aspects. The first relates to the catalysis — in this case the breaking of the glycosidic linkage. The second relates to binding the substrate. This review of the α-amylases by MacGregor et al. shows that there is a range of a-amylases, differing in this latter respect — their substrate specificity. In general there are binding sites for a varying numbers of glucose residues at either side of the bond being cleaved. This is shown in Fig. 3 of that review:

The important difference in the structure of glycogen and starch (amylopectin) — seldom mentioned in general biochemical or biology texts — is their patten of branching:

As this previous answer of mine to a different question explains, this results in a globular structure for glycogen granules in which only the ends of the chains are accessible. (The image below, from Protopedia, illustrates this better, especially if you imagine it in three dimensions.)

Hence the substrate-binding site of α-amylase does not have access to the residues that need to bind for it to perform hydroysis of glycogen, and, indeed, the enzyme that breaks down glycogen — glycogen phosphorylase — is specific for these free ends.
The α-amylases that can hydrolyse both α-1,4 and α-1,6 glycosidic links are quite few compared with those with specificity to one or the other type of linkage (see Table 2 of the MacGregor review, if you can obtain access to it). The impression obtained from following up two of the examples there is that the enzymes involved can exist in alternative conformations, the correct one of which is triggered by the substrate. An example is the glycogen debranching enzyme, the studies of which in Sulfolobus solfataricus and Candida glabrata can be read freely on-line. Although somewhat less directly relevant, the example of a Thermoactinomyces vulgaris neopullulanase is another variation on this theme.

So in summary it means that glycogen is arranged like a sphere so that only the ends of the glucose chain is exposed, hence amylase cannot work on it.

And that some amylase have active site flexible enough to accommodate both sort of linkages?

@user35897 — As regards the spherical form of glycogen, yes, and I have added another image (referenced). As regards my guess about flexible active sites, no, I was wrong. I seems that it is the enzyme overall that is flexible in being able to adopt alternative conformations. I have altered the last part of my answer with references to examples of studies with crystal structures. Good questions educate us all.

just a random afterthought but how does glycogen get digested as it goes through the gut to the small intestine, since glycogen phosphorylase is not produced in the stomach or small intestine? Some sources seem to tell me that amylase CAN indeed hydrolyze glycogen.

@user35897 — You are failing to differentiate between two different situations. One is the mammalian cell (e.g. a liver or muscle cell), from which amylase is absent, and where the breakdown of glycogen can be (and is) controlled by controlling the activity of the only enzyme in that cell able to do so — glycogen phosphorylase. The second is in the digestive system where any glycogen from a meal of meat is digested (or not). There it will presumably be exposed to, and succumb to, the same amylases that break down starch in food. [I mistakenly wrote GS, not GP in previous version of comment.]


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How exactly does a prion cause disease?
During my study of the immune system,  I came across 2 very contrasting explanation as to how prions work.
Firstly, scientific American pointed out this:
link here:

"A major breakthrough occurred when researchers discovered that the infectious agent consists primarily of a protein found in the membranes of normal cells, but in this case the protein has an altered shape, or conformation. Some scientists hypothesized that the distorted protein could bind to other proteins of the same type and induce them to change their conformation as well, producing a chain reaction that propagates the disease and generates new infectious material. Since then, the gene for this protein has been successfully cloned, and studies using transgenic mice have bolstered the prion hypothesis. The evidence in support of the hypothesis is now very strong, though not incontrovertible

However based on this website

The guess was that they infected cells by causing normal prions to become misshapen, too. That theory, though, has been proven false, though it is still commonly believed. (See Sanctuary: Bad Bad Prions from Discover, dated 9 January of this year for an example of the ongoing belief.) The first serious attack on the prion-as-infectious-agent theory was reported in Medical Hypotheses in 1997. The article makes the case that prions trigger an autoimmune response.(1) As becomes clear the more one looks into the issue, this makes sense and fits the facts as known.

The problem right now is that my campbell 11th edition textbook, which is the newest edition and just recently revised also points to the same explanation as the first source.
Which source is correct in showing the method in which prions cause diseases?

I agree with commenter Martin Klvana, but there are a couple things going on here I wanted to touch on:

I think that your second quote is making an error in saying that if prions cause immune responses that means they aren't "infectious" in the sense of propagating misfolding of homologous proteins. The standard understanding is that prions work biochemically by refolding prionogenic proteins to make more infection prion particles (see e.g. wikipedia), similar to your source 1 and your textbook. It's completely possible that these newly infectious prion particles lead to immune reactions in additional to the "infecting" particle. The key here is to separate the biochemical phenomenon (propagated misfolding of proteins) from the medical phenomenon (disease, immunological response).
To more directly answer the question: as far as I can tell from scanning a couple of articles (here, here), immune responses are not a prominent part of the best-known prion diseases, but I'm not an expert and could be wrong. I was unable to easily locate the 1997 Medical Hypotheses paper referenced by your source 2.
I haven't looked deeply into this, but that website appears to be run by an advocacy group and the "read full article" link is broken. So... I would put less stock in that source. Advocacy groups are fine and all but I don't think that their blog posts are good sources of biomedical science information.

Hope that helps.

it becomes really obvious the advocacy group articles is not written by a scientist as they talk about prions lacking a "life imperative" that viruses supposedly have. This lack of a metaphysical force is supposed to explain why it can't be an infectious agent instead it displays a lack of basic biological knowledge.


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Online resource for downloading gene variant data?
I have a long list of gene variations. For example, Here are 4 of them:
CBL Q249E
TERT H412Y
SF3B1 R625H
EGFR L747_T751delinsP
The first term identifies the gene, the second identifies the variation.
I am a data scientist with no background in biology or medicine. I am looking for an online resource where I could download synonyms, descriptive data, and other relevant info for all the gene variants.
I have seen two sites where data is offered for some gene variants, but not for others. For example, the EGFR L747_T751delinsP variant is well documented at this and this site.
While CBL Q249E is documented at the ckb.jax site but not the reactome site. Other variants are documented at reactome but not ckb.jax, etc.
Plus, there appears to be no easily downloadable file containing this data. Before I go scraping what I need off of a hodgepodge of websites, I wanted to check with you smart people to see if there is a user-freindly resource out there that has this data in a downloadable format.

Tried this one? http://dgv.tcag.ca/dgv/app/home

Seems your variants are all possibly harmful mutations to human genes, in that case ClinVar can be quite useful, it returns hits to all your variants except L747_T751delinsP. I have never used the ClinVar API so I'm afraid I can't vouch for how easy to use that is.
When ClinVar doesn't have the variant (or info about it) you need you could search EBI to see if other sites have information for this variant, when queried with L747_T751delinsP EBI actually shows us that it has been entered into Reactome twice. (welcome to the mess that is sequence annotation!).
This might be outside of your scope but if you have an interesting variant that you cannot find information on you could try to find the most similar (known) variant using BLAST.

Yes, these are all potentially harmful mutations. Although passenger genes with mutations could ultimately be beneficial (harmful to the cancer), if I understand correctly. Thanks for these great resources. Could it be that L747_T751delinsP has 2 entries at Reactome because it is a type of variation that can occur in different genes?

@ben seems like the only difference between the two entries is that the protein of "p-6Y-EGFR" entry has a bunch of phosphorylated tyrosine residues. Basically it seems the two entries cover the same gene, same variant in this gene and same protein sequence but the p-6Y entry has extra modifications to this protein. This probably does indicate difference in function but this should give you an idea of how confusing, and difficult to automate, this can get.

You can use the Table Browser.
For the variants, in the group field select variation, in the track field, select any database you are interested in, finally insert the genome position of your gene of interest and you will be able to download the relative data.
For the synonyms, descriptive data, and other relevant info for all the gene variants, in the group field select Phenotype and Literature and from the track field, select any database you are interested in. You may need to download data from multiple databases to get all the info you want, but the whole procedure is quite fast and you can do it directly from the browser.

Thanks. I do have location info for each of the genes in my data (which I got from a website--can't remember which off the top of my head right now), so I can fill in the important fields at Table Browser. Problem now is that the names of the variations given at this site do not match any in my list of variations. They all start with "rs" followed by a number, whereas you can see in the original question above the variations in my data follow a different nomenclature. Any idea how to translate between the two?

@ben It's not trivial to find the correct ID, different databases use a different one. The rs suffix is from the dbSNP database. The mutation you are looking for EGFR L747_T751>P is an indel, you can find it on the Cosmic database

I think the correct nomenclature is EGFR L747_T751delinsP, based on http://varnomen.hgvs.org/recommendations/protein/variant/delins/
You can also use a translator tool like TransVar
@smock2020 and @JAX_CKB


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Red blood cells
How can we classify red blood cells while they lack nucleus?
From my point of view i find it difficult to be classified as we have all cells with nucleus, even prokaryotic cells which have no nucleus membrane but they have a nucleus material which is DNA.
Maybe if we classify it as a type of cell which lacks nucleus and others are cells with nucleus

What do you mean by classify? Red blood cells have a highly distinctive shape, which you can use to discriminate them against other blood cells.

Human RBC develop from a nucleated cell which, clearly, is eukaryotic. They lose their nucleus at the end of their developmental pathway. It wouldn't make any sense to reclassify them. If you need an adjective to describe them it is: anucleate.

As with many types of blood cells, subsetting cell types in a heterogeneous population can be done by flow cytometry. This is really quite a nice paper because it explores the differences between erythroid lineage cells and other cell types. Based on their immunophenotyping at different stages of erythroid differentiation, you can see that the cells begin to lose discerning markers as they get closer to losing the nucleus.
Also for your reference, a chart on blood cell differentiation.
Take home point: I would classify them as erythroid cells, erythrocytes on the basis of CD235+, CD71-, CD45-, CD117- by flow cytometry. CD235 may not be present in non-primate blood (ref).
CD numbers are referred to as clusters of differentiation, or as you've described it, how do we know what a cell is if it's indistinguishable from a mixed bag? These markers are used routinely in immunology for cell classification, though as commented red blood cells are easy to spot. My only thought is you may mistake a reticulocyte for a RBC by conventional light microscopy without the appropriate stain, so it's worth being careful if you're new to viewing these cells in a microscope.
We don't need to create an entirely new classification of cell, however. Think of RBC as terminally differentiated blood cells.


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What type of guatemala beetle is this?

it was in Guatemala
it was really big like 4 inches
sorry I don't have a better photo

Search on Buprestidae family.


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Why do (many) humans like carbonated drinks?
Many/most humans like certain types of food/drink because of the psychological/physiological responses we have to consuming them. Some examples:

We like sugar because it is very energy-rich (and is relatively scarce in nature).
We like salt because it is one of the essential building blocks of our cells.

But why do we like drinking carbonated drinks? (Soda drinks like Cola, Fanta, Tonic, Dr. Pepper, etc. but also sparkling wine, cider, champagne) Except in some very rare, special springs, carbonated water does not occur in nature. Why do we like drinking it so much?

Effervescence is fun. Pop rocks, Fizzies, etc.

@anongoodnurse Yes, but why do we like it?

Because it's fun. Why do you like swinging when you're a kid?

@anongoodnurse That's circular reasoning. I like swinging (and still do :D) because of the adrenaline rush caused by the point of weightlessness when the swing is at its highest point, as well as the speed at which you can move forwards and backwards. I do agree with you that many preferences are mostly psychological, rather than physical (and thus a lot harder to quantify), but "it's fun because it's fun" is not an explanation at all. :)

Of course it is. I just didn't go into all the reasons it was fun. It's the condensed version.


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How does coconut form?
I've seen that at the earlier stage coconut is filed with water and, as time passes, the water inside the coconut escapes and a thick layer of white substance forms.
Is the water converted into that white substance?


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The insulin protein of apes & chimpanzees
How many amino acids do the insulin protein of apes and chimanpzees compose of?!

Welcome to Biology.SE! There are probably 20-30 extant species of apes (6 of them were sequenced; see here). It will be impossible to answer for every single species. Why do you say apes & chimpanzees. You are interested in all apes but in particular in chimpanzees? Why chimpanzee in particular (why not bonobo, human or a species of gorilla typically)? If you could give some background behind your interest it would be more likely people would find the question worth their time.

Chimpanzees are apes.

On the Ensembl website you can find an easy way to compare genetic sequences of the available genome references, including the one of several primates.
Here a query example:
http://www.ensembl.org/Homo_sapiens/Gene/Compara_Alignments?align=822&db=core&g=ENSG00000254647&r=11%3A2159779-2161341
For protein sequences, check the Uniprot website. For insulin, this is the page you are looking for http://www.uniprot.org/uniprot/P01308
Check the paragraph "Similar proteins", there you will find all the links to retreive the insulin sequence from all the species for which we have sequencing data.


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What type of worm is this?
Found this on the carpet in our office(North Carolina), no idea how it got there.
It is at between 8 and 12 inches long.

It looks desiccated and I think that's why it has this weird shape. Was it moving when you clicked this pic?

It was not moving.


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Found in blood sample - what is it? Hopefully not a nemotode-
After examining someone's blood - through microscope - I found these. There were some more that were not photographed. Could someone please inform me on what these are? Maybe abiotic material on the slide? Hoping that they are not Microfilariae. #3 threw me in a loop.

If you still have blood in the collection vial, I'd smear another slide that I cleaned assiduously. Also, staining would help.

A scale bar could also help quite a bit.
I second the staining, as that'd really make help make sense of what we're looking at.
Do you have any other clues about this person that could tell us what we're seeing? e.g. recent travel, exposure to anything, any symptoms etc.

The technical term is gunk. Slide 3 is the giveaway.


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Which one is true about sunflowers, "follow the sun across the sky" or "always face east"?
Which one is true :

Sunflowers follow the sun across the sky.

Or...

Sunflowers always face east.

Or are there 2 kinds of sunflowers with different behaviours?

Here at biology we like to see some effort to solve a question yourself. So: What have you found out?

@Chris : Hello chris, I was a bit surprised, when I open http://list25.com/25-science-facts-that-were-proven-wrong/2/ which stated that sunflowers do not follow the sun across the sky, so I surf the web and find out 2 different answers. so I asked about it here.


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What factors may lead to a difference in whole-cell potency compared to cell-free potency?
For studies of protein-ligand binding, the reported whole-cell potency may be higher or lower compared to measured cell-free potencies.
For decreased potency, this may represent an increase in non-specific binding of the ligand. Are there other factors that may contribute?
On increased potency, I've noticed this applied to the BACE1 protein in which the IC50 may go on the micromolar scale in a cell-free assay to nanomolar scale in a whole-cell assay. This seems counterintuitive to me. Are there possible reasons for this trend?

You are correct in saying that whole-cell potency and in vitro/cell-free potency often differ by quite a bit. There are actually a lot of factors that can contribute to this, but I'll try to give a couple illustrative examples, for increased and decreased potency (when moving from cell-free to a whole-cell assay).
When moving from cell-free to whole cell assays, decreased potency is the more common outcome. As you mention, a big reason is just that you get a lot more things the drug can bind to, so you tend to have less drug effectively engaging the target. However, there are other factors at play as well. Ultimately, the main reason that one sees decreased potency in the whole-cell format is that one is often asking for something fundamentally different than what was asked for in the cell-free assay.
For example, let's say you do some CRISPR of RNAi screen in cancer cells, and you find that if you shut down gene X, the cells die. You look it up, and gene X codes for an enzyme.
So you think, "Great! I'll design an inhibitor for the enzyme, and then kill the cancer cells with that!"
In order to screen for inhibitors and test their effect on this enzyme, you set up an in vitro with purified enzyme, substrate, and some way of measuring the generation of product. You screen, find compounds, and optimize your lead. You eventually end up with a compound that has an IC50 of 1 nM in this assay. Then you decide it is time to move into cells. You treat the cancer cells with the compound, and you notice that your IC50 for cell death is 100 nM - 100x what it was in the original assay. The reason is that you are asking much more of your compound.
In the first assay, the compound had to bind to the enzyme, which may have been the only protein in solution, and inhibit it. You were directly measuring enzyme activity. In the second assay, the compound had to diffuse through the cell membrane or find some other means of getting into the cytosol, where the target protein resides. Then, despite the complex milieu in the cell, it had to bind that specific protein and inhibit it. But inhibiting the protein isn't enough. It has to inhibit the protein enough to kill the cell. Maybe the cells die when the enzyme activity is 50%, in which case you would expect your IC50 values to be fairly close between assays. But maybe it doesn't. You may need 70 or 80% inhibition before the cells start to actually die. Plus, the cells may not go down without a fight. Maybe they up-regulate expression of drug-efflux pumps, which are ATP-powered proteins that literally pump small molecules out of the cell. This reduces the effective concentration of drug you are giving the cells. There are also many other adaptations that the cells may undergo to improve survival, which are beyond the scope of this answer. So what you are demanding from your compound in the whole-cell assay may actually be much more than in the cell-free system.
The other effect - seeing increased potency in whole-cell vs cell-free conditions is much less common. Without seeing the exact study you are referring to, it is difficult to comment. However, one thing to remember about BACE1 is that it is part of a huge complex that is embedded in the cell membrane. Reconstituting this complex in vitro is non-trivial, and it may be that the complex is not functioning the same as in the cell depending on how the reconstitution was performed. For example, maybe BACE1 binds better to the drug only when a binding partner is present that stabilizes a conformation suitable for inhibitor binding. It could also be that the inhibitor is actually targeting another protein in the complex that is not present in the cell-free system.
Anyway, I apologize if this was a bit long, but I hope this answered your question and shed a bit of light on the complexities of assay development and drug development.


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How many oxygen atoms are used up in aerobic oxidation of one pyruvate?
Please explain elaborately, if possible using the EMP, Krebs and ETS cycles.


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Why Interracial couples always give birth to colored one?
Whether couple is White male and colored female or White Female and colored Male
but they always give birth to colored one.
Why Interracial couples always give birth to colored one?

I feel you haven't looked into the matter enough.

This isn't really a biology question. It's a matter of law and politics. In some polities, a racial classification of people was carefully tracked, and children of mixed race parents were defined by law to be "colored". See for example South Africa during Apartheid, and some US states during the Jim Crow period. Children of mixed race parents may or may not inherit characteristics would lead to them being characterized as one race or another by casual observation. See the Wikipedia article on "passing".

Anecdotally: They don't.


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Histidine protonation
In histidine structure , full protonation gives a structure with only the double bonded nitrogen having been protonated in the ring and not the single bonded nitrogen. Why is that?

Textbooks tend to report structures as relatively static, whereas advanced biochemistry texts explore structural tautomerism. In essence, the histidine imidazole sidecvhain may move around it's protons and electrons when pH is roughly equal to pKa. Thus, the sidechain exists as two tautomers where the two nitrogens sort of "share" the double-bond character and the proton, like so:

And it's even more accurate to depict that the double-bond character is like so:


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Estimation of the amount of bacteria
For my first research project in microbiology I've chosen to determine the effectiveness of sanitizers and soaps in killing bacteria from our hands, however, after putting the bacteria on agar plates using cotton swabs, why do we incubate them? Won't their numbers increase and give us the wrong results?

This is a very standard method. The idea is that you have a culture of bacteria on an agar plate. During the incubation each bacteria forms a colony. After a few hours of growing the colonies grow and become visible for human eyes. So you can easily count them.
Then you can compare the number of colonies before and after washing your hands with the sanitizers and soaps and find which method has the lower amount of colonies on average and therefore whihc one is the most efficient one.

Should I use only EMB plates then, so I can identify the bacteria?

Well, there are many options from many providers. It all depends on what you are trying to identify, the cost and your budget!

When you swab the agar plate with your sample, what you're doing is spreading out all the bacteria in your sample so that each cell is able to grow separately from the other cells and form an isolated colony.
Since bacteria are microscopic and you can't actually see them directly in your sample, you need to allow them to grow a little until they form a colony and you can actually see them with your eyes. The assumption we make when we use this method to "count" bacteria is that a single cell gives rise to a single colony on the plate. That's why we call the cells "Colony Forming Units".
This might be of some help: https://en.wikipedia.org/wiki/Colony-forming_unit


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Lipids that are not found in human body
I know that human body contains FA some of which are essential and the other is not depending on the ability of the body to synthesize them in a sufficient amount, but I need a reference of the lipids types that are found at animals, plants, insects, microorganisms,....etc but not in the human body.