text:
What is the dependent variable of a relative fluorescence graph?
So it was asked what was the dependent variable of this experiment. I know that as students, we're wired to think that the y-axis is the dependent variable while the x-axis is the independent variable (probably good that way, I dunno).
However, I thought that the dependent variable in this kinetics would be time. Since this has relative fluorescence from 100 to 0, isn't the change in fluorescence for all four conditions the same, while the only affected variable being rate (which in this experiment is more dependent on change in time)?
Sorry I can't give more information about the conditions of the experiment, it's a test question that I wouldn't be allowed to post, which is why I whited-out the conditions of each line. Any help would be greatly appreciated.

When a variable is independent, it's not affected by any other variable. Relative fluorescence obviously depends on the time parameter in this case. If you stopped at 30 minutes and took readings ever 3 minutes, your data would look very different.
Without more information about the experiment, however, it's hard to tell if there are additional variables.


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How diverse are the sperm cells of an individual male due to random mutations?
Due to the sheer number of sperm cells in an individual and the rate of mutations, are they likely to be incredibly diverse and encompass most of what we see across our species?  For instance would it be likely to find sperm cells that could result in extreme height, intelligence, different skin colour,etc even if the father didn't have any of those genes in their DNA, but a sperm cell did due to mutations?

A pre-print study was recently published regarding sperm cell mutations. Contrary, to what you might expect the ratio of paternal to maternal mutations was quite stable from puberty and onward. See Gao, ..., Przeworski: Overlooked roles of DNA damage and maternal age in generating human germline mutations. They conclude that spermatogenesis does not underlie the male bias in human mutation.

source: Stack Exchange

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

sort: votes


text:
Species identification - What is this "bug"
The title says it all. What the heck is it?

Edit:
I found this on my car, in Kansas city.

Well, it's a spider. Other than that, can you post the approximate location you found the spider so we can narrow down the possible species?

After trying to dig through this list the closest I can get are the Araniella species, some of which are white. But the pattern of dots is wrong, and the leg lengths look wrong too.

@user137 I updated the question.

After conducting a small investigation, it would appear most likely that the spider captured in the attached photograph is an arachnid in the family 'Thomsidae' or 'Crab Spiders'.

Although the proposed genus of Araniella proposed above by user137 shares a superficial similarity to this family, thomsids generally do not construct webs to ensnare prey - I might hazard that the web on your car does not hold the same structure, as shown below, to that of an Orb Weaver Spider (Araniella).

From the available information it is challenging to propose a genus, let alone a species. Based on the location of the car, I may propose the sub-family Misumenoides or genus Thomisus.
The general characteristics of crab spiders are the ambush of prey as opposed to trapping prey; the inverted V-shape under the cephalothorax; and the sideways movement of certain species in the Thomsidae family. It is of interest to note that any member in the population could vary appreciably in colour.
Wikipedia article concerning Crab Spiders available from: https://en.wikipedia.org/wiki/Thomisidae
Britannica regarding Crab Spiders available from: https://www.britannica.com/animal/crab-spider
Information regarding Misumenoides is available from: https://en.wikipedia.org/wiki/Misumenoides

This answer makes sense. I grew up north of KC and saw several crab spiders, but I don't remember any white ones, I was also confused by the web, because I never saw crab spiders on any web at all. But the leg lengths look more appropriate for crab spider. If @Gogeta70 can provide more detail about size and behavior, that would help confirm the answer.

It stayed in the same spot on my car for over an hour. And the width of its long legs was about as wide as my thumb. Thanks for the answer!

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


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Are “Rings” in fish like rings in a tree?
A lot of fish have structures like the rings in a tree. Is the number of “rings” an indicator of age, as in a tree, or is it fixed?

Can you please clarify about what structure you are talking about. You could for example upload a picture with a clear red arrow pointing to the structure of interest. In any case, the answer will probably be "no, it does not indicate age".

I am VTC as unclear as the OP has not clarified what structure she is referring to.

It depends which structures you're talking about. However, several body parts of bony fish such as the scales and otoliths (earbones) generally contain a record of seasonal growth patterns. So in that sense yes, the process of ageing fish is similar to finding the age of a tree by counting rings in the wood. For different species of fish, different structures are used to determine ages.
https://www.nefsc.noaa.gov/fbp/basics.htm


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Causes of Back Dimples
What are the causes of the dimples commonly found above the buttocks?  They seem to be in line with the sacroiliac joints.  Do the joints have anything to do with them?

Back dimples or Dimples of Venus are created by a short ligament stretching between the posterior superior iliac spine and the skin. They are thought to be genetic.
Source and further reading: Kumar, Kanojia & Saili (2014) - Skin dimples

@Mesentery, thanks for editing. I took the image of Wikimedia without thinking that it might be deemed NSFW or inappropriate. Thanks again.


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Why inhbition of RTK will not help in a case of mutant EGF?
I was given the following as an example for a quiz question but i don't understand the answer. Any help will be most welcome:

Question: Iressa is a Tyrosine Kinase Inhibitor. As a young oncologe, to whome of the patients will you recommand not to take this treatment:
a. Biopsia has shown that the EGF receptor is mutant
b. Biopsia has shown that the RAS protein is mutant
c. Biopsia has shown that the MAP Kinase stays in the nucleuous permanently
d. The treatment can help each of a,b,c, cases.

The right answer should be a. Can someone see why and help here?
I know that tyrosine kinase receptor is the inside part of the EGF receptor (where the two monomeres become a dimer and phosphorelate each other).
So, if the EGF receptor is mutant, shuldn't it help inhibiting it's continuation inside the cell and thus prevent to many EGF cascades?
Thanks!

Have they given more information how the receptor is mutant?

The right answer should be A? Patients with EGFR-positive lung cancer who are also positive for mutant K-Ras don't respond to erlotinib, a common EGFR-TKI (example). This is directly because the bulk of Ras mutations are activating, which would naturally subvert the need for EGFR-RTK signaling to begin with. Thus, for mutant Ras patients I wouldn't recommend TKIs.


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How does chemical shift assignment from NMR spectroscopy is translated to three dimensional structure of protein?
I am currently involved in determination of protein structure using NMR spectroscopy. As part of structure determination I have finished the chemical shift assignment. The chemical shift information is submitted to specialized software/servers for structure determination.
My specific question is "how is the structure of a protein is determined using chemical shifts"? How do the servers translate the chemical shift information to determine fully fledged 3D structure of protein?

The chemical shift can be used to determine secondary structure, i.e. if a certain residue is part of a helix or a strand.
You’re talking about structure determination, so I assume you’re interested in obtaining the three dimensional or tertiary structure. For this, you will have to use proton-proton distances as restraints in structure calculations, not chemical shifts.


text:
How can there not be purpose movement in the fetus until week 18, when a fetus can open its mouth and suck its fingers at week 11?
According to Fetal Movement

According to an overview produced by the Royal College of Physicians
  of Edinburgh, purposive movement begins at about 18 weeks, gradually
  replacing reflex movements

but in the same article says

At week 11, the fetus can open its mouth and suck its fingers; at week
  12, it begins to swallow amniotic fluid.

I highly doubt that open a mouth and suck its fingers can be classified as "reflex movements", then how it is asserted that there is not purpose movement in the fetus until week 18 when a fetus can open its mouth and suck its fingers at week 11?

Why do you doubt that finger-sucking is a reflex?

Did you ever put a finger in an infant's mouth :) It's about as reflexive as it can be. +1 for a well researched question though

Swallowing (Nishino, 2013) and sucking (rooting reflex) are reflexes. The fingers may just happen to be in the vicinity of its oral region (they often are; Fig. 1.), and oh boy are babies keen to grab a nipple when it's close! Mouth openings can henceforth be also reflexive, being part of the rooting reflex.

Fig. 1. Fetal hands in facial area. sourceL: ABC News
Reference
- Nishino, Front Physiol (2012); 3: 4892013


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absorption time of zinc in the body
I would like to know how long it takes for the human body to absorb / digest a 10mg zinc capsule?
Note: It is recommended to take zinc  an empty stomach to gain the maximum effect. Regarding to that I think it's also a disadvantage to eat something right after taking zinc?
greetings

Zinc supplements are usually used to treat zinc deficiency or other chronic conditions, so it is not that important in what time they are absorbed but what percent of them is absorbed.
They are certain nutrients, such as calcium (for example, in milk) that can bind to zinc and partially prevent its absorption. This is why it is usually recommended to take zinc on an empty stomach (Mayo Clinic):

Zinc supplements are most effective if they are taken at least 1 hour
  before or 2 hours after meals. However, if zinc supplements cause
  stomach upset, they may be taken with a meal.

Usually there should be no significant difference between taking a pill with food, 2 minutes before or 2 minutes after the food, because in all cases the pill and the food will mix in the stomach. This is because every pill, even if you take it with water, will probably stay in the stomach for at least few minutes before it will be emptied into the small intestine.


text:
Why does the right bundle branch not have any terminal filaments in the IVS of the human heart?
Dubin's "Rapid Interpretation of EKG's" briefly describes this part of human physiology but doesn't explain the reason behind it.
Is there a specific advantage of the human heart having this characteristic, or is it a flaw/useless trait?

Why is a philosophical question, but you can see, below, the most common anatomic variation, with the ventricular septum receiving terminal branches from the septal fascicle off of the left bundle branch though it can come off the common bundle. The left ventricle is larger, and as might be expected, has a greater portion of the conducting system than the right ventricle.


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Nocturnal Animals whose Eyes Don't Shine
Are there any classes of animals which are mostly nocturnal and rely on their eyesight to a non-negligible degree whose eyes still don't shine during the night?
In other words, are there animals which have decent night vision without having a tapetum lucidum?

insects come to mind.

@John I've seen arachnids that have reflecting eyes, quite awesome.

I suspect this feature is mainly found in vertebrates (such as cats, crocodiles and bats). Try invertebrates or marine animals.


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How to find a gene sequence?
So I need to learn how to find the sequence of a gene, polyphenoloxidase. Please do not do this for me. Tell me how to approach the problem.
I have found : https://www.ncbi.nlm.nih.gov/gene and searched for polyphenoloxidase and get a list of results.
Here is one PPO page:
https://www.ncbi.nlm.nih.gov/gene/107923401
There is a FASTA sequence there under " NC_030099.1 Reference ASM98774v1 Primary Assembly" but I am not sure if PPO gene is there.

You need a gene sequence. What're you trying to accomplish? The list you get from the NCBI search notes PPO in different isoforms/types from different species. Perhaps you should first lock down your target organism and gene isoform. And so I click the top result, LOC107923401 (aka PPO-3; PPO-6; PPO-8) from Cotton. Scroll down to Genomic regions, transcripts, and products and click on the FASTA link. There is the raw sequence. Your FASTA and FASTQ files will be the result of NGS on your organism's genome.

@CKM advocado is my target organism.

If you want to blast that sequence, remove the subquery range it provides for you beside the sequence box.

@CKM Tried doing a Blast search for a PPO gene: https://www.ncbi.nlm.nih.gov/blast/Blast.cgi?PAGE_TYPE=BlastSearch&PROG_DEFAULTS=on&BLAST_SPEC=OGP__3435__73885&DATABASE=GPIPE/3435/current
However there are no matches, which may be because it is a different species with a slightly different sequence? The genome I am searching is known to contain PPO.

It doesn't appear that anyone has sequenced it. See here.

You can find the sequence in the gene database, but it is perhaps easier to search the nucleotide database if you are only looking for the sequence of nucleotides.

I used the sequence you helped me find to do a Blast search of a genome here: https://blast.ncbi.nlm.nih.gov/Blast.cgi?PAGE_TYPE=BlastSearch&PROG_DEFAULTS=on&BLAST_SPEC=OGP__3435__73885&DATABASE=GPIPE/3435/current     However there are no matches, which is may be because it is a different species with a slightly different sequence? The genome I am searching is known to contain PPO as advocados do brown.

@Dale It doesn't appear as though there is a whole genome sequence for avocado, yet.

What about: https://www.ncbi.nlm.nih.gov/genome/?term=avocado

The existence of that page doesn't mean that the entire sequence is in the database.

@Dale There are a large number of ESTs for avocado and blasting against those (tblastn) with the tomato PPO protein sequence gave some hits.


text:
How to do a blast search for similar sequences?
Tried doing a Blast search for a PPO gene in an advocado genome: https://www.ncbi.nlm.nih.gov/blast/Blast.cgi?PAGE_TYPE=BlastSearch&PROG_DEFAULTS=on&BLAST_SPEC=OGP__3435__73885&DATABASE=GPIPE/3435/current
However there are no matches, which may be because it is a different species with a slightly different sequence? The genome I am searching is known to contain PPO.

Once again, RTFM!

As stated in the comments here, there is no complete genome sequence for avocado as of yet, though people appear to be working on it.
However, there are a large number of ESTs and doing a BLAST of their translations with the tomato PPO sequence (tblastn) gives some hits.
Here is a link to that BLAST.

However there are no matches, which may be because it is a different species with a slightly different sequence?

This is precisely the problem that BLAST was designed to solve.

how did you get that link to share your BLAST search?

@Dale There is a link on the page, near the top right, called "Bookmark".


text:
On what basis is each chromosome given a number?
On what basis is each chromosome given a number? There appears to me to be no visible ordering between each pair. Is there any reason other than differentiation?

Chromosomes are generally ordered by size in terms of number of nucleotides. The first chromosome is the biggest. Note that when there are sexual chromosomes (as it is the case in mammals or birds for example), the pair of sexual chromosomes are typically considered last irrespective of their sizes.
Note that in some species the ordering has been decided and further studies have shown that the actual size order does not perfectly match the ordering. This is for example the case in humans, where chromosome 11 is actually bigger than chromosome 10 (thanks @canadianer).
Numbering is mainly just a simple naming system. It is just handy to be able to refer to a chromosome as chromosome 3 rather than having to somehow describe this chromosome for other to understand what we are talking about.

I think they were ordered by size before the number of nucleotides in each was known. Chromosome 11 is actually bigger than chromosomes 10 and 12.

Well that depends upon the species and when we got interested in their genome. It is true that for humans the ordering does not perfectly match the size order.

Good point, I forgot there were other species out there besides us :)


text:
Why the genome is divided into several chromosomes and not just a single big chromosome?
In many eukaryote species, there are several chromosomes. In humans, for example, there are 23 pairs of chromosomes.
Why are there several chromosomes and not just a join of all chromosomes into a single big chromosome?

What do you mean by the human chromosome? There are 23 pairs of chromosome in the human genome. What do you mean by chunks? Sounds like instead of "chunks", you meant "chromosome" and instead of "chromosome", you meant "genome". But then the question "why" is more than obvious. There are 23 pairs of chromosomes. There is no arbitrary decision to be made here. We just counted them. Can you please clarify your question?

After edit: Is your question why are there 23 small(-ish) chromosomes and not just a single big chromosome? If yes, is your question specific to humans or to any life forms (or any eukaryote at least) that have more that one chromosome?

Yes. why are there 23 small(-ish) chromosomes and not just a single big chromosome?. And my question is specific to humans

I rewrote your post trying to make it on-topic. Please feel free to roll back if you don't like the edit. I removed the reference to information entropy because really I don't know what you had in mind there and you would weirdly restrict the space of possible reasons by limiting the field of studies that can explain such phenomenon.

I think the answer is related to Information theory

Can you explain your thoughts for why you think that? Again, please feel free to re-edit your post as you like. You don't have to keep my edit.

Remi.b I appreciate a lot your help, and I will not re- edit your post, thank you. You are very helpful

I think the answer is related to Information theory because the genome system has : 1- redundancy by doing chomosome pairing. 2- Error Detection and error correction by base pairing (A - T & C - G)

@ManuelMilla —   This is better included in a revision of your question. Many people do not read the comments and they are not formally part of the question.

please add a paragraph that goes something like that "Based on sources (1,2,3) I think that's because of (reason 1,2,3,4). Is that correct? I dont understand why (2,3) are important" or something. In other words, show your work

@David -- When you ask for a revision in the question, Do you mean to add the reference to my conjecture about the relation between the Information theory and the genomic code?

@aaaaaa - I understand you. I will prepare the possible answer, and when it is ready I will edit the question... I will just add my conjecture at the end of the question

@ManuelMilla I think you probably know too little about both information theory and genetics to attempt relating them. There is no relevance to information theory in your question and although you listed two possible things you have not made any logical link between them and your question.

@Bryan Krause - Imagination is more important than knowledge. Albert Einstein. I have a Degree in Information systems and a specialization in Data mining and knowledge discovery. For me, asking questions is more important than answering questions. I am ignorant in many fields of the knowledge but I use my imagination in order to make questions

I agree that asking questions is important, but tags are here to help people find questions/answers appropriate to their interests; tagging a post with tags that are not relevant is not helpful.

"For me, asking questions is more important than answering questions." Fine, but that's not what SE Biology is about. It's about providing precise answers to answerable biological questions. Questions that only allow opinion, speculation or discussion belong elsewhere.

If you answer your own question (which is perfectly fine) please use the answer section. And please do it in english, as this is the language of this community. It is also not the first language of most persons here. I edited the question accordingly.

Does this answer your question? What limits chromosomal length?

The leading contender of "why" in my former lab, is that if a chromosome becomes too long, a cell cannot fully isolate the chromatid to a daughter cell. Ie in a giant chromosome, the chromosome arms trail so far behind centromere, that the arms are of two sister chromosome are still touching each other even through the centromere have reached the opposite poles of a dividing cell. This prevents nuclear reformation. It would also mean, that the size of the cell will determine the chromosome maximum size.
At present this is a hypothesis. We have only just created the method to make ultra large synthetic chromosomes. I expected an answer is 3-5 years (2021-2023). However we say there is nothing special to a chromosome number.

Related to your answer: https://biology.stackexchange.com/a/35150/6307

So your answer is "We don't know, but a plausable hypothesis is...". Possibly better as a comment.

@canadianer — a very pertinent reference. Perhaps the question should be closed as a duplicate.

Was a bit long to put in to the comments. Right now, this question has no answer, only a hypothesis. However the tools to answer it a systematic manner has been developed.

Short Answer: Humans reproduce sexually and evolution, with some random effects, has led to 23 pairs of chromosomes.
Explained:
Reproduce Sexually - Bacteria do have one large piece of DNA.  This works for bacteria because they will copy all their DNA, and split the two copies creating two "clones" of each other.  Humans, on the other hand, half the amount of genetic material in their sex cells (sperm and egg), which when combined together in a zygote sums to the full or normal amount of DNA.  This is why nearly every cell in the human body has 23 pairs, or 46 total chromosomes.  To have sexual reproduction we therefore need at least 2 chromosomes in the normal, or diploid, cells.
Randomness - While evolution is often taught as a very directed process, there is actually a great deal of randomness that shift outcomes.  The best example is that apes, our closes descendent have 24 chromosomes.  In becoming human, two of theses chromosmes somewhat randomly fused together into the human chromosome 2.  While there could be some selection advantage, what it would be is unclear.  Similarly, many other species have a variety of chromosome number.  Biologists have been unable to directly relate a cause for the number of chromosomes in each species (see UCSB and Museum of Innovation), and have therefore determined that the number is mostly based on random effects.  A good metaphor is that a chromosome is a bookshelf and genes books, the character of a library is not defined by the number of bookshelves or books, but rather the contents of the books.
Evolution - Chromosomes fill several important roles in a cell.  Firstly, during normal cell life they unravel partially and gain/lose different markers (histone marks), which can direct different proteins as to which genes should be transcribed. Secondly, during mitosis the chromosomes must become very compact, and split exactly along the mitotic plane, and during meiosis the chromosomes crossover, exchanging DNA with the other pair.  The mechanics of each event is inherently based on the size and number of chromosome.  For all of these roles, the number of chromosomes clearly has some impact, although the exact relationship is unclear.  So while evolution may select for an optimal number, the strength of the selection is likely very weak and overpowered by the random effects.

So you do not actually have an explanation. You just say that meiosis and mitosis are complicated so that it’s best for the DNA not to be too long, the only evidence for which is the circular argument that there are multiple chromosomes.

Answer has been edited.  The key key answer is that the number of chromosomes must be greater than 1, after that it is mostly random as to how many.  Although I tried to indicate that since the number of chromosome does change the mechanics of the cell, it would be a property evolution could and therefore likely has selected for.

@David: You need to remember that this is evolution, not "intelligent" design.  There might be no real reason, other than it happened to work well enough for the organisms having multiple chromosomes to survive & reproduce.  You might note that in plant breeding, at least, it's quite common to create duplicate chromosomes (polyploidy: https://en.wikipedia.org/wiki/Polyploid )  Once the duplicate chromosomes exist, they can differentiate, creating more space for genetic diversity.

@jamesqf — I found your comment puzzling, so I googled "intelligent design". It appears to be some religious superstition of the native peoples of North America in West Virginia and the like. I live in Northern Europe, in an atmosphere of scientific enlightenment. This taught me to beware of people who substituted scientific dogma for religious dogma and argued that something was so because it was so. It is possible to say "we don't yet know" without implying that it must be the work of some "god".

So your key argument seems to be that for sexual reproduction there needs to be "at least two chromosomes", in humans X and Y. But this argument does not hold because there are other animals in which sex is determined differently, e.g. in alligators, by temperature. And please do not preach to the poster. Most of your answer is patronizing biological background, rather than considered argument, let alone evidence.

@David 1. I think you are confusing sex determination with sex reproduction. Sexual Reproduction requires a 2n cell (n being number of chromosomes) becoming a n cell in meiosis.  Therefore, the total number of chromosomes must be at least 2, with n=1.  2. Intelligent design is not a West Virginia thing, but an idea at least exposed to students in many states. 3. I don't know how I am preaching

But n can = 1. (My other remark was a reply to @jamesqf.)

@David: My point is that when you ask "why", the only answer is often that it just happened that way.  If a few random chances fell out differently, life might be based on single chromosomes (or a single pair).  Now you might instead ask whether it's likely that a single long chromosome might break, whether by chance some might break in ways that allowed the organism to survive, and whether there are might be advantages to multiple chromosomes that allowed these broken-chromosome organisms to eventually become the norm.  But that's hindsight :-)

@jamesqf — In my opinion the key point is when you ask why. Often, as with the interminable evolution questions, the answer is never. It is clear that there is no way of knowing why we have five fingers instead of six etc. — we appear to agree on that point. In such cases it is better not to ask, and if the question is asked, not to answer. However for this question there probably is an answer, and there may even be experiments or an evolutionary paper trail that would support or reject the an idea such as maximum viable length. None has been yet been presented here unfortunately.


text:
Does evolution select against genetic diversity?
Only the best genotype in a species will win. So it sounds like evolution selects against genetic diversity.

I would not close this post as duplicate of "Evolution of diversity and extinction resistance".

selection of any kind reduces diversity almost by definition, without mutation to offset it evolution would quickly run out of diversity to work with. keep in mind however it a rarely a single genotype that is successfully but rather a set complimentary genotypes coexisting.

TL;DR
In a population, directional selection reduces genetic diversity.
Simple scenario
In a population, directional selection reduces genetic variance (at the loci that are under selection and other linked loci). Selection selects for variants that are associated with the highest fitness. Hence, selection reduces the number of variants (or at least the frequency of the variants that are associated with a lower fitness).
Note that, by reducing genetic variance, selection also reduces heritability (see this post for definition) for the selected trait.
Note that, for a correct terminology, you should not say that selection "selects for" low genetic diversity. Selection "selects for" variants associated with high fitness which causes a reduction in genetic diversity. Selection indeed does not "select for" any population-wide statistic but only for specific variants in the population which affect those population-wide statistics.
Selection vs evolution
You say

Does evolution select against genetic diversity?

Please do not confound "evolution" with "selection". There are a number of "drivers" of evolution other than selection (e.g. genetic drift, mutation, migration). Both selection and drift reduce genetic diversity, however, mutation and incoming migration will typically increase it.
Balancing selection
Note also that there are types of selection that maintain genetic variance such as negative frequency-dependent selection, or heterozygous advantage for examples. Those types of selection that maintain genetic diversity are called balancing selection.
Multiple populations
Imagine a scenario where two populations are present in two different environments. If there is directional selection going into opposite direction in each environment (aka local selection), then selection will still reduce within-population genetic diversity but will increase the among-population genetic diversity.
Definitions of genetic diversity
Genetic diversity is a concept used in population and evolutionary genetics. The term genetic diversity is typically defined as the probability of non-identity by state of two alleles. In a single population, this is identical as the definition of expected heterozygosity. Let $p$ be the allele frequency in a population, the genetic diversity $\pi$ at this locus in this population is defined as $\pi = 2p(1-p)$.
More info about these definitions and their relationship to $F_{ST}$ (a widely used statistics of population divergence) in Nei (1973) and Charlesworth (1998).
Definitions of genetic variance
Genetic variance is typically a term used in quantitative genetics. One could say that genetic variance is defined by the phenotypic consequences of genetic diversity. See this post for the definition
For simplicity, above, I used the terms genetic diversity and genetic variance correctly but without highlighting that they take different definitions.
Intro to evolutionary genetics
Your question is a very introductory question in evolutionary genetics. You might be interested in some intro books (have a look at the post Books on population or evolutionary genetics).

Heterozygote advantage, multiple population, balancing selection etc merely delay the problem or break it down into smaller pieces. There is no way to get around the fact that the best genotype in a population will win for the vast majority of traits.
The practical consequence is
https://www.natureworldnews.com/amp/articles/16388/20150907/endangered-species-genetic-diversity-explains-decline.htm

Some species may face extinction when they are not able to adapt as easily to changing environments or defend against new diseases. To better identify or rank threatened and engendered species, researchers from Purdue University suggest using the animals' rate of genetic diversity loss.

Of course this is attributed to more proximate causes and not evolution.

Heterozygote advantage is a type of balancing selection. Your quote is completely unrelated to the rest of the question (and comes from a non-peer reviewed source). The sentences merely delay the problem or break it down into smaller pieces. and the best genotype in a population will win for the vast majority of traits are unclear and possibly wrong.

Are you the same user as user43230 (the OP)? It is totally fine to post an answer to your own question. You do not need to create a new user for that. Changing user for that can be seen as spamming (esp. when the answer is wrong).


text:
What type of bird skull is this?
My aunt found this skull on the beach in Vancouver Canada. I believe it might be a type of bird, but I can’t place it.
It is about 5 inches (~13 cm) long and 2.5 inches (6.35 cm) wide.

Looks like a fish to me.

definitely a fish frontal/parietal. It is too long and rugose to be a bird skull part. If you change the title you might get a some fish experts, who can identify species.


text:
Rabies transmission via barking
According to CDC, non-bite exposure includes scratches, abrasion, and contamination of the mucous membrane from a rabid animal's saliva.
So, is it possible to catch rabies if a rapid animal barks near you? I mean, it can have some tiny droplets of saliva on it, right? Or the contamination of the mucous membrane should come from licks as stated by WHO?

Between 1956 and 1977, 4 human cases of rabies virus infection were
  attributed to aerosolized rabies virus;

Possible but very rare.
https://academic.oup.com/jid/article/195/8/1144/816583


text:
When is an ant colony at its loudest?
I want to make a sound recording of an ant colony located in a wood pile in a German forest (I don’t know the exact species).
To optimise this, I would like to select a time for this when the ant colony is at the height of its activity, i.e., loudest.
My naïve guess would be that noon in summer with some time after the last rainfall is best, but I could find anything to confirm or go beyond this.
Thus I am asking: When is an ant colony loudest, more specifically:

What time of the year?
What time of the day?
What weather conditions?

I believe you speak of some species of Formica spp., such as Formica polyctena (nest example)
You should mind that (i) ants are not particularly noisy insects; (ii) ant nests are 3-dimensional structures within which ants are heterogeneously distributed. So considering a microphone somewhere on the nest where you happened to see more ants, mostly you will be picking up noises from foragers stumbling into debris while moving around. And that only when that region of the nest happens to be most active, which was your original concern. In case I am wrong and you're interested in some smaller ant species (e.g. Solenopsis fugax or Lasius flavus) then you will probably record few if any significant sounds resulting from ants' activities.
Thus my first advice if you're focusing on foragers moving around the nest surface is that you record them in the afternoon of your hottest days, particularly if they're refurbishing their nest or upon disturbance. If you leave the microphone for extended periods try to find out where most foragers are coming out from (and pray they'll not damage the equipment) and leave it there in the afternoon of a dry, hot day.
Now, I am not sure about your ultimate goal, but in case you want to actually hear the ants instead of their stumbling around, then you should focus on having a tiny (protected) microphone inserted into a nest chamber. It is hard to say when the insides of a nest of unknown species will be particularly active, but usually during a fair day, under the sunlight exposure following a wet night. Finding the best region to record ants stridulating inside their nest will depend on finding the best nest location(s) and equipment.
Good luck!

Thank you for your answer. The ant colony in question is actually surprisingly loud, probably due to being above the ground, its size, and its domicile acting like a sounding box. I can still hear it from eight metres distance. This is what inspired me to attempt this in the first place.

Still this is probably their bodies moving about the vegetation, dried leaves, etc, right? If that's the sound you want (i.e. not their true sound communication) and it is so loud, then leave nearby the most busy exit at these times suggested. But I do not know too much about Germany, all the more without knowing species.

Yes, I want to capture the general sounds produced through moving, etc., not communication sounds.


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Why is plasma glucose concentration not double that of whole blood?
It is known that the concentration of plasma glucose is 12% higher than that of whole blood. But since 45-50% of whole blood is red blood cells, shouldn't the plasma glucose be almost double — since it's just the hematocrit that is missing from the denominator.
Obviously something is wrong with this line of reasoning, since it does not meet the observations. Why so? Does whole blood glucose also measure intra-cellular glucose? Is that the reason for the lesser than expected increase?

What units are you talking about — concentration or amount? Please cite values with units, then we can address your question. Otherwise it is unclear and I, for one, will vote to close it on these grounds.

@David I've edited the question, I'm talking about the glucose concentrations in whichever units.

Quoting from the paper: "Within one hour after blood collection protein-free filtrates were prepared from whole blood and plasma according to Somogyi [6] in the following modification [7] : to 2.0 ml of distilled water 0.4 ml of whole blood was added and mixed. Then 0.8 ml each of balanced zinc suiphate and barium hydroxide solutions were added, in this order, slowly and with constant mixing. The mixtures were then centrifuged for 10 minutes at 3000 rpm. (2000 X g). The protein-free filtrates were carefully sucked off with Pasteur pipettes." i.e. the measurements include intracellular glucose.


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Darwin's views on Lamarckian Heredity?
Currently I'm reading She Has Her Mother's Laugh: The Powers, Perversions, and Potential of Heredity, a fascinating book about heredity by the popular science author Carl Zimmer.
While reading this I came across this following passage, which bothers me.

It also meant that the inheritance of acquired traits - taken as a fact by Hippocrates, Lamarck, and Darwin alike - was impossible.
~ Chapter 2: Traveling Across the Face of Time

I've read Darwin's The Origin of Species, and a fair bit of other stuff on Evolutionary Biology, and as far as I know Darwin clearly opposed the idea of Lamarckian heredity. Which is why I was quite surprised to see this, from Zimmer, who's a very highly reputed author. How can he make such an obvious mistake, or is there something more to it than I know? Did Darwin ever agree with some form of Lamarckian heredity?
EDIT
Here's the passage of the book where it appears, for context.

It sounds like a weird claim to me too. Note that a book is not peer-reviewed, small mistakes are not so uncommon. Also Carl Zimmer is a reputed popular author. He is not a researcher (but I he likely has a very decent understanding of evolutionary processes).

@Remi.b yes, I considered the possibility of a small error slipping in, but I find that a little hard to buy. I've read many of his books, and he has a very good understanding of evolution, which means, this is a difficult mistake to make. There's such a fundamental difference between Darwinian and Lamarckian ideas. I've never had a formal education in biology, I'm completely self taught because I found it interesting, and even if I could find the mistake, how could a team of people dedicated to the subject, not.

From wikipedia (without reference): Weismann starts out believing, like many other 19th century scientists, among them Charles Darwin, that the observed variability of individuals of one species is due to the inheritance of sports (Darwin's term). He believed, as written in 1876, that transmutation of species is directly due to the influence of environment.. So the claim might be correct as a reference to Darwin's early thoughts.

According to Ghiselin (here): Darwin accepted the inheritance of acquired characteristics, just as Lamarck did, and Darwin even thought that there was some experimental evidence to support it

@Remi.b — this is really interesting, and should certainly be made into an answer that would be of value. It may explain something I was reading about Morgan recently to answer another question. The Wikipedia entry states Morgan "but rejected Darwin's proposed mechanism of natural selection acting on small, constantly produced variations." However I wonder if it was more that he favoured the idea of genetic mutations (as produced the first X-linked mutant, white, in 1910) being the driver of evolution, rather than aquired characteristics.

I finished reading Ghiselin's article. While some of it sounds legit, he too is guilty of the the same errors textbook authors he criticizes do; providing no or very minimal references. The only really possible way to settle this is reading both Origin and The Variation... by Darwin keeping this question in mind. I'm actually thinking of writing to Zimmer about this as well, hopefully he'll reply.

@Remi.b — Forgot to mention that I noticed and was puzzled by the word "sports" in Morgan's 1910 paper. The phrase "due to further sporting" occurs on the first (free) page. I see from Merriam-Webster that this can mean "tending to mutate freely"

This is sign of good research work :)

I wrote to Carl Zimmer, and he replied within two hours. That's pretty cool!
So I thought I'd put everything I learned about this here as an answer with all the links, and if you guys have more to add, feel free to post more answers.
My Original Email:
Currently I'm reading She Has Her Mother's Laugh, which is a fascinating book, and I'm thoroughly hooked. However, while reading it, I came across this passage that troubled me. The bit in question is in Chapter 2: Traveling Across the Face of Time.

"It also meant that the inheritance of acquired traits - taken as a
  fact by Hippocrates, Lamarck, and Darwin alike - was impossible."

From what I've read on the subject over the years, almost unanimously people agree that Darwin opposed the idea of Lamarckian heredity. I thought that Darwin's idea is that small modifications arising from random mutations (although he didn't know about DNA and genes at the time), if beneficial, were retained and accumulated over the generations resulting in new species. But is it not the case? Did actually Darwin subscribe to the idea of Lamarckian heredity?
I did a little bit of research on this, and found some conflicting and confusing information.
To start with, I've read Darwin's Origin of Species and though I remembered him opposing the idea, so I searched through the book again and found the following para.

Thus, as I believe, the wonderful fact of two distinctly defined
  castes of sterile workers existing in the same nest, both widely
  different from each other and from their parents, has originated. We
  can see how useful their production may have been to a social
  community of insects, on the same principle that the division of
  labour is useful to civilised man. As ants work by inherited instincts
  and by inherited tools or weapons, and not by acquired knowledge and
  manufactured instruments, a perfect division of labour could be
  effected with them only by the workers being sterile; for had they
  been fertile, they would have intercrossed, and their instincts and
  structure would have become blended. And nature has, as I believe,
  effected this admirable division of labour in the communities of ants,
  by the means of natural selection. But I am bound to confess, that,
  with all my faith in this principle, I should never have anticipated
  that natural selection could have been efficient in so high a degree,
  had not the case of these neuter insects convinced me of the fact. I
  have, therefore, discussed this case, at some little but wholly
  insufficient length, in order to show the power of natural selection,
  and likewise because this is by far the most serious special
  difficulty, which my theory has encountered. The case, also, is very
  interesting, as it proves that with animals, as with plants, any
  amount of modification in structure can be effected by the
  accumulation of numerous, slight, and as we must call them accidental,
  variations, which are in any manner profitable, without exercise or
  habit having come into play. For no amount of exercise, or habit, or
  volition, in the utterly sterile members of a community could possibly
  have affected the structure or instincts of the fertile members, which
  alone leave descendants. I am surprised that no one has advanced this
  demonstrative case of neuter insects, against the well-known doctrine
  of Lamarck.

If you read the last few sentences, Darwin says "accumulation of numerous, slight, and as we must call them accidental, variations,..." which to me indicates he's referring to random mutations in genes even though he didn't know what genes were. Furthermore, a little later, "For no amount of exercise, or habit, or volition, in the utterly sterile members of a community could possibly have affected the structure or instincts of the fertile members, which alone leave descendants." and "I am surprised that no one has advanced this demonstrative case of neuter insects, against the well-known doctrine of Lamarck."
To me this clearly indicates he was opposed to the idea of Lamarckian heredity. Could you please explain a little bit more about your stance? I'd love to hear the different viewpoint and the reason(s) behind it.
Since I was curious about this, I posted the same question on StackExchange biology forum.
One of the users pointed me to an article by Michael T. Ghiselin who seems to be in agreement with you regarding the matter.
While some of his points about textbook authors misunderstanding Lamarckian heredity sounds fair and valid, I can't quite see how he came to the conclusion that Darwin agreed with Lamarck. The passage he points to (Lamarck was the first man whose conclusions ...") doesn't say anything about Darwin agreeing with Lamarck about acquired traits being passed down the generations.
In Wiki page about Pangenesis, the following is mentioned just as you have in your book.

"Darwin thought that environmental effects that caused altered
  characteristics would lead to altered gemmules for the affected body
  part. The altered gemmules would then have a chance of being
  transferred to offspring, since they were assumed to be produced
  throughout an organisms life.2 Thus, pangenesis theory allowed for
  the Lamarckian idea of transmission of characteristics acquired
  through use and disuse. Accidental gemmule development in incorrect
  parts of the body could explain deformations and the 'monstrosities'
  Darwin cited in Variation."

Which indeed supports your viewpoint, but to me that seems like a direct contradiction to Darwin's own words in Origin of Species.
So which of it is true? Or, since Pangenesis theory came after he published Origin, did he change his mind later?

Carl Zimmer's reply:

Thanks for your email. I've also had to struggle to work out Darwin's
  views about Lamarck--they were complicated and changed over his
  career. Basically, the more Darwin thought about heredity, the more he
  warmed up to the possibility of the inheritance of acquired
  characters. I've attached a few good papers that may be of interest.
Best wishes, Carl Zimmer

Papers Referred by Carl Zimmer:
Gemmules and Elements: On Darwin’s and Mendel’s Concepts and Methods in Heredity.
Lamarck, Evolution, and the Inheritance of Acquired Characters.
orgThe Early History of the Idea of the Inheritance of Acquired Characters and of Pangenesis.

I haven't read those papers yet, will do so when I find time and hopefully it will shed some more light on it.
So, I'm still not quite sure about the issue, but I do think Carl Zimmer's point of view is fair enough, that it is possible Darwin's views evolved over time. Particularly, given that nobody knew what exactly even heredity means at the time, it's possible that Darwin thought it cannot just be ruled out. Besides doesn't seem like he was out campaigning for the idea, rather allowed for it with his Pangenesis hypothesis.
After all, Darwin's theory was about how small modifications accumulated over time leads to species change, not how those changes occurred in the first place. So, while it turned out to be untrue, if there was a mechanism in which experiences could be stored in the unit that transmitted heredity, you can probably incorporate that into Darwin's theory of evolution. That probably was a line of thought Darwin had.

Wow amazing. Thanks for sharing your email with C. Zimmer. If you happen to read the linked articles and wish to summarize them, it could be quite awesome to add you summary to your answer.

@Remi.b yeah I plan to read those three papers as soon as I can, and will try to summarize them here afterwards.


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What is this tiny translucent worm I found on my desk?
I found this tiny critter crawling vertically up my speakers. It seems to crawl like a caterpillar, but strangely, every now and then, it stops, rears-up and look/ feel around.
It looks sort of grey/ translucent from a distance with a maybe orange-ish head and tail-tip, however, looking at it from above, it seems to have a black center.
It was kind of hard to take a clear picture, but I hope it helps.
P.S. Got it in a glass before, just because I've never seen anything like it before. My friend said it might be an alien.

That is a lepidopteran, most likely in the family, Geometridae. An "inchworm". https://www.thoughtco.com/geometer-moths-inchworms-and-loopers-1968193


text:
What causes the preliminary changes in resting membrane potential in neurons?
Background: The neuron's membrane resting potential is maintained at a certain voltage. The neuron has a lipid bilayer with certain protein channels which allow the movement of ions in both directions (in and out). Some of these protein channels are gated by:
1) mechanical changes (stretching, pressure, etc)
2) voltage changes- regulated by electrical signals (transport of Na+, K+ through protein channels)
3) Ligands (neurotransmitters, etc)
(Guyton and Hall, Textbook of Medical Physiology, 2016)
Question: If action potentials are brought about by voltage-gated channels which are activated by the change in voltage, what brings about this change in voltage which activates voltage-gated channels?
It sounds a bit convoluted. Here's a quote from Wikipedia's Membrane Potential page:

Because voltage-gated ion channels are controlled by the membrane potential, while the membrane potential itself is influenced by these same ion channels, feedback loops that allow for complex temporal dynamics arise, including oscillations and regenerative events such as action potentials.

Hopefully this quote will help to communicate my confusion.

You have already listed two possibilities:

1) mechanical changes (stretching, pressure, etc)

and

3) Ligands (neurotransmitters, etc)

In the central nervous system, ligands and in particular neurotransmitters are going to be the overwhelming cause of most initial depolarization. Ligand-gated ion channels are the simplest mechanism: some examples include AMPA receptors, GABA-A receptors, and nicotinic acetylcholine receptors, but it is also possible to change the membrane potential via second messenger systems that open or close other channels.
In the periphery and in sensory organs, sensory-evoked potentials can be caused by mechanical gating, as you mention, as well as by specialized channels that respond to particular stimuli, for example the TRP family which includes channels sensitive to temperature (for example TRPV1, which responds to heat and also responds to capsaicin, the chemical that makes chili peppers 'hot') and to certain chemicals in food (resulting in taste).
The other category you missed is that some cells generate a spontaneous depolarization because they contain channels that are activated around the resting potential (and/or potassium channels that close, which also depolarizes the membrane). This is crucial for the cardiac pacemaker but can also be found in the central nervous system in some cell types.


text:
Does using animal models for medical research also promote veterinary research on these animal types?
I have been reading about mouse models for studying inflammatory bowel diseases such as Crohn's disease and Ulverative Colitis. For example, according to this publication, a widely used mouse model for colitis is the Dextran Sulfate Sodium (DSS)-Induced Colitis.
This got me thinking: when we induce disease in mice (or monkeys, fish etc.), is that somehow beneficial for veterinary research of these animals when they get sick (unrelated to medical research focusing on humans)? Are the data from pre-clinical trials used for that purpose in any way?

Short answer is no. Human disease take a long time to develop naturally, far longer than the lifespan of animals models used (mice, rats or fish).
Also the cost of the drugs far exceed the cost of the animal. There is little point in spending $40k to make a non-commercial anti cancer drug to save the life of a pet mouse who has developed the rare cancer.
Longer answer... some... a bit. Not quite what you expect. There are a few labs that are re purposing anti cancer drugs that failed animal (mouse) trials to treat dogs. It appears that people are willing to spend a fair amount on experimental drugs to save the life of the family dog.
Mice have increasingly been shown to be a poor model for human anti cancer drugs. Their cells grow to fast, their immune system is subtly different from humans. Stuff that work in mice often times are too toxic in human or just don't work. A longer lived animal model is needed. However dogs as experimental animals is too costly to maintain, too much red tape to use and takes too long for cancer progression (You cannot wait 2 years for a cancer experiment to finish).
However a sick family dog with cancer is another matter.

I don't follow the logic of this answer - it seems focused on the usefulness of animal models for human disease. It hardly addresses the actual question about veterinary research.

The animal models used (in research) are too short lived to be naturally affected by many of human disease that are being researched. So direct application of this research to mouse health care is very limited. Furthermore when using said research data is used on human, often we find the work not applicable. So by guess work successful mouse anticancer drugs are unlikely to be successful in other animals either. The best use of research in mice has been the use of failed (by mouse test) anti cancer drugs in pet dogs.


text:
Ligaments at the posterior superior iliac spine
In Causes of Back Dimples, it was determined that these 'Dimples of Venus' are created by

a short ligament stretching between the posterior superior iliac spine and the skin. They are thought to be genetic. (@Johnny)

The linked article in the answer to my original question says nothing more other than the fact that dimples of venus are normal dimples (not medically significant).
DrLumbago.com states:

The sacroiliac joints move together as a single unit.  From the back it is common to see a pair of dimples on the buttock near the base of the spine.  These are sometimes called the “dimples of Venus” and they are a landmark for the top portion of the sacroiliac joints.

Posterior superior iliac spine (PSIS) marked in red

Image made by DBCLS (Polygondata is from BodyParts3D) CC BY-SA 2.1 jp, via Wikimedia Commons
Ligaments of the PSIS
Cooperstein & Hickey (2016) has an image of ligaments connected to the PSIS, but unless I am mistaken, the image doesn't seem to have the ligament(s) involved with the dimples of venus.
It seems from the description in Kumar, et al. (2014) that the "dimples of venus ligament(s)" are connected to the skin, and seeing that ligaments are fibrous connective tissues that normally connect bones to other bones, I am intrigued to know more.  What is the name of these "dimple of venus ligaments" and what is their purpose?
References
Cooperstein, R., & Hickey, M. (2016). The reliability of palpating the posterior superior iliac spine: a systematic review. The Journal of the Canadian Chiropractic Association, 60(1), 36.PMCID: PMC4807681
Kumar, A., Kanojia, R. K., & Saili, A. (2014). Skin dimples. International journal of dermatology, 53(7), 789-797. DOI: 10.1111/ijd.12376

It seems from the description in Kumar, et al. (2014) that the "dimples of venus ligament(s)" are connected to the skin, and seeing that ligaments are fibrous connective tissues that normally connect bones to other bones, I am intrigued to know more. What is the name of these "dimple of venus ligaments" and what is their purpose?

First, re: what a ligament is, you're correct in your understanding that ligaments generally bind bones to bones (vs. tendons), but the term is used more broadly as connective tissue that binds things together, holds them in place, is a remnant of a fetal structure, or a mesenteric fold. Your wikipedia link acknowledges this. Some examples are:

Round ligament of the liver: a remnant of fetal structure
Broad ligament of the uterus: a mesenteric fold
Median arcuate ligament: this one actually binds two muscles together
Sternopericardial ligament: binds the pericardium to the sternum

The unnamed short ligaments Kumar describes (and wikipedia, quora, and stack exchange have repeated), are probably unnamed because they are difficult to isolate and study, and they are not clinically relevant. They may even be theoretical. There are no studies on them indexed in medline, and they aren't discussed in any anatomy text I've read. Dimples are generally thought to be caused by fibrous connections between the skin and muscle, bone, or other deep tissue. If you ever cut into the back of a cadaver or surgical patient, you'll see that there are a great number of unnamed fibrous connections to the skin. It's not unreasonable for Kumar to invoke them as the cause for these dimples.


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This strange spiral creature grew up in my cup of water after night
This grew up in my water cup over night!

Length ~ 12mm
Form - spiral made of dark dots
It does not move
Growing slowly

Can some one help identify it?

I would guess these are eggs of some animal. Just a wild guess.

Can you give us a location as well?

Yes, of course! https://www.google.com/maps/@46.3494507,48.0312648,332m/data=!3m1!1e3

Wow, what a precise location :D I didn't know that there was a city with such a name, only knew the fur with this name! For how much time that speak would grow? Did it happen something afterwards?

It was expanding for 20-30 hours, then almost completely disappeared in water.

See my comment on this question

Definitely eggs since it appeared so quickly. Caddisflies (Trichoptera) lay their eggs in spirals within a slimy blob, but some searching made me see that other animals do too. Like this https://bugguide.net/node/view/641162 that apparantly comes from midges. Perhaps someone else can come closer!

@picapicaThank you! We have a lot of Caddisflies and Chironominaes here, great guess!

It appears like the egg mass of some Chironominae species. At least searching "Chironomus eggs" returns visually similar images. @picapica can you post an answer?

See this SO question for an answer to a related question, which points to Chironomous egg masses.


text:
Which DNA would sperms contain from a transplanted scrotum?
We had a discussion at the coffee break today about transplanting a scrotum.
Let's assume that it's possible.
Would the produced sperms contain the DNA of the donor or the one that got the scrotum transplanted? Can you explain why?

What do you mean by pouch? Testicles? Penis? Marsupial pouch?

Found the correct word (I think). English is not my native language.

Possible duplicate of Is DNA replaced after organ donation?

Johnny: I'm not asking about the organ that was donated, but the sperms produced in it. Aren't they produced using elements from the rest of the body?

So you are really asking for a hypothetical testicle transplant not scrotum, the answer would still more or less be the same as given in "Is DNA replaced after organ donation?". You are not the first to ask this question, if you head over to Reddit, there's an entire thread dedicated to the subject: https://www.reddit.com/r/AskReddit/comments/czaae/if_you_had_a_testicle_transplant_would_your_sperm/
As you can see the answer is the same..

There also is an article in The Verge: https://www.theverge.com/2018/4/26/17286728/penis-scrotum-transplant-surgery-us-veteran-johns-hopkins-testicles-ethics


text:
Is there a notion of RMSD for two different molecules?
The (least) Root Mean Square Deviation is used for comparing different conformations of the same molecule. However one may be interested in comparing the conformations of two different molecules e.g. two proteins of different backbone lengths. So is there any method for comparing conformations different molecules such as a generalized RMDS?

PyMOL ("align molecule1, molecule2" returns aligned structures and RMSD). TM-align (returns aligned structures and TM-score; tmalign.py is a python module for running TM-align using PyMOL).


text:
Distinction between primary and secondary tumor
How can a primary tumor be distinguished from a secondary tumor? I tried finding it on the internet but it only said that they are found by means of immunohistology but I couldn't understand how.Please elaborate

Different tissues express different proteins, and cancers are often allocated to their primary tissue by virtue of expressing proteins specific to the type of tissue they arose in. Of course, with primary tumours there is also the advantage of imaging ; lung cancer, for example, can be localised to the lung based on a PET scan.
Sometimes though there are cancers of unknown primary , where a metastasis is picked up, but allocation to the primary tumour is not possible because it wasn't detected. In this case, it is possible to use epigenetic profiles to predict the tissue of origin for the tumours in question. See https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(16)30297-2/fulltext

The difference is pretty easy to understand. The secondary tumors is metastiesed tumor sped to enother parts of body. On the other hand the primary tumor is the source of the metastiesed.

I give you one example of this. On of the most common tumor of testicles is seminoma metastiesed to the peritonium, lungs, brain.

The secondary tumor is usually hard to distinguised with primary. But usually if there is specific antigen which can be recognised by antibody. The antibody is usually cultivated in mice. But this antibody have to be recognised by enother antibody. The second antibody to mice antibody is cultivated usually in rats. After that the secondary antibody is usually modified by fluorescent chemical. This is indirect immunohistochemistry. Direct is usually only the first antibody modifided by some fluorescent.

So first of all you have to do biopsy of that potential tumor. After that the sample is usually fixated by freazing and sliced by cryomicrotom. Than samples is usually put in to petry dish and poor with izotonic solution. Then the primary antibody is add. It take some time to react (find the antigen), thereafter is add the secondary antibody. To view the antibody you have to activated fluorescent by laser in fluorescent microscope. So if the fluorescent is in the sample, the tumor should be secondary.

Nevertheless is still hard to distinguish secondary tumor from the primery. Usually is up to experiencies with the tumors and how they are behave in body of patient. This is one of the reasons why is hard to treat the cancer.

By the way you can see the antigene as adress to cell and antibody as post man.


text:
What kind of spider is this? (Photo included)

We found this guy on the ceiling inside today. We live by Lake Erie in Ohio so we see a lot of large spiders, but this one looks different than most we encounter. It's was about the size of a quarter (~ 25 mm), and the abdomen was iridescent.

Not a spider person but I did find this useful summary of commonly encountered Pennsylvania spiders, a few of which are similar-looking.

It looks to me like a false widow spider, Steatoda grossa. It would be helpful if you could find one in their web so I could see what its web looks like.


text:
MLE estimation with Mk model in ape or phangorn?
When doing MLE with the R package ape or phangorn, is it possible to set the substitution model to Mk? If so, how does one do this?

I'm voting to close this question as off-topic because this belongs on Bioinformatics SE

SE Biology has an established question tag for bioinformatics, so that property alone should not be reason for closing the question as off-topic.

When u have a Stack Exchange website solely dedicated to bioinformatics work, I would suggest that you ask your question there.

I will do that. The existence of the Bioinformatics SE does not make this question off topic, however.

From reading though the documentation, the Mk model does not appear available.
Although the JC69 model is, which this source describes as a slightly less generalized form as Mk.  The JC69 model still assumes equal substitution rates and equal base frequencies.  To use the JC69 model in phangorn set the model to "JC" and in ape set the model to "JC69".

Of course this will not work if you have more than 4 discrete states - JC69 is a DNA model of sequence evolution. Look into using a program which isn't R. RAxML, IQ-TREE, MrBayes all allow Mk.

The R package diversitree has a large range of models including functions to optimise under Mk. Perhaps have a look at that.


text:
Should I help this young Magpie?
I found this young Eurasian Magpie in my garden:

He is just standing there, not doing anything. I believe he fell from a tree and can't fly yet and is just waiting for the feeding from his parents until he can fly, but I wonder if that’s true and if I should do anything to help.
There’s another young one on a branch of a nearby tree, also:

Call the RSPCA or whatever animal rescue service there is in your area. Posting it on SE doesn't help the critter in any way I'm afraid.

@AliceD my question was precisely if there is something I should do, or if this just normal in the bird's growing process

And my answer is precisely call the RSPCA or whatever animal rescue service there is in your area. Posting it on SE doesn't help the critter in any way I'm afraid.

@AliceD actually it does help the critter. The OP didn't know what to do, and didn't want to interfere without knowing if he/she should, so came here to ask someone who knows better, which in my opinion was a good thing to do. And you, presumably someone who knows better, said call RSPCA, which is useful information the OP received he/she didn't have before.

It's best to leave the bird alone. The parents are likely still in the area and tending to the young, including feeding and chasing away would-be predators. You're better off staying away so as to not intimidate or upset the parents. If you have outdoor pets, relocate them indoors or to an enclosed area for a few days.
Failing this, the advice given in comments to call your local animal rescue is best.

I actually saw a pair of adult magpies chasing off a hawk in the sky later, so maybe those are the parents. Thank you for the answer

check the guides "what do I do if I find a young bird on the ground"... if there are no cats it should be ok.


text:
What plant is this? (Found in Southwest Germany in June)
The picture was taken in Southwest Germany in June, and they covered the ground of a garden we were at...

Undoubtedly a Sedum, but someone with local expertise will have to give the species.  Wikipedia states there are several common species in Europe (https://en.wikipedia.org/wiki/Sedum).

I am almost sure this is Sedum reflexum (aka S. rupestre), in English prickmadam or crooked yellow stonecrop and in German Felsen-Mauerpfeffer. It usually grows at rocky or stony ground, not full of grass.
Distinctive features are the pointed leaves, which are not as round as in S. album and also the bended stem (flower stalks are always bend, hence the name reflexum). Its' flowers should be yellow.
These features can be seen well at the botanical drawing below (from wikipedia commons).

The reason I'm not completely sure is that in garden (and on roofs) exotic sedums are often planted.


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What is the carbohydrate found in almonds, cashews, pecans, hazlenuts and pistachios?
What is the carbohydrate found in almonds, cashews, pecans, hazelnuts, and pistachios? I first thought they probably have starch but I am not sure. Can someone verify this for me, and/or send a link where I could find this information?

Firstly you must realize that all the above mentioned nuts are actually the seeds of plants.
So the question now is which carbohydrate is mainly found in seeds of plants.
During the double fertilization of angiosperms, one sperm fertilizes the egg to form the embryo while the other fertilizes the endosperm nucleus to form the endosperm which acts as the nutrient storage for seeds.
The major carbohydrate for seed endosperm is Starch, often stored as granules for their property as being insoluble and compact.
However there are other carbohydrates such as free sugars, glucofructans and hemicelluoses present.
Hope this helped.
References
https://link.springer.com/chapter/10.1007/978-1-4615-2672-8_8

For the plants listed in the question (almonds, cashews, pecans, hazelnuts, pistachios) the primary storage is not the endosperm but the cotyledons. These seeds have two distinct halves, each a cotyledon, with an embryo sandwiched between. Starch is likely the most abundant carbohydrate, but there are other "nonstructural carbohydrates" as well as cellulose. Since these are intact cells that may go on to photosynthesize, these carbohydrates can be very diverse, and will differ between the species. Note, too, that these seeds will store many other nutrients, like proteins and fats.


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Is the rate of photosynthesis higher than the rate of respiration?
In photosynthesis carbon dioxide is used up and oxygen is produced and at the same time plants respire too. So oxygen is used up and carbon dioxide is produced.
Then the net exchange of gases should be zero. If this is so, then why do we say that plants maintain the level of oxygen and carbon dioxide in the atmosphere?
So, is the rate of photosynthesis higher than the rate of respiration in plants in a year(overall)? What is the net exchange of gases annually?

The net exchange of gasses in any area will be different depending on the number of plants and what plants they are.  This is because it depends on the number and size of leaves, and because chlorophyll is essential for photosynthesis, it also depends on the amount of chlorophyll in the leaves. Therefore that part of the question is very broad.
Overall, photosynthesis (oxygen production) is higher than the rate of respiration in plants during a year.
Aerobic respiration continues all the time in plant cells (in light and in darkness), using up oxygen and making carbon dioxide. Photosynthesis, in contrast, occurs only in light and uses up carbon dioxide and makes oxygen. The more light there is, the more oxygen is produced.
There is a light intensity at which respiration and photosynthesis cancel each other out. This is called the compensation point. Below this level carbohydrates are used up and the plant cannot grow.

This and more can be read in this document from the Royal Society of Chemistry


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What kind of big bird is this seen walking around Taipei?
I've seen this humorous sign warning drivers to keep an eye out for birds many times, but today I finally realized what it's talking about!
This is a large bird and I've seen it all around Taipei in gardens and green areas. It's not shy of people unless you get too close.
I'd guess it's about 30 cm tall when standing upright, but it often is bend down looking for things to eat. It takes one step at a time, sometimes very slowly, and it's head moves out-of-synch with its body as it hunts for food. I am not sure if it can fly, I've only seen it on the ground, and I've never heard it make a sound.
It's various shades of brown and tan, and just like the cartoon on the sign it has long feathers projecting backwards from its head. That can be seen in the center top of the photo montage.
Any idea what kind of bird this is?
These are cell-phone photos from the closest I could get without it getting nervous.

"Life imitates Art far more than Art imitates Life" Oscar Wilde

Does anyone know what the sign says?

@CDspace I don't have an official translation, but I'm told it doesn't match the humor of the drawing, and says something like "animal crossing; slow speed, pass slowly".

Ah, I see it now. The bird is in the foreground, and not Godzilla size picking up the car

@CDspace actually I believe it's meant to look huge. That's the style of warning signs here, often a little humorous and cartoonish to catch your eyes and not to appear too authoritative.

I am fairly certain that this is a Malayan Night Heron (Gorsachius melanolophus).
Taiwan is listed as one of the countries where the Malayan night heron can be found. Its diet consists of small reptiles, snails, chilopods, arachnids, crabs and insects. This would explain why you have observed it bend down a lot to look for food.
Needless to say you can find more information in the corresponding Wikipedia article.
Here a photo with better resolution:

Photo by: Pete Morris/Birdquest
In addition, here is a link to a video taken in Taiwan. Does this remind you of the bird that you saw?

That's a great photo, yes this certainly looks just like it, thanks! Okay I'll give the article and video a look. Tis one and the one in the video are a little darker than the ones here but that could just be regional variations. Southern Taiwan has some differences in flora and fauna.

You are welcome. I agree, it could well be that there are regional variations or that males looks slightly different to females (sexual dimorphism).


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Does gene editing have any technical cross-species limits?
How far could you go in cross-species gene editing?
Is it possible for example to introduce plant genes into human DNA and vice versa?
Question: How is gene editing limited by the "donor" and "target" species?

Putting plant cells into a human has nothing to with gene editing (and wouldn't work). I'd advise that you make clearer if you want to ask about this specific case (plants cells / genes into human) or about the general limits of gene editing.

thanks, of course cells come after all through gene experession, but fixed that now . Yes I want to know general limits of gen editing.

So, I'll assume that you are talking about gene editing in a laboratory (e.g. using a technique like CRISPR).
Theoretically, there are almost no limits to what you can do - or at least try. Fundamentally DNA is the same in all living (and non-living) things on earth, so you can absolutely take a gene from a plant and "paste" it into a human cell/genome (with some additional work needed to make the pasting work). You probably even go further and try to isolate whole chromosomes from one organism and (literally) inject them into cells of another one.
The problem with this radical approach to gene editing is, that it probably won't do much (good). A human cell likely doesn't recognise a plant gene as a gene and so just ignores it (it might still cause indirect problems for the cell though) and if you start making very drastic changes like adding chromosomes the chances that your cells will just die are super high.
This means that in practice you either need to (heavily) modify a gene you want to insert to match the structure and 'expectations' of the target organism - you basically have to make a humanised version of a given plant gene - or you can only use genes from similar enough organisms: as a general rule genes from the same kingdom (bacteria, archaea, plants, fungi, animals) are likely to retain some degree of function in another species (but how much exactly or even a general effect is almost impossible to predict).


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Difference between morphogens and evocators in development?
I am specifically interested in this within the context of 1950's developmental biology (I presume the meaning and scope of usage of the terms has changed since then), as I am reading Alan Turing's paper on 'The chemical basis of Morphogenesis'. Turing first mentions evocators in the context of 'evocators of Waddington'. I have read some articles by Waddinton to try to see what he meant by 'evocator', but have not gained clarification from the articles available online. Turing cites Waddington's "Organisers and Genes", which is not available on the web and I do not have access to.
A more recent article here states

The first element is the inducer (or evocator) defined as the signal emanating from a piece of tissue, such that when the tissue is transplanted to an ectopic position it elicits changes in the behavior of neighboring cells.13 Today, we understand that most of these inducers are secreted proteins and include morphogens belonging to the Wnt, Hedgehog (Hh), TGFβ, EGF, and FGF families.

Which seems to imply that most evocators are morphogens, although from the definition of evocator given I would say that this is exactly what a morphogen is!
Any insights would be much appreciated!

"Since the evocator Waddington and Needham discovered was ether soluble, it was considered to be a sterol, a class of molecules that includes many hormones related to later development" (https://embryo.asu.edu/pages/chemical-induction).
It seems like the termed is outdated, hopefully, you find this information useful.


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Program (on Mac) to show 3D protein structures?
I have an assignment for 6th grade biology. I have to look at a 3D structure of a protein and manipulate it so it only shows the AA I’m interested in currently.
what I already did
I already looked up the programs most used for this and they point me to JMol and Yasara but the download files are .bin files and the like and I don’t I don’t understand which file is the one I should download and how to install it.
Can someone help me please ?

Jmol: how to install
Here are instructions for getting Jmol to run on a Mac (or with a slight variation in the runtime file you need to download and the security warnings, on a PC).

Download Jmol from
https://sourceforge.net/projects/jmol/files/latest/download?source=files
The name of the file will be something like Jmol-14.29.16-binary.zip. Double-click to unzip.
The unzipped folder has a confusing variety of files. This is because most are used for setting up web pages with Jmol embedded. However there is a double-clickable desktop application without any icon and the unpromising name of: Jmol.jar. When you double-click to launch it you will most likely get a message as shown below (1):

To get round this you must either control-click or right-click and select `Open With > Jar Launcher as shown above (2).
Click ‘Open’. (Next time it will just launch without right-clicking.)

Now, in my case the program launches because I have the Java runtime installed on my machines, but you will probably have to download and install this.
Go to the Oracle Java website at http://www.oracle.com/technetwork/java/javase/downloads/jre8-downloads-2133155.html
Download and install the appropriate Java SE Runtime Environment, e.g jre-8u172-macosx-x64.dmg
Try launching jmol.jar again. It should work this time.

Jmol: how to use
Because of their emphasis on Jmol in relation to the web, the developers of Jmol do not provide an easy entry to the desktop program. However you can find a clearly illustrated series of web tutorials at the MSOI Centre for Biomoleclar Modelling. I’d highly recommend this as a starting guide.
Although I am not going to describe how you can visualize particular amino acids as that is part of the poster’s project and can be found in the instructions. there are a couple of pointers I would make about things that are not entirely obvious.

After you have loaded a protein from the file menu, you will probably want to change its representation, not least because it may be surrounded by red balls (oxygens from water). To do this you need to right click (or click on the Jmol text on the bottom right) and go through two levels of submenus to select an appropriate representation, as shown.

In order to make the selections you require you will need to issue commands in the ‘Console’. This can be selected from the File menu:

I've just updated my post with a link to a site with a well illustrated introductory tutorial. I use Jmol/JSmol myself, so I am happy to try to answer questions that member may have.

I've expanded my instructions for getting started because this is not intuitive.

You could use an online molecular viewer for this. A fairly complete list is available in Wikipedia as well as in JMol wiki.
In particular, JMol that you tried to install has also a JavaScript version called JSMol that you can use on any website that embeds JSMol:
RCSB, Proteopedia, a JSMol tutorial, and many more. To load own structure in JSMol: right click and select File > Load > Open Local File.
If you'd prefer a desktop program, there is also plenty of them: JMol, PyMOL, Chimera, VMD, CCP4mg, etc. All of these are free for non-commercial use (some are even free for commercial use) and work on Mac.
The most popular file format for storing 3D structures of protein is the PDB format. If you would not be able to make your viewer of choice to show only the amino-acids you want, you can always open the PDB file in a text editor and remove lines (atoms) that you don't need.

LiteMol Viewer, an HTML5 web application for 3D visualization of molecules and other related data.

Avogadro has a mac version you can use. https://avogadro.cc/
I found it simple.
edit:
You can view the protein you listed here, maybe?  ( I am on windows so I do not know if this web app works perfect on mac OS)
https://www.ncbi.nlm.nih.gov/Structure/pdb/1C9O
then in the bottom left corner of the structure image box, there will be a small box icon with arrow.
.
Then you can click on View Sequences and Annotations, under the window tab.

You can then click on the details tab and then left click and drag on the Amino acid sequence to highlight them on the sequence and where they are on the corresponding structure.

Crashed when I tried to load 1c9o.pdb on Mavericks.


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Glycogen replenishment after exercise
In the body, the liver holds between 90-110 grams of glycogen in storage, while skeletal muscle storage makes up another 400 grams.
If a person exercises and depletes both stores, when a carbohydrate source is consumed, which of the stores is replenished first?

What kind of conclusions would you draw from either process being faster assuming it was depleted somehow?

Would you say you eat before you workout and drink enough water? What other supplements do you take?

I eat good amount of carbs and a banana, no supplements just a multi vitamin once a day

What makes you believe it is one or the other.

I did read that "Your muscles are the secondary storage facility, filling up only when the liver has reached its storage capacity". Is this true? So the muscles will only take in carbohydrates when the liver is full?


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How to convert between Kunitz units and Enzymatic units?
I've googled around and there has been the common answer of 1.5 U = 1 Kunitz Unit, but none of those answers have come from a reputable source, so I am really doubtful. :(
The enzyme I use comes in 723 Kunitz units per mg protein, but I need 600 U per mg of DNA being used in my procedure. I do not know how to properly determine how many Kunitz units equivocate to Enzymatic Units, and vice versa.


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Hepatocytes polyploidy
Why are some hepatocytes polyploid?


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Mathematical models of gene editing using CRISPR
One confusing thing I have found when reading articles about possible CRISPR based gene therapy treatments in humans is that there is vey little discussion about what percentage of your cells will actually have their DNA edited, the rate at which the editing takes place, and how to quantitatively estimate how many edited cells would be needed to "cure" a specific disease.  (It's not so confusing how edits could be made to a small embryo, what's confusing is what is actually possible for grown patients)
Can someone provide a few basic facts that calibrate what is currently possible and what is needed.
For instance, is it currently possible to edit more than 50% of the cells of an adult  nematode (or more complicated organism) using CRISPR?  How long does it take (minutes, hours, days, weeks).
For the current list of human diseases that are possible targets for gene therapy, how many cells need to be edited for one of those diseases to be "cured" (hundreds, thousands, billions, etc)
But in general is there a name for the mathematical models that try to predict how many cells will end up being edited, how those edited cells will multiply and replace diseased tissue,  and how many edits are needed to generate a concentration of missing protein for a treatment to be successful?
cheers!

There are several probabilities that you need to take into account.

The efficiency of DNA transformation of CRISPR encoding DNA and
target DNA into the host cell (varies between cell types and
transformation agent).
Efficiency of cutting by CRISPR at target site. (varies by DNA compaction - which varies by site and cell type, and guide RNA)
Number and cutting efficiency at off targeting sites.
Efficiency of degradation of free DNA by cellular antiviral systems
(varies between cell types)
Efficiency of DNA repair machinery to fix dsDNA breaks. (thus removing CRISPR cut sites. Varies by cell type)
Efficiency of recombination machinery (homologous
recombination and microhomologous recombination) (which is used to
insert new DNA sequence).
Probability of NHEJ damaging target site. (which can delete the CRISPR cut site)

Too many things to count.
However to give you some idea. The efficiency of CRISPR making a correctly targeted knock in for DT40 (chicken lymphoma) is  ~1% of all resistant colonies (ie colonies that have taken up the DNA seq used to make the knock in), when lipofectamine reagents are use. Lipofectamin trasfromation efficiency varies depending on the size of the transformed DNA, host cell type and plating density. So for a 5kb construct that transformation efficiency varies between 30%-50%.
CRISPR is nearly 100% efficient in yeast cells, ie all knock in cells are correctly targeted. This is likely due to the high levels of HR in yeast


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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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How does one identify a seed's species & variety?
How does one identify a seed's species & variety, could it be done by some means of DNA or by use of a microscope?
Say for example, I had a pumpkin seed, I knew that it was a "small sugar pumpkin" variety, but how would one scientifically identify it to know that it was infact a small sugar pumpkin as well as a pumpkin without going through the process of planting it. Is there some kind of indicator on a DNA level that shows "This is what I am?"
My knowledge regarding biology is extremely basic, but I am very interested in knowing the full process of how this would work.

You sure, could identify plants by genotyping them. For many species, you can probably identify morphologically. For example, I am sure you are able to tell sunflower seed apart from flax seeds. Now, it will depend a bit about how accurate you want the identification to be. Sequencing would ultimately be most accurate (and most expensive) method.

@Remi.b: I disagree.  The most accurate method would be to plant it and see what grows :-)  I'm not sure sequencing would be that accurate, unless you have a pre-existing reference sequence for comparison.  Even then, I doubt that all small sugar pumpkins are genetically identical.  Could the gene(s) that differentiate a small sugar pumpkin from say an ordinary Halloween jack-o'-lantern one be reliably distinguished?

@jamesqf Ha ha that's right. Of course you;re right, identifying by genotyping will depends upon reference sequences. It will for sure be helpful to grouping related individuals in one's sample though.

Yes, their name are "molecular marker". Every gene carrying a phenotype, quantitative or qualitative, is identified as an allele of every gene encoding for proteins.
In order to identify a phenotype using just infos gained from DNA, you'll need a previous library made by these gene regions, were every polymorphism between them is associated with a phenotype. For example, a kind of marker used for this kind of work is SSR , or "Simple sequence repeats" : it is made by a simple sequence of DNA interspaced between two other region. The number of repeats of the internal sequence could be associated with a phenotype.
So, by a simple PCR you could amplify this regions:

And by a electrophoresis you could see how much repetitions are in your band, using just the molecular weight.
Here is an example of SSR used for phenotype/genotype screening


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What do Caucasians see in their peripheral vision, and how is their visual field?
I am an Asian who has no idea how much of their nose Caucasians (especially for those with extremely deep-set eyes, very prominent and low brow ridges, and high noses like Brian Shimansky or Rishi Idnani) can see. I also wonder if they are distracted by their nose.
Also, what are their visual fields (nasal, upward, and downward) in degrees?
These articles have made me think of this question: http://pizzawithrice.blogspot.com/2012/08/wondering-about-white-people-visual.html?m=1
https://www.quora.com/Not-to-be-racist-but-why-do-Asians-have-smaller-eyes-and-does-it-affect-their-vision (comment of 3rd answer by Dale Thomas: "I did always want to ask. Do Caucasian men see their eyebrows and forehead? Is there any impact on vision?")

I think we only needed to see the face from the picture!

Speak for yourself @Remi.b. Haha!

There is quite a diversity of noses among caucasians too. As a caucasian with a somewhat similar nose than the guy on the picture (but not as extreme), I can say that I am able to see the "bulgy part" of my nose if I cross my eyes. If I point my eyes toward the right and close my right eye (and vice-versa on the left), I can see a fair part of my nose. If my right eye is left open, the I can barely notice the presence of my nose. I have never felt like my nose was a distraction in my visual field, no $\ddot \smile$

@Remi.b Do you see your entire nose or just most of it? If your nose is shined on, such as by sunlight or overhead halogen lights, does it become more noticeable?

No, I don't think I can see my entire nose although that depends upon when you define being the start of the nose. There is no particular lighting that makes my nose more noticeable in my field of vision. I suspect that you can also see some of your nose as you cross your eyes (at least the tip) but it does not bother you at all. It is the same, it really never bothers me in any way.

@Remi.b I define the start of nose as the bridge of nose (glabella). Do you see your nose bridge? Where it meets the eyebrows? What about your eyebrows? Also, the horizontal skin below/behind your eyebrows (top of eye socket/bottom of brow ridge)?

I can almost see my nose bridge but not quite.

If I look up my vision is just barely obscured by my brows, particularly if scrunched up


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Does cellular/organism death happen to enable evolution?
On the topic of whether we could conceivably understand death and extend human lifespans significantly - I'm wondering if any smart folks can point me to where my thinking regarding death may be wonky.
Hypothesis: Death only exists as an evolutionary advantage, and decoding the genome would point to designed cell death
Offspring provide a chance for mutations and evolution. Bacteria, with their short doubling time, can evolve very quickly (e.g. antibiotic resistance). Humans, with a longer lifespan, cannot evolve as quickly.
While the exact metric above is not linked to lifespan directly (its actually reproductive rate), I'd argue that at stable/equilibrium population size (due to resource constraints) they are indirectly correlated.
Understandably, there are many factors that introduce mutation into a species, other than death rate. Some species may have more powerful DNA editing enzyme variants that lower mutation rates.
Some counter arguments may include 'wear and tear', the notion that no organism can live forever as any ordered matter tends to break down over time. Some cold-water fish have low metabolism rates and long lifespans.
What can I learn about this topic?

Unclear as to what you mean.  You refer to an "exact metric above," but I don't know which metric you're referring to.  "Designed cell death" is uncontroversial.  It's called apoptosis.  Designed senescence of the whole (human) organism is more controversial, but there are theories.  Take a look here:  https://en.wikipedia.org/wiki/Evolution_of_ageing#Problems_with_programmed_ageing_theories

there's a few good links in that second one, thanks. not a huge fan of the discussion in the first link, if you switch the duplicate link I will accept it and close

@sterid thank you that also added the kind of thoughts I was looking for and its helpful to ground on the term 'designed senescence'

@Nth.gol Sorry, what does "ground on the term" mean?

I was not previously familiar with the combined term 'designed senescence', its a good search term. to your first comment, the 'exact metric above' I already mentioned as reproductive rate


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Camera and the eye (filtering information)
How does a camera recreate a very similar perceptual stimulus (through the photo) for us to see compared to the person directly viewing the object of interest with their eye?
My questions stems from what I've already learned about the visual system:
1) The retina receives information from the external world, but not 100% of the photons (the form of this information).
2) This information is then passed to the superior colliculus where further filtering, and changes to this information occurs.
3) It is next passed to the thalamus and then relays it to the occiptal lobe which interprets this information (another filtering process) causing us to perceive the external world in a particular way.
Is it that the camera captures the light information on the film that would otherwise have made contact with our retina? And then upon seeing the photo, that same information (or similar since the camera would not exactly capture it, but enough for us to notice that we are seeing what we expected to see) finally makes contact with the retina and then the process occurs as described in the points above?
If so, how does the camera do this!? Because I thought the camera would also be selective in which light it uses to recreate these images. And I'm incredibly doubtful that a camera simulates the filtering processes of the human brain. Moreover, it doesn't make sense that we would perceive the expected image in the photo if it was already based on the filtered information.
I am very curious and very confused. :)
-N

I'm voting to close this question as off-topic because you are asking how a camera works, not about biology.

I disagree. This question came from a friend who disagreed with the above explanation that the light information that encounters the retina is no longer the same once it reaches our visual cortex. He couldn't believe that our vision of the external world is not a true representation (whatever that is!).
So he then argued my original question in this post. If it isn't a true representation of the external world, how is it that a photo is able to provide a stimulus for almost the same visual response of an object of interest.