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Usage of "lineage" over "species"
Remi.b has suggested here:

The concept of species is poorly defined and is often misleading. The concept of lineage is much more helpful. IMO, the only usefulness of this poorly defined concept that is the "species" is to have a common vocabulary for naming lineages.

Definition of lineage from Wikipedia:

An evolutionary lineage is a temporal series of organisms, populations, cells, or genes connected by a continuous line of descent from ancestor to descendent. Lineages are subsets of the evolutionary tree of life

If we're talking about populations, how do we know if two individuals have the same lineage?

Lineages have many levels, it is like using the word groups in some ways, they are stacked inside each other like the worlds biggest branching Russian nesting doll. All vertebrates is a lineage, all birds is another lineage, as is chickens, as is just rhode island reds. Two individuals of any earth life will always share some lineages. Lineage is not the same as clade however since they do not have to be monophyletic and usually refers to a stem line leading to a group, because of how lineage is named, it can be confusing. For instance the gorilla/human lineage could refer to basically all the great apes minus orangutans or it could refer to the sequence organisms leading to their common ancestor, or it could refer to the genetic lines to their common ancestor and back to themselves. And easy way to think of it is the outer boundaries of a lineage is not well defined. What is used to denote the lineage will help with what it is referring too.
You have to look at context. In paleontology because it is assumed you never have a direct ancestor it is used more vaguely almost like a "stem clade", in microbiology however it will be a far more precise term referring to one or more genetic lines.
The concept of species is misleading because people are trying to use our instinctual categorical thinking to describe a continuous series. It is like trying to define a color any category we invent to split the spectrum up will have many problems because it is not something with discrete differences.

So, "lineage" is a synonym of "clade" or "monophyletic group"? I would agree with this definition, however wikipedia (A lineage is a single line of descent or linear chain within the tree, while a clade is a (usually branched) monophyletic group, containing a single ancestor and all its descendants.) and @mgkrebbs (in a comment under my now deleted answer; Lineage refers to a line from one individual to another, whereas a monophyletic group is a tree of descent from one individual to many, and so is not a synonym) disagree.

It can be synonymous with clade, it is not a well defined term. For instance the theropod lineage would basically just be the clade theropoda, but say the tyrannosaur lineage  could mean the tyrannosaur clade or it could include the stem groups leading to tyrannosaurs as well. Context will usually tell you how it is being used. I'll be more clear.


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What is this slug-like thing I found in my bed?
what is this thing I found in my bed? Squishy like a slug, mildly freaked out, help? I'm in Scotland Edinburgh

it looks like your slug-like thing could be a slug! it might av gotten in stuck to your clothes (or if you have a pet, stuck to that). but a better picture would be helpful.

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sort: votes


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Amino acid structural charges

Hello,
I was wondering if i could get an explanation as to why the charge of this peptide is +2 and -2. How do you figure this out? What is it based on exactly?
Thank you

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Differences that are too small to see
Consider two identical pieces of paper.
Scenario 1: On both something is drawn in black ink. If the difference between the areas covered in black ink is sufficiently small, I cannot see the difference between the two drawings.
Scenario 2: Now imagine that the same parts are covered with ink, but their color differs. Again, if the difference is sufficiently small, I cannot see the difference.
Firstly: what causes this? I am aware of the terminology of just-noticeable differences/limina, but do not understand precisely what causes them. Is there some discretization of continuous signals going on that causes `nearby signals' to be treated the same way?
Secondly: one person may have better vision than another, but are there physical constraints that are the same for any two persons and that imply that if the difference in scenario 1 or 2 is sufficiently small, no two persons will be able to see a difference?
Addenda: I phrased the question informally by not defining what a `small difference' is, trusting/hoping that this does not lead to confusion. If desired, such statements can be made precise by adopting appropriate distance functions. In scenario 1, one way to measure distance between two areas covered in ink could be to use the Hausdorff distance; likewise, one way to measure the distance between colors in the second scenario could depend on the difference in responsivity of the three types of cone cells.

I am having problems understanding your question. Would it be possible to add an image for your example? Also note that you may increase your chances of getting an answer over at cogsci.stackexchange.com.

Thanks, I will give the cogsci site a try as well. Two concrete examples: load a digital image into your computer, change just the colour of a single pixel. This is typically not a difference you can see. Likewise, it is not clear at first sight whether the strings 0000000000 and 00000000000 are identical. Why exactly can we not see small differences?


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Why is the glomerular filtrate isotonic to the blood in the capillaries?
How can the osmolarity of the filtrate be the same as the blood in the peritubular capillary when there is no red blood cells filtered?

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Why we see black colour when we close our eyes
Why is it neccessary that if there is no light then everythimg is black and when we close our eyes we see everthing black usually when we are in black room??

Is your question: "why does the absence of light (from the physically shielding of our pupils from taking in light) appear black?" or "why do we perceive darkness as the color black? (vs., say, all white?)?" ?

Am I unusual?  Because when I close my eyes in a dark room, I don't see complete black, but darkness with some random "light shows" going on, for instance random dots of a slightly orange-tinted grey.

The mechanism of sight is as follows (ref. 1). This was shown in the 1100s by Ibn al-Haytham (ref. 2), except the 4th step which may have been proposed by Galen in the 100s (ref. 3).

Light comes from a light source
The light then hits an object
The light then bounces off the object into your eye
Your eye sends a signal to your brain. Your brain then figures out what you're seeing

So in order for us to see, you need light getting into your eye (step 3). If you're in a dark room you have no light source, so no sight (no step 1). If you shut your eyes, you're stopping light from getting into your eye (no step 3). When there's no light getting to your eye, the eye tells this to your brain. So your brain just sees black (the absence of light).

References

Duree, G. (2011). Optics for Dummies. p. 67.

Adamson, Peter. (7 July 2016). Philosophy in the Islamic World: A History of Philosophy Without Any Gaps. p. 77.

Reeves, C. and Taylor, D. (2004). A history of the optic nerve and its diseases. p. 1097.

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What happened to dead cells which still keep DNA information?
I heard that the destination of dying cells is either one of them: Apoptosis and Necrosis. Further I heard that apoptosis causes destroy of cell components and necrosis is caused by autolyses.
But we can do DNA profiling from supposedly dead cells. How is DNA stored in dead cells? Those cells not dead by any chance? Otherwise, the core occasionally remain safe even during such destroy process in Apoptosis or Necrosis?

In apoptosis, the nucleus falls apart, DNA is fragmented, and cell contents are packaged into vesicles which are then degraded by phagocytes. I suppose there might be fragments of DNA that could be sequenced before phagocytosis occurs.

@iowf Thank you for the insight. That makes sense to me. Cells are surely dead and destruction process happen but there are many cases that fragmented DNA components remain safe enough to investigate. Now this is my latest understanding.


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Average masses of atoms / amino acids
I recognized that there is some controversy about the average mass of amino acid masses in different online sources.
Expasy and Wikipedia report the same masses, but UWPR and Mascot report different ones. However, the monoisotopic masses are always the same.
Does anyone know where these differences come from or where to find a definite source for the masses?
In the end, the question boils down to the average masses of single atoms. The UWPR names UniMod as a source for their calculation. What different ways of calculation for average mass exist and who defined them?

This is chemistry not biology. If there is still any interest in the topic it should be reposted on SE Chemistry. Otherwise it is best closed.

A bit more link following reveals on the UniMod site: "All mass values in Unimod are calculated from the IUPAC atomic weights and isotopic abundances tabulated by WebElements:"
So, the answer is the isotope abundances are from the IUPAC; you can find links to references at webelements.com by drilling down in the periodic table there.

I guess confusion comes from either:

Inclusion vs exclusion of H2O (free AA vs in chain)

Averaging with
equal weight between all AA vs weight of their relative
occurrence

(EDIT) The Wikipedia link states:

Alanine  A   Ala     89.09404

ExPASy link:

Alanine (A)  71.03711

So ExPASy lists the weight without H2O, 18 Dalton lighter due to the condensation reaction in the form you would find the amino-acids in a peptide.

cannot be the cause, the differences are minimal, nothing like 18 Da. 2. No average is calculated over AA. The average weight is calculated out of the relative occurrence of different stable isotopes of the atoms. I guess that there are different reports of the relative occurrence of stable isotopes that lead to the difference in AA average mass.

I keep this answer because it might be relevant for people, who arrive here via search engines.


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Can Covid-19 virus be simply filtered out from infected patient’s blood?
Can Covid-19 virus be simply filtered out from infected patient’s blood?
If a Covid+ patient’s blood is passed through a filter, say 100 nm or a system of filters, 100 nm and 500 nm can we isolate the virus from serum including small and large blood particles? This is somewhat like a dialysis of the blood. I am particularly interested to know if graphene filters will be of help here. Has somebody worked on that? I am thinking if size can be exploited to isolate the virus (irrespective of mutants) and aid the primary treatment of the patient. I am not a virologist and new to the subject.

No, this wouldn't work, and if you think about it for a bit you'll see why. First and foremost, your 100nm filter would catch all the cells that are in the blood. Therefore, all you'd end up with is plasma, and the patient would die within several minutes of beginning "therapy" due to not being able to transport oxygen with red blood cells. On a practical note, all those cells would clog your filters, of any size, immediately.
Another reason: SARS-CoV-2 primarily infects epithelial cells in the respiratory system, and can easily transfer from cell to cell without having to use the bloodstream. In fact, it's my understanding that the serum load of virus is actually rather low. Filtering the blood wouldn't prevent any of that cell->cell transfer.
Final reason (for now): there are other things in the blood that are in the vicinity of the same size as virus particles - cholesterol/lipoprotein aggregates, larger protein complexes, platelets, etc. You'd lose all these vital components of your body with any kind of filtering scheme.

Thank you.
I was suggesting a system of three filters, 800 nm, 200 nm and 100 nm in that order. Infected blood passing through this system will isolate the virus while retaining the useful constituents of the blood. I agree that there may be blood constituents in the same size range as the virus which should be identified and replenished back. I also agree that the larger problem is in the epithelial cells which should be addressed by standard vaccination. To avoid filter clogging, if filtering is done in small quantities of blood at a time then it may not be a problem. Let me refine this.

Feel free to revise your design, but trust me - there are reasons why this is not a clinical therapy, for viral infections or anything else. I've laid out some above, but there are others. Filtering small amounts of blood at a time won't work, b/c you're always going to lose something important when you filter. Even if you can get 95% of the RBCs back, there's still that 5% gone each time, and there'd have to be many, many rounds if you want to reduce the whole viral load appreciably. It's just not a good idea.


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Should Secondary Antibody Bind better through adsorption than using an EDC Linker?
Recently, I conducted an experiment to compare the use of EDC versus passive adsorption.

I attempted to immobilize goat anti-rabbit HRP secondary antibody to Carboxylated polystyrene beads via EDC and NHS linking protocol.
As the beads were polystyrene, we used centrifugation to clean the beads in between each step. Otherwise, we followed ThermoFisher's DynaBeads protocol. After immobilizing the ligands we added 100ul of HRP substrate to each sample and measured the luminance using Molecular Device's ID3.
The Materials used are as follows:

3um Carboxylated Beads (dyed red) from Polyscience
2%BSA
ThermoFisher's Pierce Premium EDC
25mM MES Buffer (6.33 pH)
50mg/ml EDC
50mg/ml NHS

Antibody and Detection

Goat Anti-Rabbit HRP Secondary Antibody
HRP substrate

However, when measuring the luminance of the HRP substrate the passive adsorption seemed to consistently provide significantly brighter results, suggesting that the EDC linker is not as effective as I thought.

Further, when testing different concentrations of EDC I noticed that luminance decreased as the concentration of EDC increased.

These results seem consistently odd and I'm not sure what to make of them. Looking for advice, as I am completely new to this procedure.


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Looking for literature on hand-head movement coordination (not hand-eye)
sports scientists and kinesiologists, I'm a linguist working on sign languages and I'm looking for papers that discuss motor coordination of hand and head movements and potential constraints on such parallel movements (not hand-eye coordination, there's plenty of papers out there on that topic). In particular, I care about combinations of a repeated headshake and small, repeated twisting movements of wrist, as they occur in this sign in German Sign Language: https://www.sign-lang.uni-hamburg.de/.../type18133_de.html. Or head nods combined with a 'no' side-to side gesture of the dominant hand. Does anybody have clues as to why such movements might be difficult to combine? I'd be so grateful for any pointers!

consider also SE Medical Sciences, https://medicalsciences.stackexchange.com/, and maybe also fitness https://fitness.stackexchange.com/. If you do cross-post, make sure that you link each question to each other post to make it clear that you've posted in multiple places.

@MaximilianPress The guidance on cross-posting is that unless each post can be specifically tailored for the target site such that they aren't quite the same question anymore, the poster should choose one site for their question to live on, rather than posting in multiple places. It's fine to delete a question on one site to post it on another if OP changes their mind about the most appropriate venue.


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Peptide oxidation bias during sample preparation for LC-MS/MS
Problem description
In bottom-up proteomics, a commonly observed amino acid modification is the oxidation of methionine (Met-O). I wonder if the observed Met-O reflect natural protein oxidation or if they rather stem from oxidation during sample preparation.
Observations
During sample preparation, several factors could influence the Met-O:

Typical sample preparation protocols include reduction of the sample by either DTT or TCEP. This step serves to reduce disulfide bridges. I wonder if this step would also lead to reduction of oxidized methionines. Still, this reduction step seems to be used even in studies that analyse natural protein oxidation (e.g. Walker et al., PNAS, 2019, Methods)
Sample preparation takes several hours at least, typically the digestion is even prolongued over night. Several modifications typically happen during sample preparation or during the measurement, e.g. deamidations. I did not find studies about the extend of Met-O happening during sample preparation. Klont et al. report differences between Met-O in four different sample preparation methods, but it is not clear where the differences stem from. They could either happen during sample preparation or the four methods have different capacities of detecting natural oxidations.

My questions

Does the use of reducing agents modify oxidized methionines?
Do methionine oxidations occur during LC-MS/MS sample preparation and measurement? How strong is this effect?
Does anyone know a technique that discriminates native protein oxidations from those occuring during sample preparation? I found this publication, using 18O, but I cannot access it and thus cannot estimate if the protocol would be useful.

I know this was posted a long time ago and I'm not sure if you have found your answer but I am an author on two of the publications you  andcite can offer some insight.
1.) Methionine oxidation, unlike cysteine oxidation, is irreversible without the action of a dedicated enzyme or catalyst. Neither TCEP nor DTT is able to reduce methionine sulfoxide. The only reducing agent that I know of that is strong enough to reduce methionine sulfoxide is MMA.
2.) The in-vitro oxidation of methionines during sample preparation is a well documented issue in LC-MS/MS analysis and it is known that the majority of in-vitro oxidation occurs during peptide digest as well as during electrospray ionization. The strength of the effect is highly variable and dependent on how long you digest proteins. For a typical overnight digest we observe effects that range from 0%-400%, depending on the peptide.
3.) The use of 18O labelled blocking reagents is the only currently available method that can prevent the accumulation of in-vitro oxidation. I'm the first author on the publication you cite and would be happy to send you a copy if you email me (jbetting@ur.rochester.edu) I have also been working on improved methods using the same general strategy and would be happy to share those with you after publication

Hi John. Thanks for your reply. In the meantime, I found your paper on PMC. I will look into this.

could you please comment whether there was a study that directly showed that TCEP cannot reduce Met?


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Univocal identifying of a plant cell
We yesterday got our biology-exams back and there's one exercise where I don't agree with my teacher. However, since he is the expert and not me, I need the support of external sources, i.e. experts in order to justify my statement.

Now in the exercise, we first had to identify the parts of a cell (which was shown in form of an image) and then in part b) reason whether it was an animal or plant cell.

I had identified a chloroplast and a vacuole and stated that the only cell with this organelles was the plant cell. My teacher answered that I had missed the fact, that the cell had also a cell wall (which is indeed a difference between plant and animal cells).
My question is

Is the fact that the cell had a cell wall necessary in my argumentation, i.e. are there other cells having chloroplasts and a vacuole without being a plant cell?

Could you provide a source which supports, or doesn't support my statement so that I can show it to my teacher?
Thanks in advance

Your teacher is right, chloroplasts and vacuoles are not sufficient to define a plant cell.
Amoeba have both chloroplasts (McFadden et al, PNAS, 1994) and vacuoles (Day, J. Morphology, 1927) but they are not plants - and they do not have a cell wall.
Sea slugs eat algae and can "steal" their plastids and keep them working for weeks/months, effectively becoming photosynthetic animals for a while. This is called kleptoplastidy (Pillet, Mob. Genet. Elements, 2013).


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Possible combinations in the Meiosis' Telophase 1
As you might already know

Meiosis is the process in eukaryotic, sexually-reproducing animals that reduces the number of chromosomes in a cell before reproduction $^{[1]}$

One of the reasons why meiosis has been so important in evolution is variation.
As my teacher used to say: Nature rolls the dice... - It's the magic of genetics; two completely different persons might share the same parents.
So here the question:

Suppose we have a cell with four chromosomes (two couples of homologous chromosomes) in the Prophase 1. I've drawn all possible combinations that could happen - these are chosen randomly - in the Telophase 1.

Is there a genetic disorder (not only regarding humans), in which the four initial chromosomes are split, in the Telophase, into two parts, each of them containing a couple of homologous chromosomes. I.e. (referring to the image) is the combination $(\color{red}{red}+\color{blue}{blue})(\color{green}{green}+black)$ in the Telophase 1 possible?

$$$$
$^{[1]}$ Quote from https://biologydictionary.net/meiosis/

Failure to properly separate homologous chromosomes during meiosis, either by including an extra copy of a chromosome or including zero copies of a chromosome, causes gametes that are 'aneuploid', and as a result, a zygote that results from that gamete will have an extra or missing chromosome as well.
For humans, most aneuploidies are completely fatal at some point of early development, so there is not an associated genetic disorder in live births.
One common aneuploidy that is not fatal to the embryo is an extra copy of chromosome 21; this causes Down syndrome.

Thanks, @Bryan Krause [+1]. However, what I meant with the question was, if homologous chromosomes (here red+blue and black+green) could stay together in Telophase 1 (which isn't normal (or even possible???) but might be a genetic disorder)

@Dr.Mathva I explained what the result would be if/when this happens for even 1 chromosome pair, which would lead to a genetic disorder in the offspring. A genetic disorder where all of your own germ cells failed to go through meiosis properly would effectively mean sterility because nearly all their gametes would be aneuploid, and most lethally so, so such a trait would not be passed to offspring.


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Negative RNA virus
I have tried to see how this works but I can't find any helpful information. How can a negative strand RNA virus make protein during an infection?

Then you did not search enough. It took me 2 google searches to find that the virus uses RNA dependent RNA polymerase to convert -ve sense RNA to +ve sense mRNA. Also the virus particle itself contains the polymerase. Link - https://microbiologybytes.wordpress.com/2008/02/04/negative-sense-rna-viruses/


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Why antimicrobial resistance is based mainly on antibiotic use?
Why antimicrobial resistance is based mainly on antibiotics use and not so much on antifungal or antivirus drugs? Why, when someone speaks about antimicrobial resistance, refers mostly to antibiotitic resistance and not so much to antifungal resistance or antivirus resistance?
All this has to do because of the overuse of the specific drugs(antibiotic), or there are biological and genetical mechanisms that make the antibiotics the main reason of antimicrobial resistance instead of anti-fungal or other drugs?

Can you do some research first on this? We prefer well-researched questions where the OP has made some effort on their own to answer.

The answer is actually a lot simpler. Antibacterials are the most commonly used antimicrobials by far and a consequence of this is that many people use antimicrobrial and antibacterial interchangably. You're right that antimicrobials are substances that target microorganisms such as bacteria, archaea, viruses, and eukaryotes. As stated earlier, the reality is that we use antibacterials far more than any other type of antimicrobial. Other antimicrobials are either toxic to us because they target other eukaryotes like fungi or they are very limited in what they target like many antivirals. Hopefully this helps you.

Antibiotic resistance is more in the public eye because the general population is more likely to use or be prescribed antibiotics than antivirals.  Antibiotic resistance has also been in the news more lately because
1: persons infected with superbugs that resist antibiotic treatment make salacious news articles.  e.g. https://www.thesun.co.uk/news/4528838/bleach-antibacterial-soap-antibiotics-mrsa-infection/
2: it is now recognized that the use of antibiotics to promote growth in livestock is responsible for a lot of evolved antibiotic resistance - these are large populations of animals that are fed antibiotics all the time.
 In the US until very recently, 80% of antibiotics sold were used as animal growth promoters.
It does not take much googling to read about other circumstances where evolved drug resistance is a problem.  Resistance to antivirals is hugely important for persons with HIV and their caregivers.
http://www.who.int/hiv/topics/drugresistance/en/
If you are not in one of these populations you may not be aware of the issue.  Other examples include drug resistant malaria and drug resistant tuberculosis.  These diseases are not so problematic in the developed world which may be why they are less in the public eye than superbugs in the senior's home.


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Manipulating phylogenetic trees
I am looking to manipulate manually constructed phylogenetic trees (adding bootstrap values, markers to indicate trate loss/gain etc.) I came across a paper that used Macclade, however, this no longer appears to be a program that will run on almost all computers. Is there a useful alternative software package? I have tried Mesquite, but it does not appear to have the same functionality (although, I have probably just missed understood how to use it effectively).
Any help/recommendations would be appreciated

If you have some knowledge of python, you can do a lot of things with the ETE toolkit.
Disclaimer: I have used an older version of it, but in a very limited manner.

The MEGA software package is the most comprehensive software I have used, if you don't want to rebuild your tree I have used FigTree in the past but it seems to be unsupported now.


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Onion Cells or Pear Cells?

I am researching different cells under a brightfield microscope for homework and am having trouble determining whether or not these cells are Onion cells (Allium cepa) or pear cells (Pyrus) under a light microscope. I am pretty sure they are pear cells, but I just wanted to be sure!

Pear has loosely arranged spherical cells and some cells are sclereids cells. Onions cells are rectangular and almost transparent.
Honestly I'm about to vote for closing, because I don't see how this question can be important.

@MaximKuleshov No question should be closed solely because it is unimportant, but this question doesn't show any effort at in researching the question before posting. What were you expecting the difference to be? Where did you previously try to answer this question and what didn't you understand about those answers? Why are you pretty sure it's a pear cell? I think this question is close to being a very nice question.

You are correct, those are pear cells.
Onion skin cells (popularly in slide sets)

source and a hommge to onion skin cells
Pear Cells

source and also several other neat pictures of pear cells


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What is total body water and why is it inversely proportional to fat content of body?
In my textbook "Physiology" by 'Linda S. Costanzo' its written that total body water is the amount of fluid present in the body. So my question is that is it just the water content it means by "amount of fluid" or it means amount of liquid content within the body (I.e. water, oils etc.)
Secondly, i have no idea that why is it inversely proportional to fat content. Is it because the decomposition of fat release relatively lots of water molecules and thats why its inversely proportional.

Total body water is the total amount or percent of one's body that is comprised of water. It isn't the same as total body fluids, but on careful examination, it's close. For example, the average adult has a blood volume of about 5 liters (there are formulas to calculate more accurate numbers.) Blood is a fluid. It is normally about 55% plasma with the rest being mostly red blood cells. Plasma (also a fluid) is ~90% water and red blood cells   are about 70% water (estimates vary slightly), So while blood is mostly water, blood (fluid) is not equivalent to water.
Most cells have a fairly high percentage of water. The exception is fat cells/adipose tissue. Whereas muscle is ~70% water, adipose tissue is only ~10% water.
Therefore, if, say, 70 pounds of lean human tissue is (say) 70% water, and 70 pounds of (white) fat contains only 10% water, a 140 pound lean/muscular athletic male with 10% body mass comprised of fat will have more total body water (TBW) than a sedentary male of the same weight but with more adipose tissue. That's why the more fat your body is composed of, the lower the TBW.


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How long is agar agar good for?
I'm a high school science teacher, and am starting at a new school. I'd like to do some labs with bacteria and so I'll need to make plates with agar agar. I found 3 huge jugs of powdered agar in the storage cabinet, but I'm wondering if they're still good. The only one with a date said "1995" and I think that may be a bit much, but I could be wrong. Does anyone know if I should buy new agar or use the old stuff?

There's a similar post on our sister-site for cooking: seasoned-advice.

I have used 5 year expired agar, no dramas. I expect your old agar will be fine.

I don't see why it shouldn't be ok as long as it has been stored dry. If it is still powdery and white it should be ok and personally, I would have any problems to use it in the lab.

I'm assuming these labs are going to be mostly qualitative in design? If you're able to use it to make an agar plate and grow bacteria on it, seems like it's still "good". If it won't form a gel then something's wrong. If it forms the gel and doesn't grow the bacteria... save that stuff and maybe consult with someone to find what new antibiotic you've discovered :)

Use science to figure it out!
Order some new jugs.  Tell the class about the old jugs you found.  Make 2 batches of plates: old and new.  Make dilutions of bacteria.  Does the old agar support as many colonies as the new?
Even better would be to have some other kinds of agar plates.  You can have old and new.  You can have agar with extra salt.  You can have agar with extra sugar.  You can have agar with a little iodine.  You can have agar made with old coffee.  You can have agar made with water from the fish aquarium.  Each student group will have a group of plates one of each type.
Then you can pool the plates of each type.  Graph number of colonies.  Use statistics.
If you determine the old agar is good then you can use it again next year and after that.  If you determine it is bad then it gets trashed.  Either way you are using the scientific method.  Yay science!

Test it first, but it should work fine
Agar Agar powder has a pretty long shelf life, even decades expired agar still works fine.
But if the container was opened it might have picked up some moisture from the air which will weaken how well it gels. It will be pretty obvious if you mix a test batch, just mix a bit in a paper cup and see if it gels. As long as it gels it will still work fine for any lab in a school setting. Any change will be uniform so if you used it alongside fresh agar there might be a noticeable difference in say PCR, but as long as you only compare it to itself even slightly bad agar will work fine.


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What's the lowest temperature a tardigrade can remain active at?
There's a lot of information floating around the net about how tough they are & what they can survive, like "We now know that some tardigrades can tolerate being frozen to -272.8 °C".
But any details on the environmental ranges they can actually be active in rather than what extremes they can survive in one or other of their various states of metabolic suspension seem entirely absent for the casual (& not so casual, I've spent hours looking for these details) surfer.
So does anyone out there know what the temperature range of an active (rather than dormant) tardigrade is, with specific reference to the lower end of the scale.


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What is the thickness of the biosphere?
In other words, what is the vertical distance between the deepest and highest point on Earth where life is found?
Life has been discovered at the bottom of the Mariana Trench, 13 km below sea level. It's hard to get deeper than this, but I'm not sure if this really represents the bottom of the biosphere. Elsewhere at sea, microbes can be found many kilometers below the sea floor -- would we expect to find life far below the Mariana Trench?
In the other direction, the biosphere arguably reaches as high as 435 km, the maximum altitude of the International Space Station. If the ISS is disqualified, then that number would be much lower, but again I'm not sure exactly what it would be. The highest recorded bird flight clocks in at 11 km, though it's possible that microbes regularly get dragged up higher than this by wind.

Nice question, welcome!

You might also note that life is found in rocks several miles/km below the surface: http://www.bbc.com/earth/story/20151124-meet-the-strange-creatures-that-live-in-solid-rock-deep-underground

Relevant paper, referring to the 8-15 km range in the atmosphere: Microbiome of the upper troposphere: Species composition and prevalence, effects of tropical storms, and atmospheric implications.


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Are porins on the inner or on the outer membrane of mitochondria?
I've looked at multiple resources and they are saying different things.

This is not my field, but The Transporter Classification Database would appear to be a reliable source and states that:

The best characterized members of the MPP family are the voltage-dependent anion-selective channel (VDAC) porins in the mitochondrial outer membrane.

Searching through the Protein Data Bank one can find a crystal structure for human voltage-dependent anion channel 1 and the associated paper also states that it is in the outer mitochondrial membrane, so you would imagine that they should know.


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How do plant cell vacuoles form?
Does the plant cell vacuole form by the invagination of the cell membrane?


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Reference request: neocortex creating 11 dimensional structures
I've come across several pop science articles like this one that vaguely describe a method of analyzing brain tissue involving algebraic topology and 11 dimensional structures. They all seem to cite each other. One of the researchers involved was Kathryn Hess. I've searched the web, a community college library, and the UCLA library and haven't been able to find the original paper. Does anyone know where I could learn more about their methods?

Welcome to Biology.SE! You say They all seem to cite each other. It would help if you could directly tell us what papers you found and eventually why it feels like they all just cite each other.

New Frontiers is surrounded by controversy mostly becasue they have no restrictions about what they publish regardless of methodology or ethics. They also fired a bunch of their editors for trying to impose some scientific integrity. The fact the "journal" is owned by the first authors to publish in it is another bad sign. You can safely assume anything published by Frontiers is garbage.

That's a shame I thought the mathematical model that the researchers developed was really cool. I didn't pay much attention to their methods though.

I finally found the work. It was in the sources of the sources of the article that I gave as an example.

you should edit your question not answer it, especially just to add and not answer.


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Non- brown, blue,green eye colour genotypes and genes
In genetics, eye colours (brown, green and blue) are determined by bey2 and gey genes. But what about hazel, grey and amber and more? I read a webpage about hazel eye colour and saw that there is a 3rd gene called 'hey' with 'codes' H and h
Other than B(brown), G(green) and b(blue) but now what does H and h mean when there is one hazel?

Welcome to Biology StackExchange! According to the guidelines of this site, your question might seem a little bit under-researched. You should also provide references to your statements. For example: "eye colours are determined by bey2 and gey genes" is not an accurate statement because (as you can read on Wikipedia) "The genetics and inheritance of eye color in humans is complicated" and "So far, as many as 15 genes have been associated with eye color inheritance".

Therefore, I suggest you read some more (online) resources on this topic, and then try to edit your question into a more detailed and focused one, along with the references you have read :-) There are also some useful answers on this StackExchange, such as Why are human eye colours limited? and How is eye color in humans inherited?.


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What is the importance of radiation hybrid (RH) mapping in terms of genes?
I'm currently reading about radiation hybrid mapping with a TSP (traveling salesman problem) application in order to find an ordering of the genetic markers (i'm a mathematics student) and was wondering about the usefulness of the procedure. If the end result determines the proximity of certain genetic markers then we can draw inferences about genes which are in close proximity to each other and genes which are separated with a larger distance. I'm wondering for certain set of genes if they are closely related distance wise then are the properties for the genes often related to each other? I believe there are also genes which are dependent upon having other genes in close proximity in order to function properly if I am not mistaken. Is this true?
I'm also curious as to what we may say if we have for instance two genes which are separated by large distance? May this be related to the fact that the farther away two genes are the more they act like they are unlinked?
Any help is appreciated.

One might say that this question is too basic for this list, and I feel that it must have been asked before in some form, but I can’t locate an example. So here is a short answer.
First, it should be mentioned that Radiation Hybrid Mapping is an old technique which, judging by the brevity of the entry in Wikipedia, is little used today. The main reason for this is the availability of the genomic sequencing. It may make a good example for algorithms, but that’s probably about it.
However, the basic question is still valid, “Does human gene proximity suggest interaction, and lack of proximity not?”
At one time it was thought that this might be so because of the clustering of bacterial genes e.g. involved in a single metabolic pathway in operons. However, this is generally not the case in higher eukaryotes like humans. A good example is the locations of the genes for the two subunits of adult human haemoglobin which associate in the tetrameric protein α2β2. The gene for the α subunit is located on chromosome 11, whereas that for the β subunit is located on chromosome 16. Another example is the genes for the approx. 80 proteins that assemble into the protein-synthesizing organelle, the ribosome. This 1998 paper (which, incidentally, used radiation hybrids) concluded:

Though functionally related and coordinately expressed, the 75 mapped
genes are widely dispersed: Both sex chromosomes and at least 20 of
the 22 autosomes carry one or more rp genes.

So, although there may be counter-examples, no general conclusions about human genes can be drawn from mapping alone.

Thank you very much for your answer. I was wondering in relation to genomic sequencing  which also seems very much to be a quickly evolving field what are the most popular used techniques today? I assume cost and efficacy very much play a role here.

@PianoMath — That's another question. Depends what question you are asking in your research.


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Alignment given two sequence
I have two sequences and I need to perform sequence alignment to determine all possible sequence alignments. I have created the matrix and managed to find 16 alignments.
I wanted to understand if I had correctly approached this because I need to provide all possible alignment sequences and then provide the best alignment sequence/sequences out of all the ones found, however, all my found sequences have a score of -9. The sequences I have found I have placed in this pastebin link: Sequences since I did not want to make the post too large.
I was wondering if someone could help me understand if I may have gone wrong or if I am missing some sequences since all of them have a score of -9. I do not think I have gone wrong during the matrix creation phase but I am unsure. My goal is to find all sequences and not just the optimal ones.
I have asked for help from my tutor however he has been quite rude and reluctant to explain/help so I have decided to turn to the community for help and guidance. Would appreciate any insight into this. Thanks in advance.
Sequence strings:
ggaatggmeeff
gatge
Alignment matrix

The poster writes “I need to perform sequence alignment to determine all possible sequence alignments”. It is not clear whether this need is that determined by a course assignment or the poster’s mathematical  imagination. If the former, I doubt that the wording expresses the request correctly, even though this is repeated in the question as “My goal is to find all sequences and not just the optimal (highest?) ones”. The reason for doubting this is that the number of possible alignments with no restraint imposed will vary from very large to astronomical, depending on the length of the sequences.
The display presented looks at first sight like a trackback for a global alignment using the Needleman and Wunsch dynamic programming algorithm. Such a trackback is designed to find one of what are generally several possible alignments that have the highest score using a specific scoring matrix and gap penalties (different scoring systems can give different alignments). Although it is possible in general to trace alternative trackbacks of the same score manually, I do not see any in this example. This operation is not performed in any programatic implementations of the algorithm of which I am aware. Although, memory limitations permitting, one could program this, the algorithm is not designed to find lower scores (and I find it hard to see the demand for such).
However the problem with the Needleman and Wunsch trackback is that in this algorithm each cell should trackback to the single highest-scoring cell preceding it — if there are two of the same score a random choice is made. But the trackback shown, as well as having instances where the highest scoring cell has been missed, has 9 cases where the trackback is to two cells with different scores. I can think of no justification for this.
There is another fundamental defect here, which arises from the scoring system used. The match = 1, mismatch = –1, fixed-gap-penalty system is doomed to result in low alignment scores in this case: the best possible score is 5 x 1 (matches) + 7 x –2 (gaps) = –9. The PAM or BLOSUM matrix, which score similar amino acids on the basis of their likely mutational substitution and thus are better related to the realities of protein structure,  have higher numerical values relative to the gap penalty, which should actually be replaced by a gap initiation penalty followed by a lower gap extension penalty.
In conclusion I would advise anyone undertaking work of this type, first to obtain a thorough understanding of the dynamic programming algorithms used, next to specify clearly the goals he wishes to achieve, then to assess whether they are realistic, and finally be prepared to write a program himself if none already exists.

Thanks for the response. We get weekly activities for practice to compliment the lecture. The question states to find all possible alignments, followed by "provide the best alignment sequence/s". However, from my understanding and as you have mentioned, the most optimal alignments are those that go from the most bottom-right to the most top-left. I have managed to find 16, all of which have a score of -9. Since I found them all with the same score, I thought my approach might have been incorrect. My tutor is not polite when you ask for help and so I decided to turn to the community for help.

@Krellex — It's possible for a lecturer to say or write something in a lecture that's ambiguous or not exactly what you intended — I've done it myself many times — and students can sometimes get hold of the wrong end of the stick. It's difficult for someone else to tell. However the generally topic is covered on the web in many places other than the Wikipedia link I gave. Have a look round, and perhaps discuss it with your classmates. Double-check your trackback, and perhaps try a BLOSUM matrix for scoring.


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Why are homologous chromosomes similar?
I was recently studying gametogenesis (I'm a medical student), and I was thinking about meiosis and fertilization. So on the surface it sounds simple, 23 s-chromosomes from the father and 23 from the mother, and together we have 46 chromosomes and 23 "homologous pairs" of autosomes. I already knew beforehand that each chromosome has 2 copies, but today was the first time that I asked "but why are they similar"? The father and mother should be genetically non-identical, but somehow the maternal and paternal copies of chromosome 1 for example are similar actually, enough to warrant them being called homologs of each other. So why is that? I have some sneaking suspicion it involves evolutionary genetics, but I might be wrong.
Any response is appreciated!

related: https://biology.stackexchange.com/questions/98047/in-our-23-chromosome-pairs-do-the-2-members-of-the-pair-have-distinct-or-virtua

They are similar because, on average, your genome is 99.9% identical to other humans. So, while there are traceable differences on each chromosome that can be mostly mapped back to each parent, the sequence of the chromosomal pairs is nearly the same.
Each chromosome has a specific length and set of genes. Except in rare cases of intra-chomosomal recombination (and the special case of the X/Y chromosomes), each chromosome in the pair will encode the same genes, which will be nearly identical except for the parent-specific differences, and (rare) mutations that may arise alter which are unique to the progeny.

karyotype image from NHGRI
These two questions give more background about homologous chromosomes:

What are homologous chromosomes?
In our 23 chromosome pairs, do the 2 members of the pair have distinct or virtually identical sequences?


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What's the effect of prolonged threshold stimulus currents on action potentials?
I've been confused as to what exactly occurs when a current is injected into a membrane, throughout the duration of an action potential. My main source of confusion has been trying to reconcile 2 things, mainly the invariance of the action potential's magnitude, and the logic that I used during my study of action potentials to explain their origin from equivalent circuits.
To illustrate:

This is a diagram from Cellular Physiology and Neurophysiology, a textbook that I use from time to time. This diagram has been of great usefulness to me, as it provided me with an equivalent circuit description of all phases of the action potential. As you can see during B, a current is injected into the membrane, depositing a net positive charge on the membrane capacitance, causing an outward capacitive current that discharges the membrane capacitance to threshold. Immediately after reaching threshold though, the injected current terminates and the rest of the depolarization is done by the inward Na+ current, which is in a positive feedback cycle.
Now comes my problem: what happens, if I deliberately keep injecting current throughout the whole action potential? Would, say, its magnitude change? An easy answer would be "nothing", as the action potential is always the same regardless of stimulus strength & duration. However, some of my logic is making it seem like the action potential should be changed.
Allow me to explain. My problem comes at the peak of the action potential. This is supposedly a steady state, where the decreasing inward Na+ current is equal and opposite to the increasing outward K+ current. However, for our experiment, you would have to account for the constant inward injected current, which would deposit a net +ve charge on the inside of the membrane. Now comes the inevitable question: wouldn't that increase the peak of the depolarization? For a normal AP, the peak will always be a little less than the equilibrium potential for Na+, however here the presence of the constant inward injected current (and by extension the constant outward capacitive current) makes me feel as if it would nudge the peak a bit higher, before the outward K+ current can eventually eclipse it. Is that right or not? I feel like I'm missing something crucial here.
Another way to put it, in equivalent circuit terms:
. at threshold, Ic = Im + INa
. INa decreases with more depolarization, Ic
gradually decreases
. At the peak of the AP: Ic = Im (my proposed
nudge beyond ENa)
. After that, Ik > Im + INa, and should be able to repolarize the membrane.
So yeah, I guess it all boils down to me not being able to work out what happens in a neuron when a constant threshold current is injected. I'm very sorry if this is too long, and many thanks for reading! I've tried to explain things as best as I can, please tell me if something is not clear.
Diagram source: Blaustein, M. P., Kao, J. P. Y., & Matteson, D. R. (2019). Cellular physiology and neurophysiology: Mosby physiology series (3rd ed.). Elsevier.


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Is life deterministic in nature?
I am wondering, according to our current understanding, whether life is completely deterministic. To begin with, consider a single-celled organism, do we have any evidence of any single celled organism deviate from the law of cause and effect ? This, same idea applied to us raises the question, whether we have free will.

I'm voting to close this question as off-topic because it is a question of philosophy rather than biology.

If I understand your questions correctly, I would reframe it as whether life follows the laws of physics, in which case the answer is yes. Indeed, just how one defines life as opposed to other natural processes is still debated, see for example Erwin Schrödinger's "What is life?"
As to whether physics is deterministic, that depends on what you mean. Classical physics is precisely predictable if you have sufficient information, however, quantum physics has an intrinsic random component, and so could be said to be non-deterministic, although still following defined laws. As to questions about the nature of free will, I think that is better suited to a philosophy context.


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Why did Trilobites evolve armor?
The Trilobite is probably one of the most successful created which evolved in the cambrian explosion.
Though many sources stated the Opabinia has been hunting for Trilobites, this has yet been proven wrong.
Due to my research I haven't found much more animals in the Cambrian age that grow larger than Trilobites or Opabinias - so I do wonder why did Trilobites evolve such a powerful full-body armor when they're have been no clear natural enemies.

predators don't have to be larger than their prey. More importantly Opabinia could not eat them with the armor, but they could easily eat them without the armor, that would be the point of evolving armor.

Your link that says "proven wrong" includes a hypothesis that Opabinia could have eaten trilobites during their molt, simply that it would not be able to eat through their armor (all the better reason to have armor).
The best evidence we are likely to have that trilobites had predators is that they have defenses; the fossil record is incomplete, and just because trilobites are well-preserved does not mean their predators must be. Unless other evidence surfaces for an alternative explanation, the simplest reason for why trilobites evolved armor is that trilobites with armor were protected from something and therefore selected for.
Injuries seen in fossil trilobites are similar to injuries from failed predation of modern related species (see for example Bicknell et al., 2018) and seem to be widely reported (Bicknell et al. 2018 cite a variety of other sources).

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

I agree with the hypothesis at first sight. Additionally I must confess I did link an older article because I couldn't find the one I was actually pointing to in time (it was also from wired.com stating that these researchers had actually proven it wasn't possible due to further research).
The fact that there is such a high amount of Trilobite species which can be found all around the world, yet so few predators makes me wonder how an animal evolves a protection. We can agree they had a better success rate, but why would they evolve such a thing if (let's say) there is no predator yet?

Also Opibinia appeared in the middle Cambrian age, while Trilobites had evolved in the early Cambrian already.

@polarlighthouse I'm not an expert in the field, but I thought that the high number of trilobite fossils is simply because they fossilize so well and have been around so long, rather than them being the only animal around. Predators are typically outnumbered quite a bit by the species they prey on. Not having identified a definitive predator does not mean they have none.

I'm neither an expert, but since the Paelozoic age was actually the longest the earth's existence with animal life it's hard to believe there is no evidence of Trilobite predators when we have so many evidences about the amount of Trilobite species. Of course, predators are naturally less amount of their prey. I'm just wondering and it makes no sense to me to evolve something before there is a predator. But thtat's probably what we wonder about the cambrian explosion at all.

There are very few animals that can eat a turtle would you argue a turtles shell is not for protection? If he protection was not effective there would be no reason to have it.

@polarlighthouse Injuries to trilobites (see the edits to my answer) are evidence that they were indeed predated even if the specific organisms doing the predation are not specifically known. You are right that it makes little sense to evolve armor if there are no threats that armor protects against, though armor could also be protective against damage from waves+rocks.

waves/rocks/etc came also to my mind. Thank you for your answer/comments!

@john you clearly didn't understand the essence of my question.

@polarlighthouse You want to know why ammonties have armor when no predators could eat them with the armor. which ignores the alternative could the predators eat them if they did not have the armor.

Predators need not be large, nor do they need to fossilize well.  Consider the lamprey https://en.wikipedia.org/wiki/Lamprey#Fossil_record or even the common tick.


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How does common cold START?
When I searched for the causes of common cold, I found out that it's only cause is the spreading of virus and that it's a myth that you get cold when you get wet. If that is true then how does the virus start to spread if no one else is having cold? Or Simply, Can you get cold by yourself without the virus?

Related: https://biology.stackexchange.com/questions/5445/why-does-the-cold-make-us-sick

No, only virus or bacteria can cause you cold .Cold weather  causes increase in the spread of virus. Flu virus spread quickly in cold weather. Cold feet can slow down your immune system making you prone for virus attack.Means ,if you are wet you are susceptible to a viral  infection but the cause of cold then would be a virus not the cold weather itself.

Got it.. . But then if it's summer and no one has the cold, how does the virus start with 1 human ? Is my real question.@RabikJohn

It doesnot have to be cold outside to catch a cold. If you catch a cold in summer ,it would be exactly like catching a cold in winter .The rhinovirus that causes cold can spread easily in summer as in winter.So it doesn't depend on weather .Second thing ,how it spreads to other person?That's what we call ;contagious disease  (that easily spreads by water droplets when you sneeze )so any one breathing in that air containing your virus can got cold.

Just to get it cleared,  are you saying that the cold has started with the birth of humanity and since then it has never stopped ( as in saying that humans have cold everyday but it just spreads at a higher rate at some occasions)? @RabikJohn

An important detail to add is that virus can survive without a host for some time free in the environment and surfaces. You  dont forcefully catch a cold from a person that has a cold (at least not directly).

Humans donot have cold everyday ,whenever we encounter any virus ,our immune system tries to get rid of it. But sometimes immune system fails to do this so an  infection prevails. As I said earlier ;cold feet can slow down the immune system and  the virus takes an advantage of this.

@AdheshSagar I'm pretty sure we all have a few viruses even when we are healthy. Their amount is not enough to cause infection, but when immune system weakens they can spread. And then infection starts. Why do we have viruses? Well, if we got cold at least once a small portion of viruses probably will be able to survive. I don't know if these viruses can be passed to a child from mother, but I guess it's likely.

Influenza isn't the same virus as the common cold.
Rhinovirus ("nose" virus) is the main cause of the common cold. This is a virus that exists in the nasal passages of all humans. It replicates, like all viruses, by piggy-backing off the metabolism of the host cells (yours). It's present in us, a normal part of the microbiome, but harmless most of the time -- it gets ahead when you are immune compromised, exposed to temperature challenges or chemical challenges, or are infected with some other microbe.
The virus reproduces by making your cells build virus proteins, copy the virus genome, and then build the virus particles that are released to infect more cells. The ideal temperature that human Rhinovirus proteins fold up and work best is slightly below human body temperature. This limits the virus to the cooler part of your respiratory passage -- your nose.
When you are exposed to cooling -- being caught in the rain for example -- your nose and upper respiratory are cooled. This results in the virus replicating at an accelerated rate.
The new viruses leaving the host cells they were made in and invading into nearby cells causes an irritation. Your body tries to dislodge this irritant -- you make excess mucus and you the urge to sneeze
Sniffing or snorting will introduce this mass of viruses deeper into your respiratory tract. They aren't able to replicate here because of the temperature being too high, but they can irritate and invade into your cells. Your body detects this challenge and responds with inflammation, swelling, and as a side effect, pain. Your sore throat.
Ironically, the activity of the immune system responding to this actually harmless virus will compromise the tissues of your throat, and any opportunistic pathogen is more able to invade.
https://en.wikipedia.org/wiki/Rhinovirus this the wiki of the rhinovirus

BTW: There are around 200 viruses that can cause a cold, among them are Rhino-, Adeno- and Coronaviruses just to name the more important. See [wikipedia}(https://en.wikipedia.org/wiki/Common_cold#Viruses) on it.

Why didn't we evolve to leave behind that virus from our nose?

"Rhinovirus...(is) present in us, a normal part of the microbiome," Please source this. From one review article on respiratory illnesses, "up to 27% [not 100%] of asymptomatic healthy children carry multiple respiratory viruses in their nasopharynx at any given time...", "viral presence might indicate a true subclinical infection..." It's not cut and dry yet.

Although there are some minor issues, this answer doesn't deserve a -2. Stephanie, can you please address these issues pointed out in the comments and improve your answer. Also consider the fact that cold air also causes damage to the nasopharygeal mucosa and thereby promotes infection.


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What are mutator genes which cause copying errors in other genes?
Reading Dawkins' book "The Selfish Gene," I came across this line: "There are even genes--called mutators--that manipulate the rates of copying errors in other genes." (The context is his argument that such a gene is looking out for its best interest by killing off the competition.)
What are these "mutator" genes, and how do they function?

Most obvious examples are the genes directly involved in DNA mismatch repair (MMR) such as mutS, mutL, mutH, MLH1 and MLH2.


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Why is the ability to drink salt water so rare in land-animals?
Apparently, some species are capable of drinking salt water, like the sea lion and otter.
But given how rare fresh water is, and how abundant salt water is, why have more land animals not evolved to drink it? Why are kidneys capable of handling such a thing so uncommon?
I understand that evolution doesn't necessarily always do what's most efficient on a macro scale, but this drives me nuts.
So many animals live less than a five minute walk from the shores of an ocean, and such water is so abundant that they'd never be thirsty.

How can you state [...]how rare fresh water is, and how abundant salt water is[...] ?

What do you mean?

Salt water is abundant only if you live within easy walk/crawl/flying distance of an ocean.  Fresh water is common everywhere on land, except in the driest of deserts.

I mentioned (in my last "paragraph") that many animals indeed DO live within such ranges. Yet virtually none of these animals are able to drink the water.

@Sermo: But it is a useful ability only to the part of the population that lives within range of salt water.  Unless your entire population lives there AND finds it awkward to get to fresh water, as with sea lions and other marine mammals, there's really no pressure for it to evolve.

According to an answer here there is around 356,000 km of coastline on the planet. If we take an average human walking speed of say 5 km/h then our 5 minute walk takes us 0.417 km inland - giving approximately 150,000 km^2 of land conveniently supplied with sea water.
Now according to this page the total amount of land area is around 150,000,000 km^2 which according to this page is covered by somewhere in the vicinity of 117 million lakes [I'm certain a large portion of them are more accurately described as puddles but well go with that number for now], that gives on average a fresh water body every 1.3 km^2.
If we simplify things and imagine dividing the land area into 1.3 km^2 grid with ~1.14 km the distance separating each watering hole meaning the furthest distance to a watering hole across all the earths land area (ON AVERAGE) is around 0.570 km or just under 7 minutes walk (using our previous 5km/h)
So according to my very very rough calculations only around 0.1% of the land area is located within 5 minutes of sea water while 100% is located within 7 minutes of fresh water! I don't think that extra two minute walk is going to be that much of an evolutionary drive for any species.

apparently, not even the sea mammals are drinking salt water, if they can avoid it (obtaining water from food, ice or other fresh water sources): https://www.scientificamerican.com/article/how-can-sea-mammals-drink/

In addition, a great many mammals are smaller and/or slower than humans, reducing the land area close to salt water they have available.  Smaller creatures can survive on water from rain & dew, which in many places is readily available.


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How to measure the length of mitochondria from z stack fluorescent microscopy image?
I have been working on yeast cells to analyse the effect of DNA damaging agents on mitochondrial structure. I have imaged my culture treated with MMS for a period of 6 hours and while observing the images, I suspect there is fragmentation of mitochondria in later point of time. So, I am wondering if I can get measurements of mitochondria using z stack images.

Welcome to Biology.SE! Can you expand on your protocol (both to encourage answers and to make it easier for other non-experts to understand both the question and the answer)? We have been doing some z-stack imaging for a separate project (imaging viral dissemination in insect tissues) but there isn't enough in your question yet for me to tell exactly where you're having problems.

Sorry for providing insufficient information. I have stained yeast cells with mito tracker dye (for mitochondrial staining) and analysed samples for 6 hours, by taking out 1 ml of culture at every one hour. While imaging culture, I captured z stack images for these 7 time points (starting from zero hour). Now, I have been looking for applications that can provide me the measurements (dimensions) of stained mitochondria using Z stacked images.

ImageJ is usually the standard software to measure cell characteristics, a little bit of a learning curve but there is a large suite of analysis methods and image adjustments/filters.


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What is this plant/creature in my freshwater aquarium?

I've been noticing these really small creatures (or plants, I'm unsure) in my tank recently. They measure less than 1cm in length and I've only seen them at the bottom of my tank; some attached to the gravel and some to the glass. They have tentacle-like appendages on the end of their stem(?) and seem to drift with the with the water movement rather than on their own accord.
My tank is a planted tropical freshwater.
What is this plant/creature in my tank?
Any additional information on whether or not these are harmful to my fish would be appreciated.

coooool!  You are so lucky to have such cool creatures.  Feed them!

That is a hydra.
They are a kind of jellyfish, and as such they do technically have stinging tentacles. However, they're also very small, so they're not a danger to most fish or shrimp. If you're planning on breeding your fish they will eat fish fry if they get a chance. On the other hand some fish species will eat them, so it's a bit of a wash.
Generally they only thrive in tanks with extra food hanging around, so you may consider feeding a little less than you have been.


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What causes the human body to “jump” when we get a shock?
At a Remembrance parade today, a cannon was set off to mark the beginning of a two minute silence. As it went off, the crowds quite comically jumped in sync, from the shock it gave them. I’ve seen very similar reactions in other scenarios, such as a jump-scare in a horror film.
Seeing the in-sync crowd jump today made me wonder.. what is it, in the human body, that make us jump when we get a shock?


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What's the best source characterizing proteolysis cleavage sites in the phagolysosome?
I have found MEROPS and TopFIND via the survey paper Quantitative proteomics and terminomics to elucidate the role of ubiquitination and proteolysis in adaptive immunity. These look like a good start, but I'm wondering whether there's anything more specific.
Ideally, I'd like a list of human phagolysosomic enzymes and some sort of statistical characterization of their cleavage sites, such as position-specific scoring matrices.

You can try UniProt to get a list. They seem to give cleavage sites for proteases, though nothing of the statistics you're looking for.

Looking at the first entry on the list, I think those are sites at which the  subject protein is cleaved, not its substrates.

Some of the entries do contain the cleavage site for the protease, but I guess not all of them. Anyways, that list was just a thought I had… it may have been a bad one.


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Acid/basic chemicals that can be used without extraction hood?
I need to use some meat dissolvent for my thesis, I’m working in forensic anthropology, but in my university, we are not allowed to use those which might be extremely harmful (such as HF or HCl due to the fumes).
Friend of mine suggested me to use CaO and KOH, since you only need normal lab equipment. Do you have other suggestions that might come in handy?
Thank you! All the help I can get is really appreciated


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Is the cranial nerve blood supply encapsulated by the blood brain barrier?
I understand the origin of cranial nerves are within the blood brain barrier. I'm assuming as they extend distally there's a point at which their vasculature is not encapsulated by the blood brain barrier. Is this true? Any idea where the blood brain barrier stops?
Thank you.

Did you google (e.g.) Blood Brain Barrier? The Blood Brain Barrier isn't a membrane or sac, like the dura mater. It exists because of capillary structure within the central nervous system. The origin of all nerves (anything coming off the brain or spinal cord) is "within the BBB". I'm unsure of what you're asking.

Thanks anongoodnurse. I've researched it quite a bit. Although I haven't found anything to confirm or deny, I'm assuming the cranial nerves as they emerge from the Pons, etc. would be encapsulated in the BBB. I'm also assuming that the BBB doesn't extend all the way along the cranial nerves until they end, because that would mean you have a Blood Brain Barrier outside of the CNS. Somewhere along the way from the Pons to the end of the cranial nerve, it stops. Is this right?

I will ask you a question which can answer yours, though I think you still don't quite understand the BBB. How can you administer a drug which can bypass the BBB? Think cancer treatment. I'm sorry to use the Socratic method, but that's largely how doctors are taught. Teach a man to fish and all that.

I can't find a great answer to this either, but there is a known concept of a CNS-PNS transition zone, specifically as it pertains to myelination of cranial nerves. With the exception of CN 1 & 2 (which are effectively wholely CNS) the other cranial nerves are anatomically similar to spinal nerves, i.e. they're myelinated by Schwann cells and have an endoneurial blood supply. But they are also myelinated by oligodendrocytes for a short distance (varies by nerve) after taking of from their CNS nuclei before reaching that transition zone. According to this paper, that transition zone should mark the end of the astrocyte coverage which is necessary for BBB function. It's not a dead-ringer of an answer but this explanation makes as good physiologic sense as anything I've seen.
https://www.ncbi.nlm.nih.gov/pubmed/10697296


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Scaling of Ca2+/biochemical signals with dendritic spine size?
I am looking for references that discuss the scaling of biochemical signals in dendritic spines with spine size/synaptic strength. A recent paper (Walker et al. 2017) reports attenuation of NMDA receptor Ca2+ signal with increasing spine size, consistent with a scenario where increase in synaptic efficacy (AMPAR/NMDAR conductance) is overcompensated by spine volume expansion. However, it is not clear to me if this trend is also reflected in the activation of downstream biochemical signals like calmodulin (CaM) or CaM-dependent enzymes. This relates to the issue of how the threshold for plasticity might be regulated as a function of synapse strength/spine size. Would be very interested in knowing if this kind of data has been reported in the literature.


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The quality of binding sites?
Can someone please provide a human friendly explanation.
to the following:

RNAp binds a defined site (a specific DNA sequence) at the promoter
(Fig- ure 2.2a). The quality of this site specifies the transcription
rate of the gene

what is the quality of the site?

Quality is most likely related to how tightly RNAp binds to conserved sequences in the promoter, and that is related to how closely the actual sequences themselves are to RNAp's "most-preferred" sequences. The actual sequences can vary between genes, giving them different transcription rates.

thank you for your explanation
much appreciated


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biofilm model scales
I have a question about the meaning of biofilm modelling scales:
Are they microscopic, mesoscopic and macroscopic.
Microscopic means individual bacteria
macroscopic means large number of concentration
and mesoscopic means the structure of biofilm.
If there is any mistake please correct me.
Thank you

I'd have thought it rather depends on the context in which the phrase is used. Could you elaborate? Is it a large bioreactor or a petri dish?

Thank you for your response. Actually, I am using mathematical models to model bacterial biofilm. However, I am required to write about biofilm modelling scales and to be honest I ve read several papers and I am not sure if my conclusion were correct.

Just like in math, in biology you have to define your terms. "Modeling scales" are whatever someone defines them to be, within the context their definition is used. Two papers can use the same word to mean something different if they want. For your writing, you'll have to cite the actual literature relevant to your field, not an answer on StackExchange.

I am not going to cite StackExchange. Just I wanted to clarify my understanding to the concept.


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Why do our eyes not have interference from other sources of light?
When one looks forward at a glass of wine, one is seeing it via the reflection of light off of the glass. But if you have a person to your right, looking to the left side of you (still in front of your face), he can see objects across the room that are not in your peripheral vision. Considering that the light which is reflecting off of the object to your left is passing directly in front of you to your friend to the left, why are we unable to see that reflection?
In other words, why can we only see the light reflections of objects in front of us, but not the light reflections of objects which pass our eyes from our left or right?

I'm voting to close this question as off-topic because this is a better fit for the physics stack since it about basic optics and not biology.

You can see those objects not in your vision range on a mirror because it reflects the light rays coming from that object perfectly towards our eyes instead of scattering it in all direction. It is simple ray-optics and I agree with @John that this is a physics question but I guess it may to too trivial over there so I don't know if migration would be suitable.

You can't see light that goes past your eyes, only light that goes into your eyes.
Every seen a movie where there's a laser grid that's only visible when smoke is blown over it?  You can't see the laser until a photon is deflected towards your eyes by hitting the smoke particle.

Perhaps a better question for the Physics site, but light is composed of particles called photons.  (I'm ignoring the wave-particle duality for the sake of brevity, and because it doesn't really apply at this scale.)  A photon doesn't react with anything (like the light-sensitive chemicals in your eyes) unless it hits it.  So your question is like asking why, if someone throws a rock from right to left in front of you, you don't feel the rock hit you.


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What is the max amount of photons per second of the rods and cones in our eyes?
The title says it all. I just cannot find any information about this - I have tried for so long now. Therefore, I figured that I could reach out to some clever guys in this forum for help instead:)
Also, if it is possible, I would love a link to read more about it.

what did you find? It's much better if you show the information that you've found so far, it may help others to know how far you've got and where you're stuck.

Nothing, quite simple :(


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Measure of diversity, accounting for known species
I'm interested in measuring the diversity of each sample out of many independent samples. I know a priori all possible species that could appear in a sample, and expect the counts of species to be from 0 to about 10, although often times there will be none of a particular species within a sample. For example, some data might look like:
Sample # | Species A | Species B | Species C
--------------------------------------------------
1          0           4           0
2          1           1           1
3          0           1           1
4          2           2           2
5          0           1           0

The most diverse sample here is #4. The least is #5. Theoretically, #5 would also be the least diverse ever encountered (assuming there is at least one of some species in each sample).
I encountered trouble when using Simpson's Index of Diversity since that formula would make the diversities of Sample 2 and Sample 3 both 1.0. Intuitively, with this data, I am confident that #2 is more diverse. This is because I know all possible species that may show up.
I'm relying on this definition:
$$
D = \frac{\sum n(n-1)}{N(N-1)}
$$
Are there measures of diversity which account for a priori knowledge of possible species (and perhaps their bounds) and expect near-zero counts?

Without genetic data, the standard other measures of biodiversity are Shannon-Wiener index and, simply, species richness (aka. number of species). I'm afraid that both Shanon-Wiener and species richness would rank sample 2 and sample 4 equally.

There isn't a single "true" measure of diversity, and different aspects of diversity can be taken into account (abundance, evenness, uniqueness etc). Different indices also weight these aspects differently. So you need to carefully define what you are after before choosing an index.

Also, I question your calculation of D; to me the value for 2 & 4 would be 0.333 and for nr3 0.5 (i.e. 1-D equal to 0.667 and 0.5, respectively).

@fileunderwater Thanks for the comment. I realize there isn't a single "right" solution, I'm just looking for the most suitable: something that takes into account the number of unique species in addition to the overall abundance of each (perhaps with knowledge of possible species). Pardon me for not being from the biology community (this is actually a linguistics problem, but I'm reaching out to biology because there may be a fitting link)

@AlexL No worries about being from another field, especially since the diversity indices have quite wide appeal. I'm currently working a lot on scientometric data, and diversity indices (often borrowed from ecology) are common there as well. I think it would be useful for you to look at Hill-numbers, which basically are ways to rescale diversity indices (measures of entropy) into effective numbers of species. This makes it easier to compare numbers from communities/sites with differnt levels of species richness.

Simpson's estimator, which assumes that sample frequencies are not population frequencies, is unbiased on the probability scale. As @fileunderwater noted, it can be helpful to quantify diversity in terms of effective number of species, or Hill numbers. On this scale (the reciprocal of Simpson's concentration in this case), Simpson's estimator is no longer unbiased. Chao and Jost 2015 recently proposed some estimators for Hill diversity that formally rely on the total richness (of the sampled community) to estimate the true diversity of the community based on the sample, and argue that they have reduced the bias.
I sense, however, this is not exactly the same as your question. If I understand correctly, you have a known maximum diversity but not a known true cardinality/richness/total number of types within a given community/corpus whatever the pool you're looking at is called. In this case I might use maximum richness as a Bayesian prior; I might still use a Hill number as your metric but use the model to estimate that metric.
This 2014 review paper gets into these ideas a bit, or to take an Alan Turing perspective, you might find Zhang 2017 helpful.
Most diversity indices that ecologists use are not sensitive to total abundance, only relative abundance, so as Remi.b noted, classic indices (including Hill numbers) would all rank even communities with the same cardinality/richness identically; the only reason you're getting a difference between {1,1,1} and {2,2,2} with Simpson's estimator has to do with Simpson's solution to the bias in estimates of the community's diversity arising from using sample frequencies.

Thank you, this is good food for thought. The papers and book you referenced seem like valuable resources after a skim!


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I want to know the name of this water plant?

Above is an image of an unknown plant. It grows without any care.

Welcome to Biology SE! Please have a look at our policy for species identification questions and edit your question accordingly. As it stands your question is unlikely to receive a definitive answer and it may be down-voted or deleted.

what country/pond/fields/woods/height of plant/flowers is it?

@com Size is clear from the picture and if there are no flowers, you can't take a picture of them. But I agree location and habitat (probably shore of a lake or ditch) should be mentioned.

I know this plant because it is very beautiful semi aquatic and it has yellow flowers in summer. This summer it was the most amazing plant that I found in the south of france cote d'azur rivers. I have just learned what it is. It has the most lustrious foliage of nearly any plant and it looks like green metal.

@com Yeah it is nice to look at. However, it is an invasive alien species that completely overgrows the river, blocking water from flowing and costing water management a lot of work and money. See my answer below.

This is a water-primrose Ludwigia, probably Ludwigia peploides but I am not sure about the species (also because you didn't provide a location). Luwigia peploides and L. grandiflora are native to South america. However, in the rest of the world they are considered invasive weeds. In the European union L. peploides and L. grandiflora are considered "Invasive alien species of Union concern" This means EU member states should take appropriate action against these species.

Water-primrose has a high variation in the shape of the leaves, especially between vegetative and flowering sprouts. On the picture in the question the leaves are almost round. However, on the ground just left of the hand, there are lanceolate leaves, almost willow-shaped. This is the same species and the reason it is also called floating primrose-willow.


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Are drug-gene interactions predictable?
I have been reading about drug-gene interactions and pharmacogenetic tests. I haven't been able to find many resources that define the process of testing for possible drug-gene interactions without performing trial and error method. For example, drug-drug interactions can be predicted by using several parameters as noted here. Are there any parameters similar to the ones described in given paper for predicting drug-gene interactions if drug characteristics and genetic data is available? Please describe process or provide source.

You need to add more details or else the question is quite broad. Yes you can find drug-gene interactions. Google the terms pharmacogenetics and pharmacogenomics.

One can list candidate genes based on their functions.
If a drug acts by inhibiting the expression of gene G in order to reduce process P, then, gene G, all its regulatory elements and all sequences involve in process P are good candidates for such interaction and should be investigated. If there is known genetic variation in the population at these loci and if we know this genetic variation affect phenotypic variance, then definitely, those are good candidates.
However, to my knowledge, this is the extend at which we are able to go. We can list candidates but it does not mean in the absolute that a candidate must present an interaction with the drug of interest and it does not mean that a non candidate gene would necessarily not have an interaction. Only a statistical testing for such interaction would allow one to solve the mystery.

Is there a study where the above works or is this hypothetical?


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What is this salt-water worm?
We found this near Fort Pheonix in Buzzards Bay in Massachusetts. It gets long when its swimming (About 8 inches) and contracts when disturbed (2 inches).
Its head is shaped a bit like a diamond (like a cobra?). Its body looks fairly translucent and is ribbon-shaped.

Here's a short video: https://vimeo.com/240322590

It is possibly a milky ribbon worm (Cerebratulus lacteus).

source:  intertidal-novascotia.blogspot.com
They can be found anywhere and everywhere along the Atlantic coastline in healthy abundance - http://intertidal-novascotia.blogspot.com/2012/05/cerebratulus-lacteus-milky-ribbon-worm.html


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What causes weight loss and fatigue in Addison's disease?
Why would a lack of cortisol cause fatigue? In terms of normal functioning of the gland.

Cortisol is required for gluconeogenesis. So if you have low cortisol, then you will have low blood sugar, which causes fatigue. https://www.thebabbleout.com/health/cortisol/ According to wiki low cortisol causes increases lipolysis, but that part is not so clear. https://en.wikipedia.org/wiki/Cortisol


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What happens if you intake pure magnesium?
We know that body needs a certain amount of magnesium. Why are magnesium supplements in the form of magnesium oxide, magnesium citrate, etc?

Note that this is true for all the trace metals; your body uses magnesium ions, not elemental magnesium. The free metal is not found naturally, it's far too reactive.

Elementary Mg isn't available normally in the environment, only when it's chemically reduced in the lab and stored in the absence of oxygen or other oxidative sources.

I would think pure magnesium would react with the stomach's hydrochloric acid, producing magnesium chloride and hydrogen gas.  Probably not a good idea to perform the experiment on yourself, though.

Because like a lot of material we need the ion not the pure form. Pure sodium is explosive metal and pure chlorine is horribly toxic gas but change them into their ionic form and they are essential nutrients, sodium chloride, table salt.
In the case of magnesium however the problems one of reactivity and absorption. If you swallowed a solid lump of magnesium, not much will happen, the molarity of stomach acid is fairly low, it reacts too slowly to get significant amount of magnesium (or hydrogen) out of it before it passes. Your body just is not equipped to break down solid magnesium since it does not occur naturally often. We can only absorb it in it's ionized state.
More importantly we take in some ion combinations better than others, this is called bio-availability and is influenced by a number of factors. Magnesium oxide for instance has very low absorption rates and basically just passes through without doing much, while magnesium glycinate has a fantastic absorption rate, some combinations can actually be mildly toxic like magnesium sulfate. This is a reoccurring issue with dietary supplements many do not contain bioavailable forms of the mineral they list, which is how people can end up with deficiencies even while taking supplements for that mineral.

Thank you so much! I've heard magnesium is good for IBS. The question is, which form of it. You said magnesium glycinate has a fantastic absorption rate, so it seems like the perfect choice?

once it is absorbed it is basically all the same, but different compounds are absorbed at different rates.

you said magnesium sulfate could be mildly toxic. I'm wondering if different combinations have different mechanism of action?

Magnesium sulfate is a fairly powerful laxative,  that is what I was referring too.


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Common stains for fungal microscopy
I recently got a light microscope to start exploring microscopic features of fungi (and to explore microscopy in general).
What are some of the most common and easily available stains used when preparing microscope slides for fungi? Which situations are they each best for?


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Where does my extra blood volume go after giving birth?
I'm pregnant. I've learnt that during my pregnancy my blood volume will increase by 50%. https://www.ncbi.nlm.nih.gov/m/pubmed/4075604/
So I'm wondering, what does my body do to decrease my blood volume after I give birth? Where does all that extra blood go? I would imagine I lose some during labour, but I seriously doubt it's all of it.

The extra volume of fluid is due to the fluid retaining effects of high oestrogen secretion in a pregnant human female. After this high level of oestrogen subsides the extra fluid is mainly eliminated as:

urination
some is lost during parturition (labour)
lactation to some extent as well

Reference:A Textbook of Medical Physiology (South Asian Edition) Guyton and Hall

Note that this process can take some time, and in the meantime you may see some of that extra fluid show up as edema. My ankles stayed trim throughout my entire twin pregnancy, but swelled up to twice their normal width within a day of delivery. Also, you'll continue to bleed (like a heavyish period) for a couple of weeks after delivery.

The actual blood cells just get circulated out over time (e.g. broken down in the spleen). Eliminating the fluid is the easy part - consider how easy it is to drink a liter of water, absorb it and add to your plasma volume, and then filter it straight back out through the kidneys in a matter of an hour or so.

The other answer elaborates on how the fluid leaves the body, but completely glosses over what happens to the blood cells. I suggest elaborating on how the fluid leaves the body.

You phrased that very nicely.


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What is continuous selection?
I've been reading paper on ancient horse genome (Recalibrating Equus evolution using the genome sequence of an early Middle Pleistocene horse) and in abstract authors mention term continuous selection:

We also find evidence for continuous selection on the immune system and olfaction throughout horse evolution

Can someone please explain what it means? What is continuous selection? Is it selection without interruptions, but what are those interruptions?

Continuous selection is not a term; it would not be bolded in a textbook.
When studying the history of a genome/lineage, you could have two very broad hypotheses about a given trait:
1) The trait was not present in a lineage, then appeared fairly suddenly (at least on a long time scale, it could still be hundreds, thousands, or millions of generations), and since then did not change much.
2) The trait was not present in a lineage, then the trait appeared in part of that lineage, and since then, the trait has continued to change substantially among different descendants of that lineage.
You could find evidence towards (1) if, for example, you observe a trait that is fairly constant among a diverse modern taxon but you don't see a similar trait in the cousins of that taxon.
You could find evidence towards (2) if you see a lot of diversity even among recently speciated members of a taxon.
The statement in the article is just saying in plain English, rather than using a scientific terminology, that they see evidence towards (2).

As far as I know this is not a precisely defined technical term, and there's not a huge amount of additional detail in the paper. Here's the sentence from the paper that seems to correspond to the highlighted phrase in the abstract:

Finally, we identified loci potentially selected in modern horses (Supplementary Figs 11.1–11.2), focusing on regions showing unusual densities of derived mutations (Supplementary Information, section 11.1) ... Functional clustering analyses revealed significant enrichment for immunity-related and olfactory receptor genes (Supplementary Table 11.4), two categories also enriched for non-synonymous single nucleotide polymorphisms (SNPs) (Supplementary Information, section 5.2d).

And from the supplementary information:

We used quartet alignments including the donkey as out-group, one ancient horse
  and two modern horses in order to scan for genomic regions where the two modern
  horses shared unusual accumulation of derived alleles. Those could represent
  regions where alleles reached fixation faster than the rest of the genome, as a result of recurrent positive selection along the modern horse lineage or more recent selective sweeps, possibly in relation to their domestication. ... Comparing genomic scans performed with our ancient genomes enabled us to
  dissect selection regimes at two time periods predating the tMRCA of modern
  horses.

As far as I can tell without spending much time reading the paper and supplementary methods much more carefully, the authors are comparing sets of genes that differ between between two ancient horses and the modern horse in order to determine what changes occurred during different time periods e.g. between ancient horse 1 and ancient horse 2 or between ancient horse 2 and modern horses), and are concluding that in fact changes occurred approximately equally in all periods ("continuously") rather than early vs. late.

In this picture DK is the donkey  (out-group), TC21 and CGG10022 are two different ancient horses, and M1 and M2 are modern horses.

I don't think it means anything more than repeated occurrence of the selection of the prefered traits.
A trait vital for survival will always be exposed to stronger evolutionary pressure. Even if the trait is good there will always be room for improvement.
It can be seen in contrast with the introduction of a radical improvement with the introduction of a new genetic mutation. This will probably happen only once until the entire gene pool is updated.


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What is this giant insect that just bounced off a second-floor glass door?
At about 11 pm, I heard a loud impact on the nearby glass door to a second-floor balcony. I thought it might be an acorn but it'd be a very unlikely angle - it'd have to be thrown from below or be a very strange ricochet.
So I looked and encountered this rather impressive creature recovering on the balcony:

Those planks are six inches wide.
I've never seen one of these before. What is it? Are those giant serrated appendages on the front mandibles or antennae?
I expect it's not as hazardous as it looks, but is there any risk of it biting people or pets?
Do they routinely launch themselves two stories into the air, or would it have crawled up and then just bounded from the balcony floor?
Location: Southern Oregon, USA.

Searching the Internet again this morning, I think I may have identified it as a California (Giant) Root-Borer Beetle (https://www.insectidentification.org/insect-description.asp?identification=California-Root-Borer-Beetle). Yes?
They fly, and are active at night.
The disturbing serrated appendages are antennae (whew!).
It looks like I have nothing to fear from it unless I or others panic at its appearance, but it or its progeny may be bad news for nearby deciduous trees.

Species ID answers should ideally be accompanied by an image confirming the species.

Prionus californicus would have been my guess due to the serrate antenna, Trichocnemis spiculatus are another large beetle without such saw-like antenna.

Species ID answers should ideally be accompanied by an image confirming the species, and some background information to show the species' distribution matches that where the critter was found according to OP, and some links to allow other users to background-read on your sources.


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What does the word specific epithet mean?
Is the species for Rosa indica and Mangifera indica 'indica' as you can see is the same in both. What does this signify. It is obvious that it has different species as they have different genus.

See the last line of my answer here.

Thank You @NatWH that cleared things up nicely.