text:
How does the researcher deal with new data different of what they have learned?
I am currently studying the book Alberts 5 edition 2016. I was wondering how much of the info will remaining vigent in 10 years.
How does the researcher deal with this kind of things? Do they have to relearn, every new edition of every book that they have learned related to his work?

Life is their book.

Papers.... type a topic of interest: Pubmed

Most of what makes it into a textbook is fairly settled knowledge; there are always minor exceptions being found to whatever rule you think you're sure of in biology (we're not physics), but paradigm shifts make news at scale appropriate to their disruption.


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Could a bearded woman ever become pregnant?
I am referring to woman who are facing Hirsutism. So I gone through Hirsutism, there is no mention of pregnancy. So could a bearded woman ever become pregnant ?

Did you research this much before posting? A quick google shows a lot of results.

Welcome J to the community and please make sure you do a thorough search prior to posting, with that, two noteworthy items:
1- Your title is misleading. It could be modified by adding Hirsutism. "Bearded woman" may cause confusion.
2- Referring to the wiki page you mentioned:
Diagnosis of patients includes assessment of ovulation and ovarian ultrasound as well as 17α-hydroxyprogesterone. (DHEA-S) levels >700 μg/dL is indicative of adrenal gland dysfunction.
This means that the reproductive system may not have much to do with facial hair growth. The diagnosis will cover its prevalence.

There are bearded men (transgender ones) who gave birth after going through a male puberty. So even having male levels of testosterone at some point is not enough to render you incapable of giving birth.

Yes.
There is a famous Mexican family that suffers from hypertrichosis and female members of that family have given birth to children. The BBC has an article about them here

Aceves has three daughters, all of whom have been born with hypertrichosis. His eldest, Karla, is now in her early 20s.

"It's harder for the women because it's less socially acceptable for a woman to be very hairy," says Eva Aridjis. "Most of the women have been abandoned by the non-hairy partners that fathered their children. But for the men, they are actually considered virile and tend to have a lot of girlfriends...

After giving birth to a baby, she was abandoned by the child's father.

source: Stack Exchange

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How does a (stem) cell keep track of its own 'specialization'?
If I understand correctly, as stem cells divide, they become more and more specialized. The very first (fertilized) cell still can divide into every other cell in the body, but as they divide further, each cell can divide only into a smaller subset of different cell types.
However, it seems that (other than gametes) each cell contains the full genome, an identical copy of the entire DNA. So if the DNA does not get altered as cells specialize, how does a cell keep track of which parts of that DNA it is supposed to read - and how does it tell its daughter cells to change their specialization when it divides?

This is the age-old question.  Since DNA encodes all the data for growth and differentiation of cells, and since every cell; contains essentially the same complement of DNA, how does each cell differentiate from others?  In the usual answer, reference is made to transcription factors and epigenetic factors etc., but since these must also be encoded in DNA itself, the essential question remains.  Eventually reason demands some sort of deterministic approach and a corresponding mechanism. One might propose  -- and I know that this site is averse to such conjecture --...

.. one might propose a wave dynamic in which not only is DNA itself, its structure and chemical constituents -- its entire substance, in common with the rest of reality-- the function of a fundamental 'wave interference effect', but both its mechanisms of replication and transcription conform to the progressive aspect of such an oscillatory wave principle. An incremental advance in the property of wave recurrence both within the pattern of transcription itself and in its cell-to-cell aspect would permit both features of the phenomenon of cell differentiation: that each cell derives its own...

.. each cell derives its own characteristic and definitive set of both basic and more-or-less specialised proteins and that successive cells in contiguous relation to each other derive proteins which differ slightly in conformation and definitive identity as this wave effect progresses incrementally from cell-to-cell; this latter aspect in particular implicating the requisite production of transcription factors etc. commonly encoded in all DNA. Clearly such an idea requires some substantial modification of what is eventually the philosophical approach to scientific inquiry, of its paradigm.

The process of "specialization" is usually referred to in biology as "differentiation".
Largely, differentiation is a function of expression of transcription factors; these proteins determine which proteins are synthesized in a given cell by either promoting or suppressing transcription. Transcription factors can also influence the transcription of transcription factors themselves. Simplifying things a bit, imagine you have a "muscle cell" transcription factor, we'll call it "MCTF", that is only expressed in muscle cells. MCTF binds to DNA and causes transcription of muscle-related genes, including MCTF itself. It also causes transcription of not-a-neuron transcription factor ("NNTF"); NNTF binds to DNA and prevents transcription of neuron-related genes.
Epigenetic modification including DNA methylation and histone modification can also silence sections of the genome to make cell fate a bit more concrete and less likely to revert.

Thanks! So is the emergence of a new transcription factor that specializes the cell based on some probabilistic process? Like if an "arm cell transcription factor" is present on each division a cell will produce with some probability a "hand cell transcription factor"? Or how are new transcription factors introduced into daughter cells that weren't present in the parent cell?

@matthias_buehlmann That's quite complicated and too much to talk about in a single SE answer, I feel. A textbook on developmental biology would be a good place to start. Very generally, in early embryonic development there are some push-and-pull stochastic relationships, where certain molecules might signal "head" or "front" and others "tail" or "back"; "head" makes more "head" and suppresses "tail"; "tail" does vice-versa. What starts out unstable very quickly reaches an equilibrium where "head" and "tail" are clearly separate. Something similar happens at local scales, as well.

@matthias_buehlmann https://en.wikipedia.org/wiki/Cell_fate_determination is another place to start reading.

Transcription factors usually initiate the cellular changes, but it's mostly the chromatin state of the nucleus that maintains the state of a cell and stops it from changing back and forth.
Embryonic stem cells start out with open chromatin ('open' means 'accessible'). This means low DNA methylation and overall epigenetic modifications that enable transcription. This can be interpreted as "a cell with full potential", since many regions on the DNA are available for transcription.
The further a cell differentiates, the more DNA regions assume a closed chromatin state, meaning higher DNA methylation and repressive epigenetic marks that lead to DNA condensation. It's as if the 'potential' decreases, since huge regions on the DNA become 'locked up'. These huge regions on the DNA are partitioned into 'TADs' (Topologically Associating Domains) and their epigenetic state can be determined by ATAC-Seq
See this review for reading about chromatin state and stem cells.
As mentioned by Bryan, specific transcription factors are unique to a cell type. Some transcription factors bind to multiple promoter regions and initiate a complex differentiation program that orchestrates cellular/biochemical/morphological changes needed to fulfill specialized function.
The promoters involved in cell differentiation can be in a 'poised' (aka 'bivalent') state, meaning that they got both transciption -inducing (H3K27me3) and -repressing (H3K4me3) epigenetic marks, so it's as if these promoters are "ready and waiting" for a signal to decide whether to transcribe or lock up a DNA-region. And once a DNA region is locked up, the cell knows that it has lost some potential and "knows" what cell type it is. Lesch & Page 2014
Such poised promoters are not just present in embryos, but also in adult tissues, like mesenchymal stem/stromal cells (MSCs) in the bone marrow. The RUNX2 Promoter is poised and is waiting for signals to turn the MSC into an osteoblast (or chondrocyte or adipocyte). Wu et al 2017

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How to make predictions on genes not involved in a particular disease
I have one set of genes which counts about 100 such that every gene of that set is evidence based involved in a particular disease. Let's call this set A. For a machine learning project I need a set of genes that is with high probability not involved in that particular disease. Let's call this set B. Usually in science one focuses on finding a gene that is involved in a pathology and not the opposite,i.e. finding a gene that is not involved in that particular pathology. But one can eventually make predictions based on some strategy in creating the set B. Knowing the genes of set A in terms of their identity, location in the genome, expression profile in a certain tissue where the pathology arises etc., how could one propose the set B ? Can one indicate a paper or present his/her own experience with a similar question ?
Many thanks.

Simple idea: find a GWAS for the trait you’re interested in, aggregate p values across genes and take a random set of the genes with the lowest highest p-value

Thanks. The set A is not based on GWAS. It is difficult to find GWAS studies in this case.


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What came first: the ribosome in which RNA is read, or the RNA to encode for the ribosome proteins?
It's a bit like the chicken-and-egg problem. Ribosomes need proteins because they are partially made of them. Where can they get their proteins? They read the base sequence in mRNA entering them, assemble the amino acids, and spit out the proteins. The problem though is that the proteins needed for the ribosome need a ribosome in the first place.
I realize that it's a highly simplified picture I paint here, but I think its clear what I mean. Did proteins existed before RNA/DNA? Amino acids were created in a lab-soup already many decades ago, back in the previous century, and probably the same holds for RNA-kind of (small) structures. Did one of them come first? Did protein primordial life took advantage of self-replicating structures capable of storing information about proteins, or did the self-replicating structures took advantage of the primordial protein life to facilitate replication?

I suggest — and indeed this list requires — that you do a little reading on this topic, which was first raised over 60 years ago. Of course, we do not (can not) know that answer, but we do know that the ribosomal peptidyl transferase resides in the ribosomal RNA, so it is possible (likely?) that the original ribosome lacked protein, simplifying the question a little.

@David Thanks. That would simplify things. But what should be called life then? Proteins (which I assume were present), or self-replicating RNA-like stuff?

This question has also been asked several times before: see https://biology.stackexchange.com/questions/80603/what-created-the-first-ribosome


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Does beta-actin have to be consistent in Western Blots?
I have been running Western Blots on rat brain tissues from rats that have been subject to neurological disorders.
I loaded the samples on the gel to ensure that for each tissue, I had a constant mass of protein (30 ug). The volumes were determined via BCA analysis. However, the BCA analysis was performed years ago (approximately 4-5 years ago). Also, the tissues have undergone multiple freeze and thaw cycles.
In addition to the tissue, I also loaded the same volume of Laemelli buffer as tissue and I used RIPA buffer to make the volumes of each sample constant.
I probed my membrane for my protein of interest and a housekeping protein (actin). I have attached a photo of my membrane down below.

top band is actin and bottom one is my protein of interest
However, I noticed that my actin bands are not consistent (some are fainter or darker than others).
Do the actin bands have to be the same darkness for each sample? Could I still use these results and instead do a normalization?
Or would I need to rerun this sample again?
Thanks for your help!

The long and the short of it is that your actin bands do not need to be consistent so long as you can normalize and have met the quite stringent conditions for normalization to be effective. For normalization you generally need to have loaded less than 10 ug of protein, have not over-exposed any of the bands, and have them all loaded on the same gel and blot for comparison. You can not compare results across more than one blot without running inter-blot comparison controls!
Please note that this image would not probably not meet most publication requirements (in my opinion).
Please read the PDF here from Li-Cor on western blot normalization. It are the best descriptions of the conditions needed that I have come across.
However, for publication, you may have a harder time convincing reviewers that your results represent real data if the actin bands are so variable. Having a plot of normalized results is all well and good, but the eye is not very good at determining changes of less than about 50% (i.e. 2-fold) without careful consideration, so for instance your lanes 4 and 5 (not including ladder) have faint actin, but the POI is more or less consistent with the surrounding lanes - meaning that in 4 & 5, you have much more POI than in those other lanes, but it takes some thought to realize this.


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Why doesn't HIV give you cancer if retroviral gene therapy gives you cancer?

More than twenty patients have been treated in France and Britain,
with a  high rate of immune system reconstitution observed. Similar
trials were  restricted or halted in the US when leukemia was reported
in patients treated in the French X-SCID gene therapy trial.[2]  To
date, four children in the French trial and one in the British trial
have developed leukemia as a result of insertional mutagenesis by the
retroviral vector.
https://en.wikipedia.org/wiki/Vectors_in_gene_therapy#Retroviruses

HIV doesn’t seem to cause cancer directly, but over time it causes the
immune system to become weaker, putting people living with HIV (PLWH)
at  an increased risk of many types of cancer.
https://www.cancer.org/healthy/cancer-causes/infectious-agents/hiv-infection-aids/hiv-aids-and-cancer.html

Short answer: Most HIV-infected cells will die before transforming into cancer.
Retroviral gene therapy may increase risk of cancer since the integration into the cell's genome can be faulty (strand breaks, insertion into genes, cell stress and innate immune response, etc. ). Infected cells survive but might transform into cancer later in very rare cases.
HIV also causes integration into the host cell genome, probably causing errors, too. But most infected cells will die (apoptosis, overproducing viruses) before transforming into cancer. But as you said, the lack of an immune system increases risk of developing cancer in non-infected tissues.


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What animal is this from the kitchen
The following picture has been taken in August  inside a box
I’m the kitchen in a city at the center of France. What animal is this? The real size is about the size of a grain of rice

Welcome to Biology.SE. This is a common question, but hard to find the answer if you don't about image searches e.g. Google Lens — please have a look at the links posted in the comment by @theforestecologist here.

Thank you! I just tried with Google lens that suggests this is a larva of Varied carpet beetle.

it is the larva of many possible skin beetles (carpet beetles) including, possibly, the varied carpet beetle.


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They look like tiny black ants but they're not I find them only in my son's toy box
I find these only in my son's toy box not in the kitchen or not around food I have bleached all my son's toys and they still come back they are not crawling along the wall or anywhere else in the room or any other toy box in the room there is no food in the toy box as I've cleaned it thoroughly but I don't know what they are they seem to live for a little bit and then just die they only stay in the bottom of his toy box can you help me figure this out or how to get rid of them
They are tiny and black as you can see

Unless your toys include grain of some sort, it's not likely these are actually living on the toys. I'd check your food stocks more carefully, especially rice and grains. Do you have neighbors?

Check for a bag of corn, rice, wheat, cereal, etc. That's the source. They will spread through the whole house given enough time. They're small enough to crawl "under" carpet surface and so move about great distances before being found. Are pretty harmless to everything but your food other than being a "gross" infestation. Mechanical removal + sealing available food necessary to slowly eliminate.

Seeing as it has three legs to a side, which are visible towards its right side (zoom in as far as you can) relative to the rest of the picture, appears to have a protruding set of mouthparts, and has a body that's visually divided into two parts, I'm tentatively going to call that a weevil.
As Bryan Krause pointed out: check any food you might have in your house for them. Weevils like eating things.
Alternatively, it might be a member of a weevil family that feeds on dead wood. Is the toy box made of wood?

Unlikely to be Anthribidae ("family that feeds on dead wood") due to wrong habitat, size, morphology, etc..... Also, all animals "like eating things"

@theforestecologist More specifically, weevils like eating things that people would prefer uneaten.


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In drug discovery, what is an undruggable target?
The term "undruggable" is often use in drug discovery. As far as I understand it, it means "for which no inhibitor has been found so far".
It's a fuzzy, non-satisfying, definition.
What is an undruggable target?

Welcome to Biology StackExchange! Here, it is expected that you show some research on your own. Some relevant articles: Zhang, G. Strategies for targeting undruggable targets, Dang, C. V. Drugging the undruggable cancer targets.


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Is a plant's own compost better for the plant?
Does it make a difference if a plant is composted and used for its own compost ?
Meaning, let's say there is a plant "X" (example Cucumber)
Would it grow better if the compost was made from the "X" plant itself ?
Has there been a study on the same ?

There are a lot of studies about composting and plant vigor. Have you looked for a study? If so, what did you find out? Some evidence (not your claim to have done so) of prior resesarch is strongly recommended on this site, and lack thereof is a reason for close vote and down vote.

you should ask a farmer this question,they have studied this for som time(10 000 years+).


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Does Ramon Margalef really stated in 1972 general criteria for Shannon-Wiener index interpretation?
I work as field biologist in Chilean System of Environmental Impact Assesment. Several reports made by colleagues use Shannon-Wiener index for characterizing the richness study area, with the following interpretation of the result:

H
Diversity

0
minimum

0.1 <= H <= 1.5
Low

1.6 <= H <= 3
Medium

H <= 3
High

The reference that "back up" this criteria is:

Margalef, R. 1972. Homage to Evelyn Hutchinson, or why is there an upper limit to diversity. In: Growth by Intussusception. Ecological Essays in honor of G.E. Hutchinson. E.S. Deevey ed. Trans. Connecticut Acad. Arts & Sci., 44: 211-235.

I didn't find the document, but I suspect that Margalef:
a) Never established these criteria
b) It is misinterpreted
c) Established these general criteria but without enough proof
My suspicion is based on the fact that in information theory, Shannon entropy does not have a straightforward interpretation.
So, does Ramon Margalef really stated in 1972 general criteria for Shannon-Wiener index interpretation? or:
Can Shannon-Wiener index value be used for assigning a "Richness Quality" to a Study Area without comparisions?

What do you mean "without proof"? These look to me like just labels - there's nothing really to prove.

I mean an argument, evidence or something convincing to the usage of those labels

Isn't that opinion-based? It seems like you just need help finding the document, have you tried asking your librarian?

A limited index of word occurrences for that volume of Transactions is available at hathitrust.org ; the cited paper appears present, but neither Shannon nor Wiener is shown present (but OCR could be an issue).  There are many other papers on the Shannon-Wiener index.

related discussion: https://www.researchgate.net/post/Does_anyone_have_experience_using_the_Shannon_Wiener_Diversity_Index_Score

To be clear, my suggestion to ask a librarian is not meant to be sarcastic or rude: this is part of a librarian's job. See for example https://academia.stackexchange.com/questions/134634/how-can-i-find-an-old-obscure-or-otherwise-inaccessible-paper-when-the-usual-m Librarians are trained professionals and an often underutilized resource.

Thanks for the aclaration and post Bryan, but I don't have an institution for asking a librarian. However, I will stop this search for the general (and more relevant question) about diversity index interpretation.


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Ducks highest body temperature
Normal body temperature for ducks are 106-108°F (41.1-42.2°C).
Young ducks 102-106°F (38.9-41.1°C).
How hot can a duck's body temperature get?
Possible causes are fever and viruses, as well as stress hypothermic response.
Will it ever reach 113°F (45°C)?
What will be the cause?
How common is it?
Thanks a ton!

Welcome to the site. Please visit the [help] and take a [tour] for more information on what we do here and what make a good question and answer. Please also note the homework policy. In that light - what have you found out about this. A quick search leads to some very relevant papers with great detail as the top links.

The only thing I found so far was temperatures caused by injecting the duck with different pathogenic constituents for testing purposes, it also says "When they were handled to apply treatments, the ducks developed stress hyperthermic responses", but not so sure how to read those charts, looks like it reached +-43°C due to the injection. Not sure how common this is. I heard that it can reach 45°C, but cannot verify it nor the cause.
https://www.researchgate.net/publication/51150900_Body_temperature_responses_of_Pekin_ducks_Anas_platyrhynchos_domesticus_exposed_to_different_pathogens

You can probably generalize from other birds - just as you can for most mammals. Max I have seen is 46 C being fatal.


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D-Galactose effects on primates?
A lot of studies are made using D-Galactose as a accelerated aging model in rats and mice, but why not in non human primates? How much relevant is the galactose rat model for human health perpective? (in the sense that galactose can have similar bad effects in humans)

It helps to support your question with references - e.g. a review paper on use of D-Galactose as an aging model.

Have you any idea how expensive it is to do experiments in non-human primates, and how difficult it is to get ethical permission?  You generally need an extremely strong case relating to concrete high-priority human health benefits. Aging is not that.


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Has the approach of any protein digesting enzyme has been trialled for Progressive Supranuclear Palsy against a protein accumulation in brain cells?
PSP -the degenerative disorder is attributed to accumulation of a protein in brain cells. Has any work been done to approach it by digesting this protein?

We ask that questions show evidence of prior research effort.

How would you digest such a protein without also digesting other proteins in the cell. How would you get this protease into the brain and into the cells?

I think the word "digesting" is the wrong choice. You digest a meal (non-discriminatory/encompasses almost everything in your stomach. Same with your example using proteases/other.) You want to research "tau-targeted therapy".


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Do we need to underline the name of a gene while handwriting?
While teaching about the cry genes and the Cry proteins in Biology class, my teacher told us that the names of genes are always written in lowercase and should be italicized, and the name of protein coded by that gene should always start with a capital letter.
Now, while reading the notes taken in the same lectures, I am wondering whether the name of the genes should be underlined while handwriting, as we use to do while writing the biological names; or are there some other rules related to it?
Moreover please tell me that is it really necessary to write the name of a protein (I am talking about every protein) always with a capital letter at start?

Do you get graded on your notes? They're your notes; if you'll remember the difference between the gene and the protein, write them however you want. I had an extensive shorthand system (10 years of notetaking will do that); no one ever corrected me about my unique symbols.

@anongoodnurse Actually they are my own notes which I took during the lecture!

@anongoodnurse There are no grades for those notes, but I asked the question for myself knowing the right way!

They're your notes. There is no right way or wrong way to take notes. The purpose of notes is to help you remember what was said. Formal writing is different.

@anongoodnurse Actually, my question is about the formal writing only! Are there any rules for the aforementioned?

Handwriting and notes
How you handwrite is totally up to you. No important information in research science is disseminated widely with the use of handwriting anymore; whatever the conventions were, you'd be wise not to care about it one bit.
Nomenclature in scientific research
The nomenclature can be different across fields. In Drosophila genetics, the prescribed norm, which is admittedly not really often followed, is as follows for capitalizing the first letters (contrary to what you were taught):

1.2.2. Selection of lower or upper case of initial letter. Gene symbols/names begin with a lowercase letter if the gene is FIRST named for the phenotype of a recessive mutant allele, and begin with an uppercase letter if they are FIRST named for the phenotype of a dominant mutant allele. Gene symbols/names also begin with an uppercase letter if they are FIRST named for an aspect of the wild-type molecular function or activity of the gene product, which includes genes named after an ortholog or paralog.

Rules of thumb

Keep in mind the distinction between nucleic acid and protein; this usually differentiated by formatting (e.g. italics).
Keep in mind that macromolecule formatting nomenclature often specifies capitalization (entirely capitalized, first character, if non-first characters are allowed to be capitalized, etc.)
Keep in mind the difference between symbol (ID or shorthands) and full gene names.
Keep in mind that synonymous gene names and symbols exist for many genes.

The search engine is your friend. This is a good landing page on the topic.


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Is there a dataset for the optimum conditions (Temperature, humidity, light intensity, etc.) for plants growth?
I'm a student working on an automated greenhouse. I wanted to add a database for the most commonly grown plants and the optimum conditions needed (I'm mainly looking for temperature, humidity, and light intensity) for the plants' growth. I have already found a dataset on Kaggle, but I was wondering if there are any datasets that include light intensity. Any recommendations are appreciated.

All the info is out there, but you need to search for the specific plants you're growing as their optimal growing conditions may vary widely. "Commonly grown plants" is a pretty broad category, not one-(x)-fits-all and varies widely by culture and purpose.

@Belal Bahaa Did you have any luck finding what you were looking for?

The best one I found was the one in Kaggle. Thankfully, I'm done with that project!


text:
What is the mechanism behind antibiotic resistance and how can it be mitigated or prevented?
What causes antibiotic resistance, and how can we combat it? I am interested in the mechanisms behind antibiotic resistance and strategies to prevent it in bacteria.

We expect people to show at least some effort to solve a question by themselves. So, what have you found out? This is marked as homework which is used similar for low effort questions here.


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KEGG map01100: Is this ectomycorrhizae or arbuscular mycorrhizae
Just as background mycorrhizae are fungi and split into two groups ectomycorrhizae and arbuscular mycorrhizae (AM). Taxonomically these fungi groups are very distinct. Ectomycorrhizae belong to the phyla Basidiomycota and Ascomycota, whilst AM are Glomeromycota.
I am really interested in the KEGG map01100 (metabolome map) called "mycorrhizae". The question is

What phyla is the map taken from?
Where do I find out the information/reference about how (and where) this map was constructed from?

I don't know the exact answer, and a quick click around didn't yield an obvious result for the overall pathway. The KEGG annotation process is manual and may not be easy to reconstruct overall (though is generally quite high quality).
However, if you click the "Help" it tells you that there is a reference for the ko pathway view. I wasn't able to actually locate this, but I was able to follow the ko pathway view to the gene orthology view for specific enzymes, which in turn tells you which organisms it's represented in, which you can click through on to find, in this case, an Ascomycota.
I'm sure that there is a way under the hood of the KEGG API or the KEGG database view to pull this information for everything. I imagine that you will likely find a mixture of phyla because they try very hard to generalize the broad biological categories. But that's a guess!
At worst, you might be able to scrape the website to get a reasonable guess for the various enzymes of which phylum they mostly come from.
I would guess that you could ask someone at KEGG and get a more satisfying answer! I'd be interested to see how their sausage gets made as well.

Thanks @MaximilianPress the link you highlighted is cool https://www.genome.jp/entry/K19634


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Why is it essential to uproot a plant just before flowering in order to see nodules?
In my textbook it was written - Uproot any plant from common pulses just before flowering and you will see near spherical outgrowths on the roots .

It isn't necessary to pull them just before flowering. It is merely that the optimal time to check for effective nodulation is about 10-12 weeks post emergence, which also happens to be about the same time as flowering in many species.
Root nodules for the nitrogen fixing legumes develop throughout the life span of the plant. The nodules contain bacteria from the genus Rhizobium which are attracted to the root by release of certain flavenoids. The root hair tip then curls around the bacteria and forms a symbiotic relationship between the plant and the bacteria.
As the nodule formation takes some time to develop and become big enough to see, the nodules are often easily seen about the time the seasonal plants mature as this is also when the nodules get large. However, nodulation starts within 48 h post-inoculation1, so if you took a root tip and looked with sectioning and a microscope you could find nodule initiation at about 48 h.
ref:

Dasharath Prasad Lohar, Natalya Sharopova, Gabriella Endre, Silvia Peñuela, Deborah Samac, Christopher Town, Kevin A.T. Silverstein, Kathryn A. VandenBosch, Transcript Analysis of Early Nodulation Events in Medicago truncatula      , Plant Physiology, Volume 140, Issue 1, January 2006, Pages 221–234, https://doi.org/10.1104/pp.105.070326


text:
Help identifying an insect
I live in Milan, Italy in the city center. I live in this house since 5 years and I keep finding the insect pictured below.
I see it throughout the seasons (temperatures here range from -1°C to +35°C in average).
I find it mostly in my bathroom which is not well ventilated and it is the warmest room in the house (about 23°C in winter even with the radiators off and up to 35°C in summer during very hot days if I don't use air conditioning).
The size is about 7mm in length and 1mm in width (including only the main body, i.e., excluding legs and antennae).
I find it mostly during the night but maybe just because I use brighter lights and I can see it more clearly on my white walls.
What is its name so I can research more about it (i.e., does it pose any risk to my health or to my belongings in the house?)?

Looks like a species of silverfish.
https://en.wikipedia.org/wiki/Zygentoma

They eat paper, cloth and stored foods like cereal, even organic wall paste, so yes they can damage your stuff, but outside allergies they are harmless to a person.

Could it be also https://en.wikipedia.org/wiki/Firebrat ?

Zygentoma is the name of the group there are several species, look at your local pest identification.  silverfish is the common name.

@John ‘Silverfish’ is the common name for a number of species in the Zygentoma group, but not all. Firebrats are, in my experience, the primary exclusion from the term, since their defining feature is that they’re not silvery to look at, but brownish-grey. Sort of like how members of the Odonata family are mostly called dragonflies, except those that are called damselflies.

Silverfish is what immediately leaped to mind when I saw the picture.


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Why do so many aquatic plants propagate from high stem nodes rather than through the main root system?
I have recently tried my hand at aquascaping and I am watching how my plants develop in their environment. I have a mixture of plants - some small plants that will hopefully form a "carpet" (a contiguous mass of plants covering the whole substrate surface) through to stemmed plants.
What I have found really strange is that most types of plant appear to try and spread from high-up plant nodes sprouting roots rather than soil-level runners, or underground via a root system. I have some shrimp and snails in the tank causing a bit of havoc with this because they keep uprooting the small plants and I have to re-plant a few of them each morning.
This leaves me questioning the evolutionary advantage of this kind of propagation for the plant. In some cases, the stemmed plants are attempting to grow roots some 15cm or more, vertically, from a node and these roots are growing rapidly. Presumably their job is to eventually hit substrate, bury in and drag the stem down to form a new unit. However, if they put that effort into their main root system then they wouldn't be constantly uprooted and surely they could spread laterally underground to sprout a new plant?
I understand that buoyancy might make something like a strawberry plant runner more difficult to control (to remain soil-level), but the plants seem to deliberately be choosing higher-up nodes rather than ground-level.
The best explanation I can think of is that these plants are used to fast-flowing river currents that "blow" the stems over so they naturally just hit the ground, but I'm finding that hard to believe when it's happening for pretty much all of the plant species I have introduced, particularly for the tall stemmed plants. It looks like such a huge expenditure of energy to proliferate.
Is my reasoning correct here or is there some work that explains why this should be?
The carpeting plant, with vertical roots from the end-most node:

The stemmed plant (centre) and on the far left, something in between that seems to be somewhat more successful with a huge root system from the nodes:

This is just speculation, but: There's probably something to your idea about the plants being pushed over in a current (or reduced water levels) and rooting at the nodes. Similarly, the upper parts of the plant are more likely to break off and land in a new location for rooting. Different aquatic species are probably more or less resistant or resilient to being uprooted: those that are easily uprooted may be adapted to quickly root wherever they end up. (There's also the chance that your plants are seeking out some missing nutrient, but I'd consult a specialty aquaculture site for help there.)


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What kind of bubble this？

This is the MARC-145 I cultivated. Recently, many bubbles appeared in the cells. I don’t know why.

Late stage apoptosis. Specifically what you are seeing here is cells that have undergone the blebbing stage and are releasing or have released apoptotic bodies.


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Need to Identify This Bug
When I woke up this morning I found 10 or more of these tiny little red and brown bug on the window to above the kitchen sink. They must be attracted to the light as the sun was just rising. I killed as many as I could but they are very small and hard to see. They are mostly bright red. Have 6 legs and antenna.
Does anyone know what they are? Are they dangerous?
Thank you,
Hersh

Please add some information on the location where these bugs where found.

Specifically where in the world you are based - nearby major city or state will help.

This question is more about zoology than biology.

Can you explain your need to identify it? (what exactly is your need? do you need species, genus, family?) If you cannot explain your need here, please adjust your title to be more informative/specific about your post.

(these are aphids, btw... but genus and species is not obvious and would need geography to have a chance to identify)

Hello all, I am in Swedesboro, NJ USA. I want to know what the bugs are to know how to deal with them in my house.

This is an aphid, so it could be at most dangerous if you were a plant. ;)
You can recognize them by a soft, often colorful body, relatively long antennas and legs and the so-called cornicles.


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Efficiency of molecular motors vs. human-made motors
On the wikipedia page for "Molecular motor", it says "In terms of energetic efficiency, this type of motor can be superior to currently available man-made motors." without any references to back it up. Is this true in general and how would we go about comparing for example a diesel engine with the F1-ATPase, in terms of efficiency?

I think that statement is misleading because it is too vague. Yes diesel and gas engines are inefficient, however electric motors typically average between 80-95, depending on the range of rotation speed and torque, (i,e. slow speed and high torque out of design range), they can get hot and waste 20-50% efficiency. The best EV motors are currently hitting >95% efficiency at a high range of rotation speeds.
Molecular motors have been claimed to reach nearly 100% based on limited studies (ATP synthase), however most of them are in far lower ranges than electric motors " Henry Hess of the University of Washington explains that
cytoskeleton motor proteins “convert their chemical energy with >50% efficiency into mechanical energy."
https://guava.physics.uiuc.edu/~nigel/courses/598BIO/498BIOonline-essays/hw1/files/HW1-sankar.pdf

The efficiency of F1-ATPase has ben measured at so close to a hundred percent that the margin of error of the measurement  exceeds the difference.  BUT these measurements were also taken around 1999- 2000 before the highest efficiency EV existed, so the statment was true back then. of course the step right before F1-ATPase, F0-ATPase only runs at around 50% efficiency.

It is referencing an out of date study poorly.
The efficiency of F1-ATPase has been measured at so close to a hundred percent that the margin of error of the measurement, exceeds the difference. BUT this margin of error was almost 10%. The statement was accurate when the measurements were taken, around 1999- 2000. Before the highest efficiency electric motors were common knowledge, so the statement was sort of true back then. Of course the step right before F1-ATPase, F0-ATPase only runs at around 50% efficiency.
It can be really hard to measure the efficiency of individual components of a biological process, the process as a whole from sugar to ATP is around ~40% efficient. which is still high for anything that consumes a fuel.
https://www.cell.com/fulltext/S0092-8674(00)81456-7


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The meaning of atoms sign in protein structure
There are some atoms sign of protein structure in paper, like Nε2， Cε. I know this sign is for information about atoms position, but I don't know the exact meaning. The below is original words in paper, which is about structure of type3 copper proteins.
I need more information about this atom sign system.

This is the "numbering" of the atoms in the amino acids. For this purpose, greek letters are used. This follows the convention that the Cα is the carbon atom next to the carboxylic group. Cβ is the next one and so on.
ε1 and ε2 mark the positions at the end of the ring, which are carbon and nitrogen.
See this picture (from here), which shows all the positions in Histidine:

So here, ε1 is abbreviated as ε. Cε is same as Cε1.

@CharlieXiong Yes.

Examples and references for the atom names are here: https://bmrb.io/referenc/nomenclature/


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Inheritance of child behavior based on daily life experiences of the parent
Our brain is a large network of neurons connected with each other.Our daily experiences change how  our neurons are connected.Some experiences create better connections between two neurons A and B and worse connections betweens neurons A and C.When someone makes children of his own ,does the experiences in the life of the parent influence the behavior of his child for example if the parent has experienced some very traumatic situations will the child be more distant or less sociable?

Children inherit DNA from their parents, which in turn was inherited by their parents from their grandparents, and so on. Only modifications to the DNA in the germ-line cells (those producing eggs and sperm) are heritable; changes in brain cells are not heritable, because those do not involve the DNA of the eggs and sperm.
Everything else that influences a child is environmental. The nature-nurture debate involves discussion of how much genetics versus experience influences development of different traits and characteristics.
Part of the difficulty in measuring the relative contribution of genes and environment is that parents are often important contributors to the environment as well as genetics of their children. Environment starts in the womb, so some of the mother's behaviors and experiences can influence the developing fetus. After birth, a child will continue to be influenced by their environment. Their parents' presence or absence will be part of this environment.
A child will only be influenced by traumatic experiences of their parents to the degree that those experiences influence the parent's behavior around the child.

Do you feel that scientists who seem to have demonstrated generational epigenic modification are in error? E.g. mice and cherry blossoms.

@anongoodnurse You'll note the article you link has quite a bit of skepticism, too; I certainly believe epigenetic inheritance exists, but this is really just an extension of the genome beyond nucleotide sequence. The examples given like famine in the Netherlands involve exposure to a stressed maternal environment.

I agree there is uncertainty (I wouldn't say there was quite a bit), but the evidence is compelling; in vitro fertilization still produced mice who, without ever meeting their parents, were afraid of the scent. "A child will only be influenced by traumatic experiences of their parents to the degree that those experiences influence the parent's behavior around the child." this statement does not support generational epigenetic modification...

... In that respect, the child may well behave differently "if the parent has experienced some very traumatic situations..." I don't say it's highly likely, but it's not impossible.


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What torque can the human wrist take?
Say you are holding a rod in one hand with your tumb on one side and the rest of your fingers on the other. What amount of torque could be exerted onto the rod (with the axis of rotation being around your forearm) before the average person's wrist starts to hurt?
I am asking this because from my calculations it seems like mine can withstand 115Nm which seems unreasonably high. On top of that all studies I can find only measure with the axis of rotation in line with the rod itself.
I hope you guys can help me out, thanks for the effort beforehand.

"...before the average person's wrist starts to hurt?" There is no "average" person (imo); there are males and females, there are various ranges of mobility due to hormones or genetics, there is well developed and poorly developed musculature and connective tissue and everything in between, etc. There are averages in a group of similar individuals, e.g. '30 y.o. white males in good health'. Averages don't really mean that much when it comes to one individual's characteristics. (I know it sounds nit-picky, but it's true.)

@anongoodnurse, that seems fair, but what kind of range can I expect it to be in? Because the 115Nm that I got don't seem plausible.

TBH, I don't know. Speaking medically (where most of my expertise lies), it doesn't matter. I can imagine how stupid that sounds, but it's true. I do think an orthopedist or a physiatrist can answer that with some authority, but I don't think we have one on this site. Sorry to be of so little service.

The technical terms you should include in literature search are "pronation" and "supination". This article seems to measure exactly this. Also, please let us know how you derived your estimate of 115 Nm. You might have made a (trivial) mistake somewhere.

@Domen - Those are extremes before damage occurs; the OP just wants to know at which point it will start to hurt.


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Estimating the diameter of all earths biomass as a sphere
I am working on an educational resource about the relative scales of resources compared to the earth. Attached is an example of the earth compared to various elements contained within, as well as a comparison of the sum of all water and the atmospheric gasses (at standard temperature and pressure).
Such images are great for creating a sense of scale and displaying the fragility if earth's ecosystems.
I want to also include spheres of wet biomass, which I would imagine to be quite small.
However, when I do math I am faced with spheres that seem too small.
I did the math based on 3 methods and got answers of 6km to 14km diameter, based on Metric Ton estimates of 1.57E+12, 1.38E+11, 1.00E+12
Two folks on Quora estimate 10km diameter.
My questions are these:

What is the appx wet biomass of all plant and animal life on earth?
What is the appx density of it such that it can be converted to volume?
Is it really so small? I am used to being humbled, but this seems excessive. :-)

No need to be humbled. If you think about most life exists in a very thin layer about 150 m thick (about the max height for of the tallest tree species (~120 m), and about as deep as roots penetrate (~25 m)) on the surface of the planet. There's very little biomass that we know of much below the surface or up in the air.

I would be so sad if you made this calculation based on plants and animals alone. Bacteria make up the Second largest component of earth's biomass at ~70 Gt C (~15% of total biomass), mostly in the deep subsurface. Then Fungi (12 Gt C), Archaea (7 Gt C), Protists (4), and finally Animals (~2.5Gt C). Animals are barely more than a rounding error. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6016768/

The following calculation is a very rough estimation to get the sensible order of magnitude.
In 2018, Bar-On et al. estimated the total biomass on Earth at about 550 billion tonnes $(5.5\times 10^{14} \, {\rm kg})$ of carbon, $80 \,\%$ of which is stored in plants. $70 \,\%$ of this plant biomass are stems and tree trunks, which are mostly woody.
Let's assume that the whole biomass is in the wood. The authors suggest that the carbon content should be multiplied by a factor of 2 to get the dry biomass. Assuming that the average water content of wood is $80 \,\%$. This gives us the total wet biomass of $$m=2\times(1/80 \,\%) \times 5.5\times 10^{14} \, {\rm kg} = 1.4 \times 10^{15}\,{\rm kg}$$
Approximating the density of wood at $800 \, {\rm kg/m^3}$, we calculate the diameter of equivalent sphere:
$$ V = \frac{4\pi}{3}\left(\frac{D}{2}\right)^3 \implies D = \left(\frac{6}{\pi} V\right)^{1/3} = \left(\frac{6}{\pi} \frac{m}{\rho}\right)^{1/3} = 15 \, {\rm km}$$
Even though we made quite a few assumptions, note that the diameter of sphere scales with mass as $D \sim m^{1/3}$. This means that if we over- or underestimated the total wet biomass by a factor of 2, the diameter of the sphere changes only by a factor of $2^{1/3}\approx 1.26$, e.g. $D \approx (12-19)\, {\rm km}$.

There is also another interesting visualization published, although it uses the carbon biomass and not wet biomass.

Beware: The article estimated the biomass as 550 gigatons of carbon. However, biomass is not just carbon. As noted in the methodology of the paper, you can multiply the estimate by a factor of 2 to get dry mass; still, the OP is asking for wet biomass.

thanks, yeah i saw that and i was too hurried to account for it, i just corrected it.

Thank you! I appreciate the help.

@bandybabboon, I have edited your answer to more clearly state all the assumptions and include calculations. I hope you feel that my edit improves your answer, but you may of course reject it :)


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Do all monoclonal antibodies have a blocking effect?
I find a mAb targeting protein A, which has beed validated to work in wb/IHC/IP or antibody conjugating drugs. I'm wondering if this mAb could be used for blocking the protein A from binding with other proteins? This mAb is the only one antibody which could be bought without having to make it myself, so the answer is really important for me. Looking forward for your responses.

No. Not all monoclonal antibodies block binding of other proteins. This depends entirely on the antibody and its epitope though. Most monoclonal antibodies target a small epitope, somewhere between 7 and 11 amino acid residues in length. Where this epitope sits on the protein will alter whether the antibody is capable of blocking binding of another protein.
If the epitope is at an interaction site, then it is entirely possible that it will be a blocking antibody, but if it sits somewhere else, then it may or may not block depending on proximity and size of binding site of both the antibody and the interacting protein. In this second case non-direct blocking is known as steric hindrance or steric blocking and is due to molecular size.

Thansks for your really helpful reply! I wonna take this mAb in a vivo experiment. So does this mean I have to verify the blocking effect between protein A and other Abs before using? If so, wether just taking a flow cytometry staining is enough to verify the blocking effect. Is there any other experiments I have to do?

@jinyuhuang You can verify blocking using Flow and potentially by microscopy (e.g. fluorescence using tagged antibodies). You could also do it by native western (i.e. non-denaturing) for simulation of what might happen in-vivo. You do need appropriate controls in each case to ensure that the effect seen is due to blocking and not some off-target effect or secondary antibody effect for example. Look up "antibody validation" for more information about how to validate your antibody; don't assume, just because it is monoclonal, that it can't have off-target interactions.

Thanks for your suggestion again! This mAb had been used for antibody conjugating drugs which was approved by FDA. So, I guess there should be a extremely small chance of off-target interactions. I would like to investigate literature about flow cytometry, microscopy , and native western experiments as you suggest.


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Can multi-cellular organisms transform into single-cellular organisms and conversely?
If we have a multicellular organism A, can it transform into an organism B in its lifespan, so that B is single-cellular?
And conversely given a single-cellular organism B, can it become a multi-cellular organism C?
Does any organism which satisfies both of those properties in some way exist?
I don't have background in biology and this question was mostly curiosity, so this might be a bit vague.

All "higher" animals and plants (i'd have to review other types, but pretty sure mosses, ferns etc also) go from single cell to multicellular in their life cycle. Fertilized egg/ovum ->  adult. You might want to check out sponges, which can reproduce by fragmentation, but I don't recall if they need more than one cell type for this.

A model for the evolution of single-multicellularity is choanoflagellates. Here is a video lecture. They are super cool.

The unicellular protists called choanoflagellates, ichthyosporeans and filastereans are the sister groups of metazoa (animals). They are single-celled but can live in multicellular versions. Either through aggregates (genetically different cells coming together) or by clonal division (like an animal - cells are genetically identical). So right now this is a huge field of research, in which scientists try to understand the evolution of multicellularity in respect to animals (multicellularity also arose multiple times in other species, e.g., fungi, plants etc.).
Sponges are very basal animals and have very unstable cell states. Meaning, many cells can differentiate into other cell types and if you fragment a sponge (into single cells) given that a few specific cell types are present, it can simply regenerate. But as far as I know, a single cell alone can not regenerate a sponge.
So to your questions:

If you talk about reproductive scenarios then a multicellular organism does convert itself into a single-celled organism (think about sperm, oocytes or about spores etc.).
As explained before, many unicellular organisms have multicellular states (mostly triggered by some kind of stress response, e.g., starvation).
The organisms I described before switch between these states, but they are not as complex as typical animals.


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Why is it that once mould is growing, and it releases spores, it can grow in or on materials that are not damp?
My home had some flooding recently (from a burst hose connected to a tap, but I'm not sure that's relevant), and in the process of rectifying the situation, a few things were told to me. I'd like some clarification around these statements, and maybe have some misunderstanding on my part cleared up.

If the carpet's underlay, and the subfloor are not dried correctly, in a timely manner, there is a risk of mould growing.
If mould grows in the carpet, spores will be released, and the mould will start growing everywhere, even in places that are not damp. Even if the underlay is dried too late, mould will still grow.

I feel like this leads to a contradiction. I've got a couple of ideas in my head.

The mould grows in the carpet when it is damp, because there are already mould spores in the carpet, and the moisture "activates" them. But this would imply that the spores still would not grow in other places that are not damp, which contradicts what I was told. I'd also be curious as to how the spores got there in the first place.
Mould can grow spontaneously in damp places, without mould spores. This sounds quite ludicrous to me, unless perhaps dampness somehow attracts spores, or small animals and insects that carry spores and deposit them. Then once the mould grows in the damp place, spores are released, and because of their proximity, they then grow on other surfaces, despite the lack of moisture. But it requires the dampness to bring the spores in the first place.

Its not that there is no moisture, there is just less and it changes day to day. once mold has stated to grow it saturates the surrounds with spores which means as soon as conditions allow it they grow, whereas normally you need the coincidence of spores happening to be land in the right conditions.
think of it like a fireworks factory, why are they dangerous. Why are fireworks factories, absolutely insane about fire safety. Being in a factory does not make fireworks more flammable, but it does mean any spark has a much better chance of landing on a firework. there is not more sources of fire in a fireworks factory but the factory is "saturated" with something that is highly flammable.
the sheer amount of spores makes it more likely they will find the right conditions at some time during the year. A normal home is someplace mold can grow part of the time but getting those conditions at the same time a spore happens to float in is rare, most spores that make it in will not find the right conditions. Up until you have a lot of moisture, then any spore that floats in finds the right condition, and we go from saturation of moisture to saturation of spores.


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Effects of oxygenated water on bacteria
I was curious if any of you would happen to have any experience with this but any hypotheses regarding how this would turn out would be much appreciated.
I’m wondering if water fully aerated with oxygen via pressure at a low temp could be useful in food preservation and distribution. For example if soaking meats and seafood in this water could help slow down and prevent bacterial growth.
Thanks in advance

This is just some oxygen dissolved in water. What is different for this oxygen to the one in air? It is not activated or otherwise more reactive.

We expect questions to show some evidence of prior research: what led you to asking this question? Why would you think oxygen-aerated water could be useful in food preservation?

Do you want to know about oxygen being toxic at high concentrations? If yes then I guess it could be considering anaerobes cannot survive in oxygenic conditions and high levels of oxygen will also kill aerobes. The practicality, limitations etc are unknown to me.


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Why do (some?) flies aggregate on both sides of a window even when there is no passage between the two sides?
I've observed an interesting behavior in flies that often invade old houses. When flies accumulate on the inside of a window, I've noticed that other flies start to accumulate on the outside of the same window. Interestingly, this occurs even when there's no passage for air or pheromones between the inside and outside.
To eliminate some possibilities:

The inside area is dark, and the flies are attracted to the external light, so light attraction for the external flies can be ruled out.
The use of an aerial insecticide affects only the flies on the inside, confirming that there's no passage for air or pheromones between the two sides.

Is there any biological explanation for why flies would behave this way?

Aerosol insecticides are only effective at quite high concentrations. There could easily still be passage of air/scent/pheromones from one side to the other without reaching the concentrations effective to kill on the opposite side. Dilution will play a big role here. Small amounts leaking through will be diluted enough to be ineffective, but something like pheromones or other things insects are sensitive to at very low concentrations might still be detectable.

I think the answer is a compound statistical effect. First, both window sides correlate with the overall density of flies in the area, 2nd, you only notice an accumulation of flies above a certain threshold (total number), which makes it likely that there are flies on both sides.


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Caffeine tolerance
I researched about caffeine tolerance and found out that regular consumption of coffe can build caffeine tolerance even if it's 1 cup per day, within few days or a week at most. Supposedly the body builds more adenosine receptors to cancel it's effect. My question is, is there any limit to it above which it can't neutralize the effect like a sweet spot say 3 cups which is neither unhealthy nor gets canceled by the body.

Hi and welcome. This question is kind of unanswerable as posed; how strong is the coffee? How large is your cup? These vary from country to country, and even just  how it's brewed matters. Caffeine isn't "neutralized", if it were, it would not work, and absolutely there's a limit to how much one can drink, which is why caffeinism is a thing. Finally, this reads to me as a request for personal medical advice, even though it's not phrased that way.

Maybe I was not very clear, I am not asking a personal health advice or the likes of that. It is a general ques and you are free to assume anything not stated specifically as  it may seem fit to you in  a way that it helps with the ques

I think you want a frequency rather than a quantity, that is, how long do you need to wait between caffeinated beverages so that any tolerance from the previous one has decayed.

No, how much is the upper limit above which the body can't build tolerance.

"The upper limit above which the body can't build tolerance" depends on the frequency too, which is why frequency has been suggested instead of a quantity. You need to know the frequency and the caffeine concentration.

Caffeine has several effects on the human body, and as far as I recall, while some of those things can build up a tolerance, other's can't. This is true even within the brain itself.


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Does anyone know the name of this insect?
Living in São Paulo, Brazil. Thanks for helping me.

No guarantuee due to the low photo quality, but the habitus of this specimen looks like a weevil (Curculionoidea) to me.
This beetle superfamily has characteristic elbowed (geniculate) antennae and prominent snouts. Their bodies are usually rather compact and robust.
If you still have the specimen, you could check, if you can recognize these characteristics (on the right photo (Hectonichus CC-BY-SA-4.0) is a specimen of the similar-looking genus Polydrusus as comparison):


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The amount of heat produced in muscles. A wrong answer
I'm trying to find how energy is released during muscle contraction. Seeing how no work is being produced, the issue is, after working out how much heat was theoretically produced by the heaviest deadlift. First, to give context, the heaviest deadlift I know of is 502.5 kg. Assuming he lifted it up at a acceleration of .5 m/s^2, we can add the gravitational pull to get a rounded answer of 11 m/s^2. Multiplying by the weight gets 5527.5 N. Assuming he lifted it for 1 meter, we get that in joules. Then, taking that he took a second to lift it, gives an answer of 5527.5 Watts. Now, I know a lot assuming was done to get this answer, but all guessed values were rather small, so it shouldn't effect anything. Not only this, but I read that are muscles are around 25% efficient, so the amount of heat produced would be 16582.5 Watts. That's 16 kilowatts. Maybe its just me, but that seems like way to high an answer. Could someone explain?

A workout where no work is being produced would need to be isometric. Lifting barbells is work.

Welcome to Biology StackExchange! You seem to have slightly confused the basic terms in physics. To lift a weight with mass $m=500 , \rm kg$ for a distance $h=1,m$ up, you need $A=\Delta W_p=mgh = 4900 , \rm J$ of energy. With some rough assumptions, we can say that the muscle efficiency is indeed $25,%$, which means that approximately $3A=15,\rm kJ$ of heat was produced. This heat warmed the body, and also gets transfered to the environment. Note that Watts are units of power, which is $P=A/t$.


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Are all unicellular eukaryotic organisms protists?
I know that the Protists are in Domain Eukarya, and that some protists are unicellular. Are there any other eukaryotic group of creatures that are not protists that are unicellular?

Two other kingdoms contain unicellular organisms.
Some fungi, such as yeasts are unicellular.
Many algal (Plantae) species are unicellular, including the spectacular Valonia ventricosa, which is up to 5 cm (2 inches) in diameter. There is also a genus of seaweed Caulerpa, which is unicellular, though multi-nucleate that is thought to be the largest single-celled organism, being up to about 3 m (10 feet) long.

Not the kingdom decides, hence


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Plant (lamp) identification
I recently came across this lamp part and wanted to get a lamp shade in the shape of the matching blossom.
Does someone recognize the leaves?

Flower bracts are wrong, but Thistle springs to mind. May not represent a real plant after all.

It looks to be a poppy, possibly the breadseed poppy
The flower has 4 perianth segments remaining after anthesis,matching the breadseed poppy where the sepals are abscised during anthesis leaving 4 petals.
the leaves are toothed, matching *papaver somniferum *

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. Answers on this site are typically upvoted if they contain information that supports the answer - in this case you could supply some information about the poppy, possibly including photos (proper attribution of photo source required) and why you think it is a match for the item in the photo from the question.

Different people see different flowers, interesting. Although the leaves are consistent with Poppies (good guess), the head is definitely not. At no stage does the poppy resemble that "flower". I initially thought "Tulip, but the leaves are wrong" (your guess is better than mine), bob1 thought "Thistle" (a v. good guess). The flower is either a stylized version of a flower m unfamiliar with or one that is non-existent. (I've seen a lot of flowers, as I used to travel the continent to do wildflower and garden flower photography, the latter containing plenty of non-natives)

I know, I'm a the very definition of a stickler for fine detail. Also, guesses are not acceptable in answers on scientific sites like this one. We require sources for answers.Morphology, Taxonomy, Anatomy, and Palynology of the Opium Poppy (Papaver somniferum L.) Cultivation in Northern Thailand.  Note figs. 3 and 4

It may be a general rendition of a poppy rather than a specific poppy.                                               Tulips have perianths with six tepals and thistles have capitulums

Poppies have 2 sepals  (which fall off before the flower opens) and 4-6 petals, and they don't look like those. We can't identify it; it probably doesn't exist. The good news is you can make a lampshade however you want! :)

The 4 petals of a poppy match quite well with the lampshade

I will admit to being wrong if somebody shows me a better match

Why don't you post a photograph of a poppy blossom (any poppy blossom, not necessarily breadseed poppy) with pointed petals? That would help with your answer's credibility.

What do you mean by pointed petal


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What is the range of motion of a raptor wrist?
I have been trying to find out how much could raptor like dinosaurs move their wrists.
I know that this will vary between species, so let's say for example a deinonychus.
I am aware that the usual movie depiction of pronated wrists is wrong.
But I want to know the range of motion of the real animal.
Sometimes they are drawn with fingers pointing back to the tail, sometimes down to the ground and sometimes forward.
So were they able to rotate the wrist the full 180 degrees or where the truth is?
A couple of examples what I mean.
https://en.wikipedia.org/wiki/Deinonychus#/media/File:Deinonychus_Restoration.png
Fingers down:

Fingers forward (Same wiki page):

Thanks.


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species that alerts predators in order to mate
I read once about a species of animal that engages in, and please forgive me for the terminology but I cannot for the life of me think of any other way to describe it, mutually-assured destructive sexual blackmail.
If a male attempts to mate with a female, and the female shows signs that she is going to reject the male's advance, the male will start making a loud call that will attract this species' common predator.
Essentially, the male is threatening the female that they will both get eaten if she doesn't accept his advance.
I can't remember what the name of this species was and I really do not like what it's doing to my search history.
What species, if any, engage in this type of behavior?
What terminology should one use to describe this behavior?
I tried asking ChatGPT first (less judgmental) but came up empty.
There's a species of orb-weaving spider that will mimic the web vibrations of prey struggling to get free when a female seems likely to reject his advance, in the hopes that the female will accept the male's advances in order to avoid being mistakenly identified as prey.
There's the vampire jumping spider, which risks predation during courtship displays.
Neither of those quite fits the pattern I'm thinking of, where the male exposes both himself and his potential mate to predation.
If you downvote this question, I... completely understand.

A similar phenomenon occurs in begging nestling birds: https://www.nature.com/articles/nature.2013.12774

I finally found an answer, probably after getting put on some kind of watch list:
water striders.
If the female looks like she's going to reject the male, the male will tap on the water surface to attract fish.
The female, being closer to the water, is more likely to be eaten.

Excellent answer, what a memorable phenomenon. Not sure, but for the term for this you might try [english.se], with the tag [single-word-requests].


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How to understanding the mouse strains name and differences in mouse strains used in biology
I am currently working with various mouse strains in my biological research and I am encountering some confusion regarding their nomenclature and differences. I understand that the different names indicate different origins, but I am finding it difficult to decipher the specific meanings behind these names.
For instance, I frequently come across the strain C57BL/6JN. It seems that C57BL represents a common mouse strain, but I am unsure about the meaning of the slash and the 6JN. Could someone kindly elaborate on this?
Additionally, I have seen the name C57BL/6NJ referenced in some literature. Is this the same strain as C57BL/6JN, or do they possess certain distinct characteristics? I would appreciate any clarification or guidance on this matter. Thank you!
Regrads

There once was a mouse numbered "57". Someone used that mouse to make a bunch of inbred lines. One of those lines, number 6, survived well. It had a black coat.
This is the C57, black, line number 6, or C57BL/6, also called "black 6". Remember that inbreeding is typically "bad", so it takes a lot of tries to make an inbred mouse line; most turn out to have fatal diseases or poor reproduction.
The original line was and is maintained by Jackson Labs, we call that strain J. NIH started maintaining a line from that same stock. We call that strain N or 6N; sometimes JN because it started as J. These are all inbred lines so they "should" be identical, but in practice mutations happen and genetic drift can occur; this is mitigated by back-crossing within the inbred line but Jackson wasn't back crossing theirs with NIH and vice versa, so it's proper to consider them separate lines.
Jackson Labs also now has taken the NIH strain and maintained it to sell:
https://www.jax.org/strain/005304
They call this C57BL/6NJ: the 6N strain now back at J.
Other people have taken and bred lines from these strains so there are numerous others, most are less significant since they're not mass produced commercially. Jackson Labs has really good documentation on their mouse lines including known SNPs between lines, if you're ever curious I'd start there and see what they have documented before looking for other sources.
Some other references:
https://en.m.wikipedia.org/wiki/C57BL/6
https://www.jax.org/strain/000664
Bryant, C. D. (2011). The blessings and curses of C57BL/6 substrains in mouse genetic studies. Annals of the New York Academy of Sciences, 1245, 31.

Thank you for your answer that's awesome! Can I ask an additional question to confirm my understanding? Taking C57BL/6NJ and C57BL/6JN as examples, first, Jackson Labs obtained a well-characterized mouse strain C57BL/6J through inbreeding up to the sixth generation. Then, NIH acquired and maintained this strain, so the strain maintained by NIH is referred to as C57BL/6N or C57BL/6JN. C57BL/6N and C57BL/6J have the same genetic background (except for genetic drift and new mutations that may occur after separation).

Afterwards, Jackson Labs obtained C57BL/6N (also known as C57BL/6JN) from NIH and commercially sells these mice, which are referred to as C57BL/6NJ

@zhang Nothing about "6 generations". Dozens of generations. 6 is not the generation number, it's one of several lines started from the same mouse.

@zhang inbreeding typically goes on for 20+ generations to fix the genetic lines. The 6 refers to the original line - it'll be 6th attempt or 6th mouse pairing they tried to do this to, or something similar. Nothing to do with generations.


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Why do larval stages exist in the life cycles of many species? Wouldn't it be better for a species to maintain a single form?
Many organisms undergo multiple distinct developmental stages, each adapted to a different ecological niche. This division of roles can be advantageous, as it allows for both exploration and exploitation of resources. For instance, caterpillars are efficient at feeding and growing, while adult butterflies are better suited to dispersing and finding new habitats. In contrast, tunicate larvae are the ones searching for new habitats.
However, I'm struggling to understand why some species, like the Dungeness crab, produce such vast numbers of small eggs when this argument doesn't seem to apply. Adult crabs are already mobile and capable of finding new habitats. They lay millions of eggs, which hatch into zoeae, then transform into small crabs, and finally mature into adults. If any stage fails to thrive, the species could face extinction. Additionally, if one stage is the most efficient at gathering food, why not maintain that form? Is there a reason crabs can't lay larger eggs due to their exoskeleton?

This question is similar to: Why do some bad traits evolve, and good ones don't?. If you believe it’s different, please edit the question, make it clear how it’s different and/or how the answers on that question are not helpful for your problem.

To answer your last question, the crab body plan allows for significantly larger eggs than we see in dungeness crabs. The Malaysian freshwater crab Isolapotamon baunese lays ~20-80 4 mm eggs despite having a ~6 cm carapace, compared to dungeness crabs that produce millions of < 1 mm eggs with a ~15 cm carapace. These freshwater crabs also move through all the larval stages while still in the egg and hatch as small crabs. In some cases, the mother carries these small crabs long enough for at least one molt. So, if it were advantageous, marine crabs like the dungeness could presumably also evolve to use a single body plan the way you suggest.
This difference between freshwater and marine crabs is probably due to the opportunities available to a life stage as plankton in the ocean compared to the freshwater habitats of these single-form crabs. A study of crab larvae off the coast of Portugal estimated the average crab larva ended up about 70 km from where it hatched. Obviously that kind of distance is impossible in a pond or stream. Also there is a lot of nutrition available in the ocean as plankton, but harvesting it isn't efficient with the body plan of a mature crab.


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Cell Size and Morphology of Microalgae under Wastewater
Hypothetical situation ahead, I am just curious whether the cell size and cell morphology of microalgae changes when it is under the influence of wastewater. For instance, mixing the microalgae culture with wastewater. If if does happens, what potential reasons are the causes of such changes?

Welcome Kris. This is very lacking in detail at present. Please take our [tour] and refer to the [ask] section of the help centre, then you can [edit] to add details such as: 1) Specifically what you mean by wastewater and in what concentration. 2) What microalgae are you referring to and what's its natural environment. 3) To show your own research into the question as per our requirements (see the homework policy section for details).


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Does decompression sickness (the bends) ultimately come from the change in pressure in the lungs, or the actual total ambient pressure over the body?
I am not well versed in physiology, and I've found the literature available to me confusing on this point.
Mostly I'm going off of wikipedia, mind you. The article on Decompression Sickness' Mechanism Heading states:

Under normal conditions, most offgassing occurs by gas exchange in the
lungs.[53][54] If inert gas comes out of solution too quickly to allow
outgassing in the lungs then bubbles may form in the blood or within
the solid tissues of the body.

What I can't figure out is if the actual ambient pressure matters, if we suppose that that is separate from the pressure in the lungs. From what I've understood, in SCUBA diving the water pressure applies pressure to the air you're breathing (somehow? through the air hose? I'm not certain my understanding is correct) and thus the air you're breathing and the air in your lungs is also at a higher pressure. If I'm wrong about that, that may be the ultimate answer of my question.
I'd like to present a hypothetical, to clarify the exact focus of my question:
Let's say we can somehow form a perfect airtight seal around the waist of an otherwise naked human being. Setting aside the practicality of that, of course. The point is that the human is otherwise unaffected, but it blocks air.
That air tight seal around the person's waist makes it so that their lower body and legs are exposed to a very low pressure environment, maybe even pure vacuum. The person's upper body (and notably their nose and lungs) are in a standard sea-level terrestrial atmosphere.
Putting aside the vacuum bruising and painful swelling and other detriments caused by the low pressure environment on their lower body, my question is this: could the person in this hypothetical get the bends, simply because of the lower pressure on part of their flesh? Or would decompression sickness not be an issue because their lungs are pressurized?

Your scenario is impossible because of blood vessels. If you cut the lower half of the body away while sealing it, and reduced the pressure dramatically, yes, bubbles would form in the now non-functional blood vessels.

@anongoodnurse I don't understand. I'm not implying that the seal cuts physically through the body, just around it but forms a tight seal with the skin.

I understand that. But I'm saying because blood vessles keep ferrying blood to and from the lower body, your thought experiment is impossible to carry out.

If you did carry it out you wouldn't get bruising in the lower limbs, you would extrude everything in the upper body through and into the lower body. It would get very traumatic and gory very quickly.

Ah. I was under the impression that connective tissue is rigid enough to compensate for that, and that the heart would be doing its best to maintain blood pressure for at least a short time. Obviously swelling and bruising would occur, but I wasn't sure that it would necessarily follow that nitrogen would emerge from solution as in the bends.

The solubility of a gas in a liquid is proportional to the partial pressure of the gas above the surface of the liquid Henry’s Law (On the ground at sea level air pressure is about 15psi, nitrogen is about 80% of air, so the partial pressure of nitrogen then is about 12psi.)
When a diver is 32ft deep the total pressure is about 30 psi and at 64ft deep pressure is about 45psi. This means there’s twice as much nitrogen in her blood and tissues at 32ft and three times as much at 64ft.
If you are on the ground at sea level, the pressure in your lungs is also about 15psi. When you breathe in it is slightly less, and when you breathe out it is slightly more. This small difference in pressure is what makes the air move in and out of your lungs.
Because the human body is flexible, when subject to an external pressure, that pressure is experienced equally throughout the whole body. This comes from pressure on the skin - it doesn't come through the airline (though that does need to be at the same pressure of course). If you want the pressure inside to be lower than the outside pressure then you need a rigid encasement such as a submarine or bathysphere where that exterior can support the pressure difference. You can see how an air-filled balloon expands as it rises in this  video (from about 3:25)
The pressure in our arteries is a little higher than outside pressure; on average that’s about 100 mmHg or about 2 psi, as the heart has to pump blood around the body. It’s also a little higher in our tissues, as the cell walls have to keep their contents inside against the force of gravity etc. Healthy human lungs have a surface area about equal to the size of a tennis court which allows for efficient diffusion of gases across this barrier. However it takes a much longer time for gases to diffuse out of tissues into the blood stream and be conveyed to the lungs. A bubble of air inside water has a higher pressure inside than that in the surrounding water due to surface tension of the surface of the bubble which is trying to contract, the smaller the bubble the higher the pressure. This means that, in general, dissolved gases have any easier time diffusing out of a cell than forming a bubble.
According to Navy diving tables the maximum time at 60ft is about 55min without the need for decompression. But ascent should be slow at about 0.5ft/s. Longer dives at this depth do require decompression protocol. wikipedia as illustrated by Naval sea systems command - US Navy Diving Manual, Revision 6. SS521-AG-PRO-010, Public Domain
As I said, this whole process is slow, so that if there is a sudden change in outside pressure dissolved gases will nucleate and form bubbles. This can happen even when the outside pressure is originally atmospheric. For example passengers flying at great height in a plane with a pressurized cabin can experience DCS if there is a sudden decompression, as when a window blows out. So reducing the external pressure on the lower half of the body will only make the situation worse as dissolved gases will rapidly form bubbles there.
The same thing can happen to fish! recent news
Edit:  According to David Hammen’s answer to this question air on ISS there is no chance of DCS when using pure oxygen at 30kPa. which astronauts do in their EMUs. It’s nitrogen which is the big problem. They do however have to reduce the nitrogen levels in their blood before donning these suits as air in the ISS is at atmospheric pressure with 79% nitrogen.
Also, high pressure oxygen is the best treatment for DCS. Hyperbaric Oxygen Therapy
In case of rapid decompression of the EMU due to accident or failure, getting back inside the ISS would seem to be the priority.
Good luck with your suit design.

A diver who goes to 60 feet can stay underwater for about 45 minutes and ascend at a rate of half a foot per second (not per minute) with a three-minute stop at 15 feet - about 40 minutes down and 5 surfacing. Decompression is only required for deeper or longer dives.

@Eonema You're right. I'll correct that.

Your body isn't rigid. All of your blood vessels are under pressure from the atmosphere, from the pressure of the air pushing on your skin which pushes on the underlying tissue.
When nitrogen or anything else is dissolved in blood, it's dissolved under that atmospheric pressure. If that pressure suddenly drops, it bubbles out, just like the bubbles in a carbonated soda that is under pressure until you open the can. Those bubbles happening in blood vessels is bad because it blocks them. That's the bends.

That makes sense. But skin is gas-tight by itself. From what I've read about research into mechanical counter-pressure suits, it's not like we strictly need to be surrounded by an atmosphere so much as we need pressure (and air to breathe).

@Mia You can squeeze a balloon and increase the pressure inside without any gas moving into the balloon. Your body is a big balloon of biology.

Sure, yes. Swelling and bruising would occur, you'd be generally uncomfortable and in some period of time you'd die. My question is much more specific - would nitrogen come out of solution and form bubbles in your bloodstream? This is the documented mechanism of decompression sickness and it is not clear to me if it would still occur if pressure in the lungs remained unchanged.

@Mia No one would ever be able to do your experiment, it would have disastrous consequences for all of circulation. But yes, if you had just a closed system of blood with dissolved gasses in a tube and reduced the pressure, bubbles will form. That's the mechanism. It has nothing to do with the lungs. No source is talking about bubbles forming because of the lungs. The quote you have is about the other place gas can go to not produce bubbles which is that it is breathed out if the change is slow enough.

Fair enough, thank you for your responses. My mind has been on questions of pressure suit design. Wondering if hybrid designs involving a helmet-volume kept at ~100kPa to avoid the need for pre-breathing and a body-volume kept at ~30kPa for mobility purposes would be possible. It sounds like decompression sickness would still occur. Obviously the body can handle the lower pressures in general since existing designs are ~30kPa throughout the entire suit, but I guess inconsistencies in pressure over the entire body would be too big an issue.

@Mia Diving suits are flexible, they allow pressure in throughout the whole suit just like your skin, just like a balloon. If they didn't and left part pressurized and part non-pressurized, you'd force tissue into the non-pressurized area which would be very traumatic and bad. The alternative is a completely hard body, like a submarine, which can have different pressure outside and in. You absolutely cannot keep the helmet and body at different pressures otherwise you'd have 70kPa of pressure pushing your neck and head into your chest cavity.

The least-bad thing that would happen is no blood flow to the head in that circumstance; hopefully that would kill you before everything else happened.

Ah to be clear I'm talking about suits for surviving low pressure, if that makes a difference for context. The current EVA suits used by astronauts are kept at 30kPA of pure oxygen for flexibility purposes. I've also been looking at the design of mechanical counterpressure suits. https://en.wikipedia.org/wiki/Mechanical_counterpressure_suit

@Mia Exact same problem with low or high pressure; with pressure, it's differences that matter for the physics, mostly (unless you're talking chemical reactions or temperature). Counterpressure suits don't attempt to apply a different amount of pressure in different compartments; even if there's a rigid helmet the pressure is allowed to equalize between compartments (and it will equalize, so you'd rather that equalization happen by air moving rather than body parts).

Thanks again for your answers, Bryan. For what it's worth I'm not the first person to think of looking into this, I just found a study done on this at UC Berkley in 2001. Here's a link to the PDF if you're curious: https://www.lpi.usra.edu/publications/reports/CB-1106/ucb01.pdf


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Converting m/s to body lengths / s
I am trying to calculate speed of fish in body lengths / s. As of now, I have speeds for each of my individuals in m/s. To convert each individual fish's speed in body lengths / s (bl/s; using each fish's body length), from m/s, I assume I can simply divide each m/s value by the body length of the fish.
For example:
I have a speed of 0.35 m/s, Fish A's length is 0.66 m. To convert into bl/s I should divide 0.35 / 0.66 to get 0.53 bl/s.
Is this correct or is there some kind of unit conversions that come into this? Since it's relative to the fish's length, I assume this is ok? If this isn't correct, would you please show me the correct way to calculate this?

For all unit conversions, you want to learn to multiply by ratios that are equal to 1 and make things cancel. So if you have units of "x/s" and you want to express in "y/s", you need to multiply by "y/x" so that the xs cancel. To make it work, you need y/x to be equal to 1. For example, if x = 1 meter then you could use y = 100 centimeters. If you want y = 1 body length then you need x = ____ meters, whatever makes it equal to y. Whatever units you choose, when you do this you're always multiplying by 1 overall which we know doesn't change the actual number.

Thank you for the response.... so if I have 0.35 m/s and want body length (which is expressed in m) / s, I need to multiply by y/x which would be 1 body length/0.66 m... when you cross multiply this gives you 0.231 bl/s? Is this correct? What did I do wrong initially? I thought that since body length is just a ratio of 1 m, I would just need to divide to see that ratio through.

No no, no "cross multiplying". You did it correctly the first time:$$\pu{0.35 \frac{m}{s}}=\pu{0.35 \frac{m}{s}}\times \underbrace{ \frac{\pu{1 bl}}{\pu{0.66 m}}}_1=\pu{0.53 \frac{m}{s}}$$

@Domen did you mean 0.53 bl/s? (even though in this case bl is measured in m)

Arghh, yes, of course, my mistake :)

Thank you so much!


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Do right-handed helices bind to right-handed helices, and vice versa?
I know that B-conformation DNA is a right-handed helix, and most proteins that form helices form right-handed, not left-handed, helices (1). Furthermore, "Many transcription factors have an alpha-helix that binds to DNA bases in a specific fashion" (2), indicating that it is common for right-handed protein helices to bind to right-handed B-DNA helices.
Does this mean that, generally speaking, from the perspective of basic geometry, do right-handed helices bind to right- (but not left-)handed helices? And, vice versa, that left-handed helices generally bind to left- (but not right-)handed helices?
References

Novotny, M., & Kleywegt, G. J. (2005). A Survey of Left-handed Helices in Protein Structures. Journal of Molecular Biology, 347(2), 231–241. https://doi.org/10.1016/J.JMB.2005.01.037
Suzuki, M., & Gerstein, M. (1995). Binding geometry of alpha-helices that recognize DNA. Proteins, 23(4), 525–535. https://doi.org/10.1002/PROT.340230407

But the paper you quote shows that left-handed helices in proteins only span a single turn, so fair comparison with right-handed helices is not possible. The question seems to be a case of “if left-handed helices existed”, in which case it would seem a mathematical question.

@David, I'm talking about dsDNA and dsRNA duplexes in the Z-conformation, a left-handed double helix, in association with the neurofibrillary tangle paired helical filaments of tau proteins, and the amyloid-beta fibrils from Alzheimer's disease patients' brains, both of which are pairs of protofilaments with a left twist.
See references in my other comment:

Yang, Y. et al., (2022). Cryo-EM structures of amyloid-β 42 filaments from human brains. Science, 375, 167–172.
Wischik, C. M., et al., (1985). Subunit structure of paired helical filaments in Alzheimer’s disease. The Journal of Cell Biology, 100(6), 1905–1912. https://doi.org/10.1083/JCB.100.6.1905

My understanding is that protein and DNA helices show the handedness that they do due largely to the intrinsic chirality of their components. Note that in natural biomolecules L-amino acids and D-sugars predominate. This apparently leads to a subsequent bias in their respective polymers.
I believe that it has been demonstrated that artificial alpha helices constructed of achiral amino acids demonstrate inversions between left and right handed forms- these then need to be stapled with extra molecular bridges to hold left or right handed orientation.
Thus, I don't think that there is a right-to-right or left-to-left association. In all cases, I think it's just that the biased handedness is baked into the structure of natural amino acids.

Thanks, @Maximilian Press. What you're saying is true, but that's not really my question. I am NOT asking whether nuceic acids and proteins usually adopt right-handed helices because this makes it easier for them to bind to each other (nor am I suggesting this). I am simply asking, do right-handed helices bind more easily with other right-handed helices, and do left-handed helices tend to bind more readily and tightly with other left-handed helices? I'm being a bit coy because I don't want to give away my hypothesis, but I'm more interested in the LEFT-handed nucleic acid and protein helices.

@OdinTheDO I see. I would be interested in whether anyone had any data either way, but my guess on this is a solid "no". I think that the secondary structure of helical geometry of DNA and protein with respect to each other is probably low/no relevance for binding compared to the tertiary and quaternary structures. But that's purely a guess.


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Best reference book for basic concepts when working with bioinformatics
I'm starting to study Bioinformatics, I already have basic knowledge of Biochemistry and Genetics, but I want to buy a reference book, to use when I forget a concept (I'm a Computer Science student, not a Biotechnologist).
I have already had contact with the following two books (for basic concepts):

Molecular Biology of the Cell, Alberts;
Principles of Biochemistry, Lehninger.

Which is better for my use or do you have another recommendation?
I prefer a generalist book, which covers the basic concepts, and not a Bioinformatics book, which covers basic concepts in one chapter.

bioinformatics has its own stackexchange fyi. 2. bioinformatics is a huge field. what is the part of it that you want to know about? sequence alignment/assembly? structural modeling? biostatistics/clinincal trials? population genomics? generic data analysis in a biology context? pharmacology and drug development? high-dimensional data analysis./ multi-omic data integration? metabolomics? theoretical biology? energetics? imaging? microscopy? each of these might have its own foundational text! specificity is super important.