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Distribution of hearing loss
Low-frequency sounds are more penetrating, damaging. Hearing damage caused by blasts typically occurs at frequencies around 2 - 8 kHz, while age-related hearing loss starts at the high frequencies. The frequency range for noise-induced damage is biased upward, because the low-frequency conductive structures damage first.
https://www.entandaudiologynews.com/features/ent-features/post/effects-of-blast-and-acoustic-trauma-assessment-of-hearing-status-on-war-veterans
Why does hearing loss occur at high frequency first? It should occur at low frequency, because that is the more damaging sound. The distribution of hearing loss is totally incompatible with the noise exposure explanation. It could be due to growth factors, i.e., the high frequency parts die first because more distal.

Short answer
Noise-induced hearing loss affects primarily the mid-frequencies, because the inner ear is most sensitive to these frequencies.
Background
Noise-induced hearing loss occurs typically in the mid-frequencies (Rabinowitz, 2000), typically around 4 kHz (3 - 6 kHz), see Fig. 1. This can be explained by the fact that the human ear is most sensitive in this frequency range (Fig. 2). In turn this relates with the frequency range where speech understanding is most important, namely between roughly 2 and 6 kHz (Killion & Mueller, 2000). Hence, noise exposure neither targets the base, nor the apical parts of the cochlea, as claimed by asker and answerer, respectively. High-frequency hair cells in the rat cochlea have been shown to be very susceptible to damaging noise, but the low-frequency hair cells may go unscathed (source: eMedicine).
The other answerer claims that

parts of our hearing apparatus responsible for perceiving these
[low-frequency] sounds are more fragile...

Hence, the claim that low-frequency regions in the cochlea are more sensitive than the more basal parts is not a claim supported by the bulk of the literature. In fact, as a rule of thumb, cochlear damage (inner ear damage) occurs most frequently first in the base, where the high frequencies are resolved. This holds for age-induced HL where high frequencies are lost first (Ciorba et al., 2011), as well as chemically-induced HL (Campo et al, 2013, barred some specific organic solvents that apparently do not follow this rule (Cappaert et al., 2002.

Fig. 1. Typical audiogram of noise-induced hearing loss showing loss of functional hearing at the mid-frequencies (Rabinowitz, 2000)

Fig. 2. Relation between perceived loudness and intensity (equal-loudness curves) for a normal-hearing person. source: Lumen Phsyics
References
- Campo et al., Dis Mon (2013); 59(4): 119–38
- Cappaert et al., Neurotoxicol Teratol (2002); 24: 503–10
- Ciorba et al., J Laryngol Otol (2011); 125(8):776-80
- Killion & Mueller, The Hearing Journal (2010); 63(1): 10-7
- Rabinowitz, Am Fam Physician (2000); 61*(9):2749-56

One has to distinguish between the frequency of a sound, its intensity (i.e., energy that it carries), and its loudness.

Frequency, known more conventionally as the pitch, is what distinguishes high and low sounds. E.g., male voices are on average lower than female voices, i.e., male voices have lower frequency. Frequency is what changes when we hit different keys of a piano or different strings of a guitar. Frequency is measured in Hertz (Hz).
Intensity is the energy carried by a sound wave. Intuitively it is clear that the sounds of the same frequency can have different intensity, e.g., the same key of a piano can be hit stronger or weaker, producing a louder or quieter sound. It is the intensity rather than the frequency of a sound that causes hearing damage. Intensity is however not the same as loudness, as I explain below. Intensity of a sound is measured in bells/decibells (dB).
Loudness is our perception of a sound. Two sounds that we perceive as equally loud, do not necessarily have the same intensity. In fact, the higher frequency sounds have much higher energy/intensity when perceived as equally loud with lower frequency sounds.
Spectrum While musical instruments can produce continuous sounds of a specific frequency, this is not the case for many sounds that we encounter in a real life. Combination of frequencies in a sound is called its spectrum. Blasts are an extreme case of sounds that are very short and therefore combine large number of frequencies, ranging from very low to very high ones, all having approximately the same intensity.

Since lower frequency sounds generally carry lower energy, the parts of our hearing apparatus responsible for perceiving these sounds are more fragile, i.e., more easily damaged by high energy sounds. While blast is a complex physical phenomenon, it can be roughly viewed as a sound carrying many frequencies of the same high intensity, which will thus cause more damage to lower frequency hearing.
On the other hand, the loss of hearing with age reflects the "normal wear" by hearing the sounds that our ear is adapted for. Throughout our life the high frequency hearing deals with sounds of high energy and wears out faster.
Disclaimer: I admit that my answer reflects my stronger background in physics than in biology, and I will readily accept help in improving the last paragraph, (making it more precise).

I don't think there is any evidence out there that can support your claim that ...the parts of our hearing apparatus responsible for perceiving these [low-frequency] sounds are more fragile, i.e., more easily damaged by high energy sounds. I have taken the liberty to add an answer with an alternative, and probably more likely explanation.


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How good are the hematologic parameters (e,g, IL6 or others) in predicting which patients will develop a severe COVID-19 disease?
Clinical implications of the hematologic profile of COVID-19 patients including cytokine storm, coagulation profile and thrombophilic complications are starting to be recognized. Hypercoagulability could be the potential cause of death due to COVID-19:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585459/
How good is the hematologic profile, including hematologic markers (such as interleukins and others) in predicting if COVID-19 is severe, has mild manifestations or it is asymptomatic?

A recent pre-print has studied this by measuring 86 accredited diagnostic parameters and plasma proteomes at 687 sampling points, in a cohort of 139 patients during hospitalisation.

We identified 26 protein biomarkers and 14 routine diagnostic markers
(Fig. 4a, Supp. Fig. SF20) that correlate with the time between the
first sampling point and release from inpatient care. The proteomic
signature associated with longer duration of inpatient treatment and
hence more severe COVID-19 progression includes upregulated components
of the complement system (C1QA, C1QB, C1QC) and reflects altered
coagulation (KLKB1, PLG, SERPIND1) and inflammation (CD14, B2M,
SERPINA3, CRP, GPLD1, PGLYRP2, AHSG).

They used a learning classifier to then predict survival in critically ill patients:

In a last step, we established a machine learning model based on
parenclitic networks52,53 (Methods) to predict survival in critically
ill patients (WHO grade 7, n=49) from the proteome of the earliest
single time point sample at WHO grade 7 for a particular patient. On
the test subjects (the data of whom were excluded when training the
machine learning model), high prediction accuracy was achieved, with
AUC = 0.81 for the receiver-operating characteristic (ROC) curve. Of
note, the model correctly predicted survival or adverse outcome weeks
in advance (median time from prediction to outcome 39 days,
interquartile range 16 - 64 days).

The 'predictive power' can be captured (not in a perfect way) by the AUC value - a value of 0 has the worst power to separate patients and 1 has perfect power, so 0.81 is pretty good overall. I haven't read the paper fully, but from a brief scan it looks as though their methodology is at least reasonably sound.

source: Stack Exchange

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

sort: votes


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Is it possible to spread vaccine through air?
I am not a biology people. But this question has been bothering me for months.
I read the news that, even if an effective vaccine (for Covid-19) successfully created, the transport of the vaccine and its acceptance might still be a big problem; some vaccine need to be kept at extremely low temperature prior to using.
But then, what if the vaccine could cause one recipient to fall sick and the recipient spreads the mild disease to other people? This might sound bad, but then the community will develop immunity against the notorious Covid far much faster, more effectively and possibly free of charge for most of us. Instead of injecting the recipients one by one, just spread the vaccine like how Covid-19 spread.
Maybe the vaccine contains only part of the virus but not living virus, but considering those infected by mild cowpox will develop immunity against small pox, can't we just synthesize the cowpox-analogue for Covid-19? (Cowpox might not be spread through air, or from people to people, I am just saying, use highly contagious living virus that cause mild symptoms as vaccine)
Or is it because deliberately spreading viruses might be labelled as immoral so no one attempted this?

Hello. This may interest you. This question explains how the vaccines for Covid. Also note covid vaccines are not attenuated viruses. Also think about this - you have no control on the dosage each person will receive once you release a virus into the air. That does not sound ethical and healthy.

I’m voting to close this question because it is primarily a medical question and so would be more appropriate on [MedicalSciences.SE], but please do not crosspost, instead request migration. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Thanks!

I don't see how this is a medical question. However, it is poorly phrased and displays some misconceptions.

First: This is ethically completely out of question.
Then: You could of course think about a attenuated virus, but these are designed to not spread like the disease, as they might mutate back and cause problems. This was a problem with the oral polio vaccine which is not used anymore for this reason.
This virus would need a higher transmissibility than the original virus to outcompete its spread. Creating a virus that spreads more easily but is less dangerous always harbours the danger that this virus mutates into something ways more dangerous than the original SARS-CoV-2 virus. Would you want to risk this? Also: We barely know the long-term consequences of COVID, what about another virus?
So, no, this is not a possible way.

Live attenuated poliovirus vaccines are still in use in various parts of the world. And yes, I agree it is an ethical concern, resulting in (rare) polio cases from vaccine derived polioviruses, particularly in immunodeficient children.

@user1136 Yes, to clarify, the ethical issue isn't that it's a live vaccine, it's that it is a live vaccine that is transmissible, and therefore exposes people who (a) haven't consented to receive the vaccine and (b) may be harmed by the vaccine (e.g., those with certain  immunodeficiencies). For modern vaccines, transmissibility is only an issue with certain oral poliovirus vaccines.

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


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The largest Triceratops specimen
Almost every dinosaur book writes that Triceratops maximal length was about 9 meters (29.5-30 ft), see for example Thomas R. Holtz's dinosaur genus list 2011. My question is what specimen is the base or indication for that estimate, and what is its size? It could be a partial skeleton or maybe just a gigantic skull, and not a full vertebral-column specimen.
Also, what is the largest complete (or almost complete) skeleton of Triceratops? Peter Dodson in "The Horned dinosaurs" (1996) notes a 7.9 meters long skeleton at Minnesota's Nature Museum, but since then new almost complete skeletons have been found. If it is on display, please write in which museum it can be seen.
Added in edit:
The following image of EoFauna on DeviantArt and the discussion that follows suggests that Triceratops was as big as Eotriceratops, reaching a length of 9 meters and a mass of about 10 tonnes (10,000 kg) with skull about 2.7 meters long.
Added in edit 2021 December:
A specimen named "Big John" is 8 meters long and according to reports it is the largest mounted skeleton of Triceratops. It has 262 cm long skull and 1 meter long brow horns.

There's some references here https://en.wikipedia.org/wiki/Torosaurus. quote:  in 2006 Andrew Farke had pointed out that the new skulls described by him were on average even longer than Hatcher's original two: MOR 1122 has a length of 252 centimetres and MOR 981 of 277 centimetres.

here's a pic https://pbs.twimg.com/media/D6PV2vMVUAAVAmR.jpg


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Can one derive COVID-19 risk from a cheap consumer genetic test like 23andme?
Studies have found genes associated with a significantly higher risk of severe COVID-19, some of them claiming it to be 1.6 times the general risk.
They mention genes at markers such as rs35044562, rs1129183, rs679599192 to be significant.
Can people use the raw data from a consumer-grade genetic test like 23andMe to assess their risk, at least theoretically? The raw data has many gaps and the markers and their positions may not be included in the data. Can one then look at markers at positions close by, or at other markers? Does a more rare genotype imply higher risk?
Articles

https://www.nature.com/articles/s41586-020-2818-3
https://www.biorxiv.org/content/10.1101/2020.11.02.365551v1.full.pdf

I would strongly recommend talking to a genetic counselor about any results found on a genetic test, whether it be about COVID-19 susceptibility or anything else. Also, please keep in mind that personal medical questions and health advice are off-topic on Biology.SE. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice. This question is generic, so I'm not going to vote to close it, but I just wanted to make you aware in case you were planning on doing this yourself.

I suppose the answer is 'theoretically yes, but don't trust the results much'.
The 23andme genotyping array is very useful for ancestry testing, but much less useful for clinical diagnostics. I have worked in the past for Genomics England (an arm of the NHS in the U.K. which performs genetic diagnostics for rare disease). There, the samples were sequenced to very high coverage and underwent extremely stringent quality control checks which were being constantly updated. If you want to interpret a variant in a clinical sense, you have to very sure that you get the right genotype.
I believe that the details of how 23andme performs its variant calling and quality control are proprietary and therefore I would never trust their variant calls for any kind of clinical diagnostics, and neither would any clinician I know. This doesn't mean 23andme results are invalid - they are very useful and pretty accurate for testing ancestry, but they are not valid for clinical diagnostics. If your risk calculations hinges upon a few SNPs of relatively large effect size (such as BRCA), then you want to be very sure you make the correct variant call. You simply do not get this assurance with 23andme.
Secondly, like you mention, many of the SNPs you refer to aren't covered by the 23andme array. The effect size of a particular SNP on a trait is calculated for that specific SNP only. Extrapolating the effect size for one SNP in a gene to another, nearby, SNP in the same gene is likely to give you innaccurate results. In fact, the same SNP in the same gene can have pretty different effects in different people (https://febs.onlinelibrary.wiley.com/doi/pdf/10.1111/febs.14080 caused by the environment, pleiotropy).

Curious as to why this was downvoted?

No idea. It's exactly the sort of answer this type of question needs.


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Spike protein production by mRNA vaccines?
I am trying to understand the spike protein production mechanism of the mRNA vaccines, and during my research I learned that the mRNA (Moderna, mRNA-1273) vaccines hijack the cell machinery to produce spike proteins of SARS-CoV-2 by providing genetic material mRNA (which is encapsulated by lipid nanoparticle).
My question, which cells are subject to the vaccine particules (which factor determines the target cells?) Are produced spike proteins part of the cells (which interacted by the vaccine), or are these proteins emitted into the bloodstream like hormones so immune systems attack only the produced spike proteins?
I am asking this question to understand whether the cells which are used to create spike proteins are attacked by the immune system.

I am asking this question to understand whether the cells which are
used to create spike proteins are attacked by the immune system.

Yes, that is the aim of RNA vaccinations!
But don't worry, that's a good thing, as can be concluded from this review-paper, that emphasizes the advantage of RNA vaccinations to invoke cellular immune response:

Although subunit vaccines have been used successfully to elicit
humoral immunity against a wide variety of pathogens, they fail to
induce cellular immunity which is required to eradicate the
intracellular pathogen reservoir of many chronic diseases, including
viral infections such as HIV or hepatitis C.

Basically, the idea is that presented antigens from traditional vaccines are inclined to be presented via MHC2, rather causing humoral immunity, while after RNA transfection, cellularly produced peptides can also be presented on MHC1, causing cellular immunity.


text:
What does it mean to "nucleate multi-protein complexes"?
I am reading an article about the mTOR signalling pathway and I have come across the following:

mTOR nucleates at least two distinct multi-protein complexes, mTOR
complex 1 (mTORC1) and mTOR complex 2 (mTORC2).

I am not sure what is meant by "mTOR nucleates 2 multi-protein complexes". From the paper, I understand that mTOR is a component of the mTORC1 and mTORC2 complexes. I have read the definition of 'nucleate' online and it means to either "to form into a cluster" or "to act as a nucleus for". However in the context of this article, I am not clear about what is meant by "nucleates" in the above statement. Any insights are appreciated.

Here nucleation has a rather physical meaning. mTOR acts as the starting assembly point of the complex.


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WC small organisms ID?
I have reached the end of my Winogradsky Column experiment, but out of interest I have kept them for a little longer. I have noticed small bug- and worm-like organisms appearing in some of my columns. All mud and water was sourced from a nearby pond in Florida. The bug-like organisms are simply swimming/crawling around inside the column, while the worms are sticking up from the mud and wriggling. This pictured column was part of a group kept under a heat lamp.

Could anyone please provide an ID for these organisms? I think the worms are bloodworms, but I am not sure and I do not know what the small bug-like organisms could be, either.

Please always include specimen sizes for [tag:species-identification] questions. Also, each question post should only focus on 1 species. It seems your interest is in the non-worm organisms, so please edit your post to exclude questions about the worms (you may ask about them in a separate post; though, better pictures will likely be needed for ID). In fact, better pictures for this post would also be beneficial for future readers and to ensure the most accurate ID. Finally, you mention "swimming/crawling", which are very different behaviors. Could you specify which you're observing. Thanks.

Appears single-celled, but they look too big to be any kind of euglena or paramecia that I know. (again, knowing size would be helpful). Body shape doesn't immediately conform to other single-celled organisms I can think of off the top of my head, and they don't look like they're insect larva or crustaceans (e.g. daphnia). Nothing definitive stands out, but I think this is a case of poor quality photo + lacking details. Your post would really benefit from including 1) a zoomed/microscope image and 2) a gif of a video capturing their movement

the other thing that comes to mind are certain snail larvae, but again I'm not seeing detail to convince me that's what you have. More generally, do you see any appendages of any kind? (I don't in your images). Again, more detail would be great. Thanks

Alright, thank you for the advice! I unfortunately do not have a microscope but I will try to get clearer pictures with size.


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Architecture of lamellae in trabeculae in spongy bone
It is easy to find the architecture of lamellae in osteons in compact bone, they're layers of collagen fibers and each layer alternates in the angle the fibers are oriented. Is the lamellae in trabeculae similar, and the main difference that there isn't a central blood vessel to supply the bone cells with nutrients, since that is done trough the marrow instead?


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What does the term 'glycogen mobilisation' mean?
I read that glycogen is a mobilised store of glucose:

Glycogen is a readily mobilized storage form of glucose. It is a very large, branched polymer of glucose residues (Figure 21.1) that can be broken down to yield glucose molecules when energy is needed. Most of the glucose residues in glycogen are linked by α-1,4-glycosidic bonds. [Source]

When looking online, mobilisation refers to something that is capable of movement.
I think glycogen mobilisation has something to do with glycogenolysis but not sure how to easily define glycogen mobilisation.
How would you define glycogen mobilisation in the easiest definition?

It would be helpful to see the context in which you encountered the term.

I think the key to understanding mobilization in this context is in the second sentence:

[Glycogen] can be broken down to yield glucose molecules when energy is needed.

The authors are using mobilize in a figurative sense to suggest that glycogen can be quickly and efficiently metabolized to suit the energy needs of the body, like an army may be mobilized to fight a war.  See definition #2 on Wiktionary:

mobilize (verb)
2. (transitive) To assemble troops and their equipment in a coordinated fashion so as to be ready for war.

I think that @acvill more or less gets it, but I wanted to add a direct usage in context that makes clear the meaning.
I found this as the top hit when I google "glycogen mobilization". It has a lot of information and it is not straightforward, but it makes clear that mobilization is the process of breaking down glycogen into glucose. For instance, one slide says:

Glycogen phosphorylase usespyridoxal phosphate (PLP) a derivative of pyridixine (vitamine B6) as a coenzyme. B6 is required for the mobilization of glucose from glycogen.

As far as I can tell, "glycogen mobilization" means the mobilization of glucose from glycogen, therefore it is a special case of glucose mobilization in which the source molecule is glycogen. For example:

Glucose is a negative regulator of liver phosphorylase. – Glucose is not mobilized when glucose is abundant.

Additionally, wikipedia says:

...debranching enzymes mobilize glucose reserves from glycogen deposits in the liver.

and

glycogen debranching enzymes function in glycogen breakdown and glucose mobilization. When phosphorylase has digested a glycogen branch down to four glucose residues, it will not remove further residues. Glycogen debranching enzymes assist phosphorylase, the primary enzyme involved in glycogen breakdown, in the mobilization of glycogen stores.

So glycogen mobilization == glucose mobilization, in the context of human biology. That is admittedly kind of confusing.

+1 This is a good clarification

Thank you @acvill

Thank you for clarifying @Maximilian Press


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Genome-wide association study (GWAS) search engine?
I am not a biologist and came across the term genome-wide association study or 'GWAS' for the first time today.
Now I would like to see if there is a GWAS on the particular condition I am interested in finding out about. Is there a search engine that collates all known GWAS and makes them searchable?
Note: the backup plan is to use Google, but I wonder if there's anything dedicated to this particular task.

Try this https://www.ebi.ac.uk/gwas/

When researchers write meta-analyses etc. of such studies, they still use the traditional literature search tools, pubmed etc. So I don't think there is a database that has taken off just for gwas.

Thanks @Fizz (you're a human encyclopedia). Also, you may be interested in this question, which is somewhat related to another question you answered


text:
How long does foreign DNA stay intact in human blood?
How aggressively is foreign DNA in blood targeted and degraded by the human body?
I am asking because we have a metagenomics project where we want to detect parasite DNA in the human blood. The process from DNA extraction to sequencing to bioinformatic analysis is not a problem for us. But the question is if we can expect some signal in the data.

This paper may be useful https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3728338/

The De Vlaminck Lab has extensively studied the origins of circulating cell-free DNA (cfDNA) in human plasma and its utility in detecting infections and organ injury.1,2  Concerning your question of parasite DNA detection and parsing signal from noise, I don't think you'll find a better resource than their 2020 publication in Microbiome.3
If the (uncited) claims on their website are to be believed, cfDNA from all sources is cleared within one hour after release into the blood.

Our research pursues technologies and applications of cell-free DNA in infectious and immune-related disease. The great promise of cfDNA in diagnostic medicine derives from i) its abundance: 10-100 billion molecules of cell-free DNA can be isolated from just 1 mL of plasma. The combined DNA sequence of these molecules is sufficient to cover the human genome 1,000 to 10,000 fold. ii) Its origin: cell-free DNA is derived from dead cells and comprises rich information about cells in the blood and any vascularized tissue that can be accessed noninvasively. iii) Its short lifetime: cell-free DNA is cleared from the blood within 60 minutes. Cell-free DNA therefore provides a very dynamic window into health.

References

Burnham P, Kim MS, Agbor-Enoh S, Luikart H, Valantine HA, Khush KK, De Vlaminck I. Single-stranded DNA library preparation uncovers the origin and diversity of ultrashort cell-free DNA in plasma. Sci Rep. 2016 Jun 14;6:27859.
Cheng AP, Burnham P, Lee JR, Cheng MP, Suthanthiran M, Dadhania D, De Vlaminck I. A cell-free DNA metagenomic sequencing assay that integrates the host injury response to infection. Proc Natl Acad Sci U S A. 2019 Sep 10;116(37):18738-18744.
Burnham P, Gomez-Lopez N, Heyang M, Cheng AP, Lenz JS, Dadhania DM, Lee JR, Suthanthiran M, Romero R, De Vlaminck I. Separating the signal from the noise in metagenomic cell-free DNA sequencing. Microbiome. 2020 Feb 11;8(1):18.

But things like NIFT work because the foreign DNA is being constantly renewed.  Presumably non-human parasite DNA would be as well.

Thanks much! How would you inhibit the degradation of the cfDNA? EDTA and cooling? Cooling what temp?


text:
Stability of RNA including Thymine nucleobase
Does an RNA double strand containing the nucleobase T instead of U has a lower free energy?
Or more precisely: There are tabulated values for the change in free energy of the canonical neighboring base pairs here.
Do you know of any source where values for neighboring base pairs of e.g. GT/CA got compared to GU/CA?

I think you mean bond energies.

If you want you can call "free energy of neighboring base pairs" the bond energy. But I think it is less precise.

I was under the impression that you could only measure free energy changes, not free energy. And presumably bond energies would be equivalent to the free energy changes in breaking a hydrogen bond. But my chemistry is a little rusty, so do point me to sources that measure actual free energies of base pairs of any sort.

Ah no, you are right! It is change in free energy. I adapt my question.

I think my problem with bond energy is that the change in free energy is not simply the breakage of hydrogen bonds. It is an interplay between stacking (pi-pi) and hydrogen bonding.

But the stacking would depend on the neighbouring bases. There have been lots of studies in this area, but It’s not my field. Naively I would think a rT-rA bond would have a similar energy to a rU-rA bond. But do many actually occur? I would think most rT bases are in tRNA where the T is generally in a loop and has to be generated by enzymatic modification.

I would also guess rT-rA is similar to rU-rA. I don't know if rT-rA is frequently occurring. But I am not a biologist. I would like to know that more concerning prebiotic evolution.

I don’t know because I wasn’t there, but the current thinking is that thymine arose late. There is no rTTP, only dTTP. I have an answer somewhere about thymine and the RNA World hypothesis, and discuss the biochemistry. As I said, the only place I know rT occurs naturally is as a modified base in tRNA and I don’t think it’s in base-paired stem but I would need to check that.

When you say there is no rTTP you mean there is no rTTP found in current biological systems, right? I mean you can probably make it somehow in a chemistry lab.

You certainly could. But my arguments relate to the evolution of biochemical pathways. I think if you want to take this further you need to tell us what your hypothesis is, or spend some time combing through the literature of synthetic nucleic acid duplexes.

I think my question is clear though.


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Comparing maintenance energy costs of plant biomass vs bacterial biomass
Im interested if anyone has an idea if this research has been done or how you would approach it.
What is the energetic maintenance cost of (e.g) 2kg of some given bacterial cells vs 2 kg of a plant (like soybean).
Bacteria have less DNA to maintain per cell, less organelles, they dont fight gravity (not sure if this one matters), and probably have less active transport mechanisms. I guess the amount of energy they need just to maintain their biomass is much lower than a plant.

I did find this paper:
It shows the values normalized to nitrogen content prokaryotes ~150W/kgN vs plants 200 to 400W/kg N. But the study seem oh so complicated to me https://www.pnas.org/content/105/44/16994#T1


text:
What is the energetic costs in KJ/g NH3 for nitrogenase fixation
What is the energetic costs in KJ/g NH3 for nitrogenase fixation.
I want to compare Haber-Bosch vs nitrogenase.
How would I force the biological stochiometry of 8e- electrons into an energy quantity.
$N_2 + 8e^- + 8H^+ + 16ATP + 16H_2O → 2NH_3 + H_2 + 16ADP + 16P_i$

Well if your equation is correct and complete (I haven’t checked) I would start  with 8 x the standard free energy  of hydrolysis of ATP to ADP to get part of the answer in molar terms. But the equation is incomplete in so far as the donor of the reducing electrons is not specified so the redox change should be found for the half reaction, and then converted to a free energy change. This is all in a chapter in Berg, which you can find on NCBI Bookshelf. Let us know what you find.

Will check thank you for the resource


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Why do people's hands get cold for the first half an hour and then suddenly they are warm when they are doing exercise outdoors in winter?
When people do exercise outdoors in winter at temperatures less than zero degree celsius, their hands are quite cold and hurt for about half an hour. Then, there is a sudden rush of blood into the hands and they are warm afterwards, just as if they are indoors all along. Why does this happen and is there anything one can do to trigger the warmth faster?

Probably because your body is now trying to get rid of heat after 1/2 hr of exercise.

Why is it not a gradual process and happens so suddenly, like a some valve is opened and warm blood flows into my arms?

That valve being opened could be the capilliaries opening, well expanding, allowing more blood flow...

Cold extremeties are a reaction of endotherms where they reduce warm blood circulation to prevent losing core body temperature, otherwise the cold blood in your hands would lower your central blood pressure from 37'C, which makes the body less efficient and at risk of catching colds.

The reaction is called vasoconstriction.
quote:
Active cutaneous vasodilation occurs via cholinergic nerve cotransmission and has been shown to include potential roles for nitric oxide, vasoactive intestinal peptide, prostaglandins, and substance P (and/or neurokinin-1 receptors). It has proven both interesting and challenging that no one substance has been identified as the sole mediator of active cutaneous vasodilation. source
The above research can give you some clues about exercise and cold hands:

When you have exercised for 30 minutes, the above quote applies, and perhaps there is also a hormone contribution from natural opiates, endorphins, and other chemicals like nitric oxide.
quote:
The endomorphin peptides, endogenous ligands for the mu-opioid receptor, and nociceptin (orphanin FQ; OFQ), an endogenous ligand for the ORL1 receptor, have substantial vasodilator activity. source
For some very good reading on the subject, search for "thermoregulation vasodilation", the corresponding pages give advanced general knowledge of the biology.


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The Effects of Large Static Magnetic Fields on the Human Nervous System
How do static magnetic fields impact the nervous system?
I imagine with sufficiently intense magnetic fields the Lorentz force is going to change the behavior of nerve impulses, but at what field intensity do these issues occur? Which parts of the nervous system are most impacted by these fields? What specifically does the magnetic field interfere with? Are motor nerves more impacted than sensory nerves?
The WHO has some guidelines which suggest that fields of high intensity cause nerve issues, but this seems more related to MRI tech safety and doesn't really go into the biophysics of the situation. Additionally, they talk about issues which appear while moving through the fields, which seems to imply they're talking about low frequency field variation because an MRI field isn't spatially uniform.

I’m voting to close this question because whether or not something is safe for humans is more of a biology question.

What constitutes an on topic biophysics question? It seems like this question should also be closed as well then https://physics.stackexchange.com/questions/61679/effects-of-a-very-large-magnetic-field-on-the-human-body

Biophysics questions on PSE should be primarily about the physics. I agree that MRI is an important biophysics topic, but since this is Physics Stack Exchange the biophysics problems here need to mainly be about the physics.

This is absolutely primarily about physics. Nerve impulses involve the motion of charges which are deflected by magnetic fields. Presumably the nerve is capable of dealing with some level of deflection before the impulse fails to transmit. This is only something that's possible in a magnetic field, and thus a question which falls much more in biophysics than in general biology.

I agree, physics is extremely relevant in this system. I am sorry if I gave the impression I thought otherwise. I am saying that determining whether something is safe is more of a biology question. Physics will not tell you what is biologically safe.

The inhomogeneous fields that, e.g., can levitate frogs, are quite large (but not constant), yet do not seem to bother the frogs much.

@BioPhysicist Alright then. Since this doesn't seem to be desirable here could you migrate this question to bio se?

I don't have any power to migrate anything. You can raise a flag on your question to see if a moderator thinks it should be migrated though.

@BioPhysicist Done. Thanks.

I don't know anything about long term health effects. The guidelines mentions that noticeable effects begin around 2 Tesla. This is in line with what I have heard. On the other hand, this mentions public exposure limits of 40 milliTesla. Here is a paper from the NIH that discusses health effects of neodynium magnets, but doesn't mention field strength.
Keep in mind that 2 Tesla is an extremely strong field. You are not likely to find it except right next to a large superconducting magnet. Or possibly between the poles of an exceptional research grade non-superconducting electromagnet.
Keep in mind that even if a strong magnetic field has no direct effect on a normal person, it could be harmful to a person with, say, a pacemaker.
Also, a field that strong can turn a stray piece of metal into a dangerous projectile.
Motion in a magnetic field matters because it exerts a force on moving electric charges. $\vec F = q \vec v \times \vec B$. This means for example, a copper wire feels no force, unless an electric current is moving inside it. In people, nerve impules are small brief currents. This may be why people feel effects in large fields. Walking means charges are moving faster.

Two of the experimentalists at my university just use human sized water cooled electromagnets that can produce ~9+ tesla fields, so it's not that infeasible.

@Triatticus - Thanks. I was not aware of that. I updated my answer.


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How to identify the subspecies/breed of a bee
I have been a beekeeper for a number of years and originally obtained my first colonies from a guy in my neighbourhood. However, when I sell bees to someone else, they typically ask what species of the European/Western honeybee (Apis mellifera) I have/they're buying. Technically, they're after the subspecies or breed (like Italian, Carniolan, Buckfast, ...), but I don't know what to tell them. I just call them local (or locally-adapted) bees.
Is there a way that one can find out the subspecies/breed I currently have? Perhaps through DNA analysis/sequencing or some other kind of scientific analysis? Regardless, is such subspecies identification available/accessible to the hobby beekeeper (should read as being relatively inexpensive)?
Images like the following are circulated to estimate one's breed:

However, traits are hardly a definitive assessment of a breed, especially if you consider how close some of the breeds are listed above. For example, what's the difference in a trait ranked 5 and 6, say.

I am not sure about apiculture, but in academic research it is typical that people use microsatellite markers for identifying subspecies of bees. Microsatellite are repetitive regions of the genome that are useful in at identifying different species/subspecies, as well as for generating pedigrees and paternity analysis. Different species/subspecies have different numbers of repeats in a particular microsatellites, and these differing number of repeats are heritable. People use microsatellites because they are cheap, easy to run and reliable for identifying species/subspecies. Because there can be many different alleles (or different numbers of repeats) at a given microsatellite locus, so you only need relatively few microsatellites in total to identify individuals.
An example can be found in this paper. They used 7 microsatellite loci and could reliably identify between different African and European sub-species. It is worth a read of the intro:

Recent population genetic surveys in human (Bow- COCK et al.
1994;DIRIENZO et al. 1994) and other mammals (GOTTELLE et al. 1994;
TAEOR et al. 1994) and in bumble bees (A. ESTOUP,M. SOLIGNAJC. ,M.
CORNUET and A. SCHOLL unpublished results) have shown that
microsatellites are highly efficient at differentiating
populations or groups of populations. In this paper, we investigate their
usefulness for honey bee population studies by adressing the
following specific questions: Are the three evolutionary branches
inferred from morphometry and mtDNA confirmed by microsatellite
data? Are microsatellites useful for differentiating sub-species and
populations within subspecies? How does the pattern of variability of
these markers vary between branches/subspecies/populations and which
factors may be invoked to explain it? Is it possible to assign a given
colony to its population of origin from microsatellite data and how do
the individuals from this colony cluster within the population?

References:
Estoup A, Garnery L, Solignac M, Cornuet JM. Microsatellite variation in honey bee (Apis mellifera L.) populations: hierarchical genetic structure and test of the infinite allele and stepwise mutation models. Genetics. 1995 Jun;140(2):679-95. PMID: 7498746; PMCID: PMC1206644.

Are you using the first word in your post, "typically", in an indirect generalized way or from a perspective of insider knowledge/awareness of apiculture? I ask because the paper you quote only cites a single additional study of unpublished results, which doesn't support the interpretation of "typically" to mean widespread as I think is implied from your post's wording. I don't know one way or the other, but I think it'd be good to clarify your wording and possibly explicitly indicate your knowledge of the subject so that future readers know how to frame your response. thanks.

I slightly misunderstood the post and didn't notice it was talking about bee keepers in particular - I said 'typically' since microsats are (most likely - I don't have direct evidence) used in research to identify different Hymenoptera species/subspecies. I've got a reasonable amount of experience in population genetics of Hymenoptera, so that's what I'm going off. That paper is old, so the citations are out of data, but having a look here shows it is still common. Will amend the post to make it clear.

Thanks! I had a hunch that was the case. Again, I personally don't know one way or the other, and I just wanted to make sure your post was clear to others. Thanks for the update!

@user438383: You mention "cheap [and] easy to run." Can you elaborate? I'm a beekeeper without any lab access, but I'm interested in this as a side-project. Are there tools available to the laymen to perform identify these microsatellite markers?

@Werner - good question - ill edit in the answer to my post soon.

@user438383: Any update you can provide?


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Why is the consumer/producer biomass ratio higher in the oceans?
According to Bar-on et al. (2018) (see figure 2), the terrestrial consumer/producer biomass ratio is 20/450  while the marine consumer/producer biomass ratio is 5/1 (in Gton of carbon).
Why is the consumer/producer ratio much higher in the oceans?
Is it perhaps because marine animals are more efficient? Or is terrestrial plant biomass underexploited by surface animals?
 Bar-On, Y.M., Phillips, R. and Milo, R., 2018. The biomass distribution on Earth. Proceedings of the National Academy of Sciences, 115(25), pp.6506-6511.

This is certainly not a full answer, but a lot of it probably has to do with the fact that terrestrial producers put a huge amount of biomass into support structures (wood!) that's not needed in the ocean.

The paper you cited suggests an explanation:

Such inverted biomass distributions can occur when primary producers have a rapid turnover of biomass [on the order of days (34)], while consumer biomass turns over much more slowly [a few years in the case of mesopelagic fish (35)]. Thus, the standing stock of consumers is larger, even though the productivity of producers is necessarily higher. Previous reports have observed inverted biomass pyramids in local marine environments (36, 37). An additional study noted an inverted consumer/producer ratio for the global plankton biomass (16).

To explain/clarify this a bit further: there are two main processes that affect the consumer/producer ratio. One, which you have identified, is efficiency (how much of the biomass is transferred from one trophic level to the next). The other is turnover rate (rate at which biomass leaves a trophic level), which is the reciprocal of the residence time (the average length of time that a unit of biomass spends in a trophic level before transitioning to another trophic level/compartment).
At equilibrium, the biomass in a trophic level is equal to (inflow/turnover rate) or (inflow $\times$ residence time). If consumers at a particular level consume one tonne of biomass per month (assume 100% efficiency for now) and the residence time is 6 months, the standing stock or quantity of biomass at that level will be 6 tonnes. Taking some of the numbers from the paragraph above: suppose the residence time for phytoplankton is 4 days while of consumers is 400 days. If the consumers have a 10% efficiency for taking up phytoplankton biomass, then the consumer biomass will be $(400~\textrm{days}/4~\textrm{days}) \times 10\% = 10$ times higher than the phytoplankton biomass.

Phytoplankton lives for about a week and is renewed, i.e. Cocolithophoridae which clones itself every 6 days.
Terrestrial biomass lives for about 10 years. i.e. trees
Hence, there is a higher ratio of phototrophic/producer biomass on land.
reference:

There were 45 billion tonnes of new phytoplankton each year, 45 times more than their own mass at any given time. The phytoplankton would therefore have had to reproduce themselves entirely, on average, 45 times a year, or roughly once a week. In contrast, the world's land plants have a total biomass of 500 billion tonnes, much of it wood. The same calculations showed that the world's land plants reproduce themselves entirely once every ten years.

This information is useful, but only if the OP already knows about the relationship between turnover and standing stock ...


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Do hormones make it more likely to perceive sexual forms in otherwise non-sexual objects?
People can see sexual forms in many things. It seems that this varies with age, but this is not enough to claim it is because of sexual hormones. The question is: is it?

Pareidolia is a common phenomenon, and certainly is not limited to "seeing" phallic or other objects as sexualized; the canonical example is seeing objects as face-like, such as the headlights and grill of a car appearing as eyes and mouth.
There seem to be some sex-based differences in pareidolia (see Proverbio 2017) but if there is hormonal cause it is probably developmental rather than acute, and this is related to face-specific perception, not anything sexualized.
I don't see any literature on, say, puberty and sexual pareidolia, though absense of evidence is not necessarily evidence of absense. It isn't surprising that there are changes with age, but this need not be due to hormones per se but rather due to exposure to different stimuli (or their salience). I think this is probably not an area of much biological study because there isn't an associated medical concern and it's a fairly subjective phenomenon.
Proverbio, A. M. (2017). Sex differences in social cognition: The case of face processing. Journal of neuroscience research, 95(1-2), 222-234.


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Why does this study about genetic likelihood of COVID hospitalization not associate risk to base pairs?
In the study "Genetic mechanisms of critical illness in Covid-19", (free to download) the authors share their findings on which genomes seem to be associated with an increased likelihood of hospitalization when infected with COVID 19.
See Table 1 (page 9), to see that the Risk is represented by one letter. I'm not academically trained in genetics, so my only experience when reading these papers is that usually risks are associated with a base pair. Like "C/C', or "A/G".

Why is only one chemical/letter given? How does one interpret this?
*I'd like to mentioned that several genetic testing companies have the markers in this study mapped, so this could be useful information for patients and their physicians.

I'm not sure what's unclear; the table shows a Risk base and Alternative base for a SNP (aka, a substitute of one base for another) at a given location. What are you having trouble interpreting?

I’m voting to close this question because it requires reading an external paper to understand the question. This is a question and answer site about problems in biology in which any question must be comprehensible in itself. It is not a journal discussion group.

This is a quite reasonable question to ask about a style of data presentation that is not limited to a single paper.

The "Risk" is the single basepair sequence (A, C, G, or T) at the precise chromosome:position location in the column to the left of it.  "Alt" is the basepair present in the other allele.  The complementary nucleotide is still present on the other strand, but its identity is obvious and the decision of which strand's sequence to list was made when the original reference sequence was published.
The slash notation "C/C" (as in https://www.biorxiv.org/content/10.1101/2020.12.06.413971v2 ) means that the genotype for both alleles the person is carrying has been considered jointly.  In this table no such breakdown is given.  Judging by their subsequent interest in transcript level, it is conceivable their model was that the two alleles would have subtle additive effects on overall expression level with a subtle effect on Covid risk, so that incomplete dominance could be assumed... but to truly understand their motivation you need to understand high-definition likelihood inference (see the overview and paper link at https://medicalxpress.com/news/2020-07-high-definition-likelihood-inference-genetic-human.html ) which requires some study.


text:
How would our vision be improved if our photoreceptors were not backwards?
I'm curious to how much better human eyesight would be if the nerves from our rods and cones were correctly placed behind the receptors?
Are there any Animal Models with correctly placed photoreceptors that we can use as a benchmark?

Octopuses have nerves in the arrangement you want. However I do not know any more detail. Please see if you can find some literature on this topic.


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Eye Optics/Emmert's law: Where to place scaled copies of an object so they have identical images on the retina?
I read that the center of projection of the human eye is the entrance pupil. So given a light ray which intersects the objects position and the center of the aperture stop, all copies of said object when placed along that line should cover the exact same position/area on the retina (assuming they are scaled according to their distance).
However, doesn't this ignore the effect of accomodation of the human eye: If the original object is quite near, but a scaled copy along the ray is quite distant, the focal length of the lens is changed and thus a different position and area of the retina is covered.
I tried to visualize this by using the ray simulator at https://ricktu288.github.io/ray-optics/simulator/:

Image A:
Lens focussed on distance of Object A which is projected onto A' on the retina. Object copies B and C are placed at fixed distance either along a ray via the aperture stop (B) or via the center of the lens (C).

Image B:
Lens is focussed on distance of Object B/C which are projected onto B* and C* on the retina. Both are in focus (difficult to see in the picture), but B* is further away from A' than C*. Object B would appear larger than Object C.

So I guess this boils down to the question:
Given the position P of an object A and a lens system, what is the point Q which creates a ray PQ so that all scaled copies of A (A', A'', ...) at different distances along that PQ ray appear at the same position and area on the image created via the lens system.
Is there such a point Q? Is it the center of the lens (i.e. is C* == A') or one of its nodal points?
I am thankful for any pointer to help me understand this!

I suppose that you need to use the thin lens equation (https://en.wikipedia.org/wiki/Lens#Imaging_properties), but with different focal distances. Now, the focal distance is not the same as the distance to the object  - so one needs some data on how the focal distance of an eye adjusts to the distance to the object. You may try asking this question in the physics community.


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Why do apes still exist?
If we are evolved from apes, why don't all ape evolve and become human.
Or

Why the today's ape stop evolving to become a human?

Because their environmental niches suit being apes.  Evolution does not have a goal.

Okay. But why is my question downvoted?

@jamesqf Why don't all apes evolve then?

Why do you think apes don't evolve?  Like any and all other creatures, they continuously evolve to become better suited to their environment, which is why there are about 20 species of living apes, each suited to their particular environments.  And I downvoted your question because I think it is pure creationist claptrap.  If it's not, the answer is pretty obvious: why do we have different species of cats, bears, equines, or any other group?

I am not going to bother putting any references for this answer as all the information is a google search away.
Humans did not evolve from apes. Extant humans and apes developed from a common ancestor. One lineage from this common ancestor evolved and became apes. Another lineage went on to become humans.
Some study material here and here.

Unless one can describe a "common ancestor", this phylogenetic knee jerk response begs the question. Humans evolved from animals not distinguishable taxonomically from apes. Phylogeneticists invoke the common ancestor explanation because their analysis is actually a form of cluster analysis, where groups of traits split dichotomously into smaller groups of traits. This is not a model of evolution.

OK, so what is a model of evolution?

Can you provide a link to explanations of alternate and feasible hypothesis?


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What goes into a vaccine placebo, typically and in the specific case of Pfizer's SARS-CoV-2 vaccine trials?
I am curious about what actually goes into a vaccine placebo formulation, given that there were apparently some reactions reported by trial subjects who received the Pfizer SARS-CoV-2 placebo.
From what I've been able to find out online, the actual vaccine contains as principle ingredients (simplified):

mRNA (active ingredient) to make the target antigen (spike protein)
lipids (to protect the mRNA and facilitate its delivery into cells)
salt(s) to adjust pH and match the salinity of blood
sugar to address issues which occur when the vaccine is frozen

An injectable placebo could be as simple as a saline solution... if so, how could reactions be explained? Is it entirely psychosomatic?  Is the Pfizer SARS-CoV-2 trial placebo the complete formulation (or some subset of vaccine components) minus the active (mRNA) ingredient?
The lipids have been implicated in allergic reactions to the actual vaccine; would they have been present in the placebo and account for the placebo reactions?

Simple answer: This vaccine trial compared their trial vaccine against saline.
See the original publication by Biontech and Pfizer in the New England Journal of Medicine linked below. The relevant information can be found in the methods section:

TRIAL PROCEDURES
With the use of an interactive Web-based system, participants in the trial were randomly assigned in a 1:1 ratio to receive 30 μg of BNT162b2 (0.3 ml volume per dose) or saline placebo. Participants received two injections, 21 days apart, of either BNT162b2 or placebo, delivered in the deltoid muscle. Site staff who were responsible for safety evaluation and were unaware of group assignments observed participants for 30 minutes after vaccination for any acute reactions.

As far as I followed up the case of the allergic reactions, two of these have been observed in England. Both people had an epipen injector for such cases by hand, making it possible that they have underlying problems with allergies (as this is not a medical device people usually have at hand), no such cases have been reported from the trial. Allergic reactions are always a small risk with vaccinations which is the reason why this is done in a controlled medical environment.
As for the vaccine reactions in the placebo group, this can be caused by the nocebo effect, where expecting negative effects leads to a more negative reaction. As @BryanKrause mentioned, all possible effects reported in such trials are recorded as possible side effects. This leads to a lot of things being recorded which happened at the same time as the vaccination but have no connection to it.
Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine

In addition to the nocebo/psychogenic effects, I think it's worth mentioning that people experience things classified as "side effects" all the time. People get headaches, diarrhea, sneeze, cough, get stiff limbs. Ordinarily we shrug it off, blame it on last night's meal, how we slept, smells from the neighbor's cooking. But if you just got injected with something that might have been a vaccine, it's natural to attribute it to that thing that's novel.

@BryanKrause Good point. It demonstrates the old "correlation is not causation" very well.


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Did mammals evolve from something with eusociality?

Eusociality (from Greek εὖ eu "good" and social), the highest level of
organization of sociality, is defined by the following
characteristics: cooperative brood care (including care of offspring
from other individuals), overlapping generations within a colony of
adults, and a division of labor into reproductive and non-reproductive
groups.

Did mammals evolve from something with eusociality?
I'm asking because I'm curious about the possibility that mammals evolved from something for which self sacrifice of individuals generally helped their genes survive.  Eusociality seems the limit example of that (correct me if I'm wrong).

No. The only truly eusocial mammals are Heterocephalus glaber (the naked mole-rat) and Fukomys damarensis (the damaraland blesmol). Eusociality doesn't just involve an individual sacrificing their individual fitness for others, altruism is a common behavior among many species, from arthropods and worms to mammals.
Eusociality is specifically a condition where the duties of reproduction are partitioned among individuals in a social group, with some individuals contributing to breeding future generations and others never getting the opportunity to breed. I.e., an ant colony. Only the queen and drone males ever contribute genetically to the future generation, the worker and soldier ants die without leaving offspring. In the naked mole rat and the blesmol, only the queen and some males breed while the other individuals provide them with food, shelter, defense, but never get to breed.
E.O. Wilson suggested that humans can be considered quasi-eusocial because in human society we reward individuals who contribute to society but do not breed (e.g., career individuals), but E.O. Wilson was notoriously kooky with regards to anything involving human society and gender roles.

Though with humans (and perhaps other species), a lot of that supposedly self-sacrificing behavior isn't really altruism, so much as it is a a consequence of foresight.  E.g. if I risk my life to save the tribe from a man-eating lion, then if I'm successful I'm a hero and get lots of chances to breed.

@jamesqf I mean, that's the purpose of altruistic behavior in every species ever. "If I risk my life to save my offspring it will increase my chances to pass on my genes", etc. Even in eusocial species altruism has a selfish basis, or else the behavior wouldn't persist and be passed on.

I'm using the dictionary definition of altruism, though: "disinterested and selfless concern for the well-being of others".


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What is the minimum-volume : neutral-volume : maximum-volume of the molecules that make up the SARS-Cov-2 virus-fusion machine?
The "neutral-volume" is the over-lapping volume between minimum-volume & maximum-volume of the molecules that make up the SARS-Cov-2-fusion machine. Those identifying potential differences that support particle-flow inside the SARS-Cov-2-fusion machine-molecule have certain degree's of freedom. The best description of the structural dynamics of the Sars-COV-2-fusion machine that I have found was in "Scientific American", July-2020-issue/page 34,.
A base understanding of the "open-loop & closed-looped" particle-flow-symmetry is needed to explain the action of why the fusion machine of the SARS-Cov-2 virus binds to a lung-cell. The way I understand it, there is an exchange of particle-mass, starting with disorganizing lung-cell-mass by this virus at point of attachment, then re-organization occurs between the lung-cell and the SARS-Cov-2-fusion machines particle-flow grid. The SARS-Cov-2-fusion-machine may in fact accelerate into the lung cell, (to-push & bend/in the act of causing mass to dis-organize) and then deaccelerates, causing the act of organizing particle-flow between the two cells (to pull-straight/in the act of synchronizing & organizing), producing a certain closed-looped function between the virus-cell & the lung-cell. What are those unseen differentials between what is seen and what is not seen? Covalent bonding is straight-forward and well understood, except for the fact that there are other molecular actions involved. Would this be a function of two under-square vortexes, Van Der Wall-forces, Brownian motion, the action of dipoles, or something else? ALL of which may in fact contribute to an exchange of mass of which brings on those pulling forces that bind. There is a certain working-mass having a certain energy efficiency per location per time that changes the squareness of the SARS-Cov-2-fusion machine. Volume displacement of heavenly bodies plays a critical roll as to the way particles move around and through them, i.e. outer-space becoming inner-space & inner-space becoming outer-space per location per time.

I appreciate that scientists from different disciplines view problems from different perspectives, but perhaps you should consider that too if you post on lists frequented by biologists who clearly have a different perspective from you. Your concerns are not their concerns, and I cannot imagine that you will receive an intelligent answer here.  The fact that you include totally irrelevant tags such as “mutation” and “cell cycle” signals that you have come to the wrong address.

Thank you David your input is greatly appreciated and I thank biology-stack exchange for giving me the opportunity to post. I made a mistake in that I should have used the "dissociation constant" in my descriptive terminology, for I am bound to the capitalism beast and I an limited as to what I can post.


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Why don't memory cells of the adaptive immune system get activated immediately after being created?
Why don't memory B and memory T cells of the adaptive immune system get activated immediately after being created?
As this video explains they are created in the heat of the battle. Aren't the conditions for activation there? What mechanism prevents them from being activated right there and then?


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Evidence against aging caused by loss of information in genome and epigenome in humans?
After reading Lifespan by David Sinclair I'm curious if there is any evidence against aging being caused by loss of information in genome and epigenome of 3.7*1013 cells in human body.
Specifically has anyone compared the genome and epigenome of the same humans at different ages?

It's important to mention the alternate hypothesis of not loss of information but different information. Taking the telomere shortening example, that is straightforward loss, but that DNA isn't informational really; rather it plays a structural role in the cell such that when it's lost it gets hard to segregate chromosomes. The other mutations and epimutations aren't (necessarily) loss of information, but on average the substitution of different information and rearrangement of the existing information.

By loss of genome, I think he is referring to the shortening of telomeres. This
study compares the length of telomeres of human epidermal cells. The authors report that over time, the telomeres do shorten. They also report on the rate of loss of around 32 base pairs per year. Thus there is loss of some genomic information over the age of an individual.
However, the loss of epigenomic information is trickier. The primary reason for it being some regions of the genome have been shown to lose DNA methylation marks whereas others gain it. However, leaving that aside, there is comprehensive proof that DNA methylation changes with age. This study on female peripheral leukocytes shows that approximately 350 regions (known as CpG islands) which are differentially methylated with age. Of these 350, 250 loci become hypermethylated i.e. methylation increases with age while the opposite happens for the remaining 150 loci.

Thanks for the explanations. Very helpful! In the 1st paper when the scientists use 13.8±1.0 kb, does kb mean kilo bytes of base pair ATCGs so 1 kb = 1000 bytes = 8000 bits 0s && 1s representing ATCG... where A&&T = 00, T&&A = 01, C&&G = 10, && G&&C = 11 ?

@Wang-Zhao-LiuQ The kb in biology means kilo base pairs. So 13.8 kb is 13800 base pairs. In some publications the unit kbp or bp is used to avoid confusion.

Thanks! I think I should rephrase the question is aging caused by the change of genetic information? Losing 32 base pairs or gaining 32 base pairs could both contribute to expressions of genes that cause signs of aging.

Your second sentence is correct. However, keep in mind that it is not entirely clear whether loss of telomeres causes aging or is a result of aging. For example, mice have short lifespans but less degradation of telomeres compared to humans. You may want to explore some literature on how metabolism affects aging process as well.

From what I know, I would expect that no one has performed a similar experiment to what you propose. Sequencing a genome is still rather expensive and inaccurate. Some parts of the DNA can’t be sequenced at all and most methods still rely on comparing the sequencing reads to a reference genome, making these kinds of predictions harder.
Getting snapshots of an epigenome (chromatine modifications, transcription factors) to the accuracy that you can detect a notable difference after a few years is even harder.
Also, by analyzing the genome of a given somatic cell, the cell is being destroyed and not available to test it again after a couple of years to see if relevant mutations occurred.
In short: Sinclair‘s predictions are probably hard to verify at this point.

Have any ideas on how to analyze the genome of a somatic cell without destroying it? Can it be cloned perfectly && then we destroy the cloned cell for analyzing?

This runs into a similar problem: cloning a cell involves removing it from the tissue. I’m not an experimentalist though. Maybe it’s achievable with a cell culture. Using a living organism you would have to come up with something novel, probably.


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Did snow leopards lose the ability to roar or never have it?
Since snow leopards are the only species in the genus Panthera that can't roar, was this something the others developed after snow leopards diverged or something that snow leopards lost?

Interesting topic. I found a recording of all the Panthera clade roars here, and comments like "roaring and purring are mutually excusive" and " Its vocal cords lack an all-important layer of fatty, elasticated tissue, which, in other big cats, gives the vocalisations an uneven rumble that emerges as a roar" but no information to answer your query, which is very specialized zoology/big cats info.

https://www.youtube.com/watch?v=bFCv02IGtn4&ab_channel=MeowMeowTV


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What is meant by pro-acinar cell?
What is meant by "pro-acinar cell" in the following sentence? progenitors/precursors?

A transient decline in Neurog3 expression from E11 to E12 coincides with peak segregation of MPCs into proximal, Ptf1aNkx6-1+ bipotent progenitors (BPs) and distal, Ptf1a+Nkx6-1 pro-acinar cells (PACs).

Thanks

Could you include a link to the original source from the quote? Thanks.

With the help of Google Scholar, this is from https://www.sciencedirect.com/science/article/abs/pii/S1534580720300162

'Pro-' is a general Latin preposition and English prefix with many meanings, but often in biology, as in this case, it means "before".  A proacinar cell is not yet an acinar cell (a cell of the acinus) but will be.  A related usage occurs with peptides such as proinsulin.
In Latin, "acinus" means a cluster of grapes.  You can find 'acini' in many places, notably exocrine glands, but in this case the pancreas is discussed.  With the help of Ms. Elbakyan, they tell quite a beautiful story, but the answer to this question is mostly in the first sentence of the abstract:  the stem cells (multipotent pancreatic progenitor cells) can become pro-acinar cells (which become secretory tissue of the acini, producing the pancreatic digestive enzymes), or else are reserved as bipotent progenitors that create the ducts and the islets of Langerhans.

what is meant by "pro-"? like pro- in English or pro from progenitor?

Thanks for pointing out this omission!  I've updated the answer.


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Why are some bird hybrids fertile?
So, we all know that hybrids are infertile, that's the definition of a species, but how come some parrot species can interbreed and still be fertile. For instance a military macaw and a blue and gold macaw can have offspring that are fertile and can breed to make further hybrid macaws. These two species are definitely different species and not sub-species. How is this possible?

Minor comment - not all hybrids are infertile. 'Hybridisation' can occur between two e.g. breeds of the same species and can therefore produce fertile offspring.

Yes I know that sub-species can interbreed to create fertile offspring because they are in fact the same species. However, military macaws and blue and gold macaws are separate species and therefore should not have fertile offspring. Although thank you for clarifying in case it wasn't clear in my original post

"hybrids are infertile, that's the definition of a species" is not accurate - it may be a definition but certainly not the definition (and completely fails for asexually reproducers). Remi's answer at https://biology.stackexchange.com/a/39669/27148 is a good related read.

Yes but that still doesn't really answer my question. Macaws reproduce sexually and therefore still come under that definition of a species. I'm not trying to argue I've done so much digging to find an answer to this and just can't.

@RowanBlackwell-Cronie Did you read the answer I linked?

@Bryan Krause yes I did, and whole I found it interesting, I understood it as stating that whilst similar species might never normally interbreed, e.g a bird with blue feather and a bird with red feathers, but if they did they could create viable offspring. However I interperated this as meaning that those birds were actually of the same species in order to do this? But there have been cases of very different bird species creating fertile offspring. Which is what I can't understand. Please correct me if I'm wrong here

@RowanBlackwell-Cronie No, the birds in the situation Remi describes would still typically be described as different species based on their reproductive isolation, even if hybrids are actually fertile. That's the whole point of the post: the weakness of definitions of "species".

Ohhh right. Thanks for clarifying. I'll do more research into this


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Should I consider one or two DNA chains to find how many nucleotides are in a gene?
I am trying to solve an exercise.

How many nucleotides does a gene contain if information about 287 amino acids is encoded in it? What is the molecular mass and length of this gene?

AFAIK, I have to consider two DNA chains to find molecular mass, and one DNA chain to find the length of the gene (am I right here?).
But I am stuck trying to find how many nucleotides are there in a gene. Should I consider both or only one DNA chain? I suppose that both (as for the molecular mass of the gene) but I am not totally sure.

This is a bad question from two perspectives. First, counting either one or two strands are equally correct or incorrect as there is nothing in the definition of a gene that specifies strandedness ( or even DNA). Second, the length of a gene is always longer than the DNA needed to encode the amino acids. All mRNAs have 3' and 5' non-coding regions of varying length, and, of course, there is always a stop codon. I approve of making students do calculations. I disapprove of questions that are biologically stupid.

@David, thank you very much for your reply. I agree with you. But this is exactly the question asked by my school teacher. Actually, these nuances are why I got stuck with this exercise.

Only your teacher can decide what the "right answer" is to their poorly thought out question. Either consult with them directly to find out what they want or give multiple answers and state clearly what assumptions you are making for each answer. Something like "If I assume that the gene only consists of an open reading frame and is single stranded then my answer is ###. However, if it is double stranded then my answer is #### etc." This has the advantage that you might be able to teach them ...

@tyersome, thank you for the advice. I have written exactly that way)

Counting both strands is admirably correct, but most people will multiply the number of amino acids by three, not six.  For example, nucleotide positions in a reference sequence will increase by 3 for each amino acid in the presumptive coding sequence.  Besides, if you want to be that pedantic, you should say zero, since the DNA contains nucleotide residues, not individual nucleotides, as they have undergone dehydration synthesis.  I think in biology the right answer will almost never be marked correct by a machine. :)
The answer you come up with will also be influenced by whether you would like to include a stop codon (+3) to avoid nonsense-mediated degradation, and a transcriptional start site and polyadenylation sequence (in eukaryotes).  The ''gene'' itself, in the genetic sense, will include enhancer elements over a much longer region of the chromosome and regulatory 3'-untranslated regions.  And then there's alternative splicing to consider...

Thank you very much. I understand now :) You've helped me a lot!

In fact, counting the nucleotides only one chain is mathematically the correct answer! The second chain does not contain any new information, since it is unambiguously determined by the first chain. On the other hand, the second chain does contain additional mass.

Well, you could have a mismatch.  The mRNA produced will use the complement of the base on the template strand, unless mismatch repair alters it to match the coding strand.  All six positions therefore may contain some information about the amino acid.


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Is there any correlation between animal diet and blood pH?
The alkaline diet claim that as we humans have a slightly basic pH we shouldn't eat acidic food like meat (I think they claim that meat ashes are acid).
I was wondering that if carnivores animals share similar blood pH to humans and herbivores, that argument falls.
I did a google search, but I couldn't find the answer, even though it seems like basic data for a physiology textbook.
Similar questions have been posted here but without satisfactory answers.

The alkaline/acidic diet bit is all pseudoscience junk. You'll find related questions at Skeptics.SE. There are also a couple of diet pH questions here already if you search.

I know that it's pseudoscience. The question that I post is a scientific one that is meant to refute a pseudoscientific claim. I don't think the question to this specific question could be found in Skeptic.SE

Note that pH would not be the only factor to determine how much a type of food could influence the body pH. It would also be important to know the buffer capabilities of that food.


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Selective breeding of organisms to survive on Mars
It seems that there may have been life on Mars, and it's also tempting to terraform and colonize the planet. This question is about testing the hypothesis "Can primitive life survive on Mars?". This is closely linked to the lithopanspermia hypothesis, that life can be seeded from bacteria on meteorites.
The hypothetical experimental setup is as follows:

Take microorganisms that live in the upper atmosphere and can survive high radiation
Recreate their natural environment in a lab, and let them live there
Slowly change the environment to be more similar to Mars: pressure, temperature swings, radiation, relative gas concentration
See if they are able to adjust

My question is: Is this possible? Has anyone done it, or is doing it currently? I know tardigrades are being sent to the moon, but they're hardly thriving there.
My apologies if the non-expert question is off topic. If you can suggest a more appropriate place to ask, I'll keenly do so.

Some consider the invasion of extraterrestrial environments on a moral ground, but that's not what I'm asking here.

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). At a minimum, you should search on this site for related questions before posting to avoid duplicate questions. Please also see this sites criteria for "homework". Thanks!


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Wounded Pigeon in my balcony
There is a, probably wounded, pigeon (common rock pigeon) in my balcony. It is dark right now and thus, I have very little idea about its condition. But it seems it is finding it difficult to fly/move its wings because when I approached the balcony door, it 'walked' towards the farther end of the balcony while flapping its wings very slowly.
What is the right way to handle the bird and what is the best thing I can do for him/her?

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In particular, this question seems like it might be a better fit for [Pets.SE], but please do not crosspost, instead first check that site for similar questions and then, request migration if you don't find an answer. If you do find an answer please delete your question from this site. Thanks!

Call the RSPCA or whatever animal rescue is active in your country and neighborhood.

More likely to be suffering from disease, old age, or poison. Providing food and water would probably be appreciated.

If you have a cat carrier then trying to intice it inside with some food would be a good idea. Try to contact your local wildlife vet for information on whether they would be willing to treat the animal. If you think it may be injured then I wouldn't reccomened handling the bird as you may hurt it further, but if you do need to then handle it by placing both hands over the wings in order to pick it up (https://www.rspb.org.uk/birds-and-wildlife/advice/how-you-can-help-birds/injured-and-baby-birds/if-you-find-an-injured-bird/) . In addition the bird could have gotten used to its injury and learned to live with it so you could monitor it for a bit and see how it's getting on. Hope it turns out alright.
If you live in the UK here is some advice from the RSPB: https://www.rspb.org.uk/birds-and-wildlife/advice/how-you-can-help-birds/injured-and-baby-birds/sick-and-injured-birds-faqs/#:~:text=For%20most%20injured%20birds%2C%20place,how%20you%20can%20help%20it.

Well, I don't have a cat carrier. Will it be wise to let it remain there till the morning?

It'd be a good idea to wait until the morning to see how the bird is doing. If it's still in bad condition then I'd advise calling a wildlife vet, otherwise the animal will likely get used to its injury or, unfortunately, pass away

When I checked in the morning, it had already flown away. Thank you for your help:)

I hope it'll be alright. No problem!


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Beautiful blue enigmatic insect (mantid?) in Kenya
This beautiful insect was found in Kenya today - and we don’t know what it is. We think it may be a mantid of some sort?!
Nairobi kenya, croton trees, cape chestnuts, bougainvilliea, there is quite a lot of lichen on the trees.
Despite looking to be the size of someone's arm, it's about 2” long!
Needless to say, no-one had a good camera at the time. Just phones!
The colour of the insect is very similar to the lichen on the trees (hence the mention above).
Someone suggested it was a 'grizzled mantid' Gonatista grisea (Fabricius), but we didn't think they are found native to Kenya - and likewise, we don't see a protuberance on the back of grizzled mantids... Still hoping for an answer.
You can see it also has very small wings, which I hear is a feature of some mantids - micropterous mantids.
I don’t know anything about these - someone said ‘some sort of bark mantis’.
Further update - The pronotum of Tarachodes spp females has two conical tubercles. The males are mostly fully winged, whereas the females often have shortened wings.
So it's probably a female Tarachodes species found in Kenya (or thereabouts).

I don't have time at the moment for a full answer, but Patel, S., Singh, G. and Singh, R., 2016. A checklist of global distribution of Liturgusidae and Thespidae (Mantodea: Dictyoptera). Journal of Entomology and Zoology Studies, 4(6), pp.793-803. might be a helpful resource here.

Actually, the above might be less useful since it looks like some taxonomic reorganization occurred in 2015. I'd recommend exploring Epaphroditidae

@theforestecologist - thanks! I went and checked the references you gave, but supplied photos of those species all looked like mantises, whereas this one doesn’t so much!

It's indeed nearly the same as a gonatista grisea family Liturgousinae / Liturgusa, perhaps you can msg a mantid forum.

@aliental, until yesterday I didn’t know there were so many mantids, let alone forae that specialised in them!!

I'm converting my numerous comments into an "answer" -- I don't currently know the exact species, but I can at least explain some of my thoughts more completely.
Your specimen looks a lot like Gonatista grisea, a tree mantis that mimics a lichen -- as you mention in your post. However, G. grisea, is native to the southeastern USA. I could find no evidence of any reports finding this species in Africa, so we will rule it out.
If we examine some other species of the Gonatista genus (e.g., G. jaiba, G. major, G. phryganoides, and G. reticulata) we find that they are all neotropical and not found in Africa. Therefore, let's look elsewhere.
So, I would recommend examining other close members in the same family that are found in Africa.

I originally recommended reviewing Patel et al (2016) because they provide a checklist of the global distribution of other members of the Liturgusidae family. Using this guide, we could examine known African genera.

They list Dactylopteryx, Majanga (Madagascar), Theopompella, and Zouza as African genera.

However, I had not realized that there had been some taxonomic rearrangements, and Gonatista is now in the family Epaphroditidae.

The other genus in the same subfamily as Gonotista, Gonatistella, is monotypic, and G. nigropicta is not your species.

The other genera in this family, Epaphrodita and Callimantis, (as well as the now-moved genus Brancsikia) also do not seem to contain any species I could find that are morphologically similar to yours.

So maybe we should look elsewhere in the previous Liturgusidae...

Subtribe Humbertiellina in the Gonypetidae  family are just one example of another group perhaps worth investigating because it too was once contained within the original Liturgusidae family along with Gonatista and because some online evidence suggests some members of this subtribe (e.g., Humbertiella and Theopompa) share some similar physical characteristics to Gonatista.

Some non-reputable sources (e.g., here for Humbertiella and here and here for Theopompa servillei) show specimens similar to yours with labels as one of these two genera. I couldn't find consistent imagery or reputable sources with imagery to support either one as correct...
(Also, Patel et al. (2016) suggest these genera are recognized as Asian genera, and so they may be geographically unlikely anyway like Gonatista).

However, perhaps trying to solve your unknown specimen using taxonomic and trait-similarity approaches could be misleading.

According to Rivera (2010): "Whereas the monophyly of Mantodea is well supported, the evolutionary relationships within the order are still contentious. Several classification systems for mantids have been proposed...However, the natural affinities among supraspecific taxa have been extremely difficult to discern due to the highly variable and derived morphology of these insects."

According to Schwarz & Roy (2019): "As already noticed by previous authors, external morphology is highly homoplastic and does not provide useful systematic tools above subfamily level."

Schwarz & Roy (2019) do suggest that the morphology of male external genitalia may be useful for relating individuals as these traits tend to be fairly congruent with more recent molecular phylogenies. You could start there for further research.

(I myself can't discern meaningful detail of the genitalia in your photos, nor am I any type of expert on mantises, so this route of inquiry might be too much in the weeds for me...)

If you find a good key for your region, you might want to check out Brannoch et al (2017) for a "Manual of praying mantis morphology, nomenclature, and practices" to help you with all the mantid jargon. [it appears to be a very thorough and excellent resource!].
I will update this post if I find anything more definitive for you...

Citations
 Brannoch, S.K., Wieland, F., Rivera, J., Klass, K.D., Béthoux, O. and Svenson, G.J., 2017. Manual of praying mantis morphology, nomenclature, and practices (Insecta, Mantodea). ZooKeys, (696), p.1.
 Patel, S., Singh, G. and Singh, R., 2016. A checklist of global distribution of Liturgusidae and Thespidae (Mantodea: Dictyoptera). Journal of Entomology and Zoology Studies, 4(6), pp.793-803.
 Rivera, J., 2010. A historical review of praying mantid taxonomy and systematics in the Neotropical Region: State of knowledge and recent advances (Insecta: Mantodea). Zootaxa, 2638(1), pp.44-64.
 Schwarz, C.J. and Roy, R., 2019, March. The systematics of Mantodea revisited: an updated classification incorporating multiple data sources (Insecta: Dictyoptera). In Annales de la Société entomologique de France (NS) (Vol. 55, No. 2, pp. 101-196). Taylor & Francis.

Looks like a Bark Mantis. Genus Tarachodes.
https://www.inaturalist.org/taxa/570572-Tarachodes
Here is a description of the features within the Genus from the link above and why I believe your picture reflects this genus. To narrow down to species appears more challenging as there are many species in the genus:

The bark mantises and ground mantises (genus Tarachodes) are praying mantids now placed in the family Eremiaphilidae[1] that are native to the Afrotropics. They are generally light brown but more silvery on the wings. The wings are attractively reticulated, and the veins may be mottled dark and pale.[2] The head is wider than the pronotum, which is rounded anteriorly, and doesn't overlap with the rear of the head. The pronotum is depressed, with its sides more or less parallel, and only a weak supra-coxal bulge is present.[3] The anterior tibia are flattened and greatly expanded longitudinally, and the tibial claw does not fit into a pit between the 1st and 2nd external spines of the anterior femora, as in a few mantis groups.[3]

You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion and thus inappropriate for this site.

While this link may answer the question, it is better to include the essential parts of the answer here and provide the link for reference.  Link-only answers can become invalid if the linked page changes. - From Review

And also, the link points to an proposed identification. It’s definitely in the same area as the OP (Karen) but I am unsure there has yet been a species ID offered. I am pretty sure it is a mantis of some sort - but that is where my quest ran cold!


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Bug identification: Striped grub/worm, 5mm long, indoor highrise 9th floor, Ottawa, Canada
I've seen two worms like the one below tonight, but none before.  A neighbour with a dog moved in next door 2 days ago, and it is close to our wall that I've seen them.  However, she hasn't seen the bug.  I saw one on the kitchen tile floor and one on the kitchen counter.  I'm in Ottawa, Canada, in a 9th floor apartment of a highrise.  I have no pets.
Not sure if it's relevant, but it also got very cold in the last 2 days (negative teens in terms of celsius) -- never seen these grubs in previous years when it got this cold.  It's mid-December.  The grub is about 5mm long.

Does this look similar? https://biology.stackexchange.com/q/74209/16866

It might be, but I have a bit of doubt.  It's not as big (5mm vs.  18mm).  The answer in the page you cited hypothesize a dermestid carpet beetle, which seems hairier and plumper.

The larvae size information is spotty, but sizes seem varied, so the above 5mm vs. 8mm discrepancy might not mean anything.  The stripes of a dermistid beetle seem to be due in part to its segments of its body, and my bug was too small to see this, but the stripes seemed to be due to actual colour.  But if that's what it is, I'm not liking what I find about dealing with it, nor about what it can eat.

I offered the carpet beetle as an option b/c your image isn't very clear. However, after reading your description and comments with less tired eyes, I can see that even lacking a clearer image that the carpet beetle larvae is probably not the most likely candidate. Let me ask you these: did you notice any "projections" from either end of the specimen? Or does the thicker end have a broadened body segment (i.e., one that is "thicker" than the others?) Are there any type of leg-like appendages anywhere along the length? Lastly, notice any flying insects in your home lately?

Thanks for reconsidering.  I can't answer the questions beyond what I can discern from the photo because the photo is actually better than what I could see with my bare eyes (which aren't great).  So even though it may not mean much, I didn't notice any hair-like projections at the ends, and the photo shows one end thicker than the other.  I did not see any legs, and there have been no flying insects in my home.  It's beginning to look like it might not be a dermestid beetle, which I appreciate.


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Uranium based blood
Here's a hypothetical planet with complex, sapient life and a very weak magnetic field. Could they have Uranium-based blood, much as our blood is based on iron and crab's is based on copper? Deinococcus radiodurans can resist radiation extremely well. Could this hypothetical life do the same? Or would their blood accidentally cause nuclear fission?

Why specifically uranium?

This is an opinion-based question because it is asking about a hypothetical situation. From the [help/dont-ask], avoid asking subjective questions where […] you are asking an open-ended, hypothetical question: “What if ______ happened?” We expect answers to be based on verifiable facts and references, along with subject-related expertise. You may be able to get answers at [worldbuilding.se], but please read through their help center first.

Robert, if you adjust and move this question to WorldBuilding StackExchange (read their guidelines first), perhaps you may have more suitable answers to your hypothesis.

I would say it’s very unlikely. There is a difference between tolerating radiation and incorporating unstable isotopes in your organism. In metazoa, the metal ion serves the purpose of binding to another molecule (a ligand, oxygen) which needs to be moved around within the organism. There is no reason why a rare element with an unstable nucleus would be useful for performing that task. A more abundant, easier to manage element would be selected for.
SciFi speculation: I could envision a cellular mechanism able to harvest energy from the nuclear decay of unstable nuclides. On a planet where the material is much more abundant than it was here on earth during the hadean. This is purely speculative.


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Looking for source: Biologic reactions of people saying "no"
Searching for this topic is incredibly tedious because the word "no" is the main point of interest and I always end up on sites saying how "saying no is good for your health" but I am looking for the medical evidence of this claim.
I remember very faintly hearing about measurable physical effects on a person in a situation where this person says the word "no" to something.
There was an experiment where scientists (I suppose neuro-scientists?) were able to measure the effect of saying "no". Colloquially speaking the body was "closing" in a sense that the person went in some unconscious defence mode, stress levels were rising, change in muscle tone were measurable etc.
When I also remember correctly these effects were measurable even without exposing the person to a specific situation. Just saying "no" wholeheartedly triggered those effects.
Did someone hear about this one? I am looking for any clue to get more information on that.
Edit: I add to the excellent hint from Vadim: I am indeed looking for a credible source where experiments were conducted in a controlled manner and not someone sticking electrodes on people in the mall :D. And I also think this experiment would be hard to do right in the first place since you basically would have to deprive the people from any external stimuli which by itself would probably also already cause side effects.

Most of the claims that "saying no is good for one's health" are grounded in psychology. In other words, they are  not experimentally verifiable. Likewise, health here refers not only literally to physical health, but also to psychological health, which in itself is something hard to define.
Surely, in situations of high stress saying "no" can actually result in some measurable responses, in which case it can be studied within the context physiology and neuroscience. However, this would address only a small part of the situationd covered by the original claim - discarding any effects on psychological health as well as long-lasting effects on the physical health.
To summarize: for a scientific study the claim needs to be made more specific, i.e., apply to well-defined situations and responses.
Disclaimer
I feel that a clarification is needed, lest what I wrote above is interpreted as a negative view of psychology.
I am not claiming that all of the psychology is outside of the scientific method, but a big part of it is - at least outside of being possible to study in a laboratory setting. And this is by no means unimportant part, in terms of the role it plays in our society. While words not scientific often carry negative connotation, in practice any scientist should recognize that scientific method has its limitations - many phenomena (psychological, social, economic, etc.) are not sufficiently reproducible and controllable to study experimentally, yet too important to dismiss.

@user1136 I never said all/whole. I added a clarification, lest my answer is misinterpreted.

I think your claims are likely false and certainly misleading. You need to add citations to support your opinions here

@theforestecologist Could you provide a more detailed comment? The two claims that I make are a) there seems to be no proper scientific research on the subject and b) any such research should be conducted using proper scientific procedures. Your comment doesn't make much sense to me, and I would appreciate a clarification.

@Vadim sure. Overall, you make a lot of your statements sound definitive, but you don't provide much rationale nor any support for your claims. Examples: Sentence 1: you say "most" ; where is that claim coming from? Can you cite multiple studies or a review? Sentence 2: why aren't they experimentally verifiable? That seems like your opinion without any support. Sentence 3: i'd guess a lot of therapists would disagree. Etc. Also, your disclaimer is appreciated but is also narrow in scope given the immense amount of psychology research that has been done in the last 80+ years


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Where can I find free authoritative images of different species of Lagomorphs?
I would like to make an infographic showcasing the order Lagomorpha (rabbits, hares, and pikas), which contains a dozen genera and about 100 species. I want to include a picture for most species, or, failing that, a picture for each genus. The difficulty is that I'm not at all an expert on these animals -- I just find them cute and I like infographics -- so if I simply google around for pictures of them, I won't be able to verify that a picture labeled "Bunolagus monticularis" is actually a picture of a Bunolagus monticularis specimen, rather than something else.
Photographs would be ideal, but I'm fine with using sketches instead when no photographs are available. It would also be ideal if the images were free to use and in the public domain (or licensed under some version of Creative Commons)
Is there any source for images of species specimens that is generally considered trustworthy? It's fine if it's limited to lagomorphs, but if it also extends to other animals/plants, that's all the better!

Wikipedia is good for this,
The licence is what you want, and many people will have checked the animal ID.
look up the two pika species, and the rest are under
http://en.wikipedia.org/wiki/Leporidae

Good answer. I actually just finished another project like this (an infographic about foxes) using Wikipedia for images, and although I'm also not an expert on foxes, I did sort of have the feeling that it was probably trustworthy. I'll come back and accept this answer in a couple of days if there isn't a better one by then.