text:
Why don't cells double gene expression after S-Phase?
In the cell cycle (G1-S-G2-M), all of the DNA is replicated during the S or Synthesis stage. The cell may then spend some considerable time in the G2 phase before splitting in the M phase. Since there is double the amount of genetic material in the G2 phase, what mechanism if any, prevents the amount of gene expression from also doubling?

When the double strand is duplicated, the old strand (or, in other terms, the template) is methylated : this modification is enough to prevent the bind by the RNApol system and, by so, the transcription.
By methylation, DNA-repair systems are able to detect which is the newer strand, to discover and fix replication errors.
Here you can find additional infos


text:
Why do people dying of immune deficiency diseases appear sick?
Please forgive the obviously silly appearance of this question, and/or of the tenor which may come across as flippant or dismissive of real world suffering. My intention is none of the above.
As a layperson, I have always understood that the expression of our various colds/flus etc, while frequently mis-understood as being caused by the virus, are actually just manifestations of our own immunity fighting same.  In other words, all the snot, and fever and inflammation are not caused *by the virus, they are a reaction *to the virus, as we fight it off.
My question then is why do people with AIDS (or similar immunity destroying affliction) appear sick?  If they have weak or non-existent immune systems, following the above logic, would one expect to see them passing away while looking entirely healthy?

Let me see if I understand you correctly. You are asking why people suffering from AIDS show symptoms of being sick, when the body doesn't formulate any response to the virus?

@Gabriel Fair, yes, that's my question.  What brings on the "sick", given that what we experience as illness (the simptoms) is entirely the effect of our auto-immune response, and not the virus' effects, themselves.

This is arguing semantics. Viruses cause flu symptoms. That they cause them indirectly by way of several body reactions, some of them from the immune system, is just a way of viewing this. All actions and reactions in our body are mediated in some way or other. This doesn’t make them less real or causal.

@Kondrad, I beg to differ. If a person gets shot, it is not semantical to investigate what actually killed them. "The bullet" is a useless answer, though clearly semantically correct; Did they bleed to death? Did some specific organ get destroyed? etc. It is *more useful to say that a person died of blood loss, following a bullet wound. So, similarly, to say "the virus is causing the sickness" is meaningless. The virus is provoking a reaction, but the mucous is being created by the immune response. My question is what symptoms do patients exhibit who have no immune response.

Many of the symptoms of disease are indeed related to inflammation, but inflammation depends heavily (though not solely) on the innate immune response.  Patients with AIDS and some of the other immunodeficiencies lose their adaptive immune response, not their innate response.  Therefore they are capable of mounting an inflammatory response that is not effective in clearing pathogens (because it doesn't have help from the adaptive immune system) but can still cause symptoms.
More importantly, many symptoms of disease are not caused by the inflammatory response, but are related to organ and tissue damage caused by the infection.  A patient with pneumonia may have a reduced inflammatory response but will still have difficulty breathing and signs of reduced oxygen supply simply because the lung tissue has been damaged by the pathogen.

that's a much better answer than the one that had originally been given the green check mark... I'm switching to yours.

@iayork good answer. But i think a citation  or two would be appropriate and appreciated.

They appear sick because they are sick, but with other, opportunistic infections. The "immune deficiency" part of AIDS means that the immune system is not functioning normally and, thus, is unable to protect them. Typical illnesses that are more found more frequently in AIDS patients are pneumocystis pneumonia and Kaposi's sarcoma.

I'm sorry, but that's not really an answer. You don't appear sick because you are sick, you appear sick because as a response to the presence of a virus, the body starts to do all sorts of things which manifest themselves as symptoms. You develop a fever, you produce mucous, you cough, etc.  But people afflicted with immune deficiency wouldn't have such a response, right? That's the nature of their illness. So, what symptoms do patients suffering from such illness exhibit? And why?

@Dr.Dredel: Kaposi's Sarcoma gives cutaneous lesions, Pneumocystis Pneumonia gives fever, tachypnea, and respiratory distress in immunodeficient people.

@nico, So, are you saying that these illnesses have their own (non immune related) symptoms that the patient experiences, and that all the while they are *not coughing and sneezing and all the other stuff we get when we are fighting off a cold?

@Dr.Dredel: Kaposi's sarcoma is a type of cancer, one can get it even without having an HIV infection. What you may be missing is that AIDS patients have a compromised immune system, but they still have an immune system.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What is the tradeoff which makes high altitude training effective?
Intuitively (feel free to tell me if this premise is wrong), the reason humans don't all have maximally strong muscles at all times is that maintaining larger muscles is more expensive. That's why we have to work out to build muscle rather than it being the default.
Why isn't the cardiovascular benefit of high altitude training just the default state of humans? What's the cost of being in that state all the time?

It's a common misconception that evolution drives organisms to perfection. Selection pressure pretty much goes away once an organism is outbreeding its competitors. If you'll forgive the anthropomorphism, nature is searching for "good enough" not perfect.

Your premise is wrong. My muscles are not as developed as those of a manual worker because I have a sedentary occupation. A road digger who works overtime will likely have more highly developed muscles than one who doesn’t. Development of arm and leg muscles will differ with occupation. Use seems to be what determines what percentage of “maximal capacity” is reached. Given the premise of your question is wrong I suggest you withdraw it.

How can a “benefit” be a “state”? Please read what you have written before posting.

You would experience unending High-altitude de-acclimatization syndrome aka, HADAS
symptoms include: headaches, insomnia or excessive somnolence, lower limb edema, diminished reflexes,  memory loss, inadequate fine motor coordination  blood clots, heart attack and stroke
most of this is due to changes in blood chemistry and thickness of the blood which increases blood pressure. It can even lead to direct cellular damage from persistant increased oxygen levels.
https://www.scirp.org/journal/paperinformation?paperid=51517
enter link description here
https://www.sciencedirect.com/science/article/abs/pii/S0006291X24003061

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


text:
How do our muscles get tired?
I know one of the main reason why our muscles get tired is because there is too much lactic acid, but how does this lactic acid negatively affect the action of myosin on actin?

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Would the microgravity "shape-shifting" bacteria effect have anything to do with bacteria growing in a host?
Phys.org's news article Why bacteria 'shapeshift' in space describes a recently published study Phenotypic Changes Exhibited by E. coli Cultured in Space, Zea Luis, Z. et al, 2017, Frontiers in Microbiology 8:1598, doi: 10.3389/fmicb.2017.01598.
The Phys.org article summarizes some of the results:

Because there are no gravity-driven forces in space like buoyancy and sedimentation, the only way the ISS bacteria can ingest nutrients or drugs is through natural diffusion, said Zea. The large decrease of the bacteria cell surface in space also decreases the rate of molecule-cell interaction, which may have implications for more effectively treating astronauts with bacterial infections in space.
The new study also showed the bacterial cell envelope—essentially its cell wall and outer membrane—became thicker, likely protecting the bacteria even more from the antibiotic, said Zea. The E. coli bacteria grown in space also tended to form in clumps, perhaps a defensive maneuver of sorts that may involve a shell of outer cells protecting the inner cells from antibiotics, said Zea.
In addition, some of the E. coli cells also produced outer membrane vesicles—small capsules that form outside the cell walls and act as messengers for cells to communicate with each other, Zea said. When cells with such vesicles reach a critical mass they can sync up to initiate the infection process.
"Both the increase in cell envelope thickness and in the outer membrane vesicles may be indicative of drug resistance mechanisms being activated in the spaceflight samples," said Zea. "And this experiment and others like it give us the opportunity to better understand how bacteria become resistant to antibiotics here on Earth."

I'm wondering how likely the following part of the quote from the corresponding author is to be true: "...which may have implications for more effectively treating astronauts with bacterial infections in space."
If I understand correctly, *ll of the effects related to growing in space that are described seem to be related to growing in a liquid culture medium, not inside a mammalian host. I'm not sure a bacteria which has infected an astronaut or other mammal in space will experience any difference in conditions if the host is in microgravity vs being in normal gravity. The differences seem to be specific to transport mechanisms in the culture medium, and not to any effect of weightlessness on the bacteria themselves.
Am I missing something?

@GerardoFurtado can you consider posting that as an answer so I can see how well others agree with it? I believe there are several transport mechanisms in living organisms that do not exist in a culture medium, from circulation of blood down to intracellular transport. A living mammal is not the same a bottle of liquid.

@GerardoFurtado very well then, this one is for you! Species identification; clusters of big plump red bugs in Taipei


text:
Has network theory been successfully applied to protein expression within a cell?
I saw the following passage in the NPR 13.7 Cosmos & Culture commentary post The Big Idea Behind Big Data.

Using the Internet's first generation of Big Data, researchers like physicist Albert-László Barabási of Northeastern discovered hubs controlling the behavior of all large networks from protein regulation to webpages.
"Nature evolved the metabolic network for cells over 4 billion years," says Barabasi, "but that same architecture emerged in the World Wide Web after just a decade."
Different networks, same laws.

In a complex multicellular organism there is plenty of signaling between cells types and organs, and this can be viewed as a network.
But does network theory also apply to protein regulation within a cell? I should really ask; Has network theory been successfully applied to protein expression within a cell?
I ask this because it seems according to this clickable timeline template that 4 billion years ago, life was single-celled.
edit: There is a single link in the Wikipedia article that points to this paper, but the abstract is over my head, and I'm not sure if this is a one-off attempt, or if network theory is an established method that has useful success in explaining/understanding/predicting protein expression within cells.

Yes, the tools of network theory can be used to analyze protein regulation, etc., within a cell. Lots of work on this, so this isn't an answer, just a pointer in one direction. One approach is to look at protein-protein interactions, etc, and see whether certain "motifs" in the network are more likely to occur in biology than randomly. An intro to some related ideas: Uri Alon, Nature Reviews Genetics 2007: http://www.weizmann.ac.il/mcb/UriAlon/sites/mcb.UriAlon/files/network_motifs_nature_genetics_review.pdf

@AJK OK that review is a great start! I'll give it a read, thanks.

https://biology.stackexchange.com/questions/92318/where-are-there-analyzable-signed-directed-network-datasets

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


text:
Why trust vaccine statistics from the mid-20th century, if ELISA tests were not available and disease diagnoses were completely subjective?
Why trust vaccine statistics from the mid-20th century, if ELISA tests were not available and disease diagnoses were completely subjective? Any answer is helpful. Please let me know.

Diagnoses were not completely subjective; there are myriad assays besides ELISA.

what do you mean by "vaccine statistics" exactly? To me that would denote information about the number of people vaccinated, which would be standard bureaucratic record-keeping. Do you mean statistics on the incidence and/or prevalence of infectious diseases? Or estimates of vaccine efficacy/disease prevention (which would boil down to a comparison of the previous two sets of data)?

Can you please add some more details to your question? Don't simply copy paste the title in the body. Add references, your own research etc to provide background to your question.

Diagnoses were not completely subjective; there are myriad assays besides ELISA.

Not back then.
https://emedicine.medscape.com/article/966220-workup
Although the diagnosis of measles is usually determined from the classic clinical picture (see Clinical), laboratory identification and confirmation of the diagnosis are necessary for the purposes of public health and outbreak control. Laboratory confirmation is achieved by means of serologic testing for immunoglobulin G (IgG) and M (IgM) antibodies, isolation of the virus, and reverse-transcriptase polymerase chain reaction (RT-PCR) evaluation.
None of this existed in 1970.

What about Pasteur though? He determined the first vaccine via observation of resistance to symptoms. Don't his observations count as somewhat objective? https://en.wikipedia.org/wiki/Louis_Pasteur#Immunology_and_vaccination

For measles in particular, Koplik's spots, described in 1896, are a fairly reliable diagnostic indicator.

The fact that we have better, more definitive, assays now does not imply that previous assays or clinical observations were purely subjective.


text:
Why is gastrin not acing paracrine manner primarily, when it acts mainly on cells nearby its release?
Gastrin is released by G cells and stimulates Parietal cells to secrete hydrochloric acid. Why is it not acting in a paracrine fashion instead of endocrine?

Is this question based on the content of a course?

Nope, it is not.

Paracrine signalling would mean not merely that gastrin is signalling the same organ, but that it is signalling nearby cells in the same organ - so that a few parietal cells close by respond, while the others perhaps would ignore the signal because maybe the paracrine signal would be degraded.  While the distinction is not absolute - there are shades of gray in all these things - blood gastrin tests are commonly done and medically relevant ( https://medlineplus.gov/ency/article/003697.htm ).  Because you can look at gastrin level as a whole-body characteristic, it is certainly appropriate to call it an endocrine signal.
Though their role is less emphasized, bear in mind that there are gastrin-producing G cells in the duodenum as well, and gastrin affects other digestive organs.


text:
Do Angiotensin II Receptor Blockers (ARBs) or other factors control the level of ACE2 expression? [coronavirus receptor]
Because ACE2 is used by SARS-NCoV-2 to enter the cell, I am curious what factors determine its expression.  Interestingly, myocardial infarction increases ACE2 expression in the heart in an animal model ( https://www.ncbi.nlm.nih.gov/pubmed/15671045 ).  The paper found no significant effect from ramipril, an ACE inhibitor, but I don't think I can assume ARBs would work the same way.  (I am suspicious they might increase it based on the increase in the product Ang(1-7) level - https://www.nature.com/articles/hr200974 )  Note that soluble sACE2 can bind cells that did not produce it, by an RGD independent association with integrin beta 1.
Anything that influences the amount of ACE2 on cell surfaces is a useful answer.

I should follow up with some things I've found.  As a starting point, the normal expression pattern is available at https://onlinelibrary.wiley.com/doi/pdf/10.1002/path.1570 - note the staining of simple squamous epithelium in the alveoli and the endothelia of blood vessels.  Another paper details a sharp decrease in expression with age in rats, but I don't know if that extends to humans.
For regulation of expression, I was surprised to see that Google Scholar actually provides a very good assortment of search results, easier to work with than PubMed, which were topped by the MI regulation I described in the question.  Additionally https://onlinelibrary.wiley.com/doi/abs/10.1002/path.1670 (yes, that IS a different link) describes ACE2 expression in renal disease but not in normal kidney.  ACE2 expression correlated with proteinuria, but negatively with GFR. https://link.springer.com/article/10.1007/s00125-008-0988-x  There are discordant notes in some other situations: for example, subtotal nephrectomy decreased ACE2 expression in a way that was partially prevented by ramipril. https://portlandpress.com/clinsci/article/118/4/269/68827/Reduction-in-renal-ACE2-expression-in-subtotal
The mRNA and protein are both described in atherosclerotic lesions: https://onlinelibrary.wiley.com/doi/abs/10.1002/path.2357
In the lungs https://jvi.asm.org/content/79/23/14614.short describes a positive correlation with differentiation state in airway epithelium.  The regulation by HIF-1 alpha in hypoxia seems of special importance: https://journals.physiology.org/doi/full/10.1152/ajplung.90415.2008 but it is complicated (both positive and negative).
ACE2 is also expressed at high levels in placenta during pregnancy - at least in rats. https://journals.physiology.org/doi/full/10.1152/ajpregu.90592.2008
Last but not least, pharmacologic data is reviewed at https://link.springer.com/content/pdf/10.1007/s11906-008-0076-0.pdf which describes up-regulation of ACE2 by angiotensin II receptor blockers, ACE blockers, and mineralocorticoid receptor blockers.  This includes the common drugs lisinopril and losartan.  (see also https://onlinelibrary.wiley.com/doi/full/10.1111/jcmm.12573 ) Unfortunately the paper did not report substances inhibiting ACE2 expression.  But https://journals.physiology.org/doi/full/10.1152/ajpheart.00239.2008 reported that high glucose (!) or PKC inhibitors could reduce ACE2 expression.  (but the high glucose was causing kidney injury, which as described above could mean more ACE2...)  The anti-diabetes drug liraglutide increased ACE2: https://academic.oup.com/endo/article/156/10/3559/2422879  To top it all off?  SARS itself decreases ACE2 expression, and this might be part of the process injuring the lungs: https://www.nature.com/articles/nm1267
This is by no means a complete survey, and there is much I don't understand.  The relationship between ACE2 biology and the emerging COVID-19 risk groups seems apparent - as is the urgent need for research to determine which manipulations to ACE2 expression have positive versus negative effects on the prognosis of that disease.
Update: a NEJM podcast today described this biology as 'complicated' link.  It is clearly of interest, but still under investigation.  For example, losartan is presently the subject of two clinical studies news, presumably these ClinicalTrials

Perhaps take a look at the GeneCards record for ACE2 (https://www.genecards.org/cgi-bin/carddisp.pl?gene=ACE2), which contains annotations for regulatory regions (e.g., enhancers and promoters) which contain transcription factor binding sites. TFs could potentially bind to these regions to regulate the expression of this target. ChIP-seq data can help lend experimental support.

Thanks for the suggestion - I found a link there to https://europepmc.org/article/MED/15151696 which shows an increase in HUMAN heart conditions.  The transcription factor sites, well... it's hard to be sure what is meaningful.  It seems very easy to start chasing daydreams.  MITF is in monocyte-derived lineages, and macrophages produce ACE2, so ...?  But it seems like that site is everywhere.

A lot of pathways may be redundant or constitutive. I'm not sure if a deeper dive into papers related to knock-out or knock-down mutants related to ACE2 regulation (or upstream) may help? http://regulatorynetworks.com may be of interest.

It might be useful to know about the physiological role of ACE2 and its product Angiotensin (1-/). If 1 to 7 is good for you, why not over-express. Also, I wonder about some general theory on "over-expression of hormone receptors".

Over-expression of ACE2 in case of ACE inhibition has been found: Carlos M Ferrario et al.,  Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2, https://pubmed.ncbi.nlm.nih.gov/15897343/
These findings seem to be confirmed by findings that vice versa,  in the opposite situation  of high levels of AngiotensinII  downregulation of ACE2 occurs:
Deshotels MR, Xia H, Sriramula S, Lazartigues E, Filipeanu CM: Angiotensin-II mediates angiotensin converting enzyme type 2 internalization and degradation through an Angiotensin-II type I receptor-dependent mechanism. Hypertension 2014; 64: 1368–75 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231883/
Two studies, however,  apparently did not find any down- or upregulation, which is in line with the reference you cited:

Ramchand J, Patel SK,  et al., Elevated plasma angiotensin converting enzyme 2 activity is an independent predictor of major adverse cardiac events in patients with obstructive coronary artery disease. Plos One 2018; 13: e0198144
Walters TE, Kalman JM, et al., Angiotensin converting enzyme 2 activity and human atrial fibrillation (...) Europace 2017; 19 (8): 1280–7

As your question seems to be unsettled here is my individual opinion:
The feedback circle you suggest makes sense as a mechanism of  upregulation (more product leads to more production). Why not have more input if output can be made and has been generated in larger and larger amounts? However, there also is "demand or no demand" down the cascade. A large amount of product that accumulates  thus may signal a lack of its being needed - I'd cast my vote for down-regulation of the expression of input receptors, as I'd vote for "we have enough". So contrary to your answering your question I'd suggest a high amount of product Angotensin (1-7) might cause a down-, not upregulation of ACE2.
Over-expression of receptors, to my knowledge, explains drug addiction and getting used to medication.
If in surplus of ligand hormone (in that case Angiotensin II) all receptors are "filled", it makes sense to  broaden the basis and up regulate expression of ACE2. Thus,   a block of ACE (not ACE2!) by ace-inhibitors would not lead to overexpression which seems coherent with the results of  the study on blood pressure medication you cited.
Interestingly, there is an alternative pathway of ligand transformation, and an alternative product of ACE2, it's Angiotensin (1-9). It think it is a possibility that those ACE2 cells do  over-express that are engaged in the modification of AT 1-9, not AT II, as ACE-inhibitors ("beta blockers" in German) do not address or inhibit renin production which should remain elevated. Renin becomes Angiotensin I, the alternative ligand of ACE2. However, downward that alternativ pathway, it's ACE again that transforms, and its being inhibited dampens "demand".

Your post starts out by seeming to answer the OPs question including a relevant reference. I was prepared to say good job and upvote at that point. However, you then continue with text that appears to be speculative if not entirely fictional and stop including references. Are you trying to rescue your initial speculation by tacking on something like a real answer at the beginning? No matter how much you love your ideas this isn't the place for them. (Also note that "beta blockers" is not German.) Please take the [tour] and read through the [help] starting with [Answer] and [edit] accordingly.

By " your post starts out by seeming..." you refer to my edited newer version (yes, I see, 5 hours ago). So, yes indeed, no misleading as introduction. It's intension to be polite, I remember deleting "contrary" to what you suggest and refere in your answer. So without saying I think reputabel references that come to diverging conclusions that are just the opposite of each other should give the right here and now to speak up with an opinion that is frankly declared as such. Feel free to down vote. You clearly say that this is not the place for my "ideas"?

To lyersome: Also note that "Betablocker" is German, yes, it is. Are you German, too? (By the way, I can tell you you wouldn't want to say "betablockers" with an s if you want the plural.

To lyersome, again: are you offended by my clumsy use of English when I said "Here is my own personal answering"? Sorry for that, it sure aint etzetera. What I find annoying that I feel peer reviewed without peer or editor taking up on verifying if indeed there are divergent studies (which I - it's up to you as administrator of this place I happily admit to you - think is a legitimate basis to offer one's own thought. Are you serious: this is not the place for my own ideas?

To lyersome: I have revised according to your criticism as far as I could get me. Even this I "Write to the best of your ability" :-). Citation meant to be some proof of me having read your recommended help page on how to write a good answer. There, I could not find anything in favour of your point that answers should not contain any own ideads (what's more, if they are clearely declared as personal knowing, it seems just the contrary, it surely is and should be encouraged - the more if there really is no or diveregent authority!)


text:
What are the obstacles to a quick survey of statin usage in COVID-19 patients?
A recent preprint paints a grim picture of the effect of role of obesity in COVID-19 infection.  A high role of C-reactive protein (CRP) is specifically indicated as a risk for critical illness.
It is possible to reduce the level of CRP by statin administration, but statin administration raises the level of ACE2.  It is not known whether that increases or decreases the risk from the virus.  The use of statins for coronavirus patients has been suggested - so has the possibility of the discontinuation of statin use by infected patients.
Obviously I would hope to see a study of statin use in COVID-infected patients, and one does begin recruiting this month.  The entry, however, says that it will be completed in August 2021.  My thought is that surely somebody could run around the New York COVID wards with a clipboard, though I'd hope for a wiser way to do this, asking patients whether they use statins versus whether they have ever turned down the suggestion of taking statins when their doctor mooted the issue, and seeing how many of which group ended up in the ICU.  What are the factors preventing data like this, which could have such influence on the way people respond to the outbreak, from being collected and published within a couple of weeks?

Because this is not the way a clinical trial is done. If you are not blinding the patients/doctors you at least want to randomize the patients into treatment groups, otherwise you will possible severely skew the data you get out. Or select already much sicker patients for your "study" in one of the arms which will either affect the outcome or mask small effects of a drug.

I’m voting to close this question because this is a suggestion for a clinical trial of a drug, not a question about biology in the terms of SE Biology.

The problem with your setup is that by targeting an ICU ward you are already narrowing your study to those who developed severe COVID-19. A more robust design would be a retrospective cohort study, where the exposure of interest has already been recorded.
E.g. the UK Biobank (~500,000 participants) has recently incorporated SARS-CoV-2 test results into its dataset, so you could use this to:

create a case/control split based on exposure (i.e. patients' historic use of statins)*
study the effect this has on outcome (i.e. development of severe COVID-19)

In  this  study,  we implemented rapid dynamic linkage, which allows us to provide a regular feed of new COVID-19 (SARS-CoV-2) test results to UK Biobank to facilitate rapid and urgent research into the epidemiological and human genetic risk factors for severe infection in the cohort.

Dynamic linkage of COVID-19 test results between Public Health England’s Second Generation Surveillance System and UK Biobank, Microbial Genomics (2020) **

* Or any of the other thousands of variables recorded in UKB.
** Disclaimer: I have worked on this project.


text:
Are there COVID-19 citizen science projects to compare habits and outcomes?
I've seen some "citizen science" projects for coronavirus that are not really collaborations, but simply requests for processing time.  Are there any "real" projects where people who have gotten their diagnoses could go, chat with one another, volunteer to publicly disclose their virus status, test results such as O2 perfusion, and daily self-rating of symptoms, and agree on group surveys to profile what they eat and other activities they do?
I would like to see ordinary people work together toward answers to basic questions.  For example:
a) does salt intake affect symptoms?  [re: blood pressure]
b) does drinking coffee affect symptoms? [re: type II diabetes risk]
c) does exercise affect symptoms? [re: HIFs]
d) do dietary supplements such as flax, curry, and elderberry affect symptoms?
e) does the overall intake of calories, or ratio of carbohydrates/protein/fat, affect symptoms?
Of course, trying to correlate actions by a patient with immediate self-reported changes in symptoms is fraught, as is a comparison of subsequent hospitalization or death between groups of online survey respondents.  Yet such disorder on an informal basis is where ideas often come from, and citizen science might mark out candidate factors for formal validation by professionals.  Is there anything like this going on?

I think you are looking for a very specific design of 'citizen' projects. But, if we relax a bit your criteria, there are some examples. Here, and here, for instance. One worth discussing, I think, is what Google has done for mobility tracking. Yes, the users did not 'opt-in' the study, but in essence, they provided the data!


text:
Why roots have radial vascular bundles while stems have conjoint?
Why not the whole plant has the same arrangement of vascular bundle,  why there is a difference of arrangement in roots and stems (radial in root and conjoint in stem) ,  what is the purpose of this difference?


text:
How do memory cells(B-cells) encounter pathogens?
From what I understand, once the infection is handled, some of the B cells capable of producing the correct antigens are stored for the long-term in the lymph nodes.
They will start multiplying again upon encountering the pathogen again.
What I don't understand is how can these cells, that should be in relatively small numbers, can effectively encounter the pathogen ? Do all pathogens travel to the lymph nodes? Do the memory B cells travel out and encounter pathogens?

Great Question.
Location:
Memory B cells are highly abundant in the human spleen, and they make up 45% of the total B cell population in this organ. There is evidence to indicate that human memory B cells might mostly reside in the spleen, and some memory B cells recirculate in the blood [1].
Activation:
Memory B cells circulate throughout the body in a quiescent state until specific antigen is re-encountered and triggers a potent secondary immune response [2].T cell help is a strict requirement for the reactivation of memory B cells that are specific for monomeric protein antigens [3].
Sources:

Hauser, Anja E., and Uta E. Höpken. "B cell localization and migration in health and disease." Molecular Biology of B Cells (Second Edition). 2015. 187-214.
Firestein, Gary S., et al. Kelley's Textbook of Rheumatology E-Book. Elsevier Health Sciences, 2012.
Janeway, Charles A., et al. "Immunobiology: the immune system in health and disease." (2005).


text:
Why are "itch signals" transmitted so slowly from the skin to the human brain?
In the second half of the BBC radio (and podcast) program Cats and Itch;
Discovery, The Curious Cases of Rutherford and Fry Episode 2 of 5 the phenomenon and origin of the "itch" and related sensations are discussed, with input from several specialists, including "Neuroscientist Prof Francis McGlone from Liverpool John Moores University and dermatologist Dr Brian Kim from the Center for the Study of Itch at Washington University. Yes, that is a real place."
Here is an unofficial transcription of a small segment starting at about 17:30:

Until quite recently, the same nerve fibers were thought to transport feelings of both pain and itch, from the skin to the brain. In 1997, a ground-breaking discovery revealed that itch has its own separate nerves responsible for that oh-so-familliar itchy-scratchy sensation. Now, if you accidentally lean on your “hot”, the sensation will travel through your fast pain fibers at 80 miles per hour; you can almost-instantly pull your hand away.
By contrast though, itchy signals crawl towards your brain at a sluggish 2 miles per hour, so once you’ve been bitten, it takes a while for the itching to begin.

Those quoted speeds equate to about 130 m/s and only 3.2 m/s, respectively.
What causes the "itch" fibers to transmit signals to the brain so slowly? Is there thought to be some evolutionary benefit to such slow conduction, considering that the speed of most signals from skin to brain are transmitted so much faster?

@uhoh - I am flattered! Great question btw +1

@AliceD I've orphaned your comment through clean-up, but indeed this site has great moderation; a key ingredient for a successful SE site.

Cleaning up is great. Thanks for your words. Mods often get virtually yelled at. Some appreciation to balance the scales is warmly welcomed.

What causes the "itch" fibers to transmit signals to the brain so slowly? Is there thought to be some evolutionary benefit to such slow conduction, considering that the speed of most signals from skin to brain are transmitted so much faster?

The interview most likely refers to the findings of Schmelz et al., J. Neuroscience, 1997: Specific C-receptors for itch in human skin
In essence they found tested the sensitivity of unmyelinated nerve fibers (note: myelination also increases transmission speed) towards distinct stimuli. They found that some of those fibers would selectively respond to stimuli which would be perceived as itching (such as histamines). They find that:

This slow conduction velocities attributable to small axon diameters ...

Note that since they don't need to, they also don't speculate on the physiological reason, why itching should be processed by slower fibers (and some potential explanations will be recognized quite well by readers of their article).
Please also note that the original claim, from 1997, however has been softened with the years, and there appears no strict separation been stimuli like "hot", and itching, in terms of distinct fibers and transmission speeds; e.g.: Davidson et Giesler, Trends in Neuroscience, 2011: The multiple pathways for itch and their interaction with pain

Great! Thanks for the references, I'll give them a read.

OK I've looked at these references. While I can't quite say I've read them thoroughly because I don't have the background to take it all in, I've learned more about the diversity of nerve fibers, and also that in contrast to what I'd thought before, some nerve fibers do not require a myelin sheath. Thanks for your help!

From a biologist background, one consideration: a distinction between itching and other sorts of pain would be that itching usually signals to our body that we have some prolonged inflammation or stimulation, whereas our reaction to strong heat or cold should be immediate. To avoid us having to sense itching all the time (which would be uncomfortable and distracting), it would seem likely that small or temporary signals must be filtered out. By having a slow transmission this may be achievable as spreading out a signal over time can ensure that only strong and prolonged signals are registered.


text:
What does "dissection-based microscopy" mean as described here, and how can it give genetic information?
The Phys.org article 'DNA microscopy' offers entirely new way to image cells references the new Open Access paper in Cell DNA Microscopy: Optics-free Spatio-genetic Imaging by a Stand-Alone Chemical Reaction.
My question is not about DNA microscopy, but instead about the second kind of microscopy mentioned in the explanation below quoted from the Phys.org article

Until now, microscopy fit into two main categories. The first is based on optics; light microscopy, for example, dates back to the 1600s and relies on visible light to illuminate samples. Scientists have riffed on this approach, even going beyond the visible spectrum. Electron microscopes, fluorescence microscopes, light-sheet microscopes ¬- they're all based on the principle that samples emit photons or electrons, and the microscope detects the emission.
The second category is based on dissecting samples at locations defined by a microscope. Computer programs then stitch together each dissected piece into a complete picture of the intact sample. Optical imaging can offer intricate portraits of subcellular structure and action. Dissection-based microscopy can give scientists genetic information.

I don't really understand exactly what is being referenced by the 2nd paragraph. What is "Dissection-based microscopy" and how can it give genetic information?
The passage seems to repeat a few sentences in the introduction to the Cell paper:

These approaches closely mirror the two ways in which microscopic images have been acquired to date: either (1) detecting electromagnetic radiation (e.g., photons or electrons) that has interacted with or been emitted by a sample, or (2) interrogating known locations by physical contact or ablation (e.g., dissection).

This may shed some light on the question for those more familliar with the techniques discussed, but I still don't understand what technique this is really referring to.
See also NY Times' DNA Microscope Sees ‘Through the Eyes of the Cell’

I guess it refers to optical mapping (https://en.wikipedia.org/wiki/Optical_mapping). However, the text is a little bit confusing, so I am not 100% sure.

@FabioMarroni Okay, I will have a look in the morning. Thanks!


text:
Is there recent info about the hypothetical ancient two-codon genetic code?
Here is the latest I have found. link
This is the basic idea: Evolution does not look ahead and make plans. It would not create a system of mRNA with giant ribosomes to create proteins, until proteins were already useful. There must have been a simpler way to create useful proteins before, that got complexified after it was already useful.
Since enzymes can be made of RNA, presumably early life made just RNA enzymes and no proteins. It didn't matter whether RNA enzymes were as efficient as modern ones because protein competition hadn't evolved yet.
And since we now make peptides off an RNA template, probably early proteins were also made off an RNA template. It is hypothesized that particular amino acids would be attracted to particular RNA pairs, and they would be put in just the position that would help them link to neighboring amino acids. This could be slow and inefficient compared to modern protein production because again the competition was not stiff back then.
Between two pairs of coding bases, the RNA needed a noncoding base for spacing. Possibly the noncoding base might be particularly good for catalyzing the joining of amino acids.
The system did not have to use the same amino acids we use today. It could use amino acids that were good at attaching to RNA, and later after the system got changed around the modern list of 22 amino acids could have developed.
There are various ways this is a satisfying idea. For example, the machinery to make proteins is largely made of RNA. The mRNA carries the message. tRNAs decode the message. Ribosomes are giant machines which transcribe proteins efficiently, and they are largely made of RNA with a lot of little proteins that help them hold their shape etc. Presumably the first protein-building machinery was itself built entirely from RNA -- because that's what was there to build with -- and over time evolution found ways to improve that machine with protein scaffolding.
This 2005 paper link describes a reasonably plausible way it could have been once. They imagine a few alternate amino acids which might have once been part of the genetic code -- ornithine. Homoserine. 2,4-diaminobutyrate. They imagine ways that the crevices between pairs of bases could be like the binding sites of enzymes. They fit the ideas together.
Have there been advances since 2005?

I doubt it, and I doubt whether you'll find anyone here who is even familiar with the idea. However I suggest you try to answer your own question yourself by looking for papers that cite the 2005 paper.  The online PNAS site may have this, otherwise I am sure that there are tools for doing so.

@David I don't think your comments are fair or constructive. They don't help improve this valid and interesting question. The paper has been cited 75 times so it seems like research continued after 2005. The question seems like it was written after J Thomas put effort into getting an answer.

@Michael_A — On the contrary, my remarks were absolutely constructive. I told the poster how to get an answer to his question, assuming that my subjective view of the likelihood of his getting an answer here was correct. (A view based on my experience of responses to questions on protein synthesis.) You confirm that this approach will bear fruit. The poster may well have tried to get an answer, but had been adopting wrong approaches. As an educationalist on this list I try to help people to learn how to learn, rather than spoon-feeding them. (In this case I have no spoon.)

I don't find this advice insulting, and it is of course a valid approach.
I wanted to ask the question first because if someone is following the topic, they may point to great research that many of us would like to know about. While I would like to eventually study all of the literature since 2005, there is no harm in getting tips about important links.
And second, I thought that some people who are unfamiliar with the topic might like to hear about it.


text:
How do plants absorb CO2?
I see many repeated claims that plants absorb $CO_2$ from the air.
$CO_2$ goes into the stomata, while $H_2O$ evaporates and leaves those same stomata. The $CO_2$ dissolves in the water in the plant sap, and then goes to wherever it's needed.
It occurred to me that in loose moist topsoil, there is a tremendous surface area for $CO_2$ to leave air and get into the water. And that water does get absorbed by plant roots. Meanwhile there is plentiful O2 that soil bacteria can use to oxidize organic matter in the soil and convert it to $CO_2$. In my imagination, this looks like a far more efficient way to collect $CO_2$. Instead of wait for the $CO_2$ from decaying organic matter to diffuse out of the soil into the air above and then enter stomata and dissolve in water there, cut out the diffusion step. The rising sap would carry $CO_2$ to wherever it will be used.
It seems to me this would be easy to test. Grow plants in sealed containers with their stems sticking through small holes in an impervious barrier. Introduce $CO_2$ containing $C_{14}$ either into the air above with the leaves, or into the air below with the soil the roots are in. Observe which way gets more $CO_2$ incorporated into the plants.
Have experiments like this been done? My quick search did not find experiments like that. It found only the many-times-repeated claim that plants absorb $CO_2$ through their stomata.

Carrying CO2 "in the sap" is not that easy of a step, especially compared to simple diffusion: as plants do not significantly decrease the local CO2 level, diffusion is basically a free pump insuring constant CO2 concentration. Furthermore, while CO2 does dissolve into the water, its concentration is rather low naturally. (Natural fluids that transport CO2 in large quantities, such as blood, have enzyme like carbonic anhydridase to create bicarbonate for mass transport; which soil water won't have.). Also, it maybe possible to disprove this theory by just cutting a leave and using the c14.

You see many repeated statements (not claims) that plants absorb CO2 from the air through the stomata of their leaves. For example, you can read an account of this in Lodish et al., Molecualr Cell Biology. This is because the phenomena has been studied by numerous professional scientists for over 50 years. Your question shows a lack of the research required before posting on this list. If you had done that you might have discovered that typical experiments use (rootless) leaves and manipulate the CO2 concentration. I have voted to close.

Thank you for the link. This link shows that plants absorb CO2 in the mesophyll, from the air space. Water from the xylem evaporates into this space and leaves through stomata; this drives the movement of water from the roots. O2 created by plants also leaves through stomata. It does not show that the CO2 comes only through stomata and not with the water. Using rootless leaves would prevent roots from collecting CO2, though. Still, normal photosynthesis with no root and only normal CO2 air levels would plausibly say that CO2 from air is enough.

Eliane B, thank you for responding. I think that since CO2 level in soil air can reach as high as 8% during wheat cultivation, it seems plausible to me that plants might find a way to sequester that resource rather than just let it diffuse into the outer air and then concentrate it again from there. And that probably happens. https://www.nature.com/articles/415451a

For most terrestrial plants, assimilation of soil inorganic carbon seems to be quite low. This may be because RuBisCO, the carbon assimilating enzyme, is generally more of a limiting factor than CO2 diffusion.
Ford et al. (2007) found that "soil DIC [dissolved inorganic carbon] contributed ~0.8% to whole-plant C gain, and ~1.6% to belowground C gain" in seedlings of Pinus taeda exposed to 13C-labeled soil DIC. Ubierna et al. (2009) observed no contamination in leaf CO2 efflux by 13C-enriched soil watering of large conifers, despite showing that the water was taken up by the trees. However, Bloemen et al. (2012) did observe assimilation of labeled carbon directly infused into the stems of poplar trees.
Some aquatic plants in certain habitats may be adapted to assimilate much more carbon via their roots.
Plant physiology is a rich and mature field, and isotope analyses are a primary tool with a long history. Additionally, CO2 and other gas exchange can be directly measured across leaf surfaces.
The carbon flux between the soil and the rhizosphere is complex and bi-directional, but overall, more carbon is generally lost through the roots than absorbed.
There are also dozens, or probably hundreds, of studies labeling leaves or above-ground material in various ways and tracking the fate of those elements, of which this is just one.

Thank you! I'm an amateur at this and my quick lit searches didn't find this.

The water in the plant absorbs Co2 from the air, Co2 dissolved in water equals H2CO3 carbonic acid, but carbonic acid is an extremely weak acid since it does not ionize sufficiently to produce a very high hydrogen-ion concentration. Glucose production from Co2 & pure H2O requires an electron to be in two places at the same time, absorbing light energy by this electron, de-crystalizes some of the electron working-mass that is responsible for rearranging Co2 & H2O into the crystaline C6H12O6-glucose molecule. The process of photosynthesis is one of "particle-flow" within a plant molecule and molecular bulk-flow within that same plant is a process of respiration. Respiration must also have a working-mass as well, H2O is one of the primary open-loop vehicles and light is the other primary open-loop vehicle that drives the closed-looped function of a plant. Being the difference between the interference of particle-flow in an inertial frame of reference, and the interference of the acceleration & de-acceleration of bulk-flow in a non-inertial frame of reference. Photosynthesis has similar characteristics as a alternating current transformer, they both are frequency dependent and use electrons to drive the machinery that absorbs & transforms Co2 with other molecules.

Welcome to Biology.SE. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. ——— Answers should directly and clearly address the original question — yours is very hard to follow (try adding some formatting and make sure you read the entire question). Answers are also much more likely to receive a favorable response when they include supporting references (primary literature is best). Without that support, answers are indistinguishable from opinion and thus are inappropriate for this site.

@user62753, one way the CO2 diffuses into stomata and inside the leaf the exposed water dissolves CO2 which is then converted to something else that's easier stored. The other way, CO2 would diffuse into water adsorbed onto soil particles and then be taken in by roots where it would be converted into the same transport molecules. It makes sense to me it would happen both ways. The CO2 concentration in the upper air is 0.04%, while the CO2 concentration in the air near roots can reach 8%. My claim is testable, it has been tested, and it is true.

Thanks to David's comment above, I learned enough vocabulary to do a better lit search.
Yes, $CO_2$ supplied to roots is absorbed and distributed by the xylem to places where it is photosynthesized. This is not in doubt.
The remaining question is how much of the $CO_2$ used by plants comes through stomata from the outside air (where it is present in concentration around 0.04%), and how much of it comes to roots from subsurface air (where it is present in concentration that varies widely, up to 8%).


text:
Why does a cell need siRNA?
My question is about small non-coding RNAs. miRNA and siRNA are both known for mRNA regulation. miRNA can both transcriptionally inhibit and degrade mRNA by cutting it. For inhibition just a small fragment (seed) of miRNA is complementary to the mRNA while for degradation miRNA and mRNA must reach 100% match.
siRNA is almost the same molecule and its only function is to 100% match mRNA and degrade it.
So if siRNA appears to be just a subtype of miRNA, can we confirm that? Or are there any other differences that make these two molecules different kinds of small non-coding RNAs?

So if siRNA appears to be just a subtype of miRNA, can we confirm
  that? Or are there any other differences that make these two molecules
  different kinds of small non-coding RNAs?

siRNA and miRNA are not identical, but similar. It's not incorrect to consider them similar phenomena in biology, but history places them apart and there exist small differences. Both are processed inside the cell by the enzyme Dicer and incorporated into the RISC complex where their target is degraded ("RNA interference"). However, there are important differences, in case you want to be absolutely correct.
siRNA is typically exogenous (introduced from outside by viruses or by engineering). It typically has 100% complimentary to its target mRNA, because we want to reduce off-target binding. If designed well, they target only the intended target and are checked to be incompatible with any other potential mRNA targets, i.e. are designed to be specific.
miRNA is endogenous (occurs naturally within cells) and is single stranded in vivo. Its complimentary is not always 100% perfect, and often has multiple targets. This is the major difference between the two. It pairs with its target mRNA imperfectly; it simply inhibits translation (protein production from the mRNA). In rare cases where it's a perfect match, it causes the cleavage and destruction of the target mRNA just like siRNA. If I remember correctly, plants miRNAs, in contrast to animal miRNAs, usually have perfect complementarity with their targets. miRNAs are also derived from shorter stemloop RNA products than siRNA.
As you probably know, both are non-coding RNAs and do not enter ribosomes for translation. They have similar effects on gene expression. If you are interested in the very first reports of either kinds of RNA, here goes:
miRNAs discovered in 1993 in worms.
siRNAs discovered in 1999 in plants.
Notice the phrase antisense RNA in both titles. Interesting!
Further reading, in case you are interested.

Why does a cell need siRNA?

This is a very different question. Why? Probably to fine-tune the expression of its genes. Small RNA species can accumulate, aggregate, and regulate mRNA levels in ways that are probably not possible inside the nucleus at the DNA transcription level. Small RNAs are also understood to be epigenetic and function in the cytoplasm and endoplasmic reticulum!

Perhaps you would want to add a note on endogenous siRNAs and shRNAs. Also, siRNA, as we know it in the context of RNAi, was discovered in C.elegans (1998) (Fire & Mello got Nobel for it). It doesn't matter much anyway and I don't want to debate on who did it first :P


text:
How does blood react to heat when inside the body
I was wondering:
What are the possible dangers of being burned on the surface of the skin.
Does it congeal (that's what my intuition tells me)? At which temperature would that happen? How heat-conductive is human flesh?
On the other hand, there's of course been many cases of severely burned people who did obviously not die afterwards.
This question comes from an argument i had the other day, when a friend burned himself by accident and we got into talking about what was actually happening with the affected blood (i.e. at the wrists, neck etc) and if it is dangerous (if you could actually die from an occasion where you burned yourself and then get a stroke or something)


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

insects come to mind.

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

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


text:
What can I see with a microscope at what magnifications?
I'm 26 and where I grew up the schools were complete crap so I've never really used a microscope much or learned much about them. And I want to learn some science and look at some microscopic things, like organisms in water, how tiny  bugs or dirt looks up close, blood cells, and whatever else there will be to discover.
So my questions are about magnification  and what I will be able to see at various magnifications. How much magnification would I need to get a detailed look at tiny insects like a gnat or tiny aphid? Or to see microscopic organisms in water, or our blood cells, or the fibres in my microfiber glasses cleaner. And If i was looking at stuff like blood cells, or food, would i be able to see anything like viruses or diseases? (And as an extra question, any good books for self learning about microscopic organisms like that?)  I was looking on amazon and found 500x max up to 2500x max, and would like to be able to see living microscopic organisms if possible.

Decide what you want to do; A  2X to 40X binocular is fine for insects and other stuff . But things like blood cells require serious microscopes. And magnification is a small part of defining the characteristics of a microscope .

My own experience, as a complete amateur who just bought one for curiousity's sake, is that anything over 400-500X is like doing your daily commute in a car with a 500 HP engine.  All that extra power is just going to waste.
20-40X is good for looking at insects (if you can get them to hold still :-)), feathers, and various materials.  200-400X gets you to microorganisms like protozoans in pond water, blood cells (which are pretty uninteresting, IMHO) or plant cells.  I have never tried to look for bacteria, and I don't think there's any hope of seeing viruses with a light microscope.
Another thing I've discovered is that if you wear contacts, or have floaters in your eyes, you're going to have a good bit of trouble distinguishing what's on the slide from what's inside your eyes.  I think one of the USB cameras might help: I haven't tried one yet, but it's on the wish list,

You'll be able to see something that is 1 micrometer as a slightly formed (meaning you can decide whether it's more oblong ore more round) dot. So any structure that is bigger than that can be better observed. Unfortunately, viruses are far smaller, and many interesting cel organelles are too.

Also, many things (like parts of cells) are not visible until they are stained. There are many stains that are suitable for beginners (others are quite toxic or teratogenic). I'd recommend buying a book from 1970 or before (no re-issue), because many stains and chemicals are nowadays deemed too dangerous (although they are not that dangerous if used in amateur-microscopy volumes) and normal light microscopy technique has not changed since then.
With a used microscope from a reputable manufacturer (inquire beforehand whether the tubes are of a standard size so you can get replacement oculars etc.) you are on a good way. Schools and universities will sometimes purge their stock, which is where you can make incredible deals.
Get a microscope with mains-fed light, ideally LED. Some 'tricks' like Dunkelfeld are very interesting to use, but require a good light source and non-broken iris.
Also look at the table, it should have a smooth, no-hysteresis (meaning if you go left, and then right, there should be no 'slack' to take up before the picture moves the other way) x/y platform, ideally with a measure attached.
Total magnification is ocular*objective, and many microscopes offer the possibility to attach a camera, either additionally or as replacement ocular. that is a great thing, as you can take pictures and zoom in (real magnification will not change, but still, some things are easier to see that way) or later tweak the colors or contrast.
Depending on whether you mainly want to look at things that can be put between two glass slides (cells, bacteria, small parts of insects, ...) or at 3D things (insects, flowers, minerals) you can either buy a two-ocular microscope or binocular (3D) or a one-ocular microscope.
Objectives and oculars are small tubes with many lenses built into them - this means humidity and even rot can slip between those, so be sure to check used material (especially from learning institutions) for clear pictures.

I recommend no more than 40 X in a macro binocular, zoom or turret . Nikon is a good name that makes some inexpensive lines. For about $ 500 you could get a good one with light source. I have used over a hundred optical devices ( not counting birding binoculars). From 2 X hand glass to mega X scanning electron microscopes. Over 3,000 hours looking through microscopes in my 40 yr career. What you may not have considered is that for every hour on a microscope , a technician spent about 4 hours cutting , mounting, polishing and etching a metallurgical sample. Prep is just as necessary for biological samples, cutting, slide prep, staining and stuff I don't know. This expensive preparation is required for about anything viewed at 50 X and more, and maybe for lower X. Light sources also become much more expensive as you get to 50 X. So stay below 50 X to start. Or get a job in some sort of lab .


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

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

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

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

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

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


text:
Does cell compartments and cells shell have the same meaning?
I encountered these two words today. Do they mean the same thing? Does a cell shell and cell compartments refer to a cell that has been emptied of its DNA?


text:
which of these fields will cure aging?
life extension is expected to happen as a result of breakthroughs in tissue rejuvenation, stem cells, regenerative medicine, molecular repair, gene therapy, pharmaceuticals, and organ replacement. Which among the seven fields is more likely to achieve that goal in the foreseeable future?

I'm voting to close this question as opinion based. It's an interesting question for discussion, but doesn't fit the SE model.

Not even opinion based, as any answer would require a crystal ball :-)

If we knew that, then we'd just emphasize research in that area, and reduce the effort in the other areas. Qualified opinions in the matter differ, and in the end they could all be wrong!

I think the structure of this question could be less opinion based as De Novo stated above. But a recent article published by mayo clinic will help shed light on the question. Falls under the category of regenerative medicine I believe.
Senolytics Article
EDIT:
 Since links are apparently a taboo, here is the paper. Educational on current research and methods on an 'aging cure'.
Xu, Ming, et al. "Senolytics improve physical function and increase lifespan in old age." Nature medicine (2018): 1.

We frown upon link-only answers at StackExchange as a whole and here at Bio specifically because they are likely to degrade over time and not exist anymore, making your answer meaningless. However, I would also consider whether this question should be answered at all, since fortune telling is not all that scientific.


text:
A synthetic sieve organ known as kliver?
in this video at 5:28, the narrator talks about a "vat-grown all-purpose sieve organ" called Kliver that would do away with both liver and kidney transplant. But i don't seem to find online resources about the same. Is that terminology popular in scientific literature, and if so, how would synthetic biology accomplish that? articles about the same will also be appreciated.

This term is used in this book (Synthetic Biology, The National Academies Keck Futures Initiative, p.43). This book is a summary of several interdisciplinary team discussions during a  conference held in 2009.
One...

[...] team considered building artificial organs. Engineered to be hypoallergenic, these could allow for a mass production of personalized organs. Their novel and broad functions could also be useful for medical testing. In a single artificial organ, one might screen potential drugs for both toxicity and permeability.
For instance, group members proposed the idea of a "kliver", a kidney-liver hybrid. An independent "kliver" could help filter bio-compounds out of drinking water.

There are some more paragraphs revolving around the question how to build a "kliver" and a final paragraph concluding that enough necessary building blocks were available and researchers could start working on it:

Potential building blocks might be mammalian and microbial cells and their products, such as slime, fibers, small molecules and proteins. The cells might be engineered to hold new electrical, mechanical, and chemical powers.
  [...]
  Cells would be programmed to degrade their organs and DNA if they began to invade other organisms or the environment. A genetic "kill switch" aims to stop contamination or infection.

Summarising this, I wouldn't call it a "popular term".

PS: to share some Google-fu: the book popped up when searching  for "kliver kidney liver"

How would synthetic biology accomplish this?

We already have a synthetic kidney. We've had it for over 50 years. It prolongs life, but still not very well. Transplant, with all its challenges and complications, does much better.
The liver is much more complicated, and I would be very suspicious of anyone who thinks of it as primarily a sieve or detoxifying organ being able to build a synthetic liver. It certainly does some of those things, but it does much more, playing an important role in digestion, metabolism, protein synthesis, excretion, and the immune system. See Cecil Medicine Ch. 148 for an overview.   There's a reason we don't yet have a synthetic bridge to transplant for liver failure. I wouldn't rule it out, but I think you'd need to be able to build a synthetic liver before you could build a synthetic kliver.


text:
what are some examples of how evolution's limitations prevented species from climbing to the absolute highest peak on the fitness scale?
In this answer, the author argued that plants are green instead of red or any other color because of some  limitations of the evolutionary process. what are other examples in which the physical and functional characteristics of an organism were a direct result of limitations of evolution?

What does "absolute highest peak on the fitness scale" mean? There really is no such thing, unless perhaps you think of a biological grey goo sort of scenario.

The "limitations" of evolution is somewhat subjective, but a couple of the important ones include random mutation, "greediness" (chasing short-term advantage), and environment.
Evolution is a complex process by which mutations occur which either 1) benefit an organism, increasing reproductive success or 2) harm the organism, decreasing reproductive success, or 3) cause no noticeable change. Over time, these collected mutations bring about significant phenotypic changes. There's no goal or underlying purpose, though. In your example of plants, chlorophyll could certainly have evolved a structure that absorbed light in different wavelengths, but they ended up doing just fine with their current absorption spectrum.
Another example is the difference between the vertebrate eye vs the octopus eye. For mammalian eyes, the optic nerve covers part of the retina. This is commonly known as the "blind spot", and has obvious negative consequences. For Cephalopods, on the other hand, the optic nerve is located behind the retina, so they have no blind spot.
Both of these examples are the result of random mutations coinciding with ideal (or non-ideal) environmental situations. The author of the post you cited is accurate to say that evolution is not an engineer, working towards a goal. The only goal of evolution is "What maintains life?" It's merely millennia of trial and error, and occasionally calamities occur, causing extinctions and loss of genetic potential.
I really think ANY characteristic of any species you care to name could be considered a result of evolution's limitations.

The term you are looking for is evolutionary baggage.
An easy example is the crappy color vision in mammals and to a lesser extent primates, for a long time mammals were only small nocturnal insectivorous (or at least that is all that survived),  during this time mammals lost two of the light sensing pigments in cone cells, leaving only two, primates had a strong enough pressure that a mutation creating a new pigment was favored giving use three, however two of them are very close to each other and overlap, and a whole portion of the spectrum is still invisible to us (ultraviolet) but non-mammals can see it. Birds see colors everyday you and I will never see.
Another mammal example is we turned the gene that would let us keep growing new teeth into control genes that give our teeth complex shapes, which was an advantage to our ancestors who were tiny short lived insectivores, but now mammals can't just grow new teeth to replace old ones like everything else can. there is no way to get these genes back without re-evolving them from scratch or giving up genetic controls on tooth shape, the first is simply to unlikely to occur and the second would be too detrimental.


text:
How does a neuron know to which one of the next neurons to pass the signal
Looking into how neural networks are build in the brain, here are a couple of facts followed by some questions:

The neuron receives the signal through its dendrites and passes it to the terminal at the end of the axon.
A neuron can have as much as 1000 connections to other neurons.

As I understand the dendrites can be connected to multiple neurons, so the neuron we are talking about can receive signals from multiple cells.
Now the questions:

The terminals at the axons can be connected to just one or to multiple neurons?
If the axon terminals can be connected to multiple neurons, how does the neuron transmitting the signal knows to which of the further neurons to pass the signal next? Is it passing to all of them at once?
If the axon's terminal can be connected to only one other neuron (for the single axon neurons), how are the two-axon neurons working? How do they know to which axon to pass the signal next?

The neuron that sends the signal does not know which neuron to send the info to. The job of the neurons getting the signal is to identify whether it is their turn to get activated by the signal.
This is controlled by a protein. Depending on how often the neuron is used, a number of channels are formed on the surface of the dendrites. The activation happens at an optimal level of the protein present in the cell depending on the number of channels on the surface.. Each time the cell receives the signal, this some of this protein is created.
First, the neurons with most channels is activated, but if the organism does not get the memory that is wants, the earlier neuron will continue with sending more signals. Then receiving-neuron-number-1 stops activating (because peak concentration has passed) and the next one starts. This continues for all neurons.
In layman's terms, from info-1 to info-2, info-2 is chosen in the order of thoughts most associated with info-1 to least associated.


text:
Is it true that it is mostly impossible, for any kind of antibiotic, to succeed in killing off every bacteria in a very rich environment?
It is commonly believed that the resistance to antibiotics by micro-organisms is truly evolution at work, and that the recent surge in superbugs may very well be attributed to it.
When we refer to a bacteria's ability to "evolve" into resisting this antibiotic, I assume we mean that when we introduce antibiotics into the environment, a lot of bacteria die but some who by mere chance and luck didn't do so and that these lucky bacteria go on to survive and multiply, thus aiding in the creation of so-called superbugs, or rather, bacterial resistance to sophisticated drugs.
This whole situation already suggests to us, or at least to me, that there's much inherent complexity in these organisms and indeed a certain uniqueness to each.
I have, however, been troubled recently by the following question: is it truly impossible, for any kind of wholly new antibiotic which was not used before (no matter how complex), to succeed in killing off every single bacteria in any rich habitat/environment (no matter how populous)? And that there'll always be some bacteria on whom this shall not work apparently due to uniqueness in something of their structure?

If I am not completely wrong, any kind of single agent drug (this is also true for targeted therapies in cancers for example) eventually leads to resistance. The evolutionary pressure is enormous and you only need one successfull cell.

It is not bacteria surviving by pure luck that leads to resistance.  Rather, they have some variation in their makeup that makes them harder to kill.  They survive, pass this trait on to "offspring", and eventually outnumber the easy to kill variety.

@Chris this will largely be based on how aggressive an antibiotic you use, prolonged immersion in liquid salt will kill all the bacteria but would kill the host as well.

The answer is no. The antibiotic will kill all the bacteria it's intended to target, unless a special resistive variant cell(s) exist. What this means is that it is possible that non-resistive cells are not present.
Also bear in mind that it's not the drug that induces the mutation, rather it just isolates and funnels the randomly generated mutant (if present). Also remember that the vast majority of mutations are deleterious or neutral, so the probability of resistant strains even existing in a population are low. [That doesn't mean they cannot exist at all.]

Yes. It is down to mutations. DNA replication is not 100% accurate, there will be mistakes that are not corrected in the progeny produced.
Antibiotics works like a bit of gunk wedging itself into the machine of a bacteria cell but avoids jamming a human cell due to that very same shape. Gunk that wedges into both human and bacteria machines is just a really bad poison. So that gunk has a very special shape.
Resistance can be acquired by recognizing gunk of that particular shape and removing it (not something easy to evolve but very effective when it does) or just change the shape of the machine so the gunk cannot stick. Usually the altered machine doesn't work as efficiently as it can but in an environment polluted by fouling gunk, it works well enough.
And a rich environment means there are many bacteria.
So if your chances of mutating the right part of the bacteria machine to gain resistance is 1 in million, a rich environment with 10 million cells will have 10 such mutates.
Of course in reality we are talking about trillions (a million million) of bacteria cells per human (actually 39 trillion bacteria per human) and we are talking about billions of humans.  And we are not even counting the number of bacteria in the soil and in farm animals.  And it takes a few years for resistance to evolve.
When you look at the numbers involved , it is very difficult not to imagine resistances evolving. Even if the chances of that happening is 1 in hundred of trillions. It just takes a single bacteria cell to mutate and so gain resistance for it to spread and pass that resistance to other bacteria.


text:
qPCR: Huge variation in fold change of genes between biological replicates
I am trying to validate my RNAseq data by doing qpcr for which I am looking at the fold change of few genes across various timepoints of treatment conditions. I am getting huge amount of variation (in thousand folds ) in my biological replicates. I thought may be it is due to genomic DNA contamination so thats why I repeated all my experiment and did DNase treatment twice but still I am having such variations. I am using two reference genes EF and GAPDH and I also have variations in the Ct values of reference genes across various timepoints. I will really appreciate it if you could suggest me with possible problems and solutions.
Thank you, Ambika

How do your technical replicates look?

To clarify, the variation you're seeing in the qPCR isn't being seen in the RNAseq? Do the values correlate? How was the qPCR data normalized?

How are you aliquoting DNA samples into your reaction mix? You can get alot of error just from errors in the pipette. I fine a ECHO liquid dispenser makes all your troubles go away (provided your can find one somewhere) GAPDH is sensitive to metaoblic state (ie oxgyen and glucose levels.) Are you using column purification of RNA with DNAse treatment?

@RoverEye my technical replicates look good, they don't have such variation.

@CKM I made PCA plot to compare my replicates for my RNAseq data. I had 4 replicates for RNAseq in which there was clustering of  1 and 2 together ; and 3 and 4 together. But that might be due to environmental variation since I did that in different time. In qPCR I am seeing the expression of those genes but the fold expression between biological replicates do not match. They have the same trend though. I am having 1000 folds difference in some genes

@JayCkat Yes I am using column purification of RNA with DNAse treatment.And also both EF and GAPDH have 5 to 6 Ct value difference in between the samples.

@ambika Here are some things I would do: Check the data analysis, make sure everything is in FC or logFC (i.e. make sure one isnt logFC and other is linear FC). Check how data were normalized, and whether reference genes were differentially expressed (look for stable expression or lowest CV reference genes). Also note whether the results correlate, is your R2 good if you plot the two on an x-y/scatter plot? Since the two methods measure differently, it may be more important that the trend is the same rather than the result.

@CKM I normalised the data using DDCT method. I am also thinking if my reference genes are not good enough. Thank for your suggestions.

@ambika Maybe you can use your RNAseq data to find a few genes with stable expression across your samples, to use as references in further experiments.

@CKM can you please suggest how can I categorize genes. Any programs or method?

@ambika How do you mean? Like how to categorize them as reference genes? Or something different?

@CKM Now I am trying to calculate stably expressed genes using the RNAseq data. So far I calculated coefficient of variation of all genes based on count data. Now one thing that I am confused about is the list with least CV from all replicates look different. Do I have to calculate CV integrating all the replicates data?

@ambika Calculate the list of stably expressed genes from all the data together. I like to visualize it as if i were working in excel: Columns are samples, rows are genes. Calculate the CV% in a separate column by row (i.e. by gene), and sort low-to-high and pick the ones with the lowest CV%. Just remember if you use them to normalize to drop them from your analysis set.

@CKM thank you so much. I really appreciate your suggestions..

If you have 1000-fold differences between either your biological samples or RNAseq & qPCR there is very likely a problem with your data normalization (if not you need better samples). Ideally you should always use log2 normalised fold change values (qPCR / ddCT directly gives these, they should be somewhat normally distributed around 0 and represent doubling effects which are often biologically relevant).

Also as others have mentioned GAPDH expression levels can be affected by the metabolic state of the cells, so it's not always a good control/reference. Generally a control for qPCR should have similar expression levels to the genes you want to measure (this might be an issue for you, GAPDH & EF can be very high) and of course be stable between the timepoints or conditions you want to compare.


text:
Identification of beetle: black with orange stripe and 2 orange dots
I found the following beetle in a wooded area in Essen, Belgium. Does anybody know what species it is? Thanks in advance.

Looks very much like Nicrophorus investigator https://www.pinterest.com/pin/815362707508687290/


text:
Does the repellence of an insecticide affect its efficacy (measured in insect mortality)?
I am currently working on assessing the efficacy of a suspected insecticide on a particular species of insect. I happen to be looking into any repellence caused by the substance. I test for both effects at the same time by putting that insect in a no-choice bioassay. To be specific, my assay set-up consists of a petri dish, and the test article treated with the test substance is placed on one side of the petri dish. Insect species X is introduced into the petri dish, and every 24 hours, I get to count and remove the dead ones. All these are repeated for different concentrations of the test substance.
What I found is that mortality (proportion of insect X killed) initially increases with concentration, but then decreases after a particular concentration. I also found that repellence increases with the concentration of the test substance. So, what exactly is happening here? Is the repellence of the test substance having an effect on the mortality, such that repellence is causing a decrease in mortality?

Edit: I forgot to mention that I am not qualitatively measuring the repellence of the test substance. The petri dish, that is the assay, is divided into two halves via an imaginary line, and the test article is placed on one side of the assay. An index, which I call the 'repellence index', is used to measure repellence by dividing the difference of the no. of termites between the two sides of the assay, by the total no. of termites observed. Hope that clarifies my question more.

You have a good hypothesis: the decrease in mortality is mediated by an increase in repellence. It sounds like you have a measurement of increased repellence, and it's a plausible mechanism (if an insect isn't near an insecticide, it can't be killed by that insecticide). Now you should test it.
If you are measuring repellence using a different assay (e.g., a choice assay, where the insect can enter a chamber with the insecticide vs. one without), than you could use as the denominator insects that enter the chamber with the insecticide. Compare mortality of insects that enter the chamber with insecticide changes with increasing concentrations in this assay with the mortality in your no choice assay.

Edit: I forgot to mention that I am not qualitatively measuring the repellence of the test substance. The petri dish, that is the assay, is divided into two halves via an imaginary line, and the test article is placed on one side of the assay. An index, which I call the 'repellence index', is used to measure repellence by dividing the difference of the no. of termites between the two sides of the assay, by the total no. of termites observed. Hope that clarifies my question more.

@user43591 since you are quantitatively measuring the repellence, than you can quantitatively measure the mortality of exposed (vs. non-exposed) as suggested in my answer. There is, of course, more to it, but your next step would be to use the data you already have to look at mortality in the termites on the side with the test article only and see what the curve looks like there. Depending on the result, this should give more or less support to your hypothesis that the decrease in mortality above a certain concentration is due to repellence.

Whoa thanks man, never thought of that! Thank you very much!

@user43591 you're welcome! If I answered your question, feel free to mark it the answer using the checkmark to the left of it see someone answers


text:
Can we send signals to nerve?
I want to know two things.

Can we send a signal to a nerve using external source like electricity?
Can we differentiate signals sent from receptors like pain receptors, pressure receptors etc.

Yes, almost no matter what you mean.
The trivial answer is yes, if we record from them. But I'm guessing that's not what you mean.
Please clarify your question.
You may benefit from browsing related questions such as this one:
https://biology.stackexchange.com/questions/52842

Yes. One of many examples would be transcranial magnetic stimulation (TMS).
Often, yes. I work with Drosophila (fruit flies), and we can differentiate between the electrical activity of sensory neurons, even those that innervate the same structure (e.g. sensillum) based on the amplitudes in the recorded electrophysiological signal. Neurons usually fire within a certain narrow range in terms of amplitude and that's one of many ways to differentiate between different neurons, or determine how many different neurons are found in the region where you are poking your recording electrode. Of course, if two neurons fire at the same amplitude, you would not be able to tell them apart using this electrophysiological method.


text:
Is it possible to directly uploaded controlled imagery into a person's conscience?
I was wondering, is it possible to use electrical charges and/or EM waves to induce imagery directly into a person's mind?
I got this idea because since almost everybody dreams, and dreams are images created by the brain, i wondered if it was possible for an outside source to forcibly make someone see a different image without harming them.

In principle there's no reason why we shouldn't be able to do so. In practice, we do not seem to be anywhere near able to do so.
We are barely able to decode natural images from fMRI information, and before you can hope to induce imagery you should usually first be able to decode it.

This answer isn't all that different from answering a question like "Is it possible to travel faster than the speed of light?" with "In principle there's no reason why we shouldn't be able to do so" ...when physics kind of gets in the way it gets quite messy.

Except we already know that brains can be stimulated in the right ways so why would it not be possible by stimulating the appropriate regions directly?

I just think you are underselling the distance between current capabilities and what is necessary.


text:
Mushroom Identificaton(USA)
I need help identifying a perculiar species of mushroom found in my yard today. Color is orange-yellow, around 3-4 inches total radius, its a cluster of tiny to medium mushrooms. They were found near an oak tree. Location is southern Georgia, USa.

These could be specimens of Omphalotus Illudens based on the orange/yellow color, the time of the year, their association with decaying wood (an oak in this case) and your location (eastern North America)
You can read more about these species in this reference: Messiah College

I did some research on Omphalotus Illudens (Jack-o-lanterns) and found that they were bioluminescent. The mushrooms i found are not. Is there a possibility that there is a subspecies of Illundens that are not bioluminescent?

You are right about the claimed bioluminescent properties, however this phenomena is not always happening. Apparently some people that study these mushrooms sometimes have to wait hours in the dark to be able to see the glowing and some even say the bioluminescent claims are completely false ( like this reference: mushroom expert ). I unfortunately lack the expertise to say for sure if they are bioluminescent or not.

MikeKatz45, I had cut down a tree about a month ah go, about a foot away from the clusters location. I noticed that the post said "Occurrence on wood substrate: or on the ground from decaying underground roots; ". This somewhat fits in with this type since of the location and the surroundings. Could it be possible that it might actually be it?


text:
Mushroom Identification (USA)
I would like some help identifying this mushroom I found in my yard.
Location: Southeast Georgia
Near Pine trees after heavy rainfall
Color: Light brown to Dark Red, biggest is about 4 inches in radius

It is some type of boletus. You would need a spore print and a few more examples to decide which one. They are commonly found under conifers.The books say most are editable and good taste. The couple kind I have eaten had no flavor , not worth collecting. The tubes instead of gills on the bottom of the cap are an indicator of boletus group.

I agree it looks like a bolete, but your post needs to provide citations to support your claims and should ideally give a more direct answer as yoru answer currently is conjectural and not actually answering the OP's question. Please do some additional research and [edit] your post with more info. Thanks!


text:
Palaeontology and Palaeobotany
Could someone please clarify the roles and differences between palaeontology and palaeobotany. My textbook says the palaeobotanists study plant and animal fossils, but other sources say that this is incorrect.
Thanks

Paleontology is the main scientific branch, which study fossils and prehistoric times.

Paleozoology studies the fossils and biology of prehistoric animals.
Paleobotany studies fossils and biology of prehistoric plants.
Paleobiology studies the biology of prehistoric organisms.
Paleoecology studies the prehistoric ecological systems and ecology.

In fact, putting the prefix "paleo-" turns every scientific branch of biology to a branch concentrating on this subject but in prehistoric times.

For the most part a Paleontologist will be willing to study whatever their fossil site produces. Which is why many scientists who are really "paleozoologists" just call themselves paleontologists.


text:
White resin or powder on conifer needles
I often notice that certain conifers often have a whitish powder on what seems to be their youngest needles, giving them a blue green tint. Does anyone know what this is? Is it something excreted by the trees themselves, is it a yeast or some other endophytic microorganism? Very curious and unfortunately I don't have a microscope.

I believe this is actually crystallized sap which formed on and around the bud as the bud opened up and new leafs emerged.
Note that some coniferous trees have a powdery coating as part of the leaf itself, continuing on throughout the life of the leaf. Blue spruce is a good example of this, as its dark green needles appear blue/gray due to a waxy coating the needles. This wax can be easily scraped off the leaf.

Thanks for your answer! In the case of blue spruce, does the powder diminish overtime, for example on shaded needles that receive less sunlight?

Great question @DezmondGoff. I can confirm that conifers with powdery or waxy needles will have patches with significantly more or less coating, but I don't know what the causes of that are (whether it's time, sunlight, types of leaf).


text:
Etymology of eccentric/concentric contractions
I was wondering if anyone knew why the terms eccentric and concentric were chosen to refer to lengthening and shortening muscle contractions?
The basic etymology of the words are to do with alignment with the centre of something. Eccentric is derived from the Greek for "off centre" and is also commonly used in bio-mechanics, another branch of sports science, to refer to a force applied out of alignment with an object's centre of gravity. I couldn't see how this definition applied to a lengthening muscle contraction, and haven't been able to find any information on why the terms were chosen.
I'd appreciate any help.

Try a Google search for a video demonstrating sarcomere contraction.

Are you suggesting it's just to do with the direction the z-lines are moving relative to the m-lines? ie. eccentric would mean 'away from centre' as in away from the m-line, therefore lengthening?


text:
Does night mode on iPhone really help?
Okay so I know that night mode is supposed to filter out blue light that is bad for the eyes, but is it really more helpful than annoying? At night I do use it when I’m on the phone but it doesn’t make sense to keep it on during the day when it’s bright outside does it?

Helpful for what?

To protect your eyes from high energy light waves?

Different colors mean different wave lenght and energy, as displayed in the picture.
Using Planck's theory, the shorter the wave is, the more energy it carries.
On day light, all these wave lenghts are present, including UV from sun. With no sun-light, your eyes aren't hit by those, so there's no need of using higher energy waves (that's exactly how night mode on iPhone works, using only lower energy waves).


text:
Is it possible to prove that a hand sanitizer can kill 100% of a person's germs?
We have a project for Economics, and we need to advertise something that consumers will be willing to buy. My group thought of "improved" hand sanitizer. So, instead of it killing 99.9% germs, we would make it kill 100% germs. Although, we are having a hard time trying to prove that our hand sanitizer can, but we can't change what our product is anymore, since we only have a couple more weeks until we pass the commercial.
Can anyone help us? Thank you in advance.

Its been found that women have more varieties of bacteria because the wash more and men have higher quantities

I.e. women have morevspecies due to hygiene, men have more quantity. If you use alcohil, there still will be 1 or 2 of every 1000/5000 alive.

Related: https://biology.stackexchange.com/questions/61059/why-dont-antiseptic-agents-kill-100-germs

There's no realistic way to prove that your hand sanitizer can kill 100% of a person's germs. In fact there's probably no realistic hand sanitizer that can do that. The reason is that there are just so many germs. There are billions of germs on your hands. To compare, there were only a few hundred thousand people in Hiroshima when it was hit by the atomic bomb in 1945, and even that did not reach 100% fatality.
It's because it's hard to kill all germs that antibiotic resistance is a problem.

First part of the answer isn't correct at all. You could do metagenomics analysis to say if there's presence of bacteria (or other organism) into your hand sample.

@Shred not an expert on that so if you write that as an answer I'll delete this one.

As others have pointed out, you can't claim your sanitizer kills 100% of whatever, because it just isn't true. However, you could claim, "Product X kills nearly 100% of bacteria." Many readers will key in on "100%" and gloss over "nearly." Advertisers do this all the time.Another alternative is to do an experiment that has an extremely small bacteria population, apply the hand sanitizer then claim 100% effectiveness. And yet another, is to conduct several experiments with different bacterial strains, find one result where 100% of the population was killed, and then make your 100% effectiveness claim. The FDA will probably come down on you hard, but my then you've probably made more than enough profit to cover the fines.

Alternatively, you could adapt your claim to state that "sanitizer X kills 100% of bacterium Y"

As pointed by Allure, there's no way to say that a chemical agent is 100% efficient against all kind of microrganism . That's because of high rate of mutations by these, and a strong evolutionary pressure made by the use of this hand sanitizier.
To do an example: you'll make the first traitment using the hand sanitizier, and a rate of 99,9% will be killed. The remaining 0,01% will proliferate because of the ability to live and division under the hand sanitizier traitment. Consider that SDS is often used into detergent, and some strain of bacteria are capable to make the compound totally ineffective.