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Does avoiding medication that alleviates symptoms shorten the length of a cold?
People use over the counter (OTC) medications to relieve symptoms of the common cold.
However, these symptoms are part of the immune response, right? They are driven by the body responding to the virus and attempting to make the body less habitable and thus easier to kill it off.
Do OTC medications that reduce cold symptoms cause the cold to persist longer? Should such medications be avoided if the goal is to reduce cold duration rather than symptoms?

It is plausible but by no means established that antipyretics (fever suppressors) in particular could increase the duration of infection/symptoms, because fever is part of a functional immune response.
From Graham et al 1990 (a small [n=56] randomized trial of the use of antipyretic pain relievers in volunteers experimentally infected with rhinovirus):

Use of aspirin and acetaminophen was associated with suppression of serum neutralizing antibody response (P less than .05 vs. placebo) and increased nasal symptoms and signs (P less than .05 vs. placebo) ... There were no significant differences in viral shedding among the four groups, but a trend toward longer duration of virus shedding was observed in the aspirin and acetaminophen groups.

In other words, it looked like the people who took aspirin or acetaminophen had weaker immune responses and more cold symptoms. They might have been infectious for slightly longer, but it's hard to tell (also, duration of infectiousness is not the same as the duration of symptoms ...)
However, a review (Kim et al 2013) concluded that NSAIDs (non-steroidal anti-inflammatory drugs) slightly (but non-significantly) reduced the duration of illness.

In a pooled analysis, NSAIDs did not significantly reduce the total symptom score (SMD -0.40, 95% CI -1.03 to 0.24, three studies, random-effects model), or duration of colds ([mean difference] -0.23 [days], 95% CI -1.75 to 1.29, two studies, random-effects model) [emphasis added]

Here is the figure from that analysis:

In medical terms "common cold" means rhinovirus (and possibly coronavirus) infection, but when laypeople might use it to include mild influenza infections (i.e. "I had a cold last week [runny nose, cough, mild fever ...]"). An observational study on influenza A and two other infections (Graham et al 2000) found

There was a striking correlation between antipyretic therapy and duration of illness in subjects infected with influenza A and S. sonnei, but not R. rickettsii ... Multivariate analysis suggested that antipyretic therapy prolonged illness in subjects infected with influenza A, but its use was the result of prolonged illness in those infected with S. sonnei.

In other words, to the extent that one can really distinguish causality in an observational study, it seemed that taking antipyretics made influenza illness longer, but that causality went in the other direction for S. sonnei (i.e., people took more antipyretics when they were sick for longer).
The usual caveats associated with small studies and researcher degrees of freedom apply when interpreting the results of these studies ...

J Infect Dis. 1990 Dec;162(6):1277-82
Adverse effects of aspirin, acetaminophen, and ibuprofen on immune function, viral shedding, and clinical status in rhinovirus-infected volunteers.
Pharmacotherapy 2000 (20), 1417–1422.
(doi:10.1592/phco.20.19.1417.34865)  Effect of antipyretic
therapy on the duration of illness in experimental
influenza A, Shigella sonnei, and Rickettsia rickettsii
infections.
Cochrane Database Syst Rev. 2013 Jun 4;(6):CD006362. doi: 10.1002/14651858.CD006362.pub3.
Non-steroidal anti-inflammatory drugs for the common cold. Kim SY, Chang YJ, Cho HM, Hwang YW, Moon YS.

The Graham trial is still cited relatively often, but it should be mentioned that pooled analysis including Graham shows benefit for pain related symptoms, and no harm or benefit for others (including duration). Graham is also rated as moderate risk of bias. The balance of the evidence for this question (does symptom treatment increase duration of illness) is no, probably not.

Kudos on a supported answer. My only nit-pick is that Influenza (let alone the other two) is definitely not the common cold (and, no, what's true for one virus isn't necessarily true for another.) But +1 for an otherwise nice answer.

both of these comments are good points, I will revise when I get a chance.

@anongoodnurse no virus is the common cold, but influenza infection causes the common cold in 25-30% of cases. The issue with the second reference isn't the fact that it looked at influenza A

@DeNovo - We both know what we're talking about, and what we mean. Let's not quibble like this. Influenza may cause symptoms similar to the common cold, but let's be professional here and assume the OP is talking about infections with rhinoviruses, not strep, H flu, influenza, allergies, or any other etiologies that may present like rhinovirus infections at some point.

@anongoodnurse i don't mean to quibble, but we apparently have a very different opinion of what the common cold is. Though rhinovirus is the most common single cause, half or more of common colds are caused by other viruses, the second most common cause is an influenza infection that doesn't spread beyond the upper respiratory epithelia. The third is coronavirus.

@DeNovo - I understand that it's meant to be a simple question. You're complicating it. That's all I'm saying.

The common cold as a clinical syndrome is not any particular viral infection, but a cluster of symptoms that follow a stereotypical course. It's generally associated with an initial viral infection and you can isolate infectious particles early in the course of the illness, but by the time most people go to the doctor there is no active infection. Because of this, care for a common cold is directed at the symptoms. You could even say (and I do) that the common cold is the symptoms, not the infection.
The development and resolution of many common cold symptoms are unrelated to direct infection. Cough, for example, when associated with the common cold, is not due to infection directly, but reactive inflammation, and is one of the symptoms that lingers the longest. Treatment limiting postnasal drip and, in patients with reactive airway disease, any associated asthma flare up can shorten the length of the illness.
So, no, treating the symptoms in the case of the common cold is not a bad idea, and does not cause the disease to last longer. It may even shorten the disease course.
You can see some of these principles discussed in these clinical practice guidelines  and in this review of the pathogenesis of one of the viruses most often associated with the common cold syndrome.
The general principles in this answer are discussed in Cecil Medicine Ch. 369 and Bennett Prinicples and Practice of Infectious Disease Ch 58. If you're interested in the common cold, I highly recommend reading both of these chapters. Though they were from now dated earlier editions, these chapters really helped me get a grasp on how to approach clinical syndromes in infectious disease when I was starting out.
Note:
See the comments below for valid criticisms of this answer. While the common cold is simple in many ways, good evidence on this syndrome is not simple or common. Host -pathogen interactions are variable at best, and there are thousands of viral serotypes that cause the common cold (many of which cause other illnesses too). My answer here is a synthesis of treatment recommendations and a clinical approach. As @anongoodnurse says, this is probably not a good way to answer a layperson rather than a serious student of human biology via clinical medicine. The summary is pretty simple. If you use medicine that is safe to make someone with a cold feel better, you've taken care of that person's cold.  If you don't have the access or background knowledge to digest Cecil and Bennett, believing this requires you to take an anonymous internet typist's word for it. Because of that, it may not be a good SE answer.

Your links have nothing to do with the OP's question, really, except for "postinfectious". My take on the OP's question is, e.g., "if the first sign of the common cold is a runny nose, does taking a decongestant make the illness last longer?" I don't think this answer addresses that.

@anongoodnurse the key references are the chapters in Cecil and Bennett. I grant that this was mostly a frame challenge. The correct approach is treating the symptoms because the symptoms are the syndrome, not the virus.

@anongoodnurse the reason for the frame challenge is that this is a somewhat common question and an important teaching point. The answer is not a list of meta-analyses of the numerous and varied cold remedies. It's an understanding that treating the symptoms is treating the cold.

You're not teaching med students here, and Cecil is not readily available. Recommending it for a layperson asking a simple question is... I dunno, overkill? Unreasonable? I mean, it's a medical textbook, meant for people training or trained in medicine. I still believe you're off-track with this answer. I'll propose a clarification: Is the virus completely gone once the nose starts running? If it is, that should be made clear. If it's not, that should be addressed with a proper answer.

Lets take this to chat


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Lac Operon and Arabinose Operon
In the lower concentration of glucose, what among lactose and arabinose, when both are present in the growth medium, is more likely to be utilized by E. coli?

It's been done.
Both are expressed.
I remember reading about lactose as a special case. The lac operon is not induced directly by lactose, but a different enzyme present in small concentration converts lactose to allolactose, and the allolactose induces the lac operon.
I vaguely remember reading an explanation, that at low lactose concentrations a fraction of cells would randomly get enough lactose to convert to allolactose to induce the lac operon. Then those cells would transport lactose. This would reduce the lactose concentration in the medium so that other cells would not start using lactose. A fraction of the population would use it up, while the rest concentrated on other energy sources. It would be less efficient for the whole population to gear up to use lactose and then use it up fast.
I don't remember where I saw that story and I don't know whether it's been refuted.

source: Stack Exchange

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Has Epipremnum aureum lost its ability to reproduce sexually?
In this recent question the shy flowering nature of Epipremnum aureum (Golden Pothos) was discussed:
Where can I find a picture of the inflorescence of Epipremnum aureum (golden pothos)?
To summarize: (1) The two first and only observations of the plant flowering date back to the 60s and (2) genetic analysis yields a potential explanation for why the plant is so rarely flowering
Question: Is this sufficient evidence to conclude that E. aureum has lost its ability to reproduce sexually?
(Triggering thought: It is very unlikely that two specimens flower simultaneously, at a distance from each other that allows pollination, that pollination actually takes place and that the seeds germinate and successfully grow into new plants)

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Confirmation for a picidea
I am sorting some pictures and found this one taken from Swiss Jura Mountains (North part, alt ~700m) in March 2013.

The day before I saw a Dendrocopos major (Great spotted woodpecker) and without looking thoroughly before I though it would be a young one.
Now when I examine in more details the picture it seems to be a Dendrocopos medius (Middle spotted woodpecker).
Am I right? Can someone confirm this?

You are right, this must be a Middle spotted woodpecker Dendrocopos medius. It has clear stripes on its belly, and the black stripe on its cheek does not reach the beak. The beak is also  smaller, but size is always hard to judge.


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Appropriateness of PCA to visualize clusters in genetic data
In many genetic studies, PCA is often utilized to examine genetic cluster in human populations. Rarely is the % variance reported for the components. With human data it's been my experience that the first three components (which are often plotted) tend to contain very little % of the variance. How meaningful are your visual results (i.e. clustering) when the first three components cumulatively account for only (say) 10% of the variance?
To answer this question, I constructed a theory based on the following assumptions.
One theory. For human, the proportion of variation within groups (i.e. same ethnic group) account for ~85% of the genetic variation within individuals. Conversely, the variation within populations (i.e. continental scale) account for only ~15% of the genetic variation within individuals.
Even though the first three components (i.e. PC1, PC2, PC3) contained only a small fraction of the total variance, most often the magnitude of associated eigenvalues can be 50 to 70 times that of higher components. In other words, the first three components can explain substantially more (50x-70x) variance than any other component when comparing by individual basis.
While sometimes these higher components do explain hidden substructure within groups, bear in mind that individuals from the same group has ~85% genetic variation among themselves. Hence, most of the higher components might just be explaining this within groups variation. For analysis of genetic clusters, this is of no interest to geneticists. These higher components can thus be treated as background noises. Geneticists are mainly interested in variation within populations, which often is very ancient and strongly separated. Thus, when population clusters are formed in the first three components, it can be argued that they form mainly due to the variation within populations.
Summary: The low variance (<10%) cumulatively accounted by the first three components can be justified by the fact that variation within populations is only ~15% of the genetic variation within individuals.
My question is: Does the theory to my own question seem reasonable?

I'm sure you agree this is a question about statistics, not biology. Geneticists use statistics, but many of us are not experts and often require recurring reminders from statisticians on how best to interpret, analyze and visualize data, preserving both clarity and validity. I agree; the principal components should always account for as large amount of variation in the data as possible, otherwise it would make little sense - at least in my limited understanding of it. I defer to others on this question!


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What dictates which protein to synthesize at a given time?
I understand how DNA is replicated and how it directs the synthesis of proteins from amino acids through RNA polymerase, RNA and ribosomes. Now I want to understand how it works in the big picture.
With my current level of understanding, any protein can be synthesized at any time at any rate, but it looks to chaotic to work at all.
What dictates which protein to synthesize at a given time?

Regulation of gene expression and protein synthesis occur on multiple levels, and together these levels allow for fine control of when, and to what extent genes are active. It would be impossible to give a comprehensive answer for such a broad question. Here is a starter, beginning with the most important fact:
DNA is used as a template to make messenger RNA, which is exported out of the nucleus to produce proteins on structures called ribosomes in the cytoplasm.
One the level of DNA, there is a lot of regulation of which genes, and when, and to what extent, will be transcribed into messenger RNA. The name for this regulation is transcriptional regulation. For example, a network of proteins called transcription factors bind to DNA, regulating a gene's accessibility to transcriptional enzymes. Another example: the three-dimensional topography of DNA is also important. Epigenetic features may render some stretches of DNA inaccessible. The specific action of distal elements called enhancers can also affect a gene's level of expression. There are many things working in tandem on this level.
Once a messenger RNA is formed, it has to be exported out into the cell from the nucleus. In the cytoplasm it can be packaged, isolated from being translated into protein, degraded, accumulated, the list goes on. This is called translational regulation. Currently, there is a lot of focus in biomedical and basic research on microRNAs, which are RNA species which participate in regulating the amounts of messenger RNAs present in the cell. They are also found in the nucleus. Many biotechnologies are based on this concept; also, a common lab practice is to knock-down (reduce the expression of) genes of research interest by a technique called RNA interference.
Additionally, there's regulation of protein biosynthesis at the ribosome, which often complexes with other molecules in complicated ways to ensure an additional layer of tuning of how much protein is produced, and how quickly.
There are many, many other known levels of regulation. There also remain many unknown mechanisms of regulation, which scientists are busy with uncovering and understanding as we speak.
EDIT: What dictates which protein to synthesize at a given time? The history and present identity of a cell. By identity, I mean its state regarding regulation of its own gene expression, as well as other things.

Your asking how a cell or organism regulates protein synthesis. This is a complex question, with many different parts. It is well presented in Alberts Molecular Biology of the Cell, Chapter 7, on genetic switches. Here's an online section from that chapter in the 2002 edition.
There is a lot involved in regulating protein synthesis. As a general rule if you can imagine regulating it, it's regulated. Here's a figure from Alberts to get you started thinking about this:

There are some things that are required for all genes. General transcription factors, for example, and the Pribnow, or TATAAT box. The presence, absence, location, and accessibility of these things can regulate the levels of protein synthesis by the cell. Other things are going to discriminate between different genes. Under certain conditions, certain gene regulatory proteins will be produced, not destroyed as quickly, activated, allowed entry into the nucleus, etc, regulatory sequences will be exposed or not exposed, methylated or unmethylated... and transcription rates will change accordingly (increasing if those protein gene interactions stabilize assembly, binding, and transcription by the polymerase, decrease if they destabilize assembly, binding, and transcription by the polymerase).
This is just a taste of the wonderful world of gene regulation in the eukaryotic cell. As it says in Alberts, of the roughly 30,000 human genes, an estimated 5–10% encode gene regulatory proteins. And these are just the proteins that directly regulate transcription.


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If I stop consuming protein, will I still excrete urea?
Will an animal that is not eating any aminoacids stop excreting urea (or whichever other form of excreting nitrogen)? If the body is not in a position to lose nitrogenated compounds, in which processes is nitrogen inevitably turned into waste products like amonia/urea?

A hypothetical question from a new user who hasn't taken the Tour looks suspiciously like a homework question for which there is a specific policy on SE Biology. For all questions, but especially homework questions you are required to show evidence of trying to answer the question yourself. In addition your standpoint seems unclear. Your "why not?" seems to be responding to some unspoken answer. Please clarify.

The reason I am asking is because I am looking at the optimal protein intake from ratios of macronutrients for a healthy low-empty calorie diet. I want to understand what the smallest replacement amount of protein is that won't trigger autophagy and why even under autophagy one will still lose protein. I am sorry if I posed the question in a way that begs for a specific answer, but I could not really find a concrete answer to why it is that there is always some urea around even under nitrogen deficit. Seems to be because aminoacid reactions produce byproducts like ammonia that can't be reused.

Yes, you will still excrete urea, but the amount you excrete will be diminished. As you might expect, when the body is low on protein, there's a physiologic drive to hold onto as much nitrogen products as possible, in order to conserve the limited supply.
Normally, your kidneys excrete approximately 40% of the urea that is filtered through the glomerulus. (It's slightly more complicated, because there's both secretion and reabsorption that happens along the nephron, but that's approximately the end result.) However, in protein malnutrition, the kidneys reabsorb more of the urea, and that number can drop to excreting only 10% of the filtered urea. (Source) It appears that this is an active process to reabsorb the urea, rather than a passive effect from other effects that malnutrition has on the body.
However, the body isn't capable of stopping excretion of urea completely... there will still be some that is excreted. Urea transporters in the kidney aren't 100% efficient, but probably the bigger issue is that the body needs to use that urea to regulate other functions. Urea is important to the body's ability to concentrate urine, which in turn is related to the body's regulation of blood volume and sodium concentration. And in general, the body cares more about maintaining proper blood volume and tissue perfusion than anything else.

also not eating protein will not stop proteins in the body from wearing out and having to be recycled.

Despite the title I would have thought the biochemical tag indicated an interest in whether urea was actually synthesized in starvation. Irrespective I find the information you provide about urea resorption interesting — I was not aware of it. Do you know whether the resorbed urea can be converted to useful biochemical intermediates either by reversal of the urea cycle or by other means (urease?).

What I don't understand is why when a protein is recycled, it won't just return to being made of its original aminoacids. Can't the body keep those aminoacids around for further usage? What is the specific reaction family that releases ammonia/urea (not the ones triggered when the body runs out of energy storage and has to use aminoacids as an energy source). Essentially, where does deamination occur in the aminoacid cycle and how can it be reversed?

If an animal that is not eating amino acids is still eating enough nucleic acids to degrade some, that will produce ammonia and urea.
Plus some amino acids will still get degraded.

The scenario I was thinking of is one where you have plenty of sugar/fat around, so no energy deficit, but you are eating too little protein, so that the losses of nitrogen can be somehow reversed. If they can't, why is such a reaction necessary and irreversible, even with availability of energy to reduce entropy increases from protein degradation into aminoacids?


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B -Cell activation by helper T cell
When Dendritic cell travels to nearby lymph node with antigen presented on MHC II molecule, the helper T-cell residing there gets activated. But what happens to B- cell residing there? Does it get activated too when helper T-cell is activated and start producing antibodies for that specific antigen?

Naive T cells hang out in the lymph node waiting for antigen presenting cells (APCs) like DCs to present processed antigens on their MHC molecules. Naive B cells similarly hang out in the B cell zone and are capable of interacting with other T cells and follicular dendritic cells (FDCs). Antigen that ends up in the lymph ends up traveling to the lymph node, where B cells internalize, process and display them on MHC molecules. This is because B cells are also APCs.
Activated (and differentiated) T cells that were previously activated by DCs can identify some of these B cells clones through the TCR-MHC interaction. The B cells process the antigens like DCs, so the resulting heterogeneity of the processed peptides means a fair chance a T cell will recognize it. The result is that B cells receive an activating signal through the BCR and costimulatory receptors.
Differentiated T cells also secrete different profiles of cytokines. For example, Th1 cells secrete IL-12 and IFN-y whereas Th2 cells secrete IL-4, IL-5 and IL-13. Not exclusively, just predominantly or in greater amounts.
The receptor signaling in conjunction with certain cytokines can induce class switching to the resulting antibody production. This swaps the constant or Fc region of the antibody to a different isoform. So Naive B cells are IgM/IgD, and if the cells is receiving Th2 cytokine stimulation, class swtiching results in IgE antibodies, for example.
For elementary immunology I like to reference Cellular and Molecular Immunology, 8th ED. by Abbas et al., but 9th ED is out so keep that in mind. The field somewhat rapidly evolves.

There are a couple ways the adaptive immune system can be activated: Naive T cells require a co-stimulatory signal from professional antigen-presenting cells (Dendritic Cell); naive B cells require accessory signals that can come either from an armed helper T cell or, in some cases, directly from microbial antigens(NCBI, B-cell activation by armed helper T cells). So, within your question the helper T cell would activate naïve B cells through T cell-dependent activation. Though T cell-independent activation is possible (Wikipedia, B cell).
The activated B-cell would then begin producing antibodies while also undergoing clonal expansion to produce a foci of B cells that are specific for the antigen. Most of these clones differentiate into the plasma cells, also called effector B cells which produce a first wave of protective antibodies and help clear the infection, but a fraction persist as dormant memory cells that survive in the body on a long-term basis after having gone through a highly mutative and selective germinal center reaction (NCBI, Human memory B cells; Wikipedia, memory B cells).
Great visuals if you look at Google images "t dependent b cell activation".

So , Can the B-cell be activated to proliferate without phagocytosis of antigen and that antigen being presented on MHC II molecule on the surface of B-cell?

@ShawnDypx At this time I have to say no, antigen presentation is the only way that we know of that activate B-cells and they present the antigen on MHC II molecule on their surface to activate T-cells. Though we do know that interferon's can play a role with activation but they aren't what actually activate the B-cell (Keifer et. al, 2012).


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Estimating population divergence time with a single mitochondrial marker
Is it possible to estimate population divergence time with a single mitochondrial marker?
Here is additional information for my specific case:

Mitochondrial marker: Cytochrome Oxidase Subunit 1 (COI)
Molecular clock rate for COI for my taxon of interest: 1.29-1.96 % per million year
Age of the taxon: ca. 2.69 million years
Number of individuals per population: 10


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What do groundhogs and other subsurface-tunnel dwelling creatures do in heavy rains to avoid harm?
I notice groundhogs and many other tunneling creatures in my yard, the same yard which became pretty flooded during heavy rainfall. I don't see wildlife out during rain storms, but not long after, they emerge and return to their regular daily behavior.
What do the creatures living in tunnels underground do to avoid harm from flooding? The kind of harm I imagine them being susceptible to is drowning or damage to their tunnel. It could be that their tunnels get destroyed and they simply dig their way out and make a new one, in which case the only remaining question is how they avoid drowning while sheltering underground from storms. Even that question may be moot if they don't in fact shelter underground from storms, but instead shelter somewhere less susceptible to inundation like up in a tree.
I originally had groundhogs in mind with this question, but if possible, I'm interested in answers that apply to various tunnel dwellers: groundhogs, chipmunks, ants, ground wasps, etc. I know many ground-dwelling insects live there for the moisture it provides, and during storms they'll come to the surface to enjoy the moisture there and avoid drowning (e.g. slugs, worms), but I don't think this applies to all insects and certainly doesn't apply to mammals who generally seek shelter from the rain.


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What is the difference between a viral strain and a viral isolate?
Both are characterized, their genes are usually described and published, they are kept safe, they could be used as inoculum or to produce vaccine... Would it be correct to say a strain would be somehow a successful isolate ?

An isolate is a sample. It's this particular virus in this fridge, that was isolated from this, e.g., sputum sample, and cultured. A strain is more abstract -- it is a distinguishable, stable genetic variant of a species. An isolate may be identified as a particular strain of a particular species. That's how I and my colleagues use these terms, in any case, and how they're generally used in the literature. You can read more about this here and here
From the first reference (since it's behind a paywall)
Isolate

An isolate may be defined as “a sample of biological material, especially a microorganism, that has been cultured for study” which is clear, perfectly acceptable and useable by virologists.

Strain

Although there is no official definition of a strain, the strain concept is widely used and a de facto definition states “strains are viruses that belong to the same species and differ in having stable and heritable biological, serological, and/or molecular characters”.


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Why do plants need oxygen through their roots?
I was asking myself why plants die from over-watering and the simple answer was that they can't get enough oxygen through their roots. But this made me ask myself why they need oxygen in their roots since oxygen is a product of photosynthesis and plants even release oxygen through their leaves.
With this seeming surplus of oxygen, how can plants "suffocate" when their roots dont get enough oxygen from the soil?

They are mostly susceptible to stagnant water. Stagnant water gives rise to anaerobic bacteria, which use sulphur reduction and other kinds of energy chemistry. That's why anaerobic pond silt has an eggy sulphur smell. That anaerobic biochemistry can start to thrive after 2-3 days. The roots can handle low oxygen for a while, but beyone a few hours of zero oxygen pushes them into some kind of toxic cell state, which breaches the root's defenses and causes the roots to be rapidly attacked by bacteria. They benefit hugely from nitrogenated, oxygenated water.

Plants need oxygen but don't have a heart
Complex animals all have a circulatory system of some sort to get oxygen throughout the body for respiration. Plants also do respiration even though they are net producers of oxygen through photosynthesis.
Plants also have a bit of a circulatory system, but for the most part it isn't nearly efficient enough to deliver oxygen everywhere in the plant: plants don't have anything like circulating hemoglobin-filled cells we are familiar with in vertebrates, and although fluids flow in plant circulatory systems, they aren't circulating quickly like you are familiar with in your own body. This means that plants need to get oxygen near to where it is needed.
Roots, in particular, consume oxygen
The problem of a plant not getting enough oxygen through its roots isn't because the whole plant gets oxygen through the roots, it's because the roots themselves need oxygen to function. Roots do a lot of 'heavy lifting' in a plant, literally: they are pumping ions across membranes to pull in water, to concentrate other nutrients that the plant needs for survival and growth, and to pressurize the plant enough for those nutrients to make it up into the leaves. Those processes take energy, and in turn they need oxygen.
Additionally, photosynthesis isn't taking place in the vicinity of the roots: plants are both taking in CO2 and releasing oxygen from their stomata in the leaves and stems.
If roots cannot get enough oxygen, for example due to overwatering, the roots themselves are damaged, and this harms the plant as a whole.
Adaptations
Because there are always exceptions in biology, it should be noted that some plants are indeed adapted to wet environments and have better systems for promoting the diffusion of oxygen including increasing the amount of air space in the roots, where oxygen diffuses more quickly than through aqueous media. Other plants use fermentation in their roots to survive temporary hypoxia.

References
Colmer, T. D. (2003). Long‐distance transport of gases in plants: a perspective on internal aeration and radial oxygen loss from roots. Plant, Cell & Environment, 26(1), 17-36.
Drew, M. C. (1992). Soil aeration and plant root metabolism. Soil Science, 154(4), 259-268.
Justin, S. H. F. W., & Armstrong, W. (1987). The anatomical characteristics of roots and plant response to soil flooding. New Phytologist, 106(3), 465-495.
Laan, P., Tosserams, M., Blom, C. W. P. M., & Veen, B. W. (1990). Internal oxygen transport inRumex species and its significance for respiration under hypoxic conditions. Plant and Soil, 122(1), 39-46.

Great answer. This answer to a different question details differences in respiration vs. photosynthesis. Also note that anaerobic conditions around the roots can cause root rot, another pathway to death of the plant, which is related to the last adaptation you mentioned.

Plants are living things. And living things need oxygen to survive. While plants may produce oxygen as a byproduct during photosynthesis, they still require to undergo respiration, which requires oxygen.

But that doesn't explain why they cant use the oxygen they produce and have to absorb additional oxygen.

This is because photosynthesis and respiration are decoupled, they don't have an additional module to harness the oxygen produced to respire


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How does LDL leave the circulatory system and enter the interstitial fluid to deliver cholesterol to cells?
I have read that small molecules like oxygen and carbon dioxide diffuse through the capillaries, but larger structures can't fit through.
This answer indicates that some proteins go through via transcytosis.
The wikipedia article on capillaries shows that there are 3 types of capillaries, and it looks like LDL could fit through fenestrated or sinusoid, but sinusoid seem to only be found in certain organs, and if it did go through the holes in fenestrated capillaries, how would the LDL get to cells that are nearby only continuous capillaries? Would fenestrated capillaries be regularly dispersed so one is always nearby, or would the LDL just diffuse through the interstitial fluid originating wherever the fenestrations are?

I love these nobel prize questions! This is the same sort of question George Palade had, some 60 years ago :)

Many biologists had the same question for a number of years. In the 1950s, Nobel Laureate George Palade identified small vesicles in endothelial cells and postulated a mechanism whereby these vesicles would take in macromolecules from the luminal side of the endothelial membrane and transport them across the cell to release them to the tissues. His hypothesis has been tested, confirmed, and is now well documented.
Endothelial cells have LDL receptors that bind LDL in the capillary lumen, cause the cell to form a vesicle, and then transport it across to the membrane facing the tissues. There, the vesicle fuses with the tissue facing membrane, and LDL is released for uptake by peripheral tissue.

This process is called transcytosis. Endothelial cells use receptor mediated transcytosis to deliver many different large molecules to peripheral tissues in a regulated manner. You can read about this in some detail here (also the source of the figure), and more generally here.


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What is this plant, and is it edible?

After I planted some spring mix lettuce a couple of years ago, nothing survived except for this plant.  It doesn't look like any of the leaves that I am used to.  Does anyone know what it is?  Is it edible?  I am located in East Tennessee.
Thank you for any help you can give!
I just posted some more photos with measurements. The total length from base of the plant to the end of the leaf is about one foot. These plants have no flower growing from the base, however there is a separate plant nearby in the mix that does have flowers. I included a photo of it in case it is related. The original plant in question has leaves that are mostly smooth (some have tiny white or clear hairs on the backside or stem...some are smooth). They are almost as thick as spinach leaves.

Welcome to SE Biology. Can you edit your question to include where you are? It will help with the identification.

Thank you!  I just updated to include area... Chattanooga, Tennessee area / Southeast United States.

At first glance, I was thinking some species of plantago, but the leaf veins are wrong. Please provide more info: size of leaves, texture (hairy/fuzzy, smooth, waxy, thin/thick, etc), and any info on a flower if you have it

My guess would be Asteraceae, but species I don't know. Someone more familiair with the American flora might know.

BTW: lettuce is also Asteraceae.

Thank you all for your responses!  I just posted some more photos with measurements.  The total length from base of the plant to the end of the leaf is about one foot.  These plants have no flower growing from the base, however there is a separate plant nearby in the mix that does have flowers.  I included a photo of it in case it is related.  The original plant in question has leaves that are mostly smooth (but very few of them have tiny white or clear hairs on the backside or stem).  They are almost as thick as spinach leaves.  I hope this helps.  Thank you again for your help!!

This is a leaf vegetable called Cichorium, Endive in English. There are several closely related species, Cichorium endivia (also called endive), Cichorium pumilum (also called wild endive), and Cichorium intybus (also called common chicory). I think it looks most like common chicory, but if it comes from your seeds, Cichorium endivia is more likely.
Flower from Cichorium intybus

Flower and leaves of Ch. pumilium

https://en.m.wikipedia.org/wiki/File:Cichorium_pumilum.jpg
(source pictures:wikipedia)

Oh wow! That is very helpful...Thank you for your response, RHA!!

So looking again at the other leaves in the other photos, are you thinking that those are chicory too?

@steve I've added a second picture, from Ch. Pumilium, on which you can see leaves resembling yours.


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What proportion of proteins require chaperone-assisted folding?
I am new to the field of biochemistry (I am a chemist, actually).
I have long known the process of folding as the process that leads to the minimum energy conformation of a protein.
Now, I am introduced to the chaperones, that I didn't know before.
What I am wondering is: my previous view of folding, as a proces of "self-assembly" (the protein folds without external assistance as it is assembled by the ribosome) is real, or any folding process is assisted by chaperones?
If both processes exist, how frequent is the "assisted" folding, compared to the spontaneous process?

I've edited your title to remove the word "frequent" as what you are asking is not a temporal question (how many proteins per minute are folded with chaperones) but one of proportion or description (do all proteins are just some fold in this way). Do revert or modify if you don't like my change.

I'm reminded of a lovely review in Trends in Biochemical Sciences that discusses chaperone independent, partially dependent, and fully dependent proteins in prokaryotes.  The conclusion was that smaller polypeptides are less likely to require chaperone assistance. This is their figure:

That principle still holds to a certain extent (in prokaryotes), but folding assistance is now more broadly understood to include much more than just specific proteins identified as molecular chaperones. The Anfinsen postulate (that the final tertiary structure of a protein depends only on its primary structure) may still hold for small globular proteins, but folding in vivo is almost certainly always assisted. Since you're coming from the perspective of a chemist, don't think of it as a reaction between two molecules in solution. It's a reaction in a gel packed with complex sugars, lipids, proteins, and nucleic acids.
If you're skeptical of the perspective of a crowded cytoplasm, read the review I linked. It's an important but often under-appreciated aspect of in vivo biochemistry. There is much more to read about it. You might try looking up Allen Minton (AP Minton) and macromolecular crowding in your favorite database.

I would upvote your answer, but for the last two sentences. If the cytoplasm is "a gel completely packed with things" how do tRNAs, protein synthesis factors etc. diffuse to the ribosomes, and the released proteins distribute themselves in the cytoplasm. And what precisely has this to do with the protein folding? This is a serious, not a rhetorical, question.

@David did you read the serious, not rhetorical paper I referenced?

@David on re-reading, i may have phrased it a little stronger than I should have in order to emphasize the difference between dilute in-vitro biochemistry and the gel-like phase where protein biochemistry (including folding) occurs in-vivo. I removed the word completely, and added a comment about it.

— I'll check your reference out. I'm traveling in a foreign country where I'm being charged a £7 per Mb for data, so I'm dependent on rather flaky wifi reception.

Ok, I've looked at both the TIBS review and the 2012 Int J Mol Sci review. I see that the latter makes the point that the results in vitro are not always borne out by those in vitro (e.g. with mutants in the chaperones) and the authors suggest that (non-specific?) interactions with other molecules may be important. That's all I see that relates to your "gel" remark, which I now see you've clarified in your answer. The general impression I get is that it's difficult to answer the question posted with any precision, although assisted folding cetainly exists.

@David they review the good deal of evidence for the importance of other macromolecules in folding assistance. You seem unconvinced :) Read some of Allen Minton's work.

I don't doubt the role of other molecules in folding. It just seems to me from the review that the field is still in flux. That's no criticism, just an impression.


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Ambiguity about the relation between membrane potential and concentration gradient in neuron cells
I am stuck in an ambiguity about the equilibrium potentials of neuron cells. The following text is picked up from khanacademy website:
In one part it is said that:
We'll start out with K at a higher concentration inside the cell than in the surrounding fluid, just as for a regular neuron. (Other ions are also present, including anions that counterbalance the positive charge on K but they will not be able to cross the membrane in our example.)

If potassium channels in the membrane open, K will begin to move down its concentration gradient and out of the cell. Every time a K ion leaves the cell, the cell's interior loses a positive charge. Because of this, a slight excess of positive charge builds up on the outside of the cell membrane, and a slight excess of negative charge builds up on the inside. That is, the inside of the cell becomes negative relative to the outside, setting up a difference in electrical potential across the membrane.

As potassium continues to leave the cell, separating more charges, the membrane potential will continue to grow. Thus, the building membrane voltage is an increasing force that acts counter to the tendency for net movement of potassium ions down the potassium concentration gradient.
Eventually, the electrical potential difference across the cell membrane builds up to a high enough level that the electrical force driving K back into the cell is equal to the chemical force driving K out of the cell. When the potential difference across the cell membrane reaches this point, there is no net movement of K in either direction, and the system is considered to be in equilibrium. Every time one K leaves the cell, another K will enter it.

In another part it is said that:
The electrical potential difference across the cell membrane that exactly balances the concentration gradient for an ion is known as the equilibrium potential. Because the system is in equilibrium, the membrane potential will tend to stay at the equilibrium potential. For a cell where there is only one permeant ionic species (only one type of ion that can cross the membrane), the resting membrane potential will equal the equilibrium potential for that ion.
The steeper the concentration gradient is, the larger the electrical potential that balances it has to be. You can get an intuitive feeling for this by imagining the ion concentrations on either side of the membrane as hills of different sizes and thinking of the equilibrium potential as the force you'd need to exert to keep a boulder from rolling down the slopes between them.

I concluded the two following information from the above text:

The closer we get to the equilibrium state, the membrane potential
decreases because the concentration gradient decreases. (The steeper
the concentration gradient is, the larger the electrical potential
that balances it has to be)
The closer we get to the equilibrium state, the membrane potential
increases, because positive ions leave the cell.

How to solve this paradox?

Can you clarify your question? I think one of the issues here is understanding the difference between the membrane potential and the equilibrium potential. If positive ions leave the cell, the membrane potential becomes less positive/more negative. That is the only way positive ions leaving the cell will impact the membrane potential. The closer we get to the equilibrium state, the smaller the difference between the membrane potential and the equilibrium potential will be.

The closer we get to the equilibrium state, the smaller concentration gradient will be?

I interpret your question to be roughly: "the equilibrium potential is based on a concentration difference, but as ions move to create the electric potential, the concentration difference is changing. Why doesn't this in turn change the equilibrium potential such that the concentrations become equal and the potential becomes zero?"
If I'm correct...
The answer to your paradox is that very few ions have to move.
The number of potassium ions that would have to move across the membrane to establish the resting membrane potential is tiny. Electrical forces are very very strong. The imbalance in ions doesn't affect the concentrations inside and out appreciably.

For a typical cell, 1 microcoulomb of charge (6 × 10^12 monovalent ions) per square centimeter of membrane, transferred from one side of the membrane to the other, changes the membrane potential by roughly 1 V. This means, for example, that in a spherical cell of diameter 10 μm, the number of K+ ions that have to flow out to alter the membrane potential by 100 mV is only about 1/100,000 of the total number of K+ ions in the cytosol.

from Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., & Walter, P. (2002). Ion channels and the electrical properties of membranes.
However, because membranes are also a little permeant to sodium, and because action potentials and synaptic transmission allow some additional ions to flow across the membrane, if you gave infinite time, eventually the ion concentrations inside and out would equalize, and the membrane potential would eventually be zero. The sodium-potassium pump solves this problem by continuing to keep potassium high and sodium low inside the cell.

Note that I also posted a very similar answer here: https://biology.stackexchange.com/a/57066/27148 but to a moderately different question that I don't think is really a dupe. I think that Q&A is good reading though for understanding how ions actually move in establishing resting potentials.

I think this answers a common question, but not the actual question/confusion the OP has. Take a look at the way the apparent paradox was worded, at the very end of the OP.

@DanHall Indeed I may have misinterpreted what they were trying to ask since I'm used to the problem I answered in students. Care to expand on your reading of it? I should add that my assumption was that they meant membrane potential increasing/decreasing to mean absolute value.

Take a look at my comment to the OP. It's hard to say for sure without some dialogue. I didn't phrase it as an answer. Since your the neurophysiologist here, I thought it best to leave it to you.

@DanHall Okay thanks. I've added an explanation of my reading of their question, so hopefully that will either help them realize I am answering their question or help them realize how to rephrase so I can answer their actual question :)

@BryanKrause I know that the concentration gradient is not necessarily zero in  equilibrium potential. My understanding from your answer is that: because very few ions leave the cell the concentration gradient does not change, right?

Correct! Basically you should take the concentration gradient to be whatever it is and don't worry much about it changing because of ions flowing. It only matters over a relatively very long time. :)

Your first deduction is wrong. The sentence actually means with a greater concentration difference at the initial condition, eventually there should be a higher electrical potential to satisfy opposite chemical potential. The dynamic of the system can be described by an exponential function. The closer to the equilibrium potential we get, the smaller the rate of approaching to the final state i.e. the rate of electric potential escalation will be.
Note that in reality this does not really affect the concentrations since a tiny amount of ion exchange can generate a considerable amount of electric potential.

You mean the last picture is showing the initial state?

The last picture demonstrates the final states for two systems with distinct initial concentration difference; Smaller for the right one compare to the left system.


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Insect identification - is it a bed bug?
We were on holiday and got bitten by (most probably) bed bugs. We then carried them home, and I also saw a typical one: 4mm, flat, round, black. I thought it was pretty clear we had bed bugs. I smashed one:

Currently (2 weeks later) we have a lot of small insects in the house, like shown in the picture. But they don't really seem like bed bugs, do they? The big ones look like bed bugs, but the small ones don't?
What is it? It's around 2mm (others are much smaller, very tiny, less than 1mm). They can jump (or run really fast) 2cm if I try to squash them with a finger.

Update:
The small one is very similar to a psocid?!
Update 2:
They have wings.. I think they're psocids.
What I also realized, I probably have two different larves. I take some more probes..

Top photo looks like a bed bug. Bottom one looks very much like a psocid.


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Please help me identify this plant
I got a plant from friend but neither he nor I know what it is. Could anyone help me identify this? Google reverse image search could only find aloe vera and other green plants that are obviously not this species. In addition, it looks like it is dying so any help on caring it is appreciated as well.

It's some kind of succulent and it looks reasonably healthy.  Don't water it more than once a month.

Please add your location.

I would argue that house plants identification are off-topic here and such questions should rather be asked on gardening.SE.

Looks like a cultivar of Crassula ovata or Jade Plant.  A little searching will reveal that there are many out there.  Yours looks a lot like a cultivar humorously called "ET's Fingers".  Search for "crassula ovata ets fingers jade" and you'll see many images.  I won't link to any since they aren't my pictures and the sites may not be available in the future.


text:
Which vaccines are damaged by freezing?
I have noticed that many of the freeze-sensitive vaccines are antigen only vaccines, for example Hib, pneumococcus, and tetanus vaccines. Why are these vaccines damaged by freezing? Are inactivated or killed vaccines like IPV damaged by freezing? How about live vaccines?

Are vaccines made of non-antigens too?

@Tytoalba some vaccines are made of purified antigen. Others are made from an entire pathogen. I expect the OP might actually mean inactivated/killed vaccines, vs. live attenuated vaccines (IPV is an inactivated vaccine, not a purified antigen). eyadoalshaikh, if you could edit your question to clarify, that would be helpful.

OP: I've edited this question to make it answerable and resolve the comment above. Feel free to roll it back or further clarify if you'd like :)

many proteins are damaged by ice crystal formation when they freeze in an aqueous solution.  https://www.ncbi.nlm.nih.gov/pubmed/12673768

In order for a vaccine to work, antigens in the vaccine must maintain their shape and charge. Freezing a vaccine, particularly vaccines that contain aluminum, can cause antigens or other important constituents of the vaccine to aggregate. This may be what prevents them from working correctly, though we don't know for sure, and it may be something else about the freeze-thaw process. The main thing that we know, though, is that (typically in animal models, as in the last reference) for certain vaccines, if you allow them to freeze, they don't produce a sufficient immune response.
You can look at this very large table of data about which vaccines are freeze stable and which are not.  There are a few patterns to this, as the OP seems to have noticed.

Aluminum adjuvant: Any vaccine that uses an aluminum adjuvant (a chemical used to enhance the immune response) will be damaged by freezing. Polysaccharide vaccines and other purified or recombinant antigens are more likely to require an adjuvant. This is one of the reasons antigen only vaccines are more likely to be freeze sensitive. Some antigen only vaccines can be frozen themselves, and reconstituted with the adjuvant prior to administration (for example, some Meningitis polysaccharide and polysaccharide protein conjugate vaccines).
Live attenuated vaccines: Almost all live attenuated vaccines are freeze stable (e.g., MMR, oral polio). The only ones that aren't, as far as I'm aware, are influenza vaccines: flumist and the live attenuated H1N1 influenza A vaccine. This may or may not just be a precaution, as I'm not aware of immunogenicity experiments that demonstrate freeze sensitivity.
Inactivated vaccines: Most killed or inactivated vaccines are sensitive to freezing. IPV is one of them. Rabies is an important counterexample. This is entirely speculation, but since many of these vaccines are formalin inactivated enveloped viruses or bacteria with cell membranes, freezing a perforated cell membrane may further damage it's antigenicity.

You can read about the basic principles of vaccination (e.g., how a vaccine works, what an adjuvant is, when you need it, etc) in Abbas Basic Immunology Chapter 8, and Murray Medical Microbiology Chapter 13.


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What species is this beetle (trichius family)
I took this picture in Jura region (Northern Switzerland, alt: ~700m) of that beetle (July 2018). It was taking food from a flower of a Morus nigra.

It seems to be part of the trichius genus but I want to report the exact species.
In Switzerland we have mainly:

Trichius fasciatus
Trichius rosaceus
Trichius sexualis

I think by the color of the hairs it would be a Trichius fasciatus.
Can someone confirm the species and what field marks I can use to make the distinction between those three species?


text:
Can someone identify this Lepidoptera larva?
That's from Brazilian Amazon, more specifically a small mountain (300 m high) called "Morro dos Seis Lagos" (six lakes hill), at São Gabriel da Cachoeira municipality, Amazonas state, located at 0.283 North, 66.685 West.

Can you add an approximate size? 2-3cm?

@RHA Sorry, it's been 14 long years now. But I think bigger than that, between 5 and 10 cm.


text:
Can someone identify these eggs?
They were attached to a tree in a black-water inundated forest (igapó) near Manaus, Amazonas, Brazil. The photo was taken in mid June, the water level was already high, and the eggs were about one metre above the water (not sure if they had been or would be under water at some point). It's been many years now, but I think the whole group was about 5 to 10 cm long (about 2–4 inches).

That's an apple snail egg cluster. They're freshwater snails, and by placing their egg clutches above the water line they protect them from predation.
We actually have an issue with apple snails in Florida, because while the Florida applesnail Pomacea paludosa is native, three different invasive species have been introduced that are eating through native vegetation without many predators (1).
Different species produce different colors of egg mass, and a good example of the green egg masses includes Pomacea haustrum, the titan applesnail, which is present in the continental US, but actually native to Bolivia, Brazil and Peru (2, 3). Since other species also produce green eggs, it's difficult to tell exactly what snail produced those, however.

Could you provide more support/info for this answer? Thanks

@theforestecologist what sort of information would make this answer more helpful? I will add a couple neat facts, but those eggs are very distinct.

What characteristics should the OP or others be looking for for a positive ID? (in other words, how did you know they were distinctly apple snail eggs)? Also discussing their range and other interesting facts is always nice :). A picture is helpful for people visiting this post in the future, as well.

Thanks for the answer. So it's most probably an Ampullariidae, though it will be harder to know the genus for sure, since it could be native, introduced, or even something new...

@Rodrigo I'm no expert, but many apple snails are native to S. America. The only catch is many species that may be native may also produce green eggs.

Yes. If I knew the genus would be good enough. But to know the family is already much better than the state I was before (not even sure if it was Mollusca).


text:
Can someone identify this Brazilian flower?
The photo was taken in january 2004, at Parque Estadual do Rio Preto (Black River State Park), in the Cerrado (savanna-like) of northeastern-central Minas Gerais, Brazil.
The plant was herbaceous/shrub, but maybe it was because of its tender age?


text:
Dependency graph of life
This is a fascinating paper I read using Bayesian analysis to compare different graph models to genomic data.  Intriguingly, it shows that a dependency graph is a much better fit than a tree model.  However, a tree model is what we'd expect from common descent with variation.  What could make this dependency graph model, instead?
http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2018.3
For those who are worried about site cookies, here is the paper hosted on my Box.net account:
https://app.box.com/s/2mtiwafzr67hsee8o9m7bnfjr7dbmzsv

This paper was discussed by three scientists and the author here: https://discourse.peacefulscience.org/t/winston-ewert-the-dependency-graph-of-life/728. Really interesting paper, but Ewert has not yet made his case.

@Dr.S.JoshuaSwamidass Could you summarize the problems with the paper in an answer?  As a layperson, the tree model is what I've always thought of when it comes to evolution.  It is hard to imagine how common descent could result in anything else.  If you can provide explanation as to how a non-tree could emerge from evolution, that would be very helpful.

It appears the controversy stems from a misunderstanding of what the log Bayes factor in the paper means.  Dr. Swamidass states the D. Graph vs Tree result should be divided by the Tree vs Null result to show the D. Graph only explains the data 1.7% better than the Tree.
However, the author claims the log Bayes factor actually means the D. Graph is $2^{111,823}$ times better than the Tree.  Which clearly shows common descent (Tree) is a vastly inferior explanation for the data than the D. Graph.
The issue is there is an enormous amount of data, which can artificially inflate the log Bayes factor.  However, the proportion should stay stable.  Hence the focus on the 1.7%.  Explained here:
https://discourse.peacefulscience.org/t/uncommon-or-common-descent/776/86

Really?  You ask a question about a paper that doesn't seem to be in Pubmed, and then you give yourself credit for the best answer?

No other answer is forthcoming.  Do you have one?

No way am I giving a click to let some rando site put cookies on my computer. Grown-ups cite Pubmed, so everyone can see that the paper in question is legitimate.

I've hosted it on my box account if you would prefer that: https://app.box.com/s/2mtiwafzr67hsee8o9m7bnfjr7dbmzsv

Kids are curious about the world :)


text:
Is this a bed bug nymph?
hello ,
I want to know if this is a bed bug nymph or it's just an another insect? I got an issue with bed bugs few days ago in a hotel during a travel to Prague. Once home (in Germany), I washed all I had taken with me (a backpack with some clothes) under high temperature > 150 Fahrenheit. So I was confused when I found this bug on my arm today. I'll point out that I was under a tree and there were many tiny insects just a few minutes before I found this one.  This specimen was ~1 mm in length.
Thank you in advance for your help.

Please provide your location and an approximate size of your insect. Thanks

Thanks for your reponse. I'm actually in Germany and the insect size is about 1 mm.

It's hard to tell from this angle and the way the legs are positioned. Could be a bedbug nymph or a booklouse. The biggest visual difference is that a booklouse has a narrower neck; bedbugs have barely any neck. If you can get a look from a different angle and compare to some photos of booklice you'll be able to tell.


text:
Is there a specific suffix for "within a cell"? i.e. in a similar manner to how -aemia refers to within the blood
Words like hyperglycemia and hyponatremia refer to the relative level of each component in the blood, not in the cell. Is there a suffix for within the cell? For reference I would like one word as an alternative to "hyperglycemic cell".

I'm voting to close this question as off-topic because it is an English Language question that could have been answered by reference to dictionaries and scientific literature.

It is not present in dictionaries, nor scientific literature per se. In fact, the question arose after noticing that many authors wrote out the full phrase. I still agree it might also suit the English Language exchange, but on reconsideration it is just as relevant here. Biology is after all the main, if not only, context in which the word could ever be used. See below.

"Cyto"/"cytic" and similar are common prefixes/suffixes to refer to things associated with cells; however they don't necessarily specify intracellular space, they are more often referring to specific cell populations, counts, etc.
The word "intracellular" is, however, commonly used terminology for "inside the cell."
For the specific case you mention, I would simply write "high/elevated intracellular glucose" - I am unaware of any reference that uses a individual word for the same meaning. Some others have referred to "intracellular hyperglycemia" which may be a bit odd since the -emia refers to the blood, but they are specifically referring to the case where high intracellular glucose is a direct consequence of overall hyperglycemia.

i wouldn't say intracellular hyperglycemia. I'd say high or elevated intracellular glucose. The -emia suffix is still going to mean in the blood

@DeNovo Hmm that's a good point. I found a lot of cases where people used the term "intracellular hyperglycemia" but I've edited accordingly.

Just for reference I went with hyperglucous cells as it is more accurate than intracellular hyperglycaemia; much more useable than the triple combos: hyperglucocyte, hyperglucocyst, hyperglucocytic, hyperglucocytal.

There are very few medical terms that have  suffixes for body parts or compartments. The only 4 I'm aware of are -emia (in blood), -uria (in urine), -rhachia (in cerebrospinal fluid, rarely used) and -dactyly (arrangement of fingers) (medical term suffixes). For organs, prefixes are typical: gastro- (stomach), spleno- (spleen), cardio- (heart), cerebro- (brain), etc.


text:
What is the scientific name of this tree?

The tree flowers prior to the monsoon season and sheds it's leaves in Winter and regrow them in Spring and Summer.
I have seen three different colours of the flower (growing in my neighbourhood): pink, violet and white.
Place-India, Kolkata, West Bengal. Season - Monsoon.

It is Lagerstroemia, perhaps Lagerstroemia indica, the common crape myrtle.
https://en.wikipedia.org/wiki/Lagerstroemia
Myrtle in french means blueberry: "From Medieval Latin myrtillus, diminutive of Latin myrtus (“myrtle”), from Semitic: Arabic مُرّ (murr, “bitter”), Hebrew מֹר (mor, “bitterness") ." Myrtle is an unrelated family with tough spicy seed pods which are used as a condiment including eucalyptus.
Crape, refers to the frilly flowers, from Latin Crispus, Crispy: frilly, crèpe is often used to refer to frilly fabric and it also means pancake in french, which is a chapatti with butter and milk and an egg from the bible.
Because you said it is common, I checked google images for "india frilled pink flower tree", it was about 20 images in. There should be a Hindi/Indian script of the wiki page, with the Indian derived name.

I found two of them today in south france here, where temperatures reach -15 some years: https://goo.gl/maps/xM3sFJe5bpC2


text:
What happens to the complementary base when the other undergoes a base substitution mutation?
From what I know only the base pairs A and T/U, or G and C can occur due to hydrogen bonding. So if a base substitution mutation occurs, say an A is replaced by a C on the strand, does it affect only one of the strands on the DNA or does it changes the base pair entirely? Thanks.

Consider a stretch of DNA
A T C C T C
T A G G A G

Let's say that during replication a nucleotide get switched
A G C C T C
T A G G A G

Now, this does not work. The cellular machinery will find this location and try to solve it. It will either resolve it as
A T C C T C
T A G G A G

and no mutation would have happened. Or it will solve it as
A G C C T C
T C G G A G

and a mutation just happened.
You might want to read about DNA repair mechanisms.

A base substitution mutation often occur during replication of DNA. Remember that the template strand is methylated, in order to understand who will be the new synthetized strand between both.
Having this scenario, with a nucleotide substitution mutation in the 3rd position from 5' , the 5'-3' strand is the fresh synthetized.
The DNA polymerase will trait just the 5'-3' strand as something to work on : if a mutation happens the proof-reading activity of the DNA polymerase will try to cut off the wrong base, and to re-synthetize this piece of the strand.
5'- A G G T T C G -3' --> new strand
3'- T C A A A G C -5' --> template

If it isn't able to figure the mutation, it'll be fixed in the next replication process, so the mutation will be fixed into the considered DNA.


text:
Pyruvate oxidation - where did the hydrogen come from?

(source: resource12ubio at sites.google.com)
As shown in the diagram above, NAD+ is reduced and becomes NADH by gaining two electrons
Now, where did the hydrogen come from?
In the diagram, pyruvate has 3 hydrogen, but it still has 3 hydrogen in acetyl CoA.

@Astrolamb has given you a good answer here. In general, be aware that counting atoms will often result in a headache in biochemistry. There are large parts of key molecules that are often not represented.

@DeNovo is absolutely right; when looking at biochemical systems, if something doesn't seem to make sense, try to find a diagram that includes ALL the puzzle pieces.

The Wikepedia page has a really good diagram of the reactions involved. The Pyruvate Dehydrogenase Complex facilitates the removal of CO2, and the addition of two hydrogen atoms to the overall reaction come from the FADH2/FAD molecule.

This is an example of how, in biochemistry, the rules for writing a reaction equation are much more flexible, and generally based on convention. NAD+, for example, has a negative charge at physiologic pH. We write it as NAD+ to emphasize the active moeity in the oxidation/reduction reaction. H+s, in particular, are often poorly accounted for in our short hand.


text:
How do you define a gene list?
So I wrote in a chapter that I will be checking for publications with gene lists in them. I got a comment asking "How would you define a gene list and what criteria did I use". I know that gene lists are usually generated by microarray studies, NGS analysis etc but what is the best way to define a gene list?
I am running blank except maybe say that its a list of genes.
EDIT: "I defined a gene list as a list of genes generated as a result of a microarray analysis or a next generation sequencing study." Sounds good?

Correct me if I am wrong, but from your bio I suspect your background is in the numerate rather than the biological sciences. If so that would explain why your question "lacks context" (@Michael_A) or "is unclear" in SE Biology terms. A "gene list" means almost nothing, even with the rider "generated by microarray or NGS analysis". Just as a list of cars is almost meaningless, even if quaified by "generated by perusing newspapers". You must define the purpose of the experiments. Genes expressed in growing animal cells, after heat shock, after hormone treatment, in liver etc.

@David My work was to essentially get the number of publications with gene lists in them so as to make an argument that there are such a lot of lists being produced with potentially no follow up analysis being done on the majority of these lists generated in different studies. That is why I could not provide biological context to the question. Do not jump the gun, downvote and then vote to close before I get a chance to respond to your comment David.

The comment explained the down and close votes which were (and are) based solely on the question. I was not obliged to do this but felt it might be of use.

@David Of course you are not obliged, its just good practice. I hope I was able to explain the context of the question to your satisfaction. Have a good day.

The comment seems useful as your current definition of a gene list lacks context.

How would you define a gene list?

There are many different kinds of gene list. Specifying gene lists from microarray and next-generation sequencing provides some context but both technologies are used to analyse many different kinds of DNA and RNA samples. Define the molecules that are being referenced by the gene lists.
Defining DNA or RNA isn't sufficient as each gene list is compiled to perform a research task. Genomic projects may provide lists of genes that were sequenced or mutated or contained single nucleotide polymorphisms. An RNA transcript project may create lists of genes where transcription was occurring in a tissue or whose RNA transcripts were influenced by experimental factors or whose splicing was altered. Most publications also include multiple gene lists and some of those will include rows that were removed following data evaluation. Define the kind of lists that you are collecting.
There's value in defining your search criteria well. It allows you to communicate your work to others and it can provide focus to your search efforts.

What criteria did I use?

This was mostly answered above. I would also consider including some rules for the publications that you will search for gene lists.

I don't think this is an answer to a biological question, it is an explanation why the question is meaningless as it stands. Better as a comment.

On the contrary, I think your answer has given me some idea on how to address the comment and I thank you for that.

@David, Biology Stack Exchange is for people studying biology at any level. Questions are from students, academics and active researchers in biology and closely related fields. @The last Word appears to belong to that group and I think the answer provides a biological context to the question. Comments are not for answering questions.

You misunderstand me. My point is that the question is not clear, not that it is not biological.


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A human lifespan
Recently, I read an article that said a human lifespan does not have any limit and when a man turns 105 he has a 50/50 chance to survive another year. Some scientists say that a man who will reach the age of 140 has already been born. Is it possible that the length of a human's life will be prolonged over time? I know that we don't know what the limit is and if it exists at all, but it is possible to one day expect it to be completely normal for a human being to live 300 years or so? I mean, without the intervention of any "elixirs of youth", development of technology, medicines etc.?
I ask because in 2016 there was an article published in "Nature" that says we know what the limit is (115 years) and they believe that Jeanne Calment (who died at age 122) was lucky to live that long. On the other hand, another article published in "Science" this year says that we don't know what the limit is.

Welcome to SE Biology. Adding links to the articles that you discuss will improve this question.

"Nature": https://www.nature.com/articles/nature19793, "Science": http://science.sciencemag.org/content/360/6396/1459

Looking at these lists of oldest people a 'limit' of 115 seems unfounded. Also, Calment's actual age seems to be a somewhat controversial topic.


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What Genus Is This Ant Queen?
I believe she is either Lasius or Formica, but I am an amateur so thanks for any help. This queen is completely black and gray, with a gaster that kind of looks like the stone Tiger Eye but gray. There is no red or brown on her. She’s approximately 1.5 cm long and I found her in central Minnesota. She laid eggs overnight after being caught. I know the photo is terrible thanks to my phone but it was the best one I got of her.


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Is there any evidence that immunity or resistance is heritable?
Is any means by which smallpox or any other disease be heritable?
I have heard that smallpox introduced by European colonialists affected (and reduced) a significant proportion of the native American population. How were the native Americans more susceptible to smallpox? Is disease susceptibility or immunity heritable?

Susceptibility to infectious diseases is most certainly heritable. Variola is specific case. I'm off to the airport, but will be happy to give you a thorough answer tomorrow. Let me suggest, though, that you edit your question and rephrase it to remove the unnecessary political angle. I can't see how it adds anything to the otherwise useful scientific question.

So do you have an answer

A naturally-occuring disease would not lead to genocide.  Else it could equally well be claimed that the Black Death was genocide of Europeans by (probably) Chinese, or AIDS an attempt at genocide by Africans.

@jamesqf but there is evidence of intention in the case of the British and native Americans, "could it not be contrived to send the small pox among the disaffected tribes of Indians" Jeff Amherst https://books.google.com/books?id=EB4bAAAAYAAJ&pg=PA39&dq=could+it+not+be+contrived+to+send+the+small+pox+among+the+disaffected+tribes+of+Indians&hl=en&sa=X&ved=0ahUKEwj_0MKS8MbcAhULmuAKHay7Bm4Q6AEIKzAA#v=onepage&q=could%20it%20not%20be%20contrived%20to%20send%20the%20small%20pox%20among%20the%20disaffected%20tribes%20of%20Indians&f=false

I'm voting to close this question as off-topic because it calls for speculation and is presented in a provocative manner. Its main concern appears to be American social history.

TL;DR: Pre-Columbian Native Americans would have been much more susceptible to smallpox than the Europeans who spread it, because of non-heritable factors such as immunity and traditional knowledge, and also because of heritable factors. It's therefore completely believable that smallpox (and other diseases introduced by Europeans, such as measles) could have caused massive deaths among the American populations post-contact.

The title of the question makes an incorrect assumption. Resistance to smallpox would not have to be heritable to have a highly susceptible population. European populations were continually exposed to smallpox and there would have been both maternal immunity and acquired immunity in most populations, leading to a herd immunity effect that would both reduce viral spread and increase resistance among some infected people. (It's commonly believed that herd immunity needs to be very high to lead to protection, but that's a misconception -- the lower the contagiousness of the disease, the lower herd immunity needs to be to lead to protection.)

Smallpox apparently circulated as a childhood disease in northern England and Sweden, even where population densities were low and settlement patterns dispersed.

--The geography of smallpox in England before vaccination: A conundrum resolved
Cultural factors would also be important. Europeans had thousands of years of experience with smallpox, and knew that isolating victims was important to reduce spread.

We concluded that transmission was controlled in southern England by local practices of avoidance and mass inoculation that arose in the seventeenth and eighteenth centuries. Avoidance measures included isolation of victims in pest houses and private homes, as well as cancellation of markets and other public gatherings, and pre-dated the widespread use of inoculation.

--The geography of smallpox in England before vaccination: A conundrum resolved
That said, there is also evidence that European populations did have some innate resistance to smallpox that was lacking in the pre-Columbian Native Americans, and this innate resistance may be even stronger in Africa, which is (possibly) where smallpox originated:

Pathogens that diminish reproductive potential, either through death or poor health, drive selection on genetic variants that affect resistance; selection is likely to be most evident for pathogens with a long-standing relationship with Homo sapiens, including those that cause malaria, smallpox, cholera, tuberculosis and leprosy ... We noted that, for 32 viral isolates with documented mortality, death rates are lower in Africa (0.4−12%) than elsewhere (4−38%), even though all isolates were from a single phylogenetic clade. This is consistent with selection for resistance in Africa, where the smallpox virus is predicted to have evolved from a rodent-borne ancestor tens of thousands of years ago and where outbreaks of other poxviruses continue nowadays.
With smallpox eradicated, vaccine response is used as a crude phenotypic proxy for studying host resistance. Two GWASs that included European, African American and Hispanic populations identified 37 SNPs associated with cytokine response to vaccination179, 180 (P < 1 × 10−8). Most of the significant associations (65%) were found in African Americans, even though their sample size was half of that of the European cohorts, which is consistent with a larger effect due to selection in Africa.

--Natural selection and infectious disease in human populations
Some resistance alleles have been tentatively mapped:

However, when examining the population post-contact and into contemporary times, variants of the HLA-DQA1 gene experience a marked frequency change.  ... Although we were unable to precisely identify the selection coefficient necessary to drive the allele frequency change (since the likelihood surface is relatively flat, Supplementary Fig. 8), it is likely that relatively strong negative selection occurred. Such strength would be expected under a time frame of less than seven generations and correlates with the high mortality rates associated with the regional smallpox epidemics of the 1800s, which reached upwards of 70%

--A time transect of exomes from a Native American population before and after European contact

The CCR5 Δ32 mutation is a good example of an advantageous allele with a well-characterized geographic distribution. ...  The mutation is found principally in Europe and western Asia, where average frequencies are approximately 10% ... Bubonic plague was initially proposed as the selective agent [2], but subsequent analysis suggested that a disease like smallpox is a more plausible candidate

--The Geographic Spread of the CCR5 Δ32 HIV-Resistance Allele

This is good, but I wonder why you would say that immunity to an illness that requires T-cell involvement (and thus antigen presentation on the MHC) is not heritable? (top of your post, in the tl;dr summary)

Adaptive immunity is not considered heritable, even though of course it has heritable components to it. If you know enough to comment on MHC, you must have noticed the link with HLA-DQA1, which is of course an MHC allele.

I've upvoted your post, but I'd encourage you to read Casanova's excellent inaugural PNAS article. You may not consider adaptive immunity to be heritable, but as an infectious disease doctor, I can tell you it certainly is. MHC loci are among the most variable in the entire genome, this variability is heritable, and contributes a great deal to host susceptibility. There are plenty of other examples.

And yes, I noticed and appreciated the link. I was making a suggestion that you edit your statement in the tl;dr summary, where you classified immunity (in general) as non-heritable. That is a false classification. You could narrow it down to antibody response and be less wrong, but again, with class switching, it relies on T-cell involvement. It's a good post overall. I was just remarking on the one error.

@user45026 So basically yes. If you need further clarification, please spell out what's confusing you.

@user45026 Second sentence. Yes.

Well that's an assertion that you are right. The only relevant evidence you gave is that Europeans are more susceptible than africans

As usual, @iayork has a great answer. Let me add some additional context.
Host-pathogen interactions
Pathogens are not disease. The result of an interaction between, e.g., a virus and a host is variable. This is a fundamental and extremely important concept in understanding infectious disease. You can read more about it in Chapter 286 of Cecil Medicine and Chapter 119 of Harrison's Internal Medicine. The clinical outcome of a host-pathogen interaction is as much dependent on the host as it is the pathogen.

Host effects are variable and heritable
There is great interindividual and interpopulation variability in host factor side of this graph, the susceptibility/resistance to specific infectious diseases. Much of it is heritable. Sickle cell trait is an excellent example. We refer to it so often to illustrate genetic principles, that the key lesson about host-pathogen interactions is often forgotten. It was not unnoticed in the original paper. This genetic variation in susceptibility is not an exception, see Jean-Laurent Casanova's inaugural article in PNAS for an excellent discussion.
Comment on @iayork's answer
I did enjoy the discussion of the non-genetic (but certainly vertically transmitted) traditional knowledge in the susceptibility of a population to smallpox, as well as the references to single gene associations. Host susceptibility and resistance is certainly heritable, but as s/he points out, there are important non-heritable contributions to consider.


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Michaelis-Menten equation; how to find the constants from enzyme activity experimental results?
I was wondering what the constants in the Michaelis-Menten equation actually mean in experimental data of enzymes. How do I process the data to find Km and Kcat?
I did an experiment on catalase and its breakdown of hydrogen peroxide. I used a gas pressure sensor to track how much O2 was produced from the reaction over time. The following is an example raw plot of what I found. Point 0 is when I put the substrate and the reaction started (so I think I can call this the "maximum amount of substrate concentration" - in the Michaelis-Menten plot, it should be on the far right side.)

To find the speed of the reaction at each point, I thought of finding the slopes between each point, which basically equates to finding the derivative. Since the raw plot I found looks like a logarithm function, so I would predict that the derivative would look like a hyperbola (with x > 0). Indeed, this is the (crude) graph of the "derivative" of the previous plot, which looks like a hyperbola:

I believe that Kmax is the y-value of the first point in this graph - the initial velocity when the substrate is mixed with the enzyme. The substrate concentration is at highest at time 0, and the substrate concentration decreases as time increases.
So I thought, to make the Michaelis-Menten graph, I should flip the x-axis so that the substrate concentration is increasing along the x-axis. Yet, my problem was that if I do this, then the graph ends up not looking like the Michaelis curve...

What I would have wanted to find is the Michaelis-Menten curve, so that I can also derive the Km and Kcat values. Does anyone know how to do this? Or am I doing my steps wrong? Thank you very much for helping me!
Michaelis-Menten Curve:

Have you got data for different concentrations of hydrogen peroxode?
If so you should choose a time point that falls on the linear part of your time graph. And plot the rate at that time point for each substrate concentration.
That will give you a MM curve where you can calculate the values you desire. You cannot calculate them with just your time data that you have provided.

No, unfortunately I do not. That is why I was wondering whether I could do any MM calculations from what data I have. I guess I cannot then (unless I assume that substrate concentration decreases linearly across time - the only thing I know is how much H2O2 I put in at the beginning). Thank you very much for your reply anyway!

@lia the point is that you need to run this experiment multiple times, with multiple different starting concentrations of $H_2O_2$, find the initial (linear) rate for each, and then plot the rate vs. starting concentration. That's what this answer is trying to tell you.


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Microscope parameters for whole blood alalysis
I wonder, what are the minimum requirements for a microscope for blood cell analysis. I'm interested in:
-Counting erythrocytes
-Counting and differenciating all typed of leucocytes
-Counting of thrombocytes

What is the minimum magnification of the objective required?
Which type of objective is sufficient?
What is the minimal price-class of such an objective?

As I found out in medical lab-groups, the most lab-workers use 100x Objective (oil or dry Leica objectices) and 10x ocular. This results in 1000x and the images like the below.
My idea was to use 20x objective (as it is much easier to handle) and 14MP camera. The erythrocyte should have the resolution about 60x60 pixels then, which should be enough for the differentiation.


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Is this 12+ foot plant a sunflower or hogweed?
I'm trying to determine what this is. The plant is well over 12-feet tall, had huge leaves, and a very thick stalk. People near me say it's a giant sunflower plant, but it hasn't bloomed or shown sign of flowers. My moral ag-knowledgeable friends say it's hogweed, which is very dangerous. Thoughts?
This is the plant .
Here's another picture .

Looks exactly like a sunflower.  Though I've never seen hogweed in person (I assume you mean Giant Hogweed?), the leaves are much different, as in this picture: https://www.goodhousekeeping.com/home/gardening/a21598753/giant-hogweed/#15323659656822&%7B%22sender%22:%22offer-0-1WjsT%22,%22displayMode%22:%22modal%22,%22recipient%22:%22opener%22,%22event%22:%22resize%22,%22params%22:%7B%22width%22:800,%22height%22:792,%22iframeId%22:%22offer-0-1WjsT%22%7D%7D  Also, if it's a sunflower, it simply may not have bloomed yet.  Mine are just starting.

Never listen to those friends anymore (concerning plants that is).

The plant in your photo is a sunflower (Helianthus annuus).  The large, heart shaped leaves and stiff, hairy stem are very characteristic of the sunflower as seen in your plant. These form a single flower head on top when mature - about 90 days after planting.  They typically grow to 10 feet in height, so 12 feet would not be unusual.  The tallest recorded specimen was apparently 30 feet in height. Please see links below for more information.
https://en.wikipedia.org/wiki/Helianthus_annuus#Cultivation_and_uses
https://homeguides.sfgate.com/time-year-sunflowers-bloom-67915.html
http://www.illinoiswildflowers.info/prairie/plantx/an_sunflowerx.htm

That’s definitely a sunflower. Hogweed has very large lobed leaves and has more maple or oak look to it. Most sunflowers bloom at different times. For most sunflowers- August to early October is flowering time. Peak is usually September. Hope this helps.


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Allergy vs. Immunity
What is the difference between these two phenomena in our organism: allergy and immunity? Both cause producing of antibodies which struggle against antigens. Is it true, that allergy always leads to destruction of tissues and organs? If yes, why does destruction take place in case of allergy but not within immunity?

First line of wikipedia > Immune system

The immune system is a host defense system comprising many biological structures and processes within an organism that protects against disease

First line of wikipedia > Allergy

Allergies, also known as allergic diseases, are a number of conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment.

In other words, the immune system is here to defend the organism against diseases. However, sometimes this immune system misinterprets a harmless substance and start triggering an immune response against it. Such immune response against harmless substance is called an allergy. An allergy is hence a defect of the immune system. There are other defects of the immune system though, such as autoimmune diseases.


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Did the chromosomal fusion within humans affect phenotypical change compared to the separated chromosomes in the other apes?
I just read this article on the evolutionary divergence between humans and chimps, and how the most significant event was when the 24 number of chromosomes in chimps was reduced to 23 in humans due to chromosomal fusion. However, while this even significantly supports the theory of evolution, how does this affect natural selection? What phenotypical changes may have occured between these two groups because of the chromosomal fusion? And what if chromosomal fusion did not occur? Would speciation still occur by other means, e.g. geographic isolation?

A few comments. 1) Is there any reason for using the phrasing while this even significantly supports the theory of evolution, how does this affect natural selection? instead of just asking How did this large mutational event affect the phenotype and the fitness of the carrier? 2) And what if chromosomal fusion did not occur? this type of what "what if the world was different" are impossible to answer on a science website

Would speciation still occur by other means do you have any reason to think that this mutational event lead to reproductive isolation? Between which lineages then (two hominids lineages and among the pan and hominid lineages)?

Ah I see. I'm only eighteen so my question phrasing is still underdeveloped. And I believe reproductive isolation would occur due to post-zygotic barriers such as infertile offspring. The difference in chromosomes number should have an affect on offspring production, either disallowing it, lowering survival chance, or having the offspring infertile. And as for the lineages... I have not studied them haha

Are you claiming that humans with balanced Robertsonian translocations are reproductively isolated?

@swbarnes2 After a quick research, I would say I am claiming that those affected with Robertsonian translocation are reproductively isolated.

And is this claim of yours backed up by evidence?


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What happens to the ATP after it stores energy?
The title says it all. After the procceses of cellular respiration happen,  the energy is used in different activities that use it, but which are them, more specifically?

Welcome to SE Biology. Please take the Tour and read how to ask a question here. You are expected to demonstrate you have done your own research before asking a question.Yours is a basic question that is covered in many biochemistry and biology texts, such as Berg et al. on-line. If you have any specific questions after doing that, then it is OK to post them here, explaining what you do not understand. But check previous questions first.

this is one of those questions that could be answered by a quick visit to wikipedia. https://en.wikipedia.org/wiki/Adenosine_triphosphate

Well first of all, how is ATP used in metabolic processes? The build up of molecules require energy. And the best molecule in biological livijg systems is ATP.
One of the processes that require ATP is the very process that makes it: glycolysis. The body will reconfigure the shape of glycolysis, transforming it into a precursor of pyruvate. This first phase (a.k.a investment phase requires two ATPs, dephosphorylating it into two ADPs. And to recap the payoff phase, once the main molecule is split, the molecule will breakdown into pyruvate through another set of various steps. At the same time, two ADPs will be phosphorylated into two ATPS. This phosphorylation occurs for each of the two pyruvates.
So the one of the main purposes for ATP is for the build up of molecules. The energy of ATP is released when it is convenient for into ADP + P, and is transferred to the new, bigger molecule.
Another process that ATP is involved in is activation. In neuron cells, the sodium potassium pump is constantly trying to set a concentration gradient between sodium in the cytoplasm and potassium in the extracellular fluid. And because it is working non-stop, it needs ATP to continue working. However, in the scenario where an individual is deprived of oxygen through an extended period of time, brain damage may occur due to the the absence of ATP production. The sodium potassium gradient will never be restored, and the neuron will be unusable.


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mRNA Sequencing Basepair from Polyadenylation Site?
I was wondering how many basepairs are usually sequenced with mRNA/cDNA illumina methods from upstream of the polyedenlation site?
Thanks.

No one can answer this.  There are too many sequencing methods.

50-75 bp could be achieved.
Refrencing TruSeq® RNA Sample Preparation v2 Guide. My lab used random primers and read lengths were an average of 75 bp in length for an RNA seq project. But controlling distance from polyA wasn't considered in out project.
Using oglio(dT) primers you could try and control a specific length from the polyA tail.Two basic variations use either random primers or oligo(dT) primers for this reaction. Oligo(dT) primers are highly 3’ biased and mostly
suitable for mRNA abundance (expression) analysis. Random primers also result in some bias, which can be reduced by fragmentation of the input RNA.
Source: RNA Sequencing Methods Collection - Illumina, Page 8.
Different lengths can also be achieved for different needs.
Gene expression / RNA Profiling – Quantifying the coding transcriptome typically requires a short single read (often 50–75 bp) to minimize reading across splice junctions while counting all RNAs in the pool.
Transcriptome Analysis – Novel transcriptome assembly and annotation projects tend to benefit from longer, paired-end reads (such as 2 x 75 bp) to enable more complete coverage of the transcripts and identification of novel variants or splice sites. Paired-end reads are required to get information from both 5’ and 3’ ends of RNA species with Stranded RNA-Seq library preparation kits.
Small RNA Analysis – Due to the short length of small RNA, a single read (usually a 50 bp read) usually covers the entire sequence. A read length of 50 bp sequences most small RNAs, plus enough of the adapter to be accurately identified and trimmed during data analysis.
Source: Illumina (Considerations for RNA-Seq read length and coverage)


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Anyone know what this it?

More than 1 washed up on a beach in Ireland..close to some big jellyfish

Have a look at the tag info for species-identification

Maybe some barnacles?

Gooseneck barnacles
It appears to be a cluster of goose barnacles washed up onshore. This is based on the thick, distinct pedicle and the general shape of the asymmetrical valves. Without more information, that’s as accurate as I can probably get you.