How to increase the shelf life of yogurt without refrigeration? When we make yogurt at home and do not refrigerate it, it will become sour because of conversion of lactose into lactic acid by Lactobacillus bacteria, but this does not happen in case of Nestle's yogurt or any other brand until it remains air tight.

I wonder though bacteria is still present in it and continue to convert lactose into lactic acid then why does not packed yogurt becomes sour? How these companies increase the shelf life of yogurt..?

This article gives an excellent review on yogurt manufacturing, but to summarize:

-Raw milk goes through centrifugation to remove somatic cells and other solid impurities.
-Thermalization is conducted at "60–69 °C for 20–30 s, aiming at the killing of many vegetative microorganisms and the partial inactivation of some enzymes."

After this point, the milk may be inoculated with lactic acid bacteria or other microfloras.

-Then, standardization occurs which for milk refers to the standardization of fat and solid-non-fat content (SNF).  This in short affects the fermentation process ("an increase of SNF increases the duration of the fermentation process").

-The next step is homogenization, which prevents milk fat from rising to the top of the liquid.  This has an effect on the stability of the emulsion.

-I think this step is where "sterility" comes into play, "heat treatment of milk reduces the number of pathogenic microorganisms to safe limits for the consumer’s health. Various heat treatments can be applied, which are classified based on the duration and the temperature. The most common are known as thermalization, low and high pasteurization, sterilization and UHT (Ultra Heat Treatment)."  The review goes into more detail about each type and what they eliminate or don't eliminate (spores, vegetative bacteria, etc.).

-The fermentation process is the most important one for developing flavor and texture.  The two live bacterial strains of Streptococcus salivarius subsp. thermophilus (ST) and Lactobacillus delbrueckii subsp. bulgaricus (LB) are the two most basic strains used in yogurt.  LB is what metabolizes lactose into lactic acid and LB and ST acting in synergy is what causes a decrease in milk pH.  "When the pH of the yogurt approaches 5.0, activity of ST subsides and LB gradually dominates the overall fermentation process until the target value of pH is reached and the fermentation process ceases. Normally, the fermentation period is terminated by lowering the temperature to 4 °C. At this temperature, the culture is still alive, but its activity is drastically limited to allow controlled flavor during storage and distribution."  I think to answer your question, yogurt manufacturers probably have a very sensitive gauge for pH and can control temperature fluctuations finely to maintain yogurt pH and flavor (not too sour).  "After the pH of yogurt reaches the value of 4.7–4.3, the yogurt is cooled to around 5 °C. This inhibits the growth and metabolic reaction of the starter culture and prevents the rise in acidity. Cooling of yogurt can be in one or two phases. One-phase cooling involves the rapid decrease of the coagulum temperature to less than 10 °C, where the fermentation process is inhibited leading to yogurt with low viscosity. Two-phase cooling is initiated by rapidly decreasing the temperature to less than 20 °C and then gradually reaching the storage temperature of 5 °C leading to yogurt with an increased viscosity and limited syneresis. This is quite common in the yogurt manufacture process, especially when fruits are to be added."

You can read about the other innovative methods involved in yogurt making such as: Ultra High Pressure (UHP) which inactivates pathogens and microorganisms that cause milk to spoil, High Intensity Ultrasonication and Pulsed Electric Field (PEF) which all can reduce microbial content.

Edit: Forgot to mention that some DIY yogurt instructions mention that if you ferment longer and/or in warm temperatre the more sour it will be so to reduce how sour it is, either ferment it less and/or start fermentation at a lower temperature (source).

Sfakianakis P, Tzia C. Conventional and Innovative Processing of Milk for Yogurt Manufacture; Development of Texture and Flavor: A Review. Foods. 2014; 3(1):176-193.


How does sucrose protect bacterial cells in lysozyme solutions? I have a microbiology question.

When we put bacterial cells in sucrose solution with concentration higher than 0.5M we observe plasmolysis - the cytoplasmic membrane detaches from the cell wall due to water loss in order to balance the osmotic gradient.

If after that we put some lysozyme in the solution, the cells become spherical as they turn into spheroplasts, but they are still alive.

If we put lysozyme in a solution that contains bacterial cells, but no sucrose, they die. So my question is how does sucrose protect cells from lysis?

This is an interesting question and as often, it has been noted by someone before. In this case it has been a researcher named Claes Weibull, who did his research in the 1950s. He noted (as you did) that sucrose has a protective function on the generation of protoplasts from Bacillus megaterium) with lysozyme. He published the following figure (from the first paper below):

He did not really explain the phenomenon, but speculated about protective function of the sugar in solution when the bacterial cell wall is removed. This also works with PEG in solution (see the third paper below).
He published a number of papers on this (if you look him up in Pubmed, you will find more articles, but these seem most relevant):

The isolation of protoplasts from Bacillus Megaterium by controlled treatment with lysozyme
Characterization of the protoplasmic constituents of bacillus
megaterium.
Osmotic properties of protoplasts of Bacillus megaterium.

It seems also possible to cultivate these protoplasts on agar plates and let them form "normal shaped" bacteria again:

Morphological study of the reversion to bacillary form, of Bacillus
megaterium protoplasts.


Parametric Bootstrap Capture Recapture I am using the (one sample) capture recapture for estimating hidden human population. One sample method uses purely frequencies of capture to estimate population. One of my colleague suggested parametric bootstrapping method to assess the variability of the population size estimate. I tried to research online a little about this parametric bootstrap method but I just still don't understand how it is performed. I know bootstrapping is basically resampling data with replacement and then calculating the variance of it. However how do I perform parametric bootstrapping (I assume the frequencies of capture follows Poisson Distribution) on capture recapture data? Do we treat the frequencies as datas, i.e. so if f(1)=100 and f(2)=9, our data has 100x 1 and 9x 2 and then resampling this? Is probability of daily capture the parameter $\lambda$ in Poisson distribution?

I guess what I am trying to ask is, how do you perform the sampling bit of a parametric bootstrap [in capture recapture]?

I did a little research and I think it works like that:

Collect a dataset of $n$ observations.
Fit a parametric model to your data. If you want to model the recaptures, I would suggest a Poisson-GLM. You can also estimate the parameter directly from your data and simply parametrize a Poisson distribution. However, this approach would not model the random variation in your data.
Use the fitted model to draw a sample of size $n$
Calculate your desired metric based on the sample. I guess in your case this would be human population size (calculated as ${N} = \frac{nM}{m}$?)
Repeat steps 3 and 4 many times (1000+)
There you go! Now you can easily assess the variability in population size based on the estimates from your bootstrap samples.


Is there any biological evidence that is not suggestive of or seems to disprove evolution? Often, in science, when we have evidence that doesn't fit our paradigm, we bend it until the paradigm collapses.

Although there is plenty of decent evidence for evolution, is there anything that does not fit the evolutionary paradigm? Is there any biological evidence that is not suggestive of or seems to disprove evolution? Or is everything merely hunky-dorey?

Evolution is a broad field of knowledge. There are definitely a few elements of our current theory of evolution that does not perfectly match observations. However, those concern small details and might not of much interest to you. Here are a few examples

We don't know the relative importance of background selection and selective sweep at explaining genome-wide variation in genetic diversity.
We don't really have much of an idea what fraction of speciation happen in sympatry.
We don't understand well how recombination rate evolves to differ in different genders.
We don't really understand what are the limits and/or costs of phenotypic plasticity that makes phenotypic plasticity less frequent that we would otherwise expect.
We don't really understand the patterns of genetic diversity on sexual chromosomes at the intersection with the pseudo-autosomal region (PAR).
We don't fully understand how much expansion load (a type of mutation load caused by the sampling of individuals at the expansion edge of a population) there is in human population.
We don't really know whether the mitochondrion (and other double membranes organelles) was first a endo-parasite or a endo-symbiont.

If you are asking whether there are evidences suggesting that evolution is not happening or that humans and chimpanzee do not actually share a common ancestor but were created independently, then no, there is no such evidence.

You should have a look at the related post Is Evolution a fact?


Will obligate aerobic bacteria die if placed in a buffer solution even in the presence of oxygen? The electron transport chain in aerobic bacteria functions by pumping H+ out of the cell to establish a concentration gradient.
So if the bacteria are placed in a buffer solution having pH equal to the cytosolic pH of the bacteria, will they still be able to establish the required concentration gradient? Will the increase in pH of cytosol(due to loss of H+) alone be enough to drive ATP synthesis even in the absence of a pH change in the medium? i.e.Will obligate aerobic bacteria die if placed in a buffer solution even in the presence of oxygen?

Answer
No. There is ample evidence that:

Most non-extremophilic bacteria grow over a broad range of external pH values, from 5.5 – 9.0, and maintain a cytoplasmic pH that lies within the narrow range of pH 7.4 – 7.8.

The explanation for this is another matter, but, before discussing that question there are two points of possible misunderstanding in the question that require a note of clarification.
Clarifications

What the electron transport chain establishes is an electrochemical proton gradient, or proton-motive force (PMF). This consists of two components§: the hydrogen ion concentration difference, ΔpH, and the electric potential gradient, Δψ.

The source referenced in the question shows hydrogen ions being pumped from the cytoplasm, across a membrane, to a space labelled “outside”, which, according to the figure legend represents hydrogen ions “pumped out of the cell”. This is incorrect. The hydrogen ions are pumped into the space between the inner and outer membranes of gram-negative bacteria, or the space between the inner membrane and cell wall of gram-positive bacteria. It cannot necessarily be assumed that this space has the same pH as the external milieu.

How is the proton motive force maintained?
A possible explanation of why a constant or, more striking, alkaline pH does not destroy the proton motive force relates to the two-component nature of the latter. Bacteria appear to be able to compensate for any decrease (or even inhibition) of either ΔpH or Δψ by a reciprocal increase in the other (Bakker and Mangerich,1961). One mechanism that illustrates how this can be achieved in certain cases is the use of an alternative terminal oxidase, cytochrome bd:

Cytochrome bd generates a PMF by transmembrane charge separation, but
does so without being a proton pump.

However there is a complex set of anion co-transporters involved in cytoplasmic pH homeostasis which may influence the membrane potential. The situation is neither simple nor, as yet, completely resolved, as far as I am aware (but it’s not my field).

§ The treatment of electric potential gradient, Δψ, tends to be downplayed in biochemistry text books. This may be because the generation of a hydrogen ion gradient is easier to understand than that of a membrane potential, or because the texts deal with the latter in sections on nervous tissue. There is a quantitative treatment of the free energy changes involved in Chapter 18 of Berg et al. online.


Does RNA-LPX expression of antigen by DC induce only T-cell with that antigen specificity? There was a recent publication concerning use of IV administered RNA-lipoplexes with an adjusted electrical charge to encourage dendritic cells (DC) to pick up the RNA package encoding viral or mutant neo-antigens, for example, a sequence of melanoma tumor cell coded to RNA. The paper is at Systemic RNA delivery to dendritic cells

After reading that abstract and related papers (see Dendritic Cells Pulsed with RNA are Potent Antigen-presenting Cells In Vitro and In Vivo By David Boczkowski et al I came away with the concept that the RNA segment of encoded tumor protein was taken up by a DC and the DC translated that to a protein (antigen) that it presented with MHC of the appropriate class (class I I believe in these tests) to a naive T-cell, which would subsequently amplify and pursue and kill tumor cells with that antigen (by becoming CTL cytotoxic T cell leukocytes).

A quick look at my immunology text from NIH tells me that this mechanism (DC's bringing antigen to naive T-cells in lymphatic tissue) ensures "that rare antigen-specific T cells will encounter their specific antigen on an antigen-presenting cell surface."

My question is does this mean that the so-called "mutant neo-antigen" of a particular tumor in an individual must still find a T-cell receptive to that sequence (epitope) at least in part (say fractionally)? I guess I'm wondering whether there might be the case where a particularly diabolical tumor presented such novel sequences that no existing T-cell rare or otherwise could be receptive to a fraction of its sequence (even when a customized RNA delivery of a selected portion of the sequence was delivered via DC to the T-cell).

The OP (me) was unclear whether or not the new therapy had to ultimately present antigen specific to a particular naive T-cell. The answer is yes: Each T-cell is specific for a single antigenic determinant. An antigenic determinant is a small portion of an antigen, such as a certain sequence of amino acids in a protein, that the immune system (a T-cell receptor in this case) recognizes as non-self or altered self. The antigenic determinant is also known as an epitope. Typically an antigen has many different epitopes, each able to react with a specific antibody or T-cell receptor (when presented with MHC).

The confusion arose from the description of the RNA as encoding "mutant neo-antigens" (among other possibilities, e.g., viral or endogenous self-antigens). At first glance this seemed to imply that a tumor antigen constituting a novel polypeptide antigen ("mutant neo-antigen") was able to induce T-cell response (effector and memory T-cell responses) in the absence of any T-cells with a T-cell receptor specific to that neo-antigen. That would not be possible.

Through somatic gene rearrangement in development, T-cell receptors (TCR)  have a wide range of antigen specificity, such that each T-cell has a unique receptor on its surface able to recognize foreign protein antigen associated with MHC molecules. Some estimate that human TCR and antibodies can respond specifically to 10 million different antigens.

Apparently the distinction is made between classical tumor-associated antigens that typically constitute autoantigens (which may appear frequently on the surface of cancer cells in conjunction with MHC and therefore generate some antibody response, possible ineffective) and neo-epitopes, the latter being the result of the estimated 25 – 30% of antigenic mutations (mutations not normally found in the genome) in tumors that could be made to induce immune response on the single- or poly-epitopic level. It appears that autoantigens are more modified normal protein that tend to appear somewhere in the disease process on a particular class of tumor than the result of entirely novel mutations. Since tumors usually have tens to hundreds of non-synonymous mutations, the mutanome of a tumor provides many possible targets for custom poly-epitope vaccines for each individual patient. Coding messenger RNA (mRNA), i.e., synthesizing mRNA to encode multiple transcripts for synthetic poly-epitopic nucleotide sequences, is an attractive antigen delivery format.

In order to locate a sequence that would be likely to act in this capacity (that is, to select tumor mutations likely to exhibit immunogenecity), an approach like the following serial selection has been suggested: (1) next generation sequencing (NGS) of an patient's individual tumor mutanome and patient genome (2) identify triplicate sequences present in the tumor mutanome but not in the patient genome, i.e., identify the mutations in the tumor that distinguish it from normal self (3) identify those mutations that are likely to code for a protein (4) identify those mutations that are likely to cause a non-synonymous protein change (5) identify those mutations meeting all the previous criteria that a predicted to be in a peptide presented on tumor MHC. An example quantifying this selection process is that of the murine B16F10 melanoma mutanome: The NGS exome profile (coding exons) predicted 12,842 mutations; 3570 of those predicted as somatic mutations; non-synonymous mutations 962; mutated peptide predicted to bind MHC 462; 50 of those selected for testing and of those 50, about a third of those tested strongly immunogenic when encoded to RNA and transfected to dendritic cells, i.e., inducing strong T-cell response. As a test of actual anti-tumor effect, mice were immunised with the encoded mutations identified and achieved complete tumor protection and survival in 40% of the group, compared with death of all control group animals.

Generalizing, a poly-epitopic vaccine formed from a tumor mutation should be selected to be specific to the tumor and not in the patient germline genome, to occur in a protein-coding transcript, to cause a change in protein sequence and that protein be expressed in tumor cells. In order for the mutation to induce a robust T-cell response, the mutation-containing epitope must be presented on the patient's MHC molecules in the dendritic cells during vaccination (and at least one T-cell must possess a receptor specific for one of the epitopes) and in the tumor cells for recognition (on the surface of the tumor cells). With the patient HLA haplotypte, MHC-binding epitopes can be predicted with computer algorithms. The immunogenecity of the computationally predicted epitopes can be tested in vitro with T-cell stimulation.

One of the challenges to RNA delivery has been degradation by ubiquitous extracellular RNAses. The study noted [Systemic RNA delivery to dendritic cells] solves that issue by protecting the RNA with lipid carriers to form RNA-lipoplexes (RNA-LPX). This has the additional adjuvant effect (the RNA-LPX) of triggering interferon-a (IFNa) release by plasmacytoid DCs and macrophages in a manner similar to early phases of viral infection.


Is there a term to quantify how spread a character is on a phylogenetic tree? Is there a term which can quantify how 'spread out' a particular character is on a tree? I want to distinguish between a character which is only restricted to a particular clade vs. a character that occurs all over the tree.

ETA: by 'all over' I meant it may be restricted to a few branches but those branches are spread out over the tree. It need not be ubiquitous. e.g. the character marked in blue on  compared with the case where these three branches are in a small clade.

I agree with Terdon's terminology in the comment ("ubiquitous" or "widespread").

You can use clade-specific or species-specific for a restricted character.

For the characters that appear in all species of a branch and in a quantitative way you can also provide the estimated age of the last common ancestor to the branch featuring that character. This tool might help you: http://www.timetree.org/


Do humans squint more readily at green light? I know that humans won't squint their eyes even if exposed to dangerous levels of ultraviolet or infrared light because our eyes simply don't have the capability to detect it. Neither do the irises constrict.

Since the human eye is most sensitive to green light, does this mean that we will squint and/or constrict our irises more readily for green light? Perhaps even when the intensity is safe for our eyes? (Albeit close to dangerous levels)

Yes.  According to Action spectrum for photophobia Journal of the Optical Society of America A, Vol. 20, pp. 1852-1858 (2003), the most squinting-sensitive wavelength is ~510 nm, which is green.  Squinting sensitivity progressively falls above 510nm, and below 510nm squinting falls to a local minimum at 460 nm, and then rises again below 460nm, but did not reach a higher maximum in the range studied, which ended at 420 nm.


Why is proteinase K digestion performed at 50 °C? Many DNA isolation protocols use a Proteinase K digestion to remove proteins. This is often performed at 50 °C. Why is this?

In your linked wiki article: "An elevation of the reaction temperature from 37 °C to 50 - 60 °C may increase the activity (of Proteinase K) several times." The enzyme works faster at 50°C.


What is happening when we get a tan? Almost everyone nowadays wants that nice summer tan, but what exactly is going on beneath the skin? I've heard a few different theories about tanning - such as a tan is nothing but the pigmentation in your cells burning, but is this true?

My questions:

What exactly is happening to our skin as we tan?
Are pigments being burned (like I was told in school), or is pigment being produced by the cells. ?

Bonus related question:
 Why do some people burn and others tan?

Bonus related question: https://biology.stackexchange.com/questions/35719/how-does-our-tan-disappear

When our skin is exposed to the sun, this can cause some damage in the upper layers of skin. This activates DNA damage repair and also induces signalling towards the melanocytes (which produce the pigment). Signalling means the excretion of signalling molecules (mostly alpha-Melanocyte stimulating hormone, aMSH) which binds to the MC1R receptor (melanocortin 1 receptor) on the surface of the melanocyte (the cell which produces the pigment) and induces (or increases) the production of melanin. The melanin is then transferred in the melanosomes to the adjacent keratinocytes, which are then better protected from the sun. This figure (from this article) illustrates this process nicely:

Short term tans (the fast reaction) are based on the changed distribution of melanosomes (granules containing pigment) from the melanocytes to keratinocytes. Longer term suntans are caused by increased pigmentation in the skin as a reaction to the UV exposure by the accumulation of melanin and by the burning of cells. So it is no wonder that it looks like increased pigmentation, it really is. People tan differently because of their genetic background. This influences their ability to react to sun exposure.

There is relatively little known about the degradation of the melanosomes (the granules containing the melanin). What is known is that they are degraded in the lysosome, and that the melanin is most likely degraded through oxidation. There happens to be a permanent turnover of the melanosomes, and when the body is producing fewer new melanosomes than are degraded, your skin will get lighter again.

References:

Shining light on skin pigmentation: the darker and the brighter side
of effects of UV radiation.
Melanocyte biology and skin pigmentation.
Melanosome Degradation: Fact or Fiction


Is the amount of phosphoric acid added to colas enough to disrupt the function of the kidney over the long term? Both Coca-Cola and Pepsi add phosphoric acid $H_3PO_4$ to their colas to give them a signature "bite".

The kidneys use a phosphoric acid/dihydrogen phosphate/hydrogen phosphate homeostasis as one mechanism to eliminate/excrete excess acid from the body.

The issue of whether sodas containing phosphoric acid can exacerbate osteoporosis and related conditions has been explored here and in some detail on Wikipedia, but I'm more interested in direct effects on the kidney.

I'm interested to know if the overall renal physiology is adversely affected by extra phosphoric acid that long-term moderate consumption (say a single 2L bottle per week for a year) of soda would introduce (including interrupting or saturating the Na-Pi transporter)?

The phosphoric acid in cola will contribute to dietary intake of phosphate. I may be missing something, but, since the transporter functions to reabsorb phosphate that has been filtered out at the glomerulus, excess phosphate will spill over into the urine.

According to Wikipedia the RDA for phosphorus is 700 mg and the tolerable upper intake level is 4000 mg. Coca cola contains 17 mg phosphorus (as phosphate) 100 ml-1 (which is 340 mg in 2 L)

According to this source,

  in the United States, an average person drinks 412 8-ounce drinks — or 3296 ounces — of Coke per year.

This works out at 9 oz per day = 266 ml = 45 mg phosphorus

For comparison (from here):

white flour contains 595 mg 100 g-1
one boiled egg contains 220 mg
canned salmon contains 240 mg 100 g-1


Can the Hebbian theory apply to Inhibitory Neurons If I understand the basic Hebbian theory, when a neuron fires a pulse to another neuron and this pulse causes the target neuron to fire then the delta energy sent from the initial neuron to the target is increased. (Making it easier to trigger the target cell)

With this in mind is there a way for an inhibitory neuron to increase the delta energy it applies to a target neuron (reducing the excitation level of a target neuron).

If the inhibitory neuron never triggers the target then I would assume it would never increase the decrease in energy it sends to the target.

≈Yes, it's easy to conceptualize at a simple ganglionic circuit. A really good example is (I believe from Kandel's lab)demonstrated by Aplysia's gill withdrawal reflex. Repeated stimulation causes reduced EPSPs in motor neurons that innervate muscles that cause the withdrawal reflex. However when you apply a electric shock to the tail, the snail will immediately regain withdrawal reflex sensitivity. The tail sensory neuron response activates the serotonergic facilatory interneurons which have multiple IO with sensory and motor neurons.

And don't forget, interneurons can inhibit other interneurons leading to disinhibition.

For most LTP work you're probably ok using Hebbian models. Make sure to keep in mind that in more complex systems like cortical circuits.  there are some modes of communication that don't always play well with Hebb's Laws: gliotransmission, retrograde transmission, neuropeptides/GPCRs, and activation of perisynaptic receptors/receptors on adjacent cells.


Two subunits connected by only one disulfide bridge: quaternary structure? I've always simply assumed quaternary structure to be characterized by non-covalent interactions such as hydrogen bonding, van der Waals interactions and whatnot. However, if two distinct polypeptides were only connected by one covalent disulfide bridge, would this be considered as quaternary structure, assuming that non-covalent interactions between the subunits are either negligible or even repulsive?

In other words, can a disulfide bridge, on its own, convey quaternary structure?

On a side note, are there any notable examples of this type of interaction?

I don't know of any examples of this but I would say no doubt, that's quarternary structure. Quarternary isn't so much defined by the kind of interaction but much more the fact that it's between different polypeptides; all lower-level structures are within one polypeptide. (Wikipedia agrees.)


How to convert PDB file of Amino Acids to rotamer tuples list of all AAs instances Either by Python command, or via specific application (like Chimera) publicly available. Please provide example or link to one of.

I have to detect AA location within MAP (density) 3D matrix. And to verify with PDB format (which models same 3D structure). Each AA may have different rotamer (aka 3 angles usually used to describe AA exact position related to carbon C_alpha atom (the atom which AA side chain exits from). To justify inaccuracies - I need to show that (among other reasons) - inaccuracy is caused since not all possible rotamers existed in my training set (I use machine learning classification to decide what AA is it, and where it stands within cryo- EM scan).

I’m not sure if it is what you are after, but I have used Roland Dunbrack's dihedral perl script to get dihedral angles, the header of which is:

 RL_Dunbrack@fccc.edu

 usage
 dihedral.pl filename [chain]

 dihedral.pl pdb2hla.ent
     will print out all dihedrals from file pdb2hla.ent
 dihedral.pl pdb2hla.ent A
     will print out dihedrals only from chain A

I don’t know if it’s on his website as I got it from him personally. If not, or even if it’s not what you need, email him — he is likely to be able to help you.


Multi-modal distribution for gene expression data Why would some genes have more than two modes in their expression distribution? What external factors would cause this anomaly?

I'm referring to the expression distribution of a gene across different tissue samples. For example, if one was to download a bunch of data from NCBI GEO, and pinpoint one gene and plot the expression level versus the frequency for that gene across all those data sets, some genes would have more than 2 modes (2 expression levels with very high frequency). This is the only case I'm interested in: more than 2 modes - not bimodal. So what would cause more than two modes?

One trivial situation in which this can happen is when the tissue used for expression studies is heterogeneous. Different cells express different levels of the gene.

Bimodality can be observed when the system can actually occupy two stable states; i.e. a gene can either have a high expression or a low expression. When you sample the population you would get two peaks. Bistablity (two stable steady states) is a common phenomenon in biological systems and positive feedbacks generally exhibit such behavior. In bistable systems there is also an unstable steady state which lies "between" the two stable states (like a mountain separating two valleys). If the system is in the unstable state, it can fall to either of the two stable states. (See this article for an example). This concept can be extended to multistable systems but they are a little more complex than the simple feedbacks. However they can theoretically exist (I don't know of a biological example yet).

Bimodality/multimodality can be also observed in the absence of a deterministic bistability in the system. This happens because of the expression noise due to stochasticity and is observed in case of transcription bursts (See here).


Ascending loop of Henle When ions diffuse out passively or are actively transported out of the ascending loop of Henle, do those ions just hang around or do they go into the circulatory system and leave the kidney.

I ask because I know the medulla must stay salty but I always assumed that those ions were then entering blood vessels for another purpose.

Do ions in the medullary interstitium just hang out, or go into the circulatory system and leave the kidney?

Both!

You've grasped one of the fundamental principles of the renal physiology -- the medulla must stay salty. Lets start there and see if we can't work out what happens.

As the filtrate flows through the tubule, solutes are removed from the lumen at the thick ascending limb and added to the medullary ECF. This concentrates solutes in the medulla, producing the corticomedullary gradient (the medulla must stay salty). This is called countercurrent multiplication, and explains how such a large osmolar gradient occurs between the cortex and the medulla.

At steady state, with an established corticomedullary gradient, what happens? Solutes continue to be reabsorbed by the tubular cells in the thick ascending limb. In order for it to be steady state, each ion reabsorbed into the ECF needs to go somewhere. One of three things could happen to these ions:

Secretion or diffusion into the collecting duct (and excretion as urine)
Diffusion into the cortex (dissipating the corticomedullary gradient)
Diffusion into the capillaries in the medulla, the vasa recta (exiting the kidney through the renal vein)

In fact, all of these things happen to a certain extent.

Secretion and diffusion into the collecting duct (1) are regulated by changes in the expression of pumps and channels. Diffusion into the cortex (2) is kept to a minimum by diffusion into the vasa recta (3), what we call countercurrent exchange.

  I always assumed that those ions were then entering blood vessels for another purpose.

So this does happen, but remember, the main reason for concentrating solutes in the medulla is so that the kidney can, if it needs to, excrete a very concentrated urine. Ions enter the blood vessels for the same purpose, in order to prevent them from diffusing back to the cortex, dissipating the corticomedullary gradient.

The concepts of countercurrent multiplication and countercurrent exchange were proposed in the 1940s and supported by a series of experiments in the 1950s. The landmark 1959 paper by Gottschalk and Mylle in The American Journal of Physiology was reprinted in 1997 by JASN and available for download without a paywall. It's an excellent read! As they predicted, we've learned a lot more, but this model still holds up, and is what we teach in renal physiology to this day.

This is their figure:


Decomposition of human body after death What causes decomposition of human body after death? Here it says autolysis, while Here it says that bacteria decompose the body. If bacteria decompose the body, why don't they do while we are living?

Bacteria don't decompose the body while your alive (or even when your at the office)

Because your immune system keeps the population safe, by eating them.

Both autolysis and bacteria cause decomposition.

But there are 2 types of decomposition. The kind that keeps you from being able to be rescusitated happens within 5 minutes at room temp after death.
This is oncosis.

The kind where you smell like French cheese happens later, as the cells pop and disintegrate, and then get eaten by bacteria, which release stinky chemicals.


Standard practice for generating rarefaction curves from Next Generation Sequencing data We have a few million 18S reads from a particular environment. The reads have been clustered into Operational Taxonomic Unit (OTU), and the OTUs annotated against a reference database.

To generate a rarefaction curve, my understanding is that one randomly samples $n$ reads where $n$ ranges (with some step size) from 0 to the total number of reads, and counts the number of OTUs observed at each such sub-sampling.

Which of these two ways, as implemented by sequence analysis suites such as QIIME and mothur, is standard practice? Which would be best to use with the above situation?

Treat the original assignments of reads to OTUs as truth, and when resampling $n$ reads, just count the number of "original" OTUs observed in this sub-sample.
Re-cluster the sub-sampled reads, and then count the number of "new" OTUs in the sub-sample.

My sense from reading through the QIIME documentation is that method 1 is the standard, but I am not sure. I also do not quite understand why method 2 wouldn't be the better way to go, though it would be computationally more expensive.

I actually work in the same group as Chris (QIIME author), so I hope this helps: An explanation he gave to us a while back about the basis of rarefaction curves is just to give an indication of whether your sampling is reaching saturated diversity, when comparing 2 unequal samples.

If you compare 2 samples, where sample x has less information (reads/amplicons etc) supporting it, you can't be sure you've sampled all the possible diversity.

Thus, you plot the number of OTUs you see for increasing numbers of reads. If you're saturating the diversity you should see it plateau.

To bring the 2 samples inline with the 'amount of supporting data' they have, you randomly sample the data of the larger dataset, so that it is equivalent to the smaller, and then compare the number of OTUs each is reporting.


A weird-looking fish with a shield I found this photo in a local news page. The page claims that this fish is a new species that was found by a Malaysian fisherman. Is this true or is it a known fish and already has a name?

This is a species in the Peristediidae family, commonly called armored searobins or armored gurnards.

  found in deep waters around the world, with most species in tropical regions. They are related to the searobins in the family Triglidae, and some authorities classify them in that family,2[3] but they are encased in heavy scales with prominent spines. They have prominent and often elaborate barbels on their chins.

Characteristics of Peristediidae [Source]:

  The scorpaeniform family Peristediidae (armored sea robins) is characterized by (1) a body entirely enclosed by four rows of spinous bony plates (scutes) on each side; (2) a large bony head with spines and ridges; (3) each first infraorbital (lachrymal) anteriorly extending in distinct rostral projections; (4) barbels on the lower jaw, and (5)pectoral fins with the two ventral most fin rays free and enlarged (Miller 1974; Miller & Richards 2002; Richards 1984, 1999; Kawai 2008, 2013)

Specifically, this looks similar to other species in the genus Satyrichthys.

 Satyrichthys welchi (Source: Taiwan Biodiversity Informaiton Facility)

According to Pogoreutz et al. 2013:

  The genus Satyrichthys is diagnosed as follows: (1) no teeth in upper and lower jaws; (2) lateral margin of the head smooth; (3) the ventral row of bony plates on caudal peduncle extending posteriorly, separating the posterior bony plates of the lower lateral series; (4) only the posterior lip and chin barbels branched, and (5) fewer than 20 soft rays in dorsal and anal fin (Kawai 2008, 2013).

  An important character in separating species of the genus
  Satyrichthys is the number of lip and chin barbels (Miller 1964, Kawai 2008, 2013)

One similar looking species is Satyrichthys welchi (the Robust armoured-gurnard) [pictured above] found in the South China sea:

 Source: AquaMaps

According to FishBase, here are some characteristics of Satyrichthys welchi:

Dorsal spines (total): 7
Dorsal soft rays (total): 17
Anal spines: 0
Anal soft rays: 18


Dragonfly Identification I have been clearing brush by a lake in northwest Missouri and seen a lot of dragonflies. It's hard to get decent pictures because my phone camera sucks and they fly away before I get close. But here is one I managed to get:

I got one other picture of another species, but it's much lower quality.

The overall body shape of the second dragonfly looks like a Libellula (Skimmer), due to its broad flat abdomen. It also seems to have distinct bands on all four wings, dark patches where the wings connect and a light blue abdomen, which would indicate e.g. a male Plathemis/Libellula lydia (Common whitetail). The picture is blurry though, and there might be other similar species that it can be mistaken for (the wiki page mentions a couple of similar species).

(picture from wikipedia)


How does the lymphatic system filter blood? One of the main functions of the lymphatic system is to filter blood. How exactly is it done?
Its quite hard to find an exact answer.

The spleen is an integral part of the lymphatic system, and it is a major filter of blood.

The way this is done is by removing old, distorted, or antibody-coated red blood cells from circulation.

Interestingly, the spleen is enlarged with many leukemias and lymphomas.


Difference between stem cell "expansion", "repopulation", and "self-renewal"? From this paper (link:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4130805/), I read "Thus G-CSF results in the expansion of phenotypic HSCs in the bone marrow with reduced repopulating activity and self-renewal capacity."

If expansion meant population-expansion, then would that not mean the same thing as repopulation? Likewise, self-renewal occurs through asymmetric cell-division in which a parent cell divides into two daughter cells; or it can occur through symmetric cell-division in which a parent cell divides into a progenitor cell and a daughter cell. In essence, both types of cell-division maintain or increases the population of stem cells; hence, "self-renew" or "expand". Clearly, I am missing something here with the terminologies. Please help! Lastly, I thought phenotype is a noun, then what does phenotypic even mean?

After an hour of reading the paper (from 2014), if you can I recommend instead reading the below review article (from 2020). the 2014 article uses difficult to understand language.

Eric M. Pietras; Inflammation: a key regulator of hematopoietic stem cell fate in health and disease. Blood 2017; 130 (15): 1693–1698. doi: https://doi.org/10.1182/blood-2017-06-780882

https://ashpublications.org/blood/article/130/15/1693/36384/Inflammation-a-key-regulator-of-hematopoietic-stem

I found this by pasting your article's title into google scholar, hitting "cited by", sorting by date, and browsing until I found a review article.

The point of treating with G-CSF is that the stems cells divide, and can be recovered from the blood for stem cell treatments.

"expansion" . Here means an increase in the numbers of cells. But in plant biology it has the literal meaning of cells growing larger.

"phenotypic HSCs". Using the adjective phenotypic, the cells express the phenotype of HSCs. So the cells behave like HSCs

By itself, G-CSF makes the the HSCs divide for a while, then they stop dividing. That is, they become "quiescent".

This state of quiesence can then be interrupted. If the mice are treated with antibiotics to kill intestinal flora (or if mice are used that are germ-free), then the HSCs continue to divide.
The article calls this process of getting the HSCs to divide again "mitigating the G-CSF-mediated HSC repopulating defect"


Help me find out what this bird is (description, no picture) A while ago I read about this bird(s) whose species status was not confirmed. This was because they had a very large distribution and birds in adjacent population could breed with each other but birds at each end of the distribution (western Europe and South Asia I think) couldn't. I am pretty sure that they were some kind of gull and from Europe to Asia their wings got lighter, from black to grey. I think I might have read about them in a Richard Dawkins book.

Does anyone know the species I'm talking about?

You're describing a Ring Species: "a connected series of neighbouring populations, each of which can interbreed with closely sited related populations, but for which there exist at least two "end" populations in the series, which are too distantly related to interbreed, though there is a potential gene flow between each "linked" population".

The classic ring species is the Herring Gull complex, and that's probably what you read about:

  The classical example of the ring species model was originally based upon the herring gull complex (Mayr 1942). This group comprises more than 20 taxa of large gulls (Haffer 1982) which together occupy a circumpolar breeding range in the northern hemisphere. ... Mayr envisioned all taxa of the circumpolar chain to be connected by gene flow, while herring and lesser black-backed gulls in Europe, the hypothetical endpoints of the ring, have reached full reproductive isolation and now coexist as distinct species.

--The Herring Gull Complex (Larus argentatus - fuscus - cachinnans) as a Model Group for Recent Holarctic Vertebrate Radiations

However, recent genetic work shows that the situation is even more complicated than this, and it's questionable whether they really are "ring species":

  Contrary to the ring-species model, we find no genetic evidence for a closure of the circumpolar ring through colonization of Europe by North American herring gulls. However, closure of the ring in the opposite direction may be imminent, with lesser black-backed gulls about to colonize North America.

--The herring gull complex is not a ring species.


What are the biological processes of ingesting radioactive particles? As someone who has basic understanding/education in physics and how radiation works, there is something that is confusing me and which I would like to shed some light on (I posted about this previously, but the discussion diverted to the risk of radiation in North America from the Fukushima incident, rather than the biological processes of ingesting radioactive particles).

With background radiation, and even relatively high levels of surrounding radiation, I understand that the risk is non-existant to very minimal. However, it seems that lately, people and officials are saying that food near and even in Fukushima is completely safe to eat.

In the case of surrounding radiation, sitting next to something that reads 3000 μSv/h is completely different to eating food that also emits 3000 μSv/h of radiation. In the former situation, once you walk off, the exposure stops. In the latter, radiation is constantly emitted inside your body.

Even more, the amount of radiation is not absorbed by the body equally, but it is usually very concentrated in a particular area of the body, as the particles lodge somewhere and sometimes bioaccumulate. From my understanding, the exposure to the surrounding cells is therefore more intense and prolonged.

To what degree is ingesting radioactive particles in food considered safe (or if at all), such as those in food near Fukushima, when taking into consideration that a concentrated and continuous source of radiation is different from an external one?

Your question has a rather glaring assumption which is that the amount of radiation emitted by food sources is equivalent to the amount of radiation received while sitting on top of the Fukushima plant. Even if a fish was as radioactive as an equal mass of concrete at the site, the dose you are getting at the site is because of all of the other things surrounding you.

The answer is simply that the food sources near the plant have been deemed (by the officials you mention) to emit a dose of radiation that is less than the level deemed harmful (again, by the officials you mention). It is of course possible that either the estimate of the radiation dose from the food is low, or the level deemed harmful is too high; that discussion is too broad for an answer here.


Dopamine involvement in pleasure There are some psychologists who believe that dopamine is not released during pleasurable activities but before them; my understanding is that a little dopamine is released pre-reward in order to motivate us to complete the action and then a large amount is released when we consume/get the reward. Can you please explain this? Their argument is that dopamine release tells the brain that it is about to feel good and then the brain releases opioids to make us feel good. This doesn't make sense if when addicts take opioids, such as heroin, the brain is flooded with dopamine and the person feels good. In that case we could say that dopamine is responsible for the euphoria. Do you believe this to be correct?

This is an ongoing discussion, and entire textbooks are written in this field, but I will try to clear up some misconceptions and point you toward some further reading that may help.

Is dopamine pleasure?

"Pleasure" is an emotional phenomenon; dopamine is a neurotransmitter. Dopamine can be involved in the perception of pleasure, but there was a now-outdated hypothesis that "dopamine==pleasure".

More recent evidence says that this is not the case, because endogenous dopamine release occurs in some brain regions during the anticipation of a pleasurable event, and really doesn't correlate with pleasure itself at all. Instead, dopamine is currently thought to reflect a "reward prediction error": a signal that tells the brain "hey, we just got something better than we expected!"

Why is a prediction error useful?

This signal can then be used by the brain to upregulate circuits that were recently active, effectively using the heuristic: "I just got something I didn't expect, so whatever I did just before must have been a better thing to do than I previously thought! I should do that more often!"

There are 'degrees' of unexpectedness, however, which is why you get a dopamine signal when a positive event is expected. Let's say a cue, like a bell, signals a coming reward. The reward is now expected, so it won't produce an error signal, but the bell itself produces an error signal: prior to the bell, you didn't know the bell was coming, so you didn't know the reward was coming. Now you update your brain circuits to try to do things to make bells ring!

This is a powerful learning algorithm that is also used, in a form, in artificial neural networks.

Context in drug abuse

If a drug of abuse causes a release of dopamine, that's a signal to the rest of the brain "Hey, something good just happened, let's try to do that again in the future!" Dopamine is the message, not the experience.

Further reading

The two bolded works below are a recent review and a highly relevant original paper, respectively.

Peter Dayan, Wolfram Schultz, and Ray Dolan were recently awarded for their work in this field and you can find lots of popular press that describes their work, as well.

References

Schultz, W. (2013). Updating dopamine reward signals. Current opinion in neurobiology, 23(2), 229-238.

Schultz, W., Dayan, P., & Montague, P. R. (1997). A neural substrate of prediction and reward. Science, 275(5306), 1593-1599.

Fiorillo, C. D., Tobler, P. N., & Schultz, W. (2003). Discrete coding of reward probability and uncertainty by dopamine neurons. Science, 299(5614), 1898-1902.

Glimcher, P. W. (2011). Understanding dopamine and reinforcement learning: the dopamine reward prediction error hypothesis. Proceedings of the National Academy of Sciences, 108(Supplement 3), 15647-15654.

Pessiglione, M., Seymour, B., Flandin, G., Dolan, R. J., & Frith, C. D. (2006). Dopamine-dependent prediction errors underpin reward-seeking behaviour in humans. Nature, 442(7106), 1042-1045.


Do the genes encoded by the nucleus for mitochondrial proteins have introns? Mitochondria are believed to have transferred much of their genome to the nucleus. I know that mitochondrial protein-coding genes lack introns, but is this true for mitochondrial genes encoded by the nucleus as well?

Nuclear genes for proteins destined for the mitochondrion can have
  introns…

…to the extent that other nuclear genes for that organism have introns.

For certain insects there is a database of such genes entitled MitoDrome, and if you click on D. melanogaster in the side panel on the home page of that site you get to a list of such genes for the eponymous fruit fly. You can inspect each one with the ‘view’ option, and the first few I looked at all had introns. Here is an example for one of the subunits of NADH-ubiquinone oxidoreductase, ND-18:

The subunits of this enzyme complex can be examined in other species, from which one can find that in Homo sapiens these nuclear genes also have introns. A related human gene is NDUFS4. Mutations in this gene have been described, at least one of which results in a genetic desease — Leigh syndrome. One of these mutations involves abberant splicing of the five exons of the gene (Lamont et al. Am J Med Genet Part A 173A:596–600).

The homologous gene in Saccharomyces cerevisiae, NDI1, does not have introns, like most other yeast genes.


Unilateral damage to vagus nerve Context:
The vagus nerves supply the neck viscera, heart, lungs and gastrointestinal tract. They join around the oesophagus to form the oesophageal plexus.

Question: Would damage to one vagus nerve in the neck have significant impact on heart rate and gastrointestinal tract function?

Thoughts: If the heart and GIT lie below the oesophageal plexus, which then continue in the inferior direction towards the cardiac and gastric plexuses, then surely a major functional failure in either the heart or GIT would require damage to both vagus nerves (?). I'm trying to make sense of the effect of their fusion, and whether or not this provides a compensating mechanism in the event that one of the two nerves is damaged.

Would damage to one vagus nerve in the neck have significant impact on heart rate and gastrointestinal tract function?

Not that much, because fibers from both sides are fused, so each nerve carries about a 50% of fibers originated from the one side and about 50% from the contro-lateral. Consider that fibers are rewired after each plexus.

References:

 wikipedia page about vagus nerve

 wikipedia category about vagus nerve


Book-recommendation: Ethology I am looking for a book that covers the following topics in ethology:

Behaviour

Sensory filtering, reponsive-ness, sign stimuli, learning and memory, instinct, habituation, conditioning, imprinting.

Role of hormones in drive

role of pheromones in alarm spreading; crypsis, predator detection, predator tactics, social hierarchies in primates, social organization in insects.

Navigation and Biological Rythms

Orientation, navigation, homing, biological rhythms, biological clock, tidal, seasonal and circadian rhythms.

Methodology

Methods for studying animal behaviour including sexual conflict, selfishness, kinship and altruism.

Do you have any suggestions?

I can suggest three books, none of them cover all those aspects, though:

1) The Foundations of Ethology, Konrad Lorenz. The best introduction I know for the field of ethology. Lorenz is called by some "the father of ethology".

2) Sociobiology: The New Synthesis, Edward Wilson. The deepest study of animal societies I know of.

3) Evolutionary Ecology, Eric Pianka. If my memory is right, it says something about the Navigation and Biological Rythms part.


Do we actually know the molecular dynamics of any enzyme? That is right, is there a limitation, say Heisenberg's uncertainty principle or something that limits our understanding of machinery of enzymes at atomic level? Can we know how do they actually work?

As far as I can tell, there is no explanation of actual design and working principles of any enzyme at atomic scale. Even the nobel prizes are given to discoveries not related to molecular details but rather pathways in which enzymes are not the primary concern, they are just represented as simple geometric shapes.

PS: I know that we have the exact molecular structures of some enzymes discovered using crystallography techniques, but even then, do we know which parts execute which function and how?

MD simulations.
Molecular Dynamics algorithms like Gromacs and AMBER aim to simulate atomistic mechanisms of biological macromolecules.
This video shows a good example of a resulting video from such a simulation for the CmAAT1 Enzyme, CmAAT1-Hex-aCoA complex. Much more data such as energy values and electrostatic interactions is available from the simulation, but that's not as pretty as the video!

Implicative mechanisms.
There are also telltale signs of active regions of crystal structures. Software like Consurf can show conserved residues. This implies possible biochemically important features like key structural or enzymatic residues, areas of a protein. The image below is from the consurf gallery and is based on the crystal structure 3COQ. Pink is areas of conservation. It therefor appears that those residues are involved in binding DNA.

Consurf is only one of many tools for identifying key residues. After these residues are identified, mutant knockouts of the protein can be made to see exactly how the function of the protein is altered. From that, a fairly good mechanistic model can emerge.
Uncertainty

"Can we know..."

The word "know" is a philosophically ambiguous word and I've gathered that scientists generally tend to avoid it. This is particularly true when it comes to the simulation side of things. It is generally best to regard MD simulations as an approximation of what happens.


Air purifier agains bacteria and viruses? We would buy a mobile air purifier in our home.

Against the smoke of the city, etc.

It would have a HEPA + activated carbon filter. They are marketing it as:

  "filtration process captures 99.97% of airborne particles down to 0.1
  micron in size."

and having also:

  "encapsulated ion particle charging chamber"

But the question:

Would the mentioned filter+ion charger also help cleaning the air from bacteria and viruses?

Ex.: "Coronavirus/2019-nCoV" is about "Coronavirus virions are spherical with diameters of approximately 125 nm" - but I just Googled it, not from an official source. And 0.1 micron is 100 nm.

UPDATE: would it be more effective, if it would have UV-C light in the air purifier?

The aforementioned filter will filter microbes

Yes, it is routine practice to use microfiltration in labs to sterilize solutions from microbes. 0.2 micron filters will remove all typically-found bacteria most of the time, except for the odd bacteria here and there, though this is uncommon. 0.1 micron filters certainly remove all stray bacteria that may make it through upon a single 0.2 micrometer filtration. Here is a nice read on the appropriateness of 0.2 and 0.1 microfilters, which simply states that 0.2 micro filters are usually more appropriate since they additionally guarantee a better flow rate.

The aforementioned filter will NOT ensure filtration of viruses

These filters are not used, suitable nor effective for viruses, however. You ask specifically about the coronavirus. From a 2015 study:

  Coronaviruses are members of the Coronaviridae group and contain a
  single-stranded, positive-sense RNA genome surrounded by a corona-like
  helical envelope (Ryan 1994). The SARS virus genome consists of 29,751
  base pairs. Approximately 41% of the genome is GC base pairs while 59%
  is TA base pairs. Coronaviruses have a size range of 0.08-0.15
  microns; with a mean size of 0.11 microns (see Figure 1).

This means 0.1 micron filters will not protect you from these viruses. They may help you reduce viral count in the air, which may of course be sufficient, but this would not be an adequate measure in a biological safety facility.

The cost-effectiveness of commercial air-purifiers for biosafety vs. pollution

On a advice-related note: I do not think air-purifiers are going to help you in a cost-effective manner to avoid viruses (e.g. Rhinoviruses that cause the common cold, for instance), lest you stay at home all the time. You expose yourself outdoors, and carry plenty of viruses indoors on your body and in your respiratory tract; these will bypass your filtration system on the daily. Being healthy and lucky enough to avoid exposure to viruses outside the house is still the best bet. I think an air purifier has a greater potential to help with smog and urban pollution, those particles are typically larger than the diameter of most microbes.


Does blood carry metallic nanoparticles? I find this particular chart about constituents of blood very informative and interesting. Looking through the different components, I see metals such as copper, zinc, etc. Are these only carried as ions or conjugated to proteins, or does blood carry nanoparticles of these elements as well?

It is very unlikely to have metallic nanoparticles in blood under normal circumstances.

Reasoning:

There are specific proteins that strongly bind metal ions: transferrin and ferritin for iron,  zinc transporters (Zrt) for zinc, metallothioneins as a catch all for most heavy metal ions etc.  These tend to be intracellular so most of the metal would be bound inside cells.  Any particles would be endocytosed and oxidized to the ionic form (probably in peroxisomes), then the metal would be bound to proteins.
Metal nanoparticles as well as free ions (of metals with more than one oxidation state) have considerable catalytic activity which is non-specific (and therefore quite toxic).  They can serve as a redox catalyst as well as generate ROS from oxygen.  That's probably why metal-binding proteins have evolved.
Lastly, iron in particular is a limiting nutrient for many pathogens.  Extracellular iron is very tightly controlled as part of non-specific pathogen defenses.  There is only exactly as little iron in blood plasma (bound to transferrin) as absolutely necessary to move it to the cells that take it up.  It's unlikely there would be any free iron, because there wouldn't be any fast, specific way to take it up the way the transferrin receptor does.


Identifying a spider from coastal Virginia A spider recently put up a web in my room in coastal Virginia, USA (on the left in the photo).

Rounder/taller body than most species I've seen. Dark brown, not quite solid-color coloration. If laying flat, it looks like its body would be about the size of an American dime. Tends to hang with its underbelly pointed upwards, and the times I've watched it feed it has never attempted to wrap prey in silk –- instead, it immediately eats and discards them.

My best guess from what I was able to find online was Araneus diadematus, but the coloration on all the examples of that species I can find seems much more varied than what I'm seeing, and I'm not particularly well-versed in spider identification, so I'm not sure.

The spider on the right was new this morning, I'm less curious about it and presume it was just a male of the same species.

These are very likely one of the common spiders that gets called House Spider, but this variety is one of the comb-footed spiders; the Theridiidae.  They're sometimes also called Tangleweb Spiders or something along those lines.  They make those messy webs, and hang upside down just as you show.  You can tell these guys aren't Araneus or one of the other Araneid orbweavers, because they're not hanging vertically in an orbweb.  This particular spider is probably the very variable and common Parasteatoda tepidariorum, and the smaller one is, as you guessed, a male.  They will share the web for a day or so until he mates and moves on.  You should be aware that the related Black Widow has this same general body shape and habit, and may be stripy and have banded legs like you see in the photo when the females are young.  I suspect that was why TFE was asking for better photos - although you probably would have noted the red hourglass before if that was the case.  I'm inclined to go with P. tepidariorum, for two reasons: Latrodectus generally (but not always) are sensitive to disturbance, where the common House Spiders don't seem to mind, and the abdomen of the female seems to be a little more randomly patterned (as best we can see) than I would expect for a Latrodectus.
Here's a photo of P. tepidariorum with a snack:

https://bugguide.net/node/view/6919/bgimage


How do cats shed their fur? Dogs shed their fur twice a year, so I assume this is the same with cats.

What is the mechanism whereby the change in temperature (assuming this is what causes the shedding) leads to the falling off of fur? Is it the same mechanism as balding?

Basic reasons as to why cats shed fur can be found in this link and this link.
An elaborate understanding of shedding in animals including cats can be obtained from this link. Hope that helps.


are female bonobos "always" pregnant? Given that bonobo chimps are more sexually active then humans, are the females almost always pregnant? if not how not?

also are they so sexually active in the wild as well or is it just in captivity?

In most species, females are pregnant as often as they can be. Since the availability of sex is rarely a limiting factor, it seems likely that female bonobos are as "always" pregnant as other chimps and socially living primates. The actual rate of pregnancy will be hormonally limited by things such as reduced fertility during lactation and so on.


Why do I see an inverted image of an object when I close my eyes? If I stare at an object for a long time and close my eyes, at first I can still see the object with my eyes closed. But the image I see with my eyes closed is inverted: dark colors appear as light and light colors appear as dark. Why is that?

I think it is because of light adaptation. The rods that are perceiving strong light, downregulate their response. But when the light is suddenly withdrawn then the rods that are adapted to perceive bright light cannot immediately sense dim light.

There are two forms of adaptation- fast and slow. The fast one is Ca²⁺ dependent- decrease in Ca causes cGMP to increase which in turn depolarizes the cell. Calcium modulates this process by other means also. This article suggests that slow adpatation is  because of an allosteric binding of cGMP on transducin-phosphodiesterase complex, which stabilizes this transition state and delays the signaling.

Adaptation can also happen because of photobleaching of rhodopsin.

I don't know how an image "remains" in the eye for a while. I believe it is because of asymmetric slow light adaptation between different spatially distributed rods(some rods take a while to readapt to dim conditions).

Similar effect you can feel with colour vision also. You keep staring at green for a while, then when you see something else it appears reddish.


How can insects survive without an adaptive immune system? How can insects survive in a world full of pathogens that are able to defeat the innate immune system?

There is not really a definitive explanation for why, although it's important to note that many mammalian pathogens are not adapted to insects and vice-versa. Insects need to survive insect pathogens, and they have a number of defenses for this purpose. Animals and their pathogens co-evolve and exert selection pressures on each other.

Killing the host (or killing the host quickly) is often not in the pathogen's best interest. Pathogens evolve towards their own successful reproduction as much as animals do. Success may ultimately mean evolving towards a less pathogenic state that improves a pathogen's chances of being transmitted.

As animals develop new defenses, they gain an advantage (relative to others of their own species) in surviving various pathogens. Pathogens evolve to escape these defenses, and a new equilibrium is established. An animal lacking this defenses is likely to be more susceptible to dying of infection, as the new equilibrium is dependent on them having these protections.

Here is an interesting paper on this view: http://hedricklab.ucsd.edu/PDF/HEDRICKImmunity113.pdf


Can Anyone Identify This Bug I am looking for someone to identify this bug:

It is an ormányosbogár species. :D
Curculionidae in Latin. I don't know the exact species, but it is common here in Hungary.

It is something like Mecinus janthinus, but it seems like shorter. Probably Mecinus pyraster or another Mecinus species.

Figure 1 - Mecinus janthinus - source

I think it is Sitophilus granarius aka. wheat weevil, but it is hard to decide because of the poor quality photo...

Figure 2 - Sitophilus granarius - wheat weevil - source


Can a brain be damaged by overstimulation? I am wondering what, if any, long term health effects there are from high levels of brain activity.

I don't mean cases where a brain is being artificially stimulated, but rather where there is a high (as in the high end of normal, not as in shell-shock) sustained level of sensory input, or simply that the brain in question is "thinking too much".

Assuming a person could sustain high levels of neural activation, is there a chance that the brain could "strain" itself or somehow "wear out" or come to some other kind of harm?

(This is such a difficult question to begin answering in any satisfactory manner, though I think can be addressed for pedagogical purposes in line with the aims of this SE.)

Before we address the question, I think it is prudent to think about the difference between stimulation and activity. A neuron can be self-activating without external stimulation, or it can be highly stimulated by sensory input and yet have low or inhibited activity. You do not specify, so I think the discussion must necessarily be very incomplete on this topic.

Your question is also naturally a little unclear and difficult to answer methodically, especially because 'damage' in this case is a very subjective term. As with all biological systems, there are self-protective mechanisms and reflexes and feedback circuits in place to prevent 'you' or your brain from overdoing anything. A dysregulation in neuron activation, or activity, would probably be a state of illness, such as having a seizure. I don't think it is possible for a typical person to expose themselves to sensory extremes without consequently feeling tired or bored as a result (e.g. looking into a strobe light or listening to loud music for inordinate amounts of time), which may be the result of an internal homeostasis, just like blood pH or blood sugar level, though regulated through physiologically-dependent behavior (sleep, concentration levels, apathy, etc.)

More strictly and scientifically speaking, all activity wears all tissues, including the brain. This would make 'brain activity' a process contributing to aging. However, once again, one can interpret anything as 'damaging'; breathing is damaging (oxidation! the cellular definition of wear-and-tear), but it also sustains you. Calories sustain you, but caloric restriction extends lifespan in virtually all animal models.

A recent publication in Nature (Oct 2019) suggests that the global inhibition or decrease of all neuron firing seems to be related to increased longevity which may suggest the opposite case to your question: lower neural activity may lead to extended lifespan. This suggests, though does not demonstrate, that over-activation may contribute more 'damage' and accelerated aging, compared to lower levels of activation. This conclusion is also based on evidence associated with a global - whole-central nervous system - effect, and does not indicate that one should under-stimulate parts of their nervous system to achieve the same result. Also, keep in mind that stimulation and activity are entirely separate things, so such a conclusion does not answer your question.


How did the felines get to America? I don't know if the felines got originated on America or on Africa, but I do know there are species of cat in America and Africa that belong to the same family and genus (Felidae & Panthera).

How did the evolution of these animals beat the vastness of the ocean? The same way as Homo sapiens? Or did they coexisted before Pangea split?

Short answer
It is believed that low water levels occurring several times during the last ten million years facilitated migration and divergent evolution of the felids. The North-American ocelot, lynx, puma, leopard cat, and domestic cat are believed to have evolved from a common ancestor that crossed the Bering land bridge between 5 to 9 million years ago from Eurasia. Note that Pangea broke apart 175 million years ago, way before the Age of Mammals even started, 65 million years ago.

Background
It is believed that modern felids arose in Asia with the divergence of the genus Panthera 10.8 million years ago (Mya) and the bay cat lineage 9.4 Mya. These dates correspond to the low sea levels that occurred during the late Miocene (Fig. 1). Between 8.5 to 5.6 Mya a progenitor of the caracal lineage arrived in Africa. The common ancestor to five felid lineages (ocelot, lynx, puma, leopard cat, and domestic cat) migrated across the Bering land bridge to North America, referred to as the New World migration. This period is also believed to have facilitated migrations of the Eurasian carnivores (ursid, procyonid, mustelid, and saber-toothed felids) to North America.

Additional Pliocene/Pleistocene migrations paved the way for the differentiation of the cheetah, originating from the North American puma and migrating to central Asia and Africa. Reversely, Asian Panthera species spread into America (jaguar, lion) and subsequently into Africa (lion and leopard).

Fig. 1. Global migrations of felids. source: Johnson et al., (2006)

Reference
- Johnson et al., Science (2006); 311: 73-7


What is the speed of blood? The speed of blood may vary from one place to another and may be quite low in the tiniest vessels compared to the biggest one. What is the speed of blood while exiting a normal human heart?

As you note yourself, this depends strongly on the vessel that you are studying. I found this table in reference 1:

It lists speeds between 34 and 45 cm/sec for the inferior vena cava and 12 to 16 cm/sec for the superior vena cava.

For the capillaries I found this table in reference 2, which measured the blood velocity in cats. Nevertheless I think this approach is also useful for an approximation for humans since the capillary system should be comparable:

It lists velocities between 0,2 and 2,7 mm/sec.

References:

Velocity of blood flow in normal human venae cavae.
Regulation of blood flow in single capillaries.


If silver nanoparticles kill bacteria by penetrating the cell membrane, why don't they also kill human cells on contact? Apparently, the silver from the nanoparticles can penetrate the cell wall of bacteria and kill them from the inside. Why, then, doesn't the same happen to human cells, e.g. the skin on my foot when I wear nanosilver-coated antibacterial socks, or the stomach lining when people drink nanosilver-treated water? Is it because the cell wall is different in bacteria than in multicellular organisms?

The nanoparticles from your sock will most certainly not reach to your foots cell membrane (Walls are for plants/fungi)  because of the thick layer of dead skin, oils, than about 30 cell thick cornified layer (stratum corneum) build up from practically dead cells (with no nuclei or organelles) but lots of filamentous keratine. This is the most outer shell of your epidermis followed by layers and layers of 4 other tissue types , then comes the "actual" skin dermis and the hypodermis beneath.

If some of the silver-sock -nanoparticles would actually make it through there to basal tissue and reach the cells plasmamembrane, they enter via endocytosis, and start to release Ag+ they break all kinds of things, because Ag+ is cytotoxic it induces ROS, damages you Mitochondira, disturb some pathways... you get the point.

However this was proven to happen within human in vitro celllines.

a few in vivo studies showed that Ag-NPs cause adverse effects on reproduction, malformations, and morphological deformities indifferent non-mammalian animal model.

Says "Review: A systematic review on silver nanoparticles-induced cytotoxicity: Physicochemical properties and perspectives
https://doi.org/10.1016/j.jare.2017.10.008


If life began at sea, why organisms are less salty than the sea? We may take it for granted that a fish, a seaweed, or clams are not too salty to eat, although the sea around them is salty. I know about the existence of a mechanism which prevents their body from becoming as salty as the sea itself, but this raises an important evolutionary question.

As life evolved from single-celled organisms, those organisms started as very simple cells with the bare essential metabolic functions. Possibly their DNA had no nucleus, and obviously they could not (yet) balance the salts within their body. In theory, this would say that their metabolism should have evolved to function is a salty environment. Yet, we see that this is not the case of modern organisms.

Which of the following scenarios describe the evolution of marine creatures with no excess salts in their body?

1- Metabolism may have started in a salty environment, cells have later "discovered" that less salt makes metabolism more efficient, and therefore the energy expended to clear-out the salts is worth the effort.

2- The time it took for salts to accumulate in the seas allowed marine creatures to adjust to a gradual increase in salinity.

3- Fresh water bodies (Rivers and lakes) are better suited for life to evolve. Eventually, some of the rivers will pour into the sea with all their content, including any living thing facing the challenges of salty sea water. This article mentions "ponds", but larger bodies of water are a better means of transporting those organisms to the sea.

What do we know about the timeline of changes in oceans salinity vs. timeline of evolution? Do we have fossil records that show the salinity content of the organisms?

Many biological processes require regulation of the salts (or more precisely ions) in fluid compartments of an organism. These processes include muscle contraction, filtration of the blood by the kidneys, and so on. Without these processes, a fish would certainly be dead. So it's not necessarily that regulating ions aids evolution or metabolism, nor that the sea changed salinity - the reason is that many biological processes required for an organism's survival wouldn't work without proper regulation of ions.

One such important process is active transport. In essence, by creating gradients of ions across a cell membrane, you can let the flow of ions into the cell drive other processes. This is a bit like how the flow of water through a water wheel can drive other machines.

I've never come across any reference to a cell with an ion concentration of its intracellular fluid greater than that of the ocean, though I'd slightly doubt that to exist since it would disrupt active transport. I'd also doubt that you could discern the ion concentrations of any fossilized cell since ions need to be dissolved, but how would you see this in a fossil?

I'm not sure whether I've completely answered your question, so let me know if something's still unclear.


Help ID this plant, quite possibly a weed I found this plant near my South Indian home in Kerala, India. Most probably it could be some sort of weed. Anyhoo, is this plant of any medical or commercial value? Is it a remedy for something?

It has a white tap root with little veins off the main root
It has a really small yellow flower
It's leaves are similar to that of a clover, except for that it has three to five leaves

Merci d'avance!

(P.S. Forgive me if this is some very common plant that I should know about, I'm in 7th grade.)

I presume it is Cleome viscosa, the Asian spiderflower.

It is commonly found in rainy season.

Medicinal uses:

The crushed leaves have been investigated as a treatment on stored seeds of cowpea, to prevent weevil infestation.
The leaves are use as external application to wounds and ulcers. The seed are anrhelmintic and carminative Juice of leaves is used as remedy against discharge of puss from the ear.

Identified by the following features-

Palmate leaves

Colour of flower especially the brown part at the base

Herbaceous habit

References:

Wikipedia
Flowersofindia.net


Is human face more resistant to cold than other body parts? Walking outside tonight in -15˚C I realized an interesting observation: While I felt cold on most part of my body, my face (although the only uncovered part) didn't really feel cold. It registered the temperature of course, but it wasn't a negative perception.

I wonder, what is an explanation? Is it simply because our faces are used to the cold, because we almost never cover them? Or is it some evolutionary phenomenon?

In response to cold your body causes blood supply to the skin to drop in the whole body. This is to conserve heat, but results in us feeling really cold. Exercising reverses this, resulting in an increased blood supply to the skin in order to remove excess heat and in this case we feel hot.

As mentioned, the head receives a large blood supply, and continues to do so despite other tissues being restricted. This is particularly as a result of the brain requiring a lot of oxygen and glucose. This keeps our head warm.

This phenomenon is why hats keep us warm and are important in cold weather, we lose a lot of heat from our head.

It is also likely that the skin on our head contains less cold receptors, as these aren't likely to be required. However the other parts of our body, particularly the soles of our feet and anterior surface of our hands have many sensory receptors. They are likely to make first contact with anything that may be harmfully cold.


Are the sister chromatids exactly the same? I'm having doubts about whether the sister chromatids are exactly the same or not. I know that they are the arms that carry the information genes (the alleles), but I don't know if they are exactly the same and / or in what these arms differ, since in a partial exercise they ask me the following:

Explain briefly why the sister chromatids are not exactly the same and the homologous chromosomes are different. To answer, consider the origin of both structures.

Nor do I understand quite well when the statement clarifies "take into account the origin of both structures."

Thank you very much for the help!

A new chromatid is synthesized by copying the other chromatid. As such two sister chromatids are (quasi) perfectly identical.

Why did I say quasi? Because there are sometimes "errors" when replicating DNA. These "errors" are called mutations. As far as I know, most mutations occur during meiosis though and only very few occur during mitosis. So, to a pretty good approximation, yes sister chromatids are identical.


How does cancerous tissue break down radioisotopes faster than normal tissues? Apparently, many medical practitioners use radioisotopes to detect cancer in patients. From my textbook (McGraw Bio 12, pg. 10);

  Using a method called radioisotope tracing doctors can inject
  radioactive material into a patient and trace its movement in the
  body. For example, cancerous tissues in the body are characterized by
  a much higher level of activity than healthy tissues. Consequently,
  cancerous cells take in more glucose—a common cellular energy
  source—than healthy cells. Injecting a patient with radioactive
  glucose and then performing a positron emission tomography (PET) scan,
  such as the one shown in Figure 1.1, is one method to diagnose a
  cancerous tumour

Apparently, cancerous tissues break down radioisotopes at a much higher rate than normal tissues. But how?

Cancerous tissues break down glucose faster, not radioisotopes. Doctors use PET technique to detect breakdown of glucose, and "hot spots" are investigated as potential tumors.

Glucose can be labeled with radioisotope to show up on PET scan. Normal glucose is "invisible".

Hence, candidate for tumor will breakdown any glucose, but radioactive glucose will show up on scan.


People say the cardiac cycle depends on blood pressure? How so? I know what the cardiac cycle is. There are two phases diastole and systole. One is the relaxed, and the other is the contracted form of the heart. The diastole is where blood is pumped to the ventricles and systole is when blood goes to the aorta, and lungs. But what is the connection to blood pressure?

There are two levels to take your question at.  The first is simpler but I'm not sure if it is what you are looking for:

If you imagine the heart and all the blood vessels in your body as a closed plumbing system with no leaks (not entirely accurate) then when the heart contracts and squeezes the blood from the ventricles the total surface area the blood is pushing against has decreased - there is more blood in a smaller space.  This means that the pressure on the arteries from the blood has to increase when the heart contracts - in systole blood pressure is much higher than in diastole.

The second level is a little more in depth:

Cardiac output (a measure of how much blood is being pumped around the body to the organs where it is needed) is defined as the product of stroke volume and heart rate.

$$CO = SV \times HR$$

Heart rate is the number of times the heart beats per unit time
Stroke volume is the amount of blood that is pumped out of the heart in one beat. It is this that is related to blood pressure.

The relation of stroke volume to blood pressure is defined by Starling's Law.  This states that the more blood that is in the heart, the more its walls are stretched.  The more the walls are stretched, the harder the heart contracts in response.  This increases blood pressure as again more blood is displaced from the heart.


How is the flicker fusion rate interpreted as an on-off rate? In our experiment we use a fly to determine the flicker fusion frequency, i.e., that frequency where the fly starts perceiving a pulsating light as a constant light source. The human eye also has a flicker fusion frequency. For example, most people cannot see the flickering of a fluorescent tube, which equals the main frequency (60 Hz in Europe & USA).

Our experimental light source needs two input durations, namely how long the light is ON and how long it is OFF for. The input is provided in ms. From what I found out so far is that the unit Hz equals the frame rate, namely pictures per second. So a frame rate of 50 Hz is 50 pictures during 1 second.

But in my experiment it is about flashes of light, namely a light phase and a dark phase. Does the dark phase then count as a picture? So what I mean is whether 50 Hz represents 50 times lights ON + 50 lights OFF, or does it mean 25 times lights ON and 25 OFF?

Also, how long is then each light pulse?

My assumption is:
50 Hz are 25 lights on and 25 lights off within 1 second.
50 pictures in 1000 ms
1 picture per 20 ms
20 ms / 2 = 10 ms lights ON, 10 ms lights OFF

Short answer
A light flashing at 50 Hz means there are 50 flashes of light per second. The unit hertz means cycles per second. 1 cycle is the time it takes for the light to be ON and OFF. 50 Hz cycle time means a cycle time of 20 ms. If light ON and OFF times are equal, then the ON and OFF times are both 10 ms each.

Background
The unit hertz (Hz) is a frequency unit in the International System of Units (SI) and is defined as

  one cycle per second

A textbook example where the unit Hz finds its use is a sine wave (Fig. 1). 1 cycle per second would be 1 Hz. A cycle, as can be seen in the figure, is a complete wave consisting of a positive phase followed by a negative phase.

In the right panel of figure 1, a square wave is shown. Again, a cycle time is the time it takes for one complete square wave to develop, i.e. a positive phase and a negative one.

Fig. 1. Sine wave (left) and square wave (right) sources: Simon Fraser University, Integrated Publishing

Now, in your example, you can depict the lights ON as the positive block in the square wave in Fig. 1 above, and the lights OFF as the negative phase. Together (light ON + OFF phases) they form one cycle. So a light pulsing at 50 Hz means it flashes ON and OFF 50 times.

The cycle time then is 1 second/50 = 20 ms. If we assume that the ON and OFF times are equal, which they obviously do not have to be, then light ON is 10 ms, lights OFF is 10 ms.

On the wikipedia page on the hertz unit, a flashing light example is actually illustrated and explained.


Why is Thermus aquaticus and Taq Pol stable? What is the molecular basis of the stability of the bacterium Thermus aquaticus and the enzyme Taq Pol it produces ?

I have tried googling this but did not get a good answer.

Here is an article from Razvi and Scholtz that help you understand the thermostability found in thermophilic proteins. They compared protein stability of thermophilic proteins and their homologous versions in mesophilic bacteria (i.e., bacteria that grow in more normal temperature ranges), and compiled these proteins into a database. Their method was to make estimates of protein stability curves for each of these proteins through a model of free energy based on the known physical parameters of these proteins. From the article:

  [...] the most common way to attain a higher [melting temperature] in proteins from thermophiles is to raise the stability curve to higher values of ΔG (higher intrinsic stability) at all temperatures."

This is achieved through mutation of just the linear sequence of the protein. Fundamentally,

  "...each of the methods of stabilization are results of features like an increased number of hydrogen bonds, salt bridges, improved core packing, shorter and/or tighter surface loops, enhanced secondary structure propensities, or oligomerization."

Also, everything I have seen about the genus thermus places them as Gram negative bacteria.

Razvi and Scholtz. Lessons in stability from thermophilic proteins. Protein Science, 15(7) 2006.


What is the number of influenza strains occurring at a given time? My question was initiated by reading on mock-up influenza vaccines. I understand that the manufacturer pre-prepares a certain vaccine and tries to get it tested and ready before it is actually needed, by taking a novel virus strain that has infected a few people, and could potentially cause a pandemic.

My questions:

How many different influenza strains are there at any given time at one geographical spot (say, one US state? - narrow down at will). I always thought there would be just one novel strain appearing each year, explaining why people get sick time and again of the 'same' virus. However, the mock-up virus vaccine production seems to imply there are various strains occurring at once?
Do influenza strains vary on an annual basis, or is it a continuous process (like evolution), and is a new strain re-named after it becomes potentially dangerous (like speciation?) - i.e., what is an influenza strain? It seems, given the vaccine preps, that various strains occur at once, and strains survive for extended periods? Any hard evidence for these indirect assumptions?

And as a side -

Do vaccine manufacturers prepare a whole bunch of mock-up influenza vaccines on a yearly basis just awaiting to identify a dangerous strain and start manufacturing it once people get sick? Or are mock-up vaccines combined into a cocktail mix containing many strains and are these cocktails re-vamped annually? Or is a yearly shot necessary because immunity only lasts a year?
I might have to re-post this last question at Health.SE as a dedicated question, but since related to above I prefer to leave it here for now. Grab me in chat if need be!

Antigenic drift in the coding portions of the genes that involve antibody binding sites accounts for the seasonal variability of flu strains, i.e. they mutated enough that the antigens require new antibodies, hence a new strain. The process is as you said constant, like evolution, and in an analysis of pandemic H1N1 the authors are able to note 1 - 18.1 mutations per genome per replication cycle (ref). Because of this, flu vaccines tend to have more A strains than B strains due to the greater mutability of influenza A, at approx. 30% more mutations per site per infectious cycle (ref). At current It will take me time to research the remaining questions.

Interestingly enough, however, and I've never looked at this but CDC offers weekly influenza reports that detail by region what they're finding (CDC):

Source: CDC's so-called FluView

Beyond that, I'm pretty sure they take this weekly data, see what strain is on the rise in hospitals, and manufacture the vaccine to mirror the "popular" cocktail of strains.


How is the appropriately-stratified gut microbiome acquired in organisms performing horizontal transmission? I am studying horizontal transmission of primary symbionts in insect reproduction. This reminded me of an earlier question I had asked, in which I learned that humans analogously acquired their particular microbiomes. It is also known how the human gut can be stratified in microbial content along the digestive tract. My question is what mechanisms are employed in ensuring that organisms acquiring their microbiomes from outside sources via horizontal transmission acquire the correct microorganisms in the correct parts of the gut? As the human gut metagenome does show "homology" between individuals, it can be safely assumed that the process can't be due to random chance.

tl;dr it really might be due mostly to random chance, in terms of intentional mechanisms at least.

One thing that is important to remember about the gut tube is that conditions of life for microflora vary dramatically from one end to the other. This is true of nutrient availability, pH, and antimicrobial load. For example, the bacterial load of the lower intestinal tract is approximately seven orders of magnitude higher than the upper GI tract (stomach). They're just completely different places.

In some cases you can try to impute the bacterial assemblage in some part of the gut to a specific biological cause furnished by the host, for example the role of bile salts in controlling which organisms are able to colonize certain locations.

But a more parsimonious explanation is that the bacteria are growing in the places where they are good at growing. This brings up the old ecological saying: "Everything is everywhere, but the environment selects." We aren't necessarily trying explicitly to reinforce a certain assemblage, that's just the assemblage that works in niches with very low pH, very high nutrient load, bile salts, etc. And most of those features are unavoidable consequences of the gut's main function, digestion/excretion.

It certainly doesn't seem that e.g. behavioral strategies for exposing yourself to the "right" microbes gets you the right microbes in the right places. Recall that fecal microbiome transplant is one of the most successful strategies- just take some healthy poop and put it into a sick person's GI tract, they get better! That's not a very controlled horizontal transmission strategy.

You could propose that there is some second-order selection going on in which we have constructed GI niches in such a way that they encourage certain assemblages. Certainly, dysbiosis occurs and is bad in such cases as e.g. C. difficile infection, we would like to avoid those. Probably some coevolution has occurred between host and microbe, for example immune responses and butyrate production. That Foster paper has some more examples of possible mechanisms for a couple of specific cases, for example mucus. But they are probably not sufficient to explain the full compartmentalization of the microbiome in the way that you seem to be asking.


What do lower case nucleotides mean in this gene sequence? The following table (image linked below) shows promoter sequences recognized by different sigma factors. The sequence given for, e.g. sigma B is "GTTTaa"; why are the "a"s lowercase?

(from "A sigma factor toolbox for orthogonal gene expression in Escherichia coli", Bervoets et. al. 2018)

The case refers to the degree of conservation of a particular nucleotide in the consensus sequence. Highly conserved nucleotides are written in uppercase. At positions where the sequence varies, the most common nucleotide is given in lower case. That said, I'm not sure what the cut-off would be between "highly conserved" and "most common" and, in my opinion, is something that should be explained in the paper (though, in this case, it does not appear to be). This paper, for example, uses uppercase where a base is conserved in four of the five sequenced promoters. There may be some convention I am unaware of.


Species of this White Dove I visited a bird enclosure close to where I live in Australia. The enclosure had several different species. The birds that stood out most were these doves sitting right along the fence railing, making a deep "Wo-wo-wo-woo" sound. That and also I thought they looked and sounded similar to Spotted Doves.

Does anyone know what the species of this birds may be?

I think this is a Barbary dove (or Ringneck dove). See this image (from the here):

More information can be found here and here. The second pages shows also images of different color variations.


How do you call the species that gives its name to a upper-level clade? Just a silly question: I don't remember how the species giving its name to an upper-level clade is called.

e.g. the name of family Canidae derives from Canis lupus

You could say it is the "name-giving" species, but I'm certain a specific term exists.

I guess you are looking for the type species.
Although it is defined to be a "name giver" for the genus or subgenus level you could potentially extend this to higher up levels.

EDIT: After looking this up and actually reading the full article myself, yes, at least in zoology you can extend it to higher levels by for example using the type genus.


What is the medical definition of death? What is the medical definition of death? And how do medical examiners determine whether a person has really deceased, as opposed to for example a condition like brain death?

Ok. So when a doctor declares a person dead, it is when their heart or brain is totally not working, and won't start working no matter what they do.

This is legal death.

If your heart stops cold, you are clinically dead. This is reversible, if you are lucky. This definition basically only exists so people can say they "died". It has no real biological significance, except for the fact that your heart is not pumping blood and providing you with oxygen. This will cause...

Biological death:
Within 5-10 minutes at room temp you have reached the event horizon of biological death. Biological death is real death.

Once this time threshold is crossed, there is almost always no going back.
This is because Cells in the brain are destroyed by oncosis, and other mechanisms and forces far beyond me.