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Why proprioceptive fibres (of CN V) have their cell bodies in mesencephalic trigeminal nucleus?
It's seen that GSA (General Somatic Afferent) fibres (of CN V) have their cell bodies in trigeminal ganglion. But the proprioceptive fibres' peripheral processes terminate at mesencephalic trigeminal nucleus, making it the only nucleus in CNS where cell bodies of 1st order neurons are present.
Why this is so?

if you are satisfied you may accept the answer for the future reference.

The mesencephalic nucleus of trigeminal nerve is involved with reflex proprioception of the periodontium and of the muscles of mastication in the jaw that functions to prevent biting down hard enough to lose a tooth. To subserve this reflex protective function, mechanoreceptive nerves in the periodontal ligament sense tooth movement and project to the mesencephalic nucleus.

The functional significance of this anomaly is unclear, although there is a hint of special neural processing in the fact that, unlike DRGs and normal cranial nerve ganglia, MesV neurons receive synaptic input. Another hint is that while at spinal levels opposing extensor and flexor muscle blocks are roughly equal in size, in the orofacial motor system there is asymmetry. Jaw-closing muscles, the flexors, are massive and powerful with rich muscle spindle and Golgi tendon organ innervation. The jaw-opening muscles, the extensors, are small and delicate and lack muscle spindles and Golgi tendon organs

Reference

It is responsible for unconscious proprioception that stems from muscle spindles in the muscles of mastication and other muscles of the head and neck. It is thus essential in the process of receiving sensory information about tooth pain, helps prevent excessive biting that may break a tooth, receives information about stretch sensation from the muscles of mastication, and serves as the afferent limb of the jaw jerk reflex.
Reference


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Partial pressures of different gas in human blood and how they are calculated?
In Respiratory Physiology, we use the $P_x{O_2}$ and $P_x{CO_2}$ in blood at different regions of the peripheral circulation. From my Chemistry knowledge I know that $P_x$ of a gas in a solution is the fraction of total pressure caused due to the gas dissolved. But in blood $O_2$ is present mostly as $OxyHb$ and $CO_2$ is also present as $CarbaminoHb$ & $HCO_3^-$. In blood their dissolved state fraction is very low. Now my question is how do we measure the $P_x$ of any gas ($O_2$ or $CO_2$) in blood and what is the logic here? [x means either arterial blood or venous blood]
Here is the data I'm talking about.(https://i.sstatic.net/lA1M5.jpg)

As a notation note, I never seen your $P_a{O_2}$ notation used except for referring to arterial partial pressure ($P_v{O_2}$ would be venous). Generically, partial pressures are usually noted as, for example, $P_{O_2}$.
When we talk about partial pressures in biology, we literally mean the partial pressures: that caused by dissolved gas.
Hemoglobin-bound oxygen is not the same as gaseous oxygen, nor is carbonic acid the same as carbon dioxide. Neither contribute to the partial pressure. They do relate to the total oxygen/carbon dioxide carrying capacity of blood, but this cannot be measured directly through partial pressures.
See this Q&A for a situation this comes up: Why is arterial pO2 normal in carbon monoxide poisoning?
In medicine, it is common to use oxygen saturation as an alternative measure of blood oxygen concentration; this refers to the percentage of oxygen binding sites of Hb that are saturated.
It is important to realize that the partial pressures of dissolved gases will eventually reach equilibrium with the surrounding atmosphere; the lungs are a great gas exchange organ (that's their entire job), so blood leaving the lungs should have partial pressures that approximate those inspired air (in practice, there is some discrepancy because the lungs are very humid and also are constantly refilled with $CO_2$ from blood, so water vapor and carbon dioxide contribute a substantial gas pressure that pushes out other gases: see the similarity between arterial blood and alveolar gas in your data table and the differences between atmospheric gas and alveolar gas).
Clinically/in a lab, we measure these things with a machine that just magically gives the numbers. I looked for a simple description of how these machines actually function, and found https://acutecaretesting.org/en/articles/understanding-the-principles-behind-blood-gas-sensor-technology to be useful. In summary, $CO_2$is measured by exposing a captive solution to the gas and measuring the pH, giving an indirect (but accurate) measure of $CO_2$. $O_2$ is measured with a reducing current. It's also possible to measure concentrations of arbitrary compounds more directly with gas chromatography - colleagues of mine have used this for anesthetic gases, for example.

Extremely sorry for using wrong notations. But $CO_2$ is more soluble in water than $O_2$. So then wouldn't that imply $P_{CO_2}>P_{O_2}$ ?

@A.N.Ψ No, it would not imply that. If you want you could ask about why that is on the Chemistry stack exchange, since it's unrelated to biology.

source: Stack Exchange

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

sort: votes


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How to choose an assay for detecting virulence factors?
When looking for a protein of interest, an ELISA is being administered. I read this article about the different types of ELISAs and the advantages/disadvantages.
However, I am conflicted about whether a sandwich ELISA or a direct ELISA would be best detecting a protein virulence factor in a serum sample. The thought behind the sandwich was the antigen would not need to be purified before measuring.
Any advice as to choosing an ELISA for the detection of a specific virulence protein?

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


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DNA Inheritance- Math vs. Biology
After doing some statistical analysis of the raw math involved in DNA contributions, I would like to understand the scale of the biological factors.  I know that 99% of the human genome is identical in all human beings, so genetic recombination and gene conversion should be irrelevant in those areas.  I know that recombination occurs at different rates depending on the chromosomes and loci.  But what is the average order of magnitude?  That is, if I know that a chromosome mainly came from Grandma, how much of it is likely to be from Grandpa?  .1%, 1%, 10% ?  And, does the age of the male affect the rate of recombination to a measurable degree (in spermatozoa only, as body cells would not affect inheritance).

What do you mean by "the scale of the biological factors"? And what do you mean by "the average order of magnitude"? As you just said, differences are tiny between any two randomly drawn humans (in DNA sequence), so if this is your 'metric' there can't be any differences in 'orders of magnitude'. If you only ask about the fraction of the particular DNA (in chromosomes) that was copied into your own genome from your ancestors, then it is roughly half from your parents, a quarter from your grandparents, and so on.

DNA tests are done only on the variable segments:  It would be pointless to say "you're a 99% match to this other sample, it must be your identical twin."  Using the "average" of the actual distribution is misleading.  Only 32.24% of people inherit between 23.91% to 26.09% from a grandparent while 90.69% inherit somewhere in a range of 17.39% to 32.61%.

Agree, so, what is that you are asking then?

DNA testing is in its infancy, and different labs use different protocols for their tests and different models to report results.  2 samples from ME will not show a 100% match to MYSELF.  The zygote that turned into my mother, say, had 23 intact chromosomes from each of her parents.  When my zygote was formed, recombination may have occurred in the specific ovum that made me.  Take chromosome 1- the main body of which came from her father.  Is it likely to be 99.9% grandpa with .1% recombined from grandma, or more in the 90% grandpa 10% grandma range?

So, at core (it seems) you are interested in the rate of recombination events and the magnitud of their occurrences. This would be the only source I can think of that would give you information about the 'composition' of one chromosome (other than brute-force sequencing).
As you seem to know, recombination is an important factor that 'shuffles' some specific areas of the chromosomal DNA during meiosis (process needed to produce gametes). There is a technique developed by T. H. Morgan almost a century ago, that measures the rate of this 'recombination' events by comparing how two (or/and more) particular loci co-ocurr across generations (when recombination occurs, it is more likely to break co-occurrences of distant loci, as opposed to close loci). Thus, we can use this distance measure as a measure of recombination. In fact, in honor of Morgan, the units used to measure recombination rates are called 'centiMorgans', and abbreviated cM. A cM is the probability for a particular loci (it can be a gene or a smaller sequence) to co-occurr with another loci (to be 'linked' to). Thus, is a relational measure: every particular sequence is related to another, and by transitivity (if A and B are close, and B and C are also close, then A and C will probably be close -this is a generalization-). When done in chromosomal or genomic scale, we can build linkage maps.
In modern times, there's quite more resolution, from whole genome studies at gene/chromosome resolution, and even higher resolutions (remember that a 'loci' can be any unit of your interest in the DNA).
Being all that said, recombination rates, and thus the probability of inheriting certain DNA features from parents/ancestors based on recombination, vary quite a lot. There are many 'hot-spots' and other regions seem to be 'protected' from recombination (for instance, regulatory DNA). According to the work I cite here, the probabilities of recombination can vary within about an order of magnitude (the most likely recombination occurring at 10 times higher probability than the less likely), but this varies a lot.
I hope this helps a bit. I am still not sure what do you mean by "biological factors", but for sure recombination is one of the important factors influencing the identity of each chromosome across generations (others are, of course, point and chromosomal mutations).

I reviewed my understanding of centiMorgans.  It appears to be the measurement of a rate, but the units used are a distance.  To me, this is like estimating travel time by considering only the distance, with no regard as to terrain, weather or traffic.  As you said, there are known hot-spots in the genome.  With a cM being a .01 probability, and rounding to about 7,000 cMs in a human, that would be an average of 70 instances of genetic recombination in a single generation, and that's a non-directional switch, as opposed to conversion.  With variables you point out, only general ranges matter.

It gives a rate because the probability of 'linkage' between any loci can only be in the [0,1] range. So, even though it is thought of as a 'distance', in reality (both as conceived by Morgan, and in real 'physical' terms) it reflects the frequency of recombination events. So, to me, it is a bit like the inverse of your metaphor: we get traveling times, yet we like to talk about it as a 'distance traveled'; the weather, traffic, etc, are implicit to the traveling times observed (the linkage).


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Inheritance percentiles
I am aware that the average DNA contribution from each grandparent is 25%, while the possible range is 0%-50%.  I found a source citing 18%-32% as the "normal" range but this was undefined.  I assume it must be referring to a percentile based on the distribution in a Gaussian curve.
After searching in vain for a chart showing "normal" ranges for each level of consanguinity (sibling, grandparent/aunt, great-grandparent/cousin etc.), I started doing the calculations myself on an Excel spreadsheet... and soon went back to searching.  Surely this information is available somewhere, and there must be generally accepted norms.  The math formulas are well established.
Where should I look to find the results summarized in a compact format?
I want to first know, essentially, the statistical results of flipping 23 identical immutable coins to represent the various generational probabilities.  The facts that the chromosomes are not identical, and that recombination is more likely at certain loci on certain chromosomes, are to be considered later as adjustments to the non-biological math.
I will pursue a statistical answer elsewhere if I can get the "biological" answer as to what percentile is accepted as the "normal" range.  (The 25% average for grandparents has a vanishingly small probability of actually occurring, as it would require enough recombination to equal an inheritance of 11.5 chromosomes from each grandparent.)

Good question +1. The actual probability distribution will depends upon the recombination rate and the number of chromosomes. Are you talking about the human genome only? The distribution in recombination rate might matter too but that would make things too complex for a simple calculations so anyone giving it a shot would probably want to assume constant recombination rate. Sexual chromosomes might also make things more complicated.

For your edit, that part is now a (fairly trivial) statistical question involving the binomial distribution with p=0.5 and n=23.

I have seen a spreadsheet with percentiles with real data. I cannot recall where it was, but that resource exists.

Setting up the binomial distribution:
For generation F1 each parent (F0) has a 50% chance of contribution the chromosome (under your simplified model), i.e. p=0.5, n=46 for the binomial distribution. I assume that when you say the 'normal' range you are looking for the mean +- 1 standard deviation? For p=0.5, n=46: mean=23 with standard deviation=3.39116 which helps define: Pr(20≤X≤26)=0.698. So in about 70% of cases a child will inherit 20-26 of their chromosomes from one parent.
For generation F2 each grandparent has a 25% probability of contributing a chromosome so we use p=0.25, n=46 which gives: mean = 11.5, standard deviation=2.93684 Pr(9≤X≤14)=0.6936. So in about 70% of cases a grandparent will have contributed 9-14 chromosomes.


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Public fermentation/cell cultivation database?
I am wondering if there are any large collections of fermentation or cell cultivation data publicly available.
I am interested in all cell types used within industrial biotech and biopharma, especially the most common ones, e.g. CHO, yeast, e.coli, bacillus, lactis.
I am interested in this from a process understanding point of view. So I am very interested in the conditions throughout (pH, nutrients, dissolved oxygen, media comp, turbidity, etc.) as a time series. If manual (offline) measurements are made, CFU, amount of metabolite produced, etc. they would also be incredibly interesting to have.
I have looked around without luck.
I guess the 'perfect' database probably doesn't exist, but I haven't been able to find anything.
So I would really appreciate help finding any dataset on fermentation data, even if it doesn't have all that I am looking for.

I found this article: Bio-Ferment A Database on Bioreactor and Fermentation from 2011, but I cannot find the actual database.

What kind of data are you seeking? Growth conditions? OD? Something metabolic?

What kinds of cells? Yeast, human, bacterial? What do "online" and "offline" mean? What kinds of fermentation? What is the readout- metabolite production, cell density, biomass?

@tyersome I am especially looking for growth conditions and OD. I have re-phrased the question so that it is hopefully more informative.

@MaximilianPress online means that the measurements are made continually - e.g. a probe sitting in the tank. Offline is when someone manually takes a sample and makes the measurement outside the tank.


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What pH ranges are used in industrial scale fermentation?
When reading

Hans-Peter Meyer, Wolfgang Minas, and Diego Schmidhalter (2017) Industrial-Scale Fermentation. Industrial Biotechnology: Products and Processes, First Edition. Edited by Christoph Wittmann and James C. Liao.
  © 2017 Wiley-VCH Verlag GmbH & Co. KGaA. Published 2017 by Wiley-VCH Verlag GmbH & Co. KGaA.

I came across the following passage describing industrial up-scaling of fermentation processes (in general):

1.3.1
Process Development – Scale-Up Starts at Laboratory Scale
Process scale-up should be considered early on while the biological expression
  system is still under development. Factors such as genetic stability for at least
  the number of generations needed for a scaled-up production, and the need and
  impact on the environment of selection markers, should be evaluated before
  process development is started. The use of antibiotics as selective markers in the
  production medium should be avoided. Throughout development of media and
  cultivation conditions, it is important that parameter settings remain realistic and
  scalable, always indicated with upper and lower limits reflecting the safe operating
  range (process design space), for example, pH 7 ± 0.3.

I am quite surprised about the narrow pH range specified (pH $7 \pm 0.3$). I assumed that the pH range would be much wider, similar to lab scale. Is this really common practice?

Fermentation pH will differ a great deal depending on the bacteria or fungi being used and the process. But it is not uncommon to have a relatively narrow range of pH as a target. Remember pH is the -log[H+] so the pH scale is not linear. Also some fermentation reaction involve very expensive pharmaceuticals or intermediates, a single fermentation batch may have a value in the hundreds of thousands of dollars so keeping +/- 0.3 range in pH is trivial.


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What is the pH of cytosol? And plastids?
My teacher ask this question, and I answered 7 to 7.4, but she said it's wrong.
I read a lot and found the same answer (wikipedia)
I'm here asking for confirmation of this and the pH inside & outside of the tilakoidal membrane.

What kind of plastid and which part(s) of the plastid? The wikipedia article on chloroplasts contains relevant information ...

Thanks, that is kindly useful. Now, I just need a litle more confirmation.

The optimum cytoplasmic pH for performing physiological activities in
plant cells is a neutral pH of around 7.2 to 7.4.
The pH of apoplastic space outside plasma membrane and vacuolar pH is
acidic ranging between 5 to 7.
The thylakoid lumen is more fluctuating which varies during light /
dark cycles and is highly acidic.
The mitochondrial compartment and chloroplast maintains a basic
conditions of about pH 8 for optimization of biochemical reactions
occurring in these two particular compartments.

(Via: https://www.frontiersin.org/articles/10.3389/fpls.2017.02079/full#:~:text=Plastid%20stromal%20pH%20could%20only,cytosolic%20pH%20(around%207.3).


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Enzymes extracted from diferent tissue, may have diferent $K_m$ values under the same conditions?
My laboratory team has been used succinate dehydrogenase (1.3.5.1) from Gallus gallus domesticus breast (the most meated part of the chicken, where you will obtain nuggets) to determine $K_{m}$ and $V_{max}$ under 3 linearization methods.
But, in BRENDA page, I found various values for many organisms, like Bos taurus, and they select other tissues like liver tissue.
Why the difference?
PD. Any reference about where to find this values for Gallus gallus mesticus will be very appreciated.
EDIT: The reaction consists on dehydrogenating succinate to fumarate, on the tricarborxilic acid cycle. Include the creation of a trans-double bond.
Describing my laboratory practice, we macerate the meat with glass sand, and divide this mixture on 2 kinds: one with methylene blue and trichloroacetic acid (TCA) and one without TCA. Now I know that TCA is a protein precipitant, and methylene blue is an indicator; the less blue, the less succinate. So, with absorbance tests, we can elucidate [Succinate] vs time plot, and approximate the ratio $V_{max}/K_m$ from the michaelian equation for substrate concentration decay:
$$S(t)=S_0 e^{-\frac{V_{max}}{K_m}t}$$
Also, i think it will be possible modeling instantaneous velocity with its derivate and make the linealization plots, but i'm not very sure of this.
EDIT2: Thanks for the help with my practice report (I really appreciate it), but I still wanna know if it's possible to have different $K_m$ values on the same enzyme, only changing the tissue for reaction.

Can you please [edit] your question to add an example of such enzymes from BRENDA?

Also note that succinate dehydrogenase is a part of a complex and catalyzes many coupled reactions. A simple MM kinetic model won't apply in this case, I believe. Which reaction are you interested in?

As far as I know Brenda lists experimentally determined values, if they come from different studies/sources the differences are much more likely to be due to that than due to different tissues

I need experimentally values reported, so data in BRENDA is usefull. But I duno why it will be different values on different tissues. This is not possible, under the same conditions?

user1136 thank, I didn't know about the protein precipitation effect of TCA. That changes everything, since the Rx have a non-competitive inhibition.

user1136 In fact, I didn't found different values for $V_{max}$, I found different values only for $K_{m}$ and the ratio. If you know a website or a book where I will found it, can you tell me, please?

My teacher derived that formule from Michaelis-menten eqn assuming that $K_m >> S_0$ and omitting it at denominator. Then: $$V_0=\frac{Vmax . S_0}{Km} = -\frac{dS_0}{dt}$$ but this is not my question. Maybe I need to open another question for linealization?

I'd like to do that. That was i'm thinking. But my partners, who have re-coursed enzymology, used another method using an equation that I don't even know. If you are interested, i let you the link to the report, but is in spanish and i can't explain it to you at all. [  https://1drv.ms/w/s!AtNW_8yW8ySxgkGDfKg4KoHaWzbp ] You know, mathematics don't have a language. They are a language.

You would not expect the same enzyme from different tissues to have different Km values if the enzymes are truly identical.
In addition, you would not expect the Km value to change during purification: the Michaelis constant for the purified enzyme should be the same as that determined with a crude sample.  If this is not true, it might mean that the enzyme has become modified during purification, perhaps by proteolysis (not something you want your examiner to point out or suggest!).
One advantage of the Michaelis constant is that it is independent of enzyme concentration (and so does not depend on the degree of purity).
Having said that, I think it would not be considered too unusual for enzymes isolated from different tissues to have different Km values.
Possible reasons are:

The assay conditions are not really the same. pH, ionic strength, temperature and buffer composition may all affect  Km.  The Michaelis constant determined at pH 7 in 100mM phosphate at 37oC may be very different from that determined in 50mM Tris pH 7 and 25oC
Post-translation modification may be important.  The enzyme from one tissue may be phosphorylated, for example. One laboratory may have isolated the modified from, whereas another laboratory may routinely include phosphatase inhibitors.
Proteases present in the crude tissue preparation may have modified the enzyme.

In the case of succinate dehydrogenase, there are two other important considerations.

Succinate dehydrogenase is a membrane-bound enzyme (containing a covalently bound flavin) and the method of extraction will be all-important, and a key area to examine is whether extraction conditions may account for the difference in Km.
Finally, and this one is important I think.  SDH is a two-substrate enzyme and the Km for substrate A will depend on the concentration of substrate B ! To determine the 'true' Michaelis constant for a two-substrate enzyme (assuming no substrate inhibition), we must extrapolate to 'infinite' concentrations of the co-substrate. Otherwise we are dealing with apparent Km values.

I'll bet the last point is important. Is the problem that at least some of the reported Kms are apparent values, ie the concentration of co-substrate is different under the different experimental conditions?

One advantage of the Michaelis constant is that it is independent of enzyme concentration (and so does not depend on the degree of purity).   This is strictly true in the limit of dilute enzyme concentrations and saturating substrate concentrations, $[S]{tot} >>[E]{tot}$ which is usually the case but not necessarily feasible at all stages of purification. If Km is determined in subsaturating conditions (or concentrations that cause protein aggregation) it will apparently change over the purification.

"... which is usually the case but not necessarily feasible at all stages of purification" ?? In my experience,  [S]o will always exceed [E]o at all stages of purification This is one of the simplifying assumptions of the steady-state approximation, under which Km is usually defined. Can you give an example where this is not feasible during purification. (ii)  "If Km is determined in subsaturating conditions" Subsaturating concs of what? Of [S]o ?  This has to be the case if a rate is determined at sub-Km concentrations.  Of [E]o?? But the usual assumption is that Eo << So (always)

Can you give an example where this is not feasible during purification.  If the substrate has low solubilities (for example, gualylates, methyxanthines) then at high enzyme activities the maximum feasible substrate concentration can be subsaturating. If the enzyme has a high specific activity, for example superoxide dismutase, then obtaining saturating substrate concentrations can also be difficult. There are some obvious technical solutions to these problems but, if they aren't implemented correctly, the apparent Km will change over the purification.

If the substrate has a low solubility it may be impossible to determine the Michaelis constant at all stages of purification if the highest conc of substrate that can be obtained in the assay is way below Km. But this does not mean that the Km has changed during purification.  As long as assay conditions differ only in the degree of purity of the enzyme, and as long as the steady-state approximation applies, one would not expect the Michaelis constant to change during purification.  The purified enzyme will be typically diluted to ensure steady-state conditions, for example

i didn't say Km actually changed I said it can apparently change over a purification.

A Km can change over the course of  a purification. Solubilization of a membrane-bound enzyme could change the Km, as could proteolysis. I have made this point.  This is an undesirable (but perhaps unavoidable) outcome as the enzyme is no longer in the 'native' state. But if the Km is determined under steady-state conditions there is no problem whatsoever in determining a Km with a crude sample, as Km is independent of enzyme concentration (under SS conditions). This is what allows us to compare.  Most of the early work on enzyme kinetics, for example, was done with impure preparations.


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Why does brain invert the image formed on retina?
I have been studying about the human eye and it's working in school for some time. I came across something. I have been taught that the image formed on the retina of the eye by the lens is inverted and the image is made erect by the brain so as for correct perception. But how does the brain know what is erect or inverted? Why doesn't it just keep the image as it is? Please note that I am asking why the brain reverses the image and not about the nature of image formed on retina.

No. My question is completely different

https://psychology.stackexchange.com/questions/337/why-would-the-brain-flip-the-images-perceived-by-your-eyes is also relevant and may be helpful though it repeats from the duplicate marked here.

Thanks I got the answer


text:
Could Racemic Epinephrine be used to Treat Anaphylaxis?
To be clear, this question is not a personal health question nor a question seeking health advice, it is only a theoretical question born of a curiosity for the pharmacology and biochemistry of adrenalin/epinephrine... I have never in my life had any kind of allergic reaction and your answer bears no effect on my health or anyone else's health.  The answer will only serve to help a fictional story be as scientifically accurate as possible.
My question is: In theory, is racepinephrine (the active ingredient in Asthmanefrin) compatible as an emergency replacement for epinephrine to combat anaphylaxis?
As a side question, what effect if any, does benzyl alcohol have on epinephrine?
Thank you for your time I certainly appreciate it!


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Why do some insects which are able to fly unusually do it when they are threatened?
I have killed cockroaches and beetles several times in my house. Sometimes I miss the insects and they run fast, but they don't fly most of the time. Even when I touch a beetle it just continues its walking and don't flies. It just produces a bad smell.
Why don't these insects fly when they are threatened?

Bad smell sounds (smells) like a "stink bug"/shield beetle- they have defenses that don't necessitate flying. As for other beetles, it all depends on the type; some will, some won't.

But flying is fleeing. It's also a defense.

Yes, but if the beetle can get away with not flying (because they aren't great at it) and use a repellent, in the case of stink bugs, instead, they might use that. Cockroaches are very good at hiding and very good runners, but poor flyers. Them having their wings out means it is harder for them to hide.

Just a guess. how do they know what's a predator and what's another beetle? they specialize in hiding.  natural predators are the same sizes or a bit bigger, so they are very fast, and flying away is slower than running, i.e. for beetles, perhaps. also consider that these animals almost always live in leaves or grass or natural scenarios where running a short distance usually means invisibility under a leaf or in a chaotic wildlife substrate. Also consider that they may get disturbed fairly often by other beetles, spiders, cockroaches and flying takes a lot of energy.


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What are these worm-like creatures?
I was reading a book in the balcony and I encountered these animals. They look like worms but I don't know if they are worms or insect larva.
I investigated a little and I found a dead pigeon at the balcony of the upper floor which had a lot of these creatures inside its body.
They have a black thing under their skin near the head and they move like drunken people on the ground.
Also, at the mouth they have a tiny black proboscis-like thing (not present in the picture).
Are these worms or insect larva?

most likely fly larvae, also known as maggots, don't know which species.


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adverse effects of reduced food variety on microbiome
We often see, in science fiction, food being produced from, say, algae or yeast. Any idea what could be the effect of such a limited diet on the gut microbiome? Could there be any side-effect that would have an influence on the brain?
I know that gut microbiome has been tentatively linked to the autism spectrum in some cases, and that heavily processed food may affect it (don't worry, I don't equate "natural" with "good for you"). I'm thinking that food designed only with the needs of human metabolism in mind might ignore the needs of gut bacteria.
I understand this is very speculative, I'm just hoping someone would know of any research in that field.

Hi, and welcome to the site!  Unfortunately, this question is way too broad to be answerable in a specific way... You would have to narrow it down to a very specific diet, and ask about a specific issue that that diet could cause in order for us to be able even to adress the issue.  And even at that, I have a feeling that there will be a lot less solid answers than simple speculation, since science fiction is generally not the realm studied by scientists.  :)  Anyhow, please [edit] to make your question more specific.  Thanks!

In addition to following the guidance from @rotaredom, I encourage you to take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I interpret your question as essentially asking this:
What is the effect of a limited diet on the gut microbiome? Can a limited diet affect the brain via the microbiome?
To simplify the answer, let's make some assumptions --

This "limited" diet is nutritionally complete, meaning that it contains all the macro- and and micro-nutrients needed for human metabolism.  This includes all nutrients that we normally receive via microbiota, such as vitamin K2. Said another way, this diet only affects host health via the microbiome, and there are no effects of malnutrition that would confound our inferences.
There is no flow of genes between organisms in the gut microbiome or introduction of new organisms from outside sources, i.e. only the organisms that are present at the start of the dietary change will be present throughout.  Thus, all observed changes are directly attributable to changes in species abundance.  In reality, there is extensive horizontal gene transfer in the gut microbiome, with new genes obtained from endogenous and exogenous sources.
Following the logic of point 2, there is no mutation.  The microbes present at the end of this diet are clones of the microbes present at the beginning.  Likewise, competitive exclusion does not lead to the disappearance of low-fitness microbes in the microbiome, just a reduction in their relative abundances.
The human host of this microbiome is healthy and not undergoing the physiological changes associated with aging during adherence to this limited diet.

In this simple system, the only things that will change are (1) the total number of microbes and (2) the relative abundances of microbial strains.  Different microbes contain different genes for metabolizing different food sources.  For example, if this simple diet contains carbohydrate A that is metabolized exclusively by the enzyme encoded by gene α, then microbes that both contain and express gene α will grow in abundance.  Some different microbes may then be able to use the products of the metabolism of carbohydrate A, and those microbes may also grow in abundance.  The metabolic interaction network of the human gut microbiome is extremely complex, as it includes both microbe-microbe and host-microbe metabolite cycling.  Eventually, with the same limited dietary input, the microbiome will reach an equilibrium state where the abundance of each microbe is essentially fixed.  The microbes that are best able to utilize the nutrients provided by the food will maintain a high abundance and can be said to be "very fit" in this particular niche.
Keep in mind that this system is extremely simplified, and that microbial fitness in a particular context depends on gene copy number, expression level, enzyme efficiency, microbe-microbe antagonism, and a menagerie of other factors, notwithstanding regulatory signals from human epithelial cells.
Even if we had two people eating the exact same diet with the exact same initial composition of their microbiomes, human genetics plays a role in the carbohydrates available to commensal microbes, as can been seen with salivary amylase copy number.
...
Considering the "brain" part of your question, I suggest you Google "Gut Brain Axis".  Here's a good summary article with references at the end.


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Are there organisms that "branch more" near the leaf?
(I'm a computer scientist)
Tree branching is a fractal patterns in nature. I know stems typically branch in two at each level (self-similarity). I guess there are plants or other organisms that branch in 3 at each level (still self-similar).
But are there organisms where the stem first branches in 2, then at the next level branches in 3 or more? And maybe at the next (maybe the last) level branches even more, say in 7? It doesn't need to be the stem of a plant, it could be any part of any organism (fungi,...), e.g. the "flower part" of a plant, or a micro-organism.
I'm looking for places where just the branching factor changes, but otherwise little else. What I'm not looking for "branch by 2, branch by 2, branch by 2, and then the very final step is one level of fascicle where branching is 5". I would be fine it's "branch by 2, branch by 3, then fascicle where branching is >3".
I'm trying to find if there is something in nature (e.g. organism, geological, or physical structure) that follows this pattern found in a computer science algorithm, RecSplit, which I co-authored.
Like the following: it first branches in 3, and then branches in 8. The actual numbers don't matter to me, it might as well be branch in 2, then in 3, then in 5, or so.

Welcome to Biology Stackexchange! Could you directly link a picture of the branching you describe? I think i found it in the linked paper, but it'd be easier if you can directly link it. Additionally your questions title starts with tree's but the question focuses more on all plants - and I don't think tree's will show the pattern you are looking for so this might mislead people a bit (other plants or maybe fungi might?, not really my area of expertise).

Thanks a lot! I added a picture, and changed the title... I'm not sure what labels would be best. Feel free to edit my question!

https://en.wikipedia.org/wiki/Fascicle_(botany)

Thanks @John for the link! Do you consider this an answer to the question, or is it just the correct term for my awkward / clumsy description "flower part of a plant"?

@ThomasMueller I don't know enough about plant development to turn it into a full answer, but I know what you were asking existed so I want to leave the link.

I think I understand what you mean, but I'm afraid the fascicle is only one level of branching... Sure you could say the plan is branching before that, say branching factor 2, and then the fascicle branching factor is 5... but I'm looking for two levels of branching of the same type, and one is wider...

Can you add some information about why you are interested in such an example? Branching in most plants completely is different from what is seem in your example or in phylogenetic trees. In vascular plants branching is typically from lateral buds rather than splitting of the growing tip so your question as currently formulated doesn't apply to most plants. In most plants these lateral buds are associated with the axils of leaves and thus the branching pattern primarily depends on the phyllotaxis. ...

However, not all lateral buds grow out to form branches, so the observed branches will be a subset of those potential branches. Finally, while some plants produce leaves (and buds for branches) in whorls (all initiated at the same time and position along a stem) many produce leaves (buds) one at a time. Depending on your goal for this, I think your question may need to be rewritten to do one of the following: 1) focus on the minority of plants that show dichotomous, trichotomous, or polytomous branching, 2) allow for branching in whorls, or 3) deal with leaves/buds rather than actual branches.

Note that there may also be fungal hyphae that show "chotomous" branching. However, while I know little about that subject it seems that lateral branching is also the predominant form in that kingdom.

It looks like Penicillin might be what I'm looking for: G in https://www.researchgate.net/figure/Conidiophore-branching-patterns-observed-in-Penicillium-A-Conidiophores-with-solitary_fig2_266395536 -

@tyersome Thanks a lot! If you want to write an answer (link in my comment) I can give credit to you. (I will still create a bounty tomorrow, maybe there are better examples.)

If you're satisfied by "any organism", how about humans?  The single bone of your upper arm/leg branches into two bones in the lower limb, then into five finger/toe bones.

I can't say that your question is very clear to me, but perhaps something of interest to you would be a common type of inflorescence called an umbel. specifically, a compound umbel with associated umbellets.
Compound Umbel:

 Source: Educational Technology Clearinghouse
Some examples can be found here
Again, since your post is not clear to me, I'll also include images of other complex inflorescences:

 Source: texaswildbuds.com   [the compound cyme might be of interest to you]

Thanks a lot! Yes, this is interesting, however it looks like the number of branches are the same on each level (8 for Compound Umbel). I'm looking for something that branches lesscloser to the root (e.g. branch by 2), and branches more near the "top". Chervil does look OK to me.

One case seems to be Chervil.
Another case Penicillin, specially figure G.

Technically Penicillin is a fungus not a plant - though I'm not sure if OP cares about the distinction for his question.

I'm the OP :-) Organism is fine. Actually, a geological structure or even physical would be fine as well - anything in nature.


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Quantifying the Genetic Basis of Complex Diseases
In general, there are 2 types of diseases for which we understand "causality" very well:

Infectious disease, where there is some etiological agent that causes the disease and
Monogenic genetic diseases (e.g. cystic fibrosis), where there are a set of mutations that make specific proteins that are very important non-functional.

My question is not about these diseases. Rather it's about the diseases like T2D (type two diabetes mellitus). Simply put, are complex, chronic diseases like this always traceable to genetic causes? For a given complex disease state, is there always a set of genotypes that leads to the disease? Large-scale GWA (genome-wide association) studies of course have upturned tons of disease-associated variants in complex conditions like T2D, most with tiny effect sizes.
But is it possible to get the disease with none of the disease associated variants (even assuming that you had a list of all disease associated variants; of course you don't actually have this list, but I'm just trying out an intellectual exercise)? If yes, what is the causal pathway for this way to 'get' the disease?
EDIT: To clarify my question as per comment suggestions: Do all (complex) diseases have a genetical background/causative mutation or can they arise for other reasons?

Welcome to the Biology StackExchange, if you haven't already take a look at the tour. I think you are asking a good, but also pretty difficult and potentially broad question. I think the core of your question is 'do all (complex) diseases have a genetical background/causative mutation or can they arise for other reasons' - if I'm right maybe edit this clarification into your question. Also, like David allured to, T2D is not a common abbreviation and you should explain it.

"what is the causal pathway" - very broadly: the environment. But, I think it would be impossible to find a disease that is truly only dependent on the environment: it's always a matter of degree, and there will be some genetic component that increases or decreases susceptibility. In some cases, this component may be trivially small in the extant population.

@Nicolai Thank you for your comment and apologies if I broke some rules. I agree the question is broad, but I figured I didn't know of a better forum to ask it since it's a basic question that I haven't seen directly answered in technical literature (textbooks and papers). Happy to delete the question if necessary. I also edited the question to fix the abbreviation and clarify the main thrust of my question.

I'm not sure what you mean by "complex", but many diseases are known to arise due to exposure to toxins or to an absence of essential nutrients in the environment.
Toxic metals:
A good example of this is exposure to some metals including arsenic, lead, and mercury.  See for example this information from the US NIH and the wikipedia article on metal toxicity.
In the case of arsenic, some of this poisoning is even "natural" — i.e. due to toxic levels of this metal in ground water that hasn't been contaminated by human activity.
Diseases that have been linked to such exposures include cancer, heart disease, diabetes, and anemia.1,2
Deficiencies:
Another class of diseases that are more-or-less purely environmental are those due to nutrient deficiencies — i.e. a diet lacking in minerals or vitamins.

References:

Byrns, M. C., & Penning, T. M. (2011). Environmental toxicology: carcinogens and heavy metals. The pharmacological basis of therapeutics. McGraw Hill, New York, 1853-1878.
Tolins, M., Ruchirawat, M., & Landrigan, P. (2014). The developmental neurotoxicity of arsenic: cognitive and behavioral consequences of early life exposure. Annals of global health, 80(4), 303-314.


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Frameshift Mutation
With regards to LMNA frameshift mutations further downstream in the tail region, specifically (p.Arg455Gln fs*5) which has yet to be found/recorded in any medical literature...Does anyone have any knowledge regarding frameshift mutations (esp. concerning LMNA)? Is it possible that this is a "background mutation" and of little consequence?

Check in gnomAD. It is not in the population. It truncates the protein and the protein has a pLI of 1. So it does not tolerate LoF mutations. This mutation removes the lamin tail domain.


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Why did isopropyl alcohol not work as a disinfectant for E. coli in this experiment?
I recently performed a lab to test different concentrations (20-99%) of isopropyl alcohol and its inhibition of E. coli growth. My control was an antibacterial disk, and what I did was I dabbed the disk in each concentration and put it on the agar with the E. coli. I dabbed it enough so it wasn't soaking wet but it still had some liquid.
Unfortunately, I had no results at all from the alcohol-soaked disked, but I know the experiment should work because the antibacterial disks for all Petri dishes worked.
I don't know why the alcohol did not work at all though, especially since it is proven to be effective as a disinfectant at least for E. coli.
If anyone has a link with this exact lab being tested, or something similar (isopropyl alcohol and effect on zone of inhibition in bacteria labs) that would be amazing.
Concentrations 20,30,40,50,60,70,80,99%
-Disk diffusion, I put the bacteria by streaking across the quadrants
-I dipped the disks until it was soaked then dabbed enough to make sure it wasn't dripping
-Negative control:sterile disk In the middle, positive control: antibacterial disk on quadrant A
-I was going to measure zone of inhibition but there was none produced for all 12 plates except for quadrant A containing the antibacterial disk.

At 70 - 80% EtOH should work for sure. Can you give us details of the concentrations EtOH used, the  kind of plates/medium used, the method of plating (colonies or smooth surface of evenly distributed growth), the contact time of EtOH, the way EtOH was removed (evaporation/drying/etc), the strain of E.coli, and so forth, the study design (what was your negative and positive control), and last but definitely not least, the outcome measure used to determine the #cells left after treatment?

Just a thought: isopropanol is quite volatile and might just evaporate from the disk rather then diffuse into the agar, especially at 37C. I'm not sure the disk diffusion method is appropriate for testing microbial sensitivity of volatile liquids.

@AliceD This is all I know:
-Concentrations 20,30,40,50,60,70,80,99%
-Disk diffusion, I put the bacteria by streaking across the quadrants
-I dipped the disks until it was soaked then dabbed enough to make sure it wasn't dripping
-Negative control:sterile disk In the middle, positive control: antibacterial disk on quadrant A -I was going to measure zone of inhibition but there was none produced for all 12 plates except for quadrant A containing the antibacterial disk.
Thank you for your fast reply, I didn't expect there to be an answer so I'm sorry this is late

@canadianer I am thinking the same but do you know any references I can cite? I have to evaluate my procedure but I have no way to cite any of my assumptions :(


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How much does 10g of glucose raise the blood glucose level?
If you would calculate it:
~5 liters of blood = 50 deciliters
10g glucose = 10000 milligram
so the glucose level raises by 10000mg/50dl = 200mg/dl
However, it is known that ingesting 10g glucose only raises the blood glucose level by ~40mg/dl
Why?

@rotaredom I was talking about putting the glucose in through ingestion, that probably solves the problem. thanks!

This is nearly a personal medical question, since you're asking about your blood glucose level, but it does seem like your interested in the physiology here. I'd suggest depersonalizing this question, doing a little more research, and clarifying the actual physiology question here. To point you in the right direction, you might ask yourself how plasma concentration in a living organism is different from concentration in a beaker.

@DeNovo the 40mg/dl are actually not personal, it's an average of most diabetics.

The "I" statements are a problem, and the statement of personal experience. If you depersonalize, you'll be more likely to get an authoritative answer

If you get an intravenous injection containing 10 g of glucose, all glucose will enter the blood within few seconds and your blood glucose level will temporary rise by ~200 mg/dL.
If you take 10 g of glucose by mouth, the glucose will be dissolved and distributed within the stomach and small intestine and will be gradually absorbed into the blood, let's say within 30 minutes. In this time, some glucose will already move from the blood into the cells, so you will never have 10 g of additional glucose in the blood at a given time.
The actual blood glucose rise after ingestion of 10 g of glucose is not a fixed number, but a range that depends on several factors:

The gastrointestinal tract plays a major role in the regulation of
  postprandial glucose profiles. Gastric emptying is a highly regulated
  process, which normally ensures a limited and fairly constant delivery
  of nutrients and glucose to the proximal gut. The subsequent digestion
  and absorption of nutrients are associated with the release of a set
  of hormones that feeds back to regulate subsequent gastric emptying
  and regulates the release of insulin, resulting in downregulation of
  hepatic glucose production and deposition of glucose in
  insulin-sensitive tissues. These remarkable mechanisms normally keep
  postprandial glucose excursions low, regardless of the load of glucose
  ingested.** (Role of Gut in Glucose Homeostasis, Diabete Care, 2016)

Not to mention there are other fluid compartments, two other sources of incoming glucose, outgoing glucose through utilization and storage, and  even renal spillage at a certain level, a well as many many gluco-regulatory hormones (beyond insulin) that control these processes, in part, to maintain a narrow window of plasma glucose concentration regardless of acute differences in oral intake.

Even in a fully uncontrolled type 1 diabetic state, with ketoacidosis,  it's not the glucose that gets you into (acute) trouble. It's the fluid shifts, the cerebral edema and hypokalemia. So even without any insulin, the plasma compartment doesn't act like a beaker.


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How do I carry out an in silico PCR on a bacterial genome (target:16S rRNA)? Unable to find any bacterial genome on UCSC Genome Browser in silico PCR
I could not find any bacterial species in the drop-down list for genomes in https://genome.ucsc.edu/cgi-bin/hgPcr
Any kind of help would be appreciated. Other links for in silico PCR did not really work or perhaps I do not know the procedure well. Hopefully this query aids others in the future seeking a similar solution.
Edit: I wanted to check the primer pair 27F and 1492R which are part of Oxford Nanopore 16S library prep kit (SQK-16S024) on a bacterial genome.

Your question lacks clarity and detail : what is the purpose of the PCR ? What would you want to do with the amplicons ?

Need to check why the Oxford Nanopore 16S024 kit's primer pair (27F and 1492R) is resulting in two bands instead of a single band of 16S rRNA gene. Once I get the amplicons, there's library prep followed by sequencing on Nanopore to understand which bacteria were present in the samples of interest.

What size bands? This primer set has been found to amplify some 18s eukaryotic rRNA genes, especially when using a lower annealing temp that is more permissive to minor mismatches. TestPrime is a good in silico PCR tool, but it only runs on the Silva SSU and LSU rRNA databases (not whole genomes). https://www.arb-silva.de/search/testprime/

@MikeyC The size of the band should be around 1500 bp since these primers are for full-length V1-V9 16S region. And you are correct, I did come across literature which talk about cross-reactivity of 16S primers with eukaryotic 18S genes. I was not aware of this until now so thank you very much! I shall check out your suggestions and if you want to know, I could keep you posted, formally.

I would suggest using NCBI's Primer-BLAST tool. Formerly I would have recommended their e-PCR tool, but it has been retired. This retirement link has a lot of instructional information for how to use the tool.
You can upload your own assembly/accession, or very likely most well known species of bacteria will be in their database or in refseq.

Thank you for the response. I shall try to learn how to effectively use the Primer-BLAST. I tried it but could not follow well. In the meantime, could you give more pointers? I am supposed to upload a reference genome as template, right? I tried that with the primers but it did not work.

@RahulDhargalkar You could upload a reference genome, or you could select one of the included genomes that is in RefSeq. I'd suggest following the instructions here: https://ncbiinsights.ncbi.nlm.nih.gov/2017/06/28/e-pcr-is-retiring-use-primer-blast/. I can try to add a working example later when I have more time.


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What is this yellow sticky excretion from a moth? Details in photos
Saw this moth on some grass the other day and took some bad phone photos. I'd like to know what the yellow excretion is. I believe it is an excretion from the moth (as opposed to for example, some bubble gum someone dropped on the ground), because it was attached to the tail end of the moth instead of its whole body.

I tried to label the pictures as best I could, you may have to look closely. You can only see a tiny portion of the moth wing in the first picture, below.
The yellow thing was quite sticky but not as hard as bubble gum, as it stopped the moth from flying away. It was frantically flapping its wings trying to get away from some ants, which seemed to be very attracted to the yellow thing. At first I thought the swarm of ants were eating the dead moth, but the moth was alive and the ants were more interested in the yellow sticky thing. I got a thin stick and pulled away some of the sticky stuff and the moth was free enough to crawl away, taking the yellow sticky thing with it, leaving a thin trail behind, like when you stretch out bubble gum. It seemed to be very sticky to the moth and my stick, and very tensile, because unlike a spider's web, I was able to draw it out more when I tried to pull it away from the moth to free it.
I am so curious to know what it might be. I don't think it was made by ants, because it seemed to be attached to, or coming from the actual moth, although, the ants did not seem to be stuck to it.

Please add "moths" to the tags if you have enough 'reputation level' to do so.
Thank you

Some moths exude a yellow lymph excretion when they are threatened.
https://www.nature.com/articles/219747a0
The photo is not very clear, It's difficult to see the species of moth. what did the moth do after? did it fly away? If the moth was looking ill, it could be that it had a parasite.
https://www.insidescience.org/news/meet-moth-produces-both-bird-and-ant-repellants

Just going to mark this as the answer as I am satisfied with this explanation. The moth was trying to get away from the ants, but it was unable to fly away or spread its wings. It was rather difficult to get better photos. Thanks!


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Which member of the Hemiptera family could this bug belong to?
Today I found this little bugger on the outside stucco near Vienna (AUT). Though I'm a big fan of bugs in general, certain members of the Pentatomidae, or their super-family the Pentatomoidea, especially the Palomena prasina (European shield bug) is not one of my favourites since their stink glands on the abdomen can secrete a foul-smelling and long-lasting secretion.
To my surprise, this quite beautifully ornamented bug with a length of about 7-8 mm didn't seem to tend to secretion even when stressing him a bit with a cotton swab (Disclaimer: no bugs were harmed during this test).

Can anyone help me identify this bug which seems to belong to the Hemiptera family (just my assumption, please correct me if I'm wrong).

Nezara viridula, Green Vegetable Bug (and other names).
Probably fifth instar, as the body is mostly green.
http://en.wikipedia.org/wiki/Nezara_viridula
Found by searching images using the terms:
green stink bug with four rows of yellow dots

Photo by Charles Schurch Lewallen, under Creative Commons license. Found at https://bugguide.net/node/view/8819

Thx for your id and the link, looks like the one I photographed is the Fifth instar. I didn't know they moult five times before reaching maturity and have different color morphs - quite impressive!

You are right, I change my answer.


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How come Draq5 stains cytoplasm and membranes under confocal
Just an imaging question on the back of my head.
For nuclear counter stain, Draq5 has been an excellent choice for many people over many years. And I too love it.
The working principle of Draq5 is the nuclear dye Draq5 binds to doubles strand DNA, especially d-A and d-T. That is to say it is very specific to stain nucleus DNA, minimal binding to mitochondria DNA, and no binding to RNA. It is also a very good live cell permeant dye.
In practice, we use it to stain cell nucleus and then perform image analysis, the primary objective in image analysis is identification of the cell object, usually through nucleus staining. No problem, Draq5 does this perfectly, I can see my image crispy clear.
Next, it comes to the estimation of the entire cell, that is to find cell membrane boundaries. A huge advantage of Draq 5 is it also stain cytoplasm and cell membrane weakly, allowing the accurate detection of cell boundaries. Comparing this to Hoechst dye, which also stain nucleus and weakly cytoplasm only for estimation of cell boundaries. This is unlikely a Draq5 non-specific binding, since data from resistant cancer cells that have membrane drug pumps still retain Draq5 very well.
I'm not a chemist so that one thing in the back of my head is:
Why does Draq5 bind cytoplasm and outlines cell membranes that well? Given it is highly specific to bind A/T in double strand DNA grooves. Presumably the dye is binding to its cytoplasm target and membrane target via different mechanisms. Can someone explain that?

Welcome to Biology.SE! Please provide more details and tell us what you already know (this provides context for answers and helps demonstrate that you have done the expected prior research). In particular, if you are seeing an unexpected pattern of staining it would be helpful to include images showing 1) the expected pattern (e.g. from prior research published using this dye — make sure you include reference information and links for these) and 2) what you are seeing (including details of the cells type/tissue, growth, and staining). ——— Off-hand I would guess that you are seeing an artifact.

Unsure if question ultimately seeks practical advise. If so: Ensure application to living cells and avoid fixing and permeabilization. If problem persists: do saturation curve with concentrations spanning some orders of magnitude.

Sorry, I was just lost in my thoughts and posted the half baked idea. Here I have updated my thinking. @tsttst, the staining of cytoplasm and cell membrane happens within its working range, this is actually the advantage of Draq5. In my own experiment Draq5 intensity far from saturation, I can see it over the range set by 16 bit camera, intensity is about the same as my TMRE.


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What Kind of Bug is This
I found this bug in southern Florida in February. It was approximately 1cm long or less, fully extended.  What type of bug is this?

Please [edit] your post to include an approximate size of the specimen. Also, if you have additional information about where you found it or clearer photos, you should update to include that info as well.

It's probably the larval state of a tortoise beetle, or a closely related beetle. They are known to build a "faecal shield" at the end of their tail, sometimes including shed exoskeleton and any debris that sticks to it. They hold this shield over their bodies for defensive purposes that aren't fully  understood.
Lacewing larva look somewhat similar and also cover themselves with debris, but their legs are longer and their head and mandibles look quite different.
Here's an image of a thistle tortoise beetle larva:

Amazing detective work, looks just like it! Thanks so much!


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Is there more biomass on earth today than there was in the past?
Is there more, (or less) matter on earth sequestered as a part of biological systems than there was at any(arbitrary) time in the past?
Edit:
I realise I don't have a specific question, and was looking for a lesson of sorts on what is the footprint of life and will the new not come if the old doesn't die and dissolve(biologically atleast).
If you could suggest me good sources to study this, that would be great.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. As written the answer to your question is almost certainly yes and no depending on those arbitrary times. Rewriting your question so that it is clearer, more focused, and indicates why you want this information is likely to get a better response. We also encourage you to do some research and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

All the coal, limestone, and other bio-deposited stuff on Earth attests to the fact that past life has left behind a giant, cumulative mass of modified matter.  Even components of our atmosphere would be part of that mass.  Some of all that gets recycled by living organisms, and some gets modified by geological processes so that it may be hard to distinguish from "non-biomodified" matter.

@S.McGrew I am not talking about bio-modified matter as much as matter which forms the bodies etc. of living organisms.

Then that would include limestone, coal, & peat.  Marble is metamorphosed limestone.

Due to the massive extinction event humans are causing, especially in the oceans likely less, biomass today. disrupted ecosystems are often below capacity.

But often it is wild plants and animals going extinct, and their habitat replaced by domesticated plants and animals, like in Amazon rainforests. It is bad for diversity, but still biomass i guess

It is both more and less than at other times in the past.
You can research biomass assessment from the carboniferous and other notable times:
https://www.google.com/search?q=biomass+phanerozoic?tbm=isch
check the images there are various research graphs giving accurate responses to you query.

We expect answers here to be relatively self-contained; you can (and should!) link and reference other sources, but simply providing a Google link is not sufficient. If there are images and various graphs that give accurate responses to the query, you could provide those answers and link to the specific graphs to make a good answer.

cheers, sorry, the Stack Exchange image system does not work for webp or url's from the given sites, so I can't add images and their description, i just put links. Webp is the latest image format after JPG it uses 25% less bandwidth and that's many terabites of storage and transfer for sites like FB, Goog, Bing, Wiki, Elseiver, and if Stack still after 1 year of webp becoming a dominant image format, they can't let me share images, then it lowers responses.

I would guess there was more in the past during warmer periods.  For example, imagine if Antarctica was covered in lush jungle rather than ice, then all else equal, there'd have been more biomass back then.  But  I don't think all else would have been equal, as it seems warmer temperatures promote more developed ecosystems in general, so all the rest of the continents would likely have had more biomass.  And of course, with tectonic drift, there were likely times when the large desert areas like the Sahara would have been in different areas with more rainfall and more biomass.  Plus, certainly during past periods of dramatic volcanic activity, all of the nutrients landing in the ocean would have led to much more phytoplankton which would have supported more ocean biomass as well.  Currently, many parts of the ocean simply can't support that much life since there aren't any nutrients in the water.


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Problem with epoxy silane (Random results in glass silanization). What are crucial points to look at?

I`m trying to immobilize an antibody onto the glass surface by means of GPTOMS (glycidoxypropyl trimetoxy silane). Using the same protocol (silanization in toluene or acidified ethanol (see below)) I get different results any time, what are key points to check?

Looking through literature on immobilization, I see a lot of articles where authors use APTES (aminopropyl triethoxy silane) and only a few using GPTOMS, why? Epoxy group seems so atractive...

For toluene:

Rince slides with water
Ultrasonicate them in isopropyl alcohol for 3 min, dry them
Put for 3 minutes into piranha solution
Rinse with distilled water
Treat with oxygen plasma for 3 min
Slowly put slides into 2 or 4 % silane solution in toluene, incubate for 3 min
Rince with toluene and isopropyl alcohol.
Put them on dry heater (max temp. of ours is 97 C, most protocols say 110 C), incubate an hour

For ethanol:

Rince slides with water
Ultrasonicate them in isopropyl alcohol for 3 min, dry them
Put for 3 minutes into piranha solution
Rinse with distilled water
Treat with oxygen plasma for 3 min
Put slides slowly into 2% silane in ethanol solution (silane + alcohol + acetic acid (pH 4,5-5,5)), incubate 3 minutes
Rince slides with ethanol
Put them on dry heater (max temp. of ours is 97 C, most protocols say 110 C), incubate an hour

Please [edit] your question and post the protocol you are following. We can't help if we don't know what you're doing.

please take a look


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Why might long telomeres be selected for in laboratory mice?
In a recent episode of The Portal, Eric Weinstein sits down with his brother Bret Weinstein to discuss Bret's Reserve-Capacity Hypothesis. It's an incredible story of scientific discovery and academic injustice.
One prediction of the hypothesis was that laboratory mice, known at the time to have abnormally long telomeres for their lifespan, were not a representative sample of the wild mouse population because the environment the lab mice were being bred in was selecting for longer telomeres. This had serious implications for drug safety testing.
My surface level understanding as a non-biologist from listening to the Podcast goes like this. Please point out any misunderstandings.
Antagonistic Pleiotropy Hypothesis for Senescence
George Williams predicted that pleiotropic (multi-purpose) genes which are advantageous early in life but detrimental later in life will be selected for in nature since organisms often die or reproduce long before the disadvantageous effects manifest themselves. This is an evolutionary theory for aging, which argues that trade-offs exist between early life and later life fitness. This effect was observed, but no gene had been known to be the cause. This was the "missing pleiotropy".
The Hayflick Limit
Telomeres are repeating, non-coding regions of DNA at the end of each chromosome which aid in cell division. Each division, the telomeres shorten. Telomeres are counters of sorts, which provide a hard limit (the Hayflick limit) to the number of divisions a cell can undergo. Any cell that started dividing uncontrollably (cancer) would eventually reach its Hayflick limit and die. Aging (senescence) is the manifestation of cells in an organism reaching their Hayflick limit.
The Reserve-Capacity Hypothesis
This is Bret Weinstein's work. The way I understand it is that Weinstein pointed out that the missing pleiotropy was not a gene at all, but telomeres. Weinstein observed that there existed a trade-off which was reflected in telomere length. Long telomeres allow cells to repair themselves many more times, slowing the effects of aging, but simultaneously leave the organism vulnerable to cancer, as cells which begin to divide uncontrollably will never reach their Hayflick limit. The length of telomeres is the result of a trade-off between dying of cancer, or dying of old age.
The JAX Lab Scandal
One critical prediction of the Reserve-Capacity Hypothesis was that mice (which were at the time thought to have abnormally long telomeres for their lifespan) don't naturally have long telomeres. Instead, it was specifically the mice coming from the Jackson (JAX) Laboratory (which supplied a significant percentage of North America with mice) which had abnormally long telomeres. Since JAX Lab had economic incentive to breed as many mice as possible as quickly as possible, they were artificially introducing selective pressures on the mice. Namely, the pressure of breeding the mice early in their lives. This meant that any late-life disadvantages, such as susceptibility to cancer as a result of longer telomeres, were not playing an important role since the mice were bred well before they were likely to develop cancer. Since telomeres are a non-coding region of the chromosome, variation can happen very rapidly (no need for the traditional timescales of Darwinian selection). Over time, long telomeres became dominant in the mice population, and so research being done on mice purchased from JAX lab concluded that mice had very long telomeres.
The primary gap in my understanding is the following. Why was it that longer telomeres were selected for? It is unclear to me how discounting the late-life disadvantages of long telomeres would result in long telomeres becoming dominant in the population. If anything, telomere length should become irrelevant. If so, we'd see a wide distribution of telomere length. That is, unless longer telomeres provide benefits to organisms early in life. Is that the case? If not, how can we explain long telomeres becoming not just common, but dominant?

That is a very good and well-stated question, outside my knowledge set.

Their arguments for increased telomere length in lab mice are:

Rate of tumour formation is dependent on the number of cells within an organism. Additionally, tumours take time to form. Therefore, small animals that only need to reproduce early in life, like lab mice, are less prone to tumours and there is then less selective pressure favouring telomere shortening.
Senescence has a negative effect on reproductive success, even early in life, and there is therefore selective pressure favouring increased telomere length that reduces senescence.
While the lack of selection on senescence due to the short window for reproduction could have the opposite effect of reducing telomere length, point 2 is the dominant factor.

To be frank, this all sounds extremely speculative to me and the supporting evidence they did provide was not entirely convincing (though I am far from an expert in the field). Keep in mind that it’s a hypothesis only.
In case you don’t have access to their article, I quoted the relevant section below:

The unusual telomere system of lab mice may be an unintended consequence of captive breeding. Retirement of breeders after 8 months eliminates selection on late-life effects. Tumor-forming mutations take time to occur, tumors take time to become lethal, and the likelihood of tumor initiation is presumably a function of the number of cells in the body, so in small bodied animals like mice, tumors may be rare and inflict minimal cost in the first eight months of life, even absent a telomeric fail-safe. Further, selection for sustained high reproductive output (beginning early and maintained for 8 months) should strongly favor a reduction in senescent effects occurring in that window. Selection acting to eliminate senescent effects and increase early reproductive output may tend to elongate telomeres. Because of the inextricable connection between tumor suppression and somatic maintenance, telomere elongation should dramatically increase the risk of eventual tumor formation, but any effects manifesting after the breeding cut-off will be selectively irrelevant. By our model, selection for early high rates of reproduction in the absence of selection for longevity or tumor suppression should produce long telomeres and a strong propensity for eventual tumor incidence. Despite diminished senescence, we expect these mice to have reduced maximum longevity compared to wild conspecifics. At all ages, lab mice (with elongated telomeres) should be more likely to die of tumors than wild mice. These mice should also be unusually resilient to somatic damage and show few signs of aging other than tumor formation.
...
The hypothesis that an 8 month breeding cut-off should select for non-senescent, tumor prone mice seems paradoxical. One might expect the elimination of selection on late life effects to accelerate senescence, not retard it. But in lab mice, selection for high, sustained rates of breeding appears to be the dominant factor. The tumor fail-safe has effectively been turned off, condemning these animals to form tumors, but leaving an early-life window of reproduction within which there is minimal senescent decline.

Thanks. A couple of follow up questions: How does senescence negatively effect reproductive success early in life? How might the elimination of selection on late life effects accelerate senescence, assuming no other factors were at play?

@aRockStr (1) This may warrant a separate question, or a better answer to this question. Either way, I don’t have a good answer. Check out this paper and specifically the section titled “Cellular senescence and ovarian aging”; it might give some insight. (2) I think their idea is that without selection on late life effects, selection against tumour formation would be dominant and therefore favour shorter telomeres, which would accelerate senescence.

(2) is the argument that if aging is a non-issue, the telomere trade-off is dominated by tumour defense?

Yes that’s my understanding of it.

I think I understand then. The whole argument relies on the existence of a trade-off between defence against cancer and 'defence' against aging. If one of these factors are removed from the system, the other will dominate. This was Bret Weinstein's contribution.


text:
What is this blue insect?
I found this insect in my garden

It's the first time I see this insect, so I'm wondering what it is.
It has blueish, purplish reflections, a head like an ant or wasp but it's the size of a thumb (4-5cm)
I am located in Hungary if it can help identify it

I am pretty sure that this is an oil beetle (also known as blister beetle) of the family Meloidae. In this special case this is probably the violet oil beetle (Meloe violaceus), although this does not completely coincide with the size you mention. The slightly different color is probably caused by the different lighting.
See the image from this Wikipedia for comparision:

Be careful with them, as they can secrete a poisonous substance making blisters on the skin (hence there name) when they feel attacked. For more information see also here.

That's definitely the same as the picture just a big one. http://bugoftheweek.com/blog/2013/1/7/look-but-do-not-touch-blister-beetles-epicuata-and-meloe-spp


text:
Reasons why this protein is not suitable as an immunogen?
In a paper entitled "Progress and Prospects on Vaccine Development against SARS-CoV-2", the authors write the following in section 2.5:
"Compared with S, N, and M protein, E protein is not suitable for use as an immunogen. For one reason, it consists of 76–109 amino acids in different coronaviruses with channel activity, thus the immunogenicity is limited. Studies have shown that SARS-CoV E protein is an important virulence factor, and the secretion of inflammatory factors IL-1β, TNF, and IL-6 are significantly reduced after
knocking out E protein"
Question
Why does the fact it consists of 76–109 amino acids in different coronaviruses with channel activity imply its immunogenicity would be limited?

https://www.sciencedirect.com/science/article/pii/S0168170215001136 in 2015 thought the E protein would be a good target. I dont understand.

@PolypipeWrangler Thanks for your comment. Doesn't that paper comment on how removing the E protein weakens the virus and therefore SARS-CoV with the E protein removed might be a candidate for an attenuated vaccine? It doesn't discuss whether the immune system can be trained to go after the E protein itself.

You are right, viroids without E protein were weakly infectious. I will try to follow the citation chain forward to see if anything interesting turns up.

@PolypipeWrangler I actually think it's useful to keep your comments because that is how we all learn.

https://virologyj.biomedcentral.com/articles/10.1186/s12985-019-1182-0 is a 2019 article on c-virus proteins. out a year ago.

i find the article in google scholar, then use the "cited by" button to see who cites the article. then order by date.

@PolypipeWrangler Are you able to answer the specific query I had in my question? If so, you should post an answer.

Firstly, for better immunogenicity, we should select short peptide of approximately 20 amino acids.  Longer peptide will definitely increase the immunogenicity, but that also increase the possibility of cross-reactivity. So, shorter peptide is more specific.
And secondly channel activity means, it contains more hydrophobic amino acids, so that it can form the transmembrane domain. But hydrophobic residues will decrease the solubility of a immunogenic peptide in the aqueous solution.
Reference: https://www.proimmune.com/custom-peptides/

The article implies E proteins are quite different between the previous known strains - so a vaccine targeted against E protein may only affect a limited range of strains.
But when I do a BLAST search on CS079032.1 I find nearly all the protein sequences are identical (results below).

Thanks for posting an answer. Maybe I have misunderstood, but I don't see how this answers the specific question I asked though?

Thats OK. The line from the article about 76-109 amino acids implies that the E proteins are too diverse for a useful vaccine - but that is not what I am finding.

I could be wrong but aren't the authors of the paper in my question implying the E protein won't provoke a strong immune response (not that it's not useful as an immunogen due to variation between strains)? I'm trying to understand the reasoning underlying their claim the immunogenicity would be limited.

I hadn't found evidence that the E protein has reduced immunogenicity. I dont know why they say so.


text:
Clarification regarding a statement in "The Selfish Gene" by Richard Dawkins
In the third chapter of The Selfish Gene: Immortal coils, Dr.Dawkins makes the following statement while arguing for the case that ultimately "the gene" as he defines it is the unit of natural selection.

Natural selection in its most general form means the differential
  survival of entities. Some entities live and others die but, in order for
  this selective death to have any impact on the world, an additional
  condition must be met. Each entity must exist in the form of lots of
  copies, and at least some of the entities must be potentially capable of
  surviving—in the form of copies—for a significant period of evolutionary time. Small genetic units have these properties: individuals,
  groups, and species do not.

I am not sure what "impact on the world" he is talking about. Could someone explain this? He then goes on to say..

An individual body seems discrete enough while it lasts, but alas,
  how long is that? Each individual is unique. You cannot get evolution
  by selecting between entities when there is only one copy of each entity!

Whereas in his other book, The Blind Watchmaker, he describes a computer drawing program EVOLUTION where he does precisely that, i.e, select between entities (here, computer drawn insect-like figures) of which there is only one copy and allows them to evolve. This seems contradictory to his above statement in The Selfish Gene. Could somebody explain?
tl,dr: Why must there be many copies of entities that are being selected for evolution to be possible?

"impact on the world" is referring to the cumulative effects of natural selection, the progressive alteration of a lineage. If every "unit of selection" was completely unique there would be no cumulative effect of selection, individuals would die and it would have no effect on the next generation. Bodies are unique but genes are not, a body is produced by genes that are mostly conserved from generation to generation. He is drawing attention to the fact there must be something heritable that is conserved from generation to generation for section to have a lasting effect. That heritable thing is what is being acted on, for life one earth that thing is our genes.
The computer program further illustrates his point, the "genes" (code) are carried from generation to generation mostly intact, even though each body is created new and unique from those genes, just like many organisms. that is why they can evolve just like lineages of biological life.
there is a weird dichotomy in how evolution functions, it is a step removed process.  The genes are the things being altered by a process that can only interact with them through their products, bodies, but it is the genes that get altered it is the genes that are evolving.

"Impact on the world" is just his writing style.  Dawkins means "evolutionary significance".  For example, all the intermediate forms leading up to the modern horse have been evolutionarily significant because they contributed to survival of the lines of descent that are still present.  Any tiny evolutionary branch that dies out would have little significance or impact.
In the first part of your second question, the answer is again Dawkins' writing style plus the fact that he's writing for popular consumption.  And, his own thoughts have a way of evolving just as they should; so we shouldn't expect perfect consistency between what is said between sequentially written books.  The Blind Watchmaker was written to convince people that evolution can produce complex organisms without any pre-existing goal to do so, using a relatively simple process.  The Selfish Gene was written to promote his idea that the unit of evolution is the gene. (Note that his idea is not necessarily correct.)
In the second part of your second question you ask:Why must there be many copies of entities that are being selected for evolution to be possible?.  The answer to this is that it is NOT necessary.  It's simply a much more easily implemented - and generally better- evolutionary strategy.  If there is only one organism, and selection means killing it if it is unable to adapt to a given environmental change, then failure to adapt puts an end to it and all its possibilities.  If, on the other hand, that one organism produces a series of single copies (offspring) and each of them has some random genetic variation that's subjected to selection, there's a chance that some will make it past the selection process.  That's equivalent to the one organism producing a lot of offspring at the same time, each with its own genetic differences.
This is a slightly SiFi perspective on the above, but: In general, it's a lot safer to test a disposable copy of oneself against a new danger, than to test oneself directly.  If the copy passes the test, it's safe to face the danger directly.  If the copy fails, then you can test a slightly modified version of yourself against the danger.  If that modified copy passes, then if you're able to do so, you could make the same modifications to yourself and go face the danger.  However, there are now two identical new modified copies of you.  One of you is superfluous, so you flip a coin to decide which survives.
In the SiFi scenario, we have one organism evolving safely up one possible branch of an evolutionary tree.  But if that organism reaches a dead end from which there is no escape, its branch dies.  On the other hand if all the other branches are allowed to continue (that is, if you let both copies survive and evolve independently), there's a far better chance at least one branch will still be growing and branching far in the future.
I personally think Dawkins "Selfish Gene" idea fails when we try to fit it into that picture.

Your hypothetical falls apart for several reasons, not the least of which is copies take resources to make as much as the original took to make, and a copy is not superfluous, otherwise asexual reproduction would not exist, it is no safer to test on your copy as yourself, unless your copy is not a copy, which does occur , see skin cells. You are needlessly anthropomorphizing selection in your example.

It is pretty difficult to say anything about evolution in layman's language without being accused either of anthropomorphizing or of invoking a diety.  Please clarify "it is no safer to test on your copy as yourself, unless your copy is not a copy".

First that whole section is irrelevant to the the questions, but to answer you if the "copy" and the original are identical it doesn't matter which one is sacrificed, the loss is the same.

if they are not identical what you can "test" is pretty limited, the more capable the copy the closer it is to an identical copy and the more impactful the loss of time and material, and we already see such behavior, it is essentially r strategy,  make lots of low cost copies and spam the environment. similar is  multicellular life where only a few cells get to reproduce the rest only being beneficial in their ability to facilitate that. .

What you're saying is correct, but a bit beyond the scope of the question.   IMHO, only the OP knows if an answer fits the intent of the question.

Btw, take a look at my last name, blacksmithing, spokane.  We have some background in common.  Evolution is a big piece of it.

Let us continue this discussion in chat.


text:
How can stat major get into bioinformatics?
I'm in my first semester of phd in information science and
I want to work with bioinformatics professors.
As a stat major, what should I prepare for before contacting some of them?
I thought about completing some coursera courses in bio but will they count?

I know little of the subject, so not an answer, but you can take a look at our dedicated sister site: [bioinformatics.se], they might be able to give you a few pointers. Please take their tour and have a look at their help centre before posting to ensure that your query is on-topic.

I suggest moving this question to Bioinformatics or Academia communities.

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and delete or [edit] your question accordingly. In particular, please note that opinion based questions such as this are not appropriate — questions should be about biological processes or mechanisms and have factual answers. This is neither and thus is likely to keep accumulating down and close votes.

Thank you Rogue and Roger.

In addition to what I said above, you now seem to be crossposting this on Bioinformatics SE. Cross-posting is impolite and your post is off-topic for the same reasons there as it is here.

People, you cannot on the one hand tell a new OP that something should be moved  to another SE and then call them out for crossposting. That is toxic behaviour. Better just recommend to switch to a completely different community such as Reddit and Biostars where opinion-based answers are accepted and make a closing vote.

@ATpoint: There is no toxic behavior here only standards and the SE model in action. 1) The first user who suggested moving also said to check the help before posting — if the OP had done so they would have found that this post is off-topic here and there. 2) I never suggested moving this post (and would have mentioned not crossposting if I had) and directed the OP to appropriate resources for details about how to use this site, which they do not appear to have consulted. 3) If you wish to discuss this site and how it works then please use [meta].

Bioinformatics is still rather open to people with various backgrounds - biologists, mathematicians, statisticians, physicists, computer scientists. Solid base in math and/or software development is greatly appreciated.
The usual entry paths are:

Doing Masters in bioinformatics after having done previous studies in another field (usually biologists learn a bit of math and programming, while computer scientists learn a bit biology)
Doing a PhD in bioinformatics - this seems to be your case. So it may be a good thing to contact potential supervisors for doing a thesis in bioinformatics.
Doing a postdoc in bioinformatics (similar to the previous option, but later in the career and with less opportunities outside of the academia).

Remark: In English-speaking academia one more frequently talks about Computational biology rather than bioinformatics - it is a broader term, encompassing many useful areas of research (see this thread). It has however limited use outside of academia or in other languages.