Are the chemical constituents of human bodily fluids similar to sea water? I have heard a comparison of human bodily fluids to sea water from various sources in the past. The most notable was a teacher who claimed, if I remember correctly, embryonic fluid is comparable in chemical content to sea water. I am wondering if this claim has any scientific basis. If not, is there another bodily fluid known for this characteristic? I tried doing some google searches and did not find any supporting evidence. If this is a myth, has anyone else heard such a claim and how it may have begun?

Let's just consider mineral salts, since obviously sea water does not contain animal proteins or cells, and (fortunately) our bodies don't contain phages, micro-algae etc.

Sea water is very salty; on average about 0.5mol/L of NaCl (the main salt dissolved in sea water).

On the other hand, human biological fluids like plasma and the intracellular space are at least 2-3 times more dilute.

Unless some other human bodily fluids are exceptionally salty, it seems that there is a pretty big difference and it is not very accurate to say that bodily fluids and sea water have close chemical compositions.

There are not many fluids that are very close from bodily fluids in term of composition. Popular culture tells the tale of emergency transfusions of coconut water during WWII, but that's not supported by medical literature; even though more recently, in exceptional emergency cases, it has been reported to be possible as a short term solution because of the similarity of osmolarity between plasma and coconut water.


Lifeless Lake in Siberia There is a lake in Siberia called Lake Pustoye. No life exists in the lake. There are no fishes and no plants and even trees around the lake die . No birds even visit this lake .The lake even has bubbles in it like champagne .The water has been tested and there is nothing in the water that makes it harmful to life.  It even tastes like champagne and yet life cannot exist in it .Fish were introduced into the lake but they quickly died off . So why can't any life form survive in this lake ?

https://www.researchgate.net/publication/200464654

This is a detailed comparison between two lakes in the Trans-Volga region in Russia, one of them being Lake Pustoye. I'm not sure if the Lake Pustoye in this article is the same lake being referred to by the op as it isn't in Siberia and there's no mention of champagne-like water, but it does bear the same name and has a curious lack of fish. The authors found that while there is an absence of fish, there is by no means an absence of life in the waters of Pustoye. In the article, they catalog the seasonal shifts of biodiversity in the waters of both lakes. The pH was observed to be low in Lake Pustoye which they implicated to be the likely cause for the lack of fish, though they indicated that more research would be needed to determine the exact cause of the acidification.


What I can do in order to improve the folding of the protein? I am struggling with the expression of the certain protein. It seems that it is not properly folded and thus, it is not active. I tried to express it at the lower temperature and for the longer time, but it did not help. Can anyone give me a clue what I can try to do?

The size of the protein is around 55 kDa. I know that I have some soluble protein as I run western blot. The protein contain His-taq on the C-terminus so I started with Ni-NTA column chromatography. Steps of purification:

Incubation the lysate with resin (30 min/4°C)
Unbound proteins were collected as the ‘Flow-through’ fraction
Wash 1 with buffer: 50 mM NaH2PO4, 1M NaCl, 10 mM Imidazole
Wash 2 with 10% buffer B in buffer A
Elution with buffer B: 50 mM NaH2PO4, 1M NaCl, 250 mM Imidazole

Because the protein is co-purified with something else in size around 57 kDa (which might be a chaperone protein) I tried also:
1. add ATP to first wash in concentartion of 2.5 mM and incubate column for 1h/4C
2. add ATP to first wash in concentartion of 2.5 mM and incubate column overnight in 4C
3. add ATP to first wash in concentartion of 2.5 mM and incubate column overnight in room temperature
4. add ATP and glycerol to first wash in concentartion of 2.5 mM for ATP and  4M for glycerol and incubate column for 2h in 4add ATP to first wash in concentartion of 2.5 mM and incubate column overnight in 4C

All the method end up with two close to each other bands (only one of them is my protein) and protein is not active.

If you have over-expressed an eukaryotic full length protein or the enzymatic part, then E. coli does not necessarily provide a good environment for its folding so you need to express it in the same system which the original protein came from, e.g. mammalian or Drosophila etc. E. coli over expression is mostly used to generate wast amounts of protein for the purposes of protein sequence based Ab generation amongst other things. Look at this review for some of the solutions it offers for proteins not folding correctly in E. coli when over-expressed (http://www.biomedcentral.com/1472-6750/4/32).

The remainder of your question is a duplicate of this question (Ni-NTA purification, problem with the chaperone protein), which I have provided an extensive answer/comments to!

In addition, since the lack of enzyme functionality is a potential indication of errors in its state/3D structure, it is however not a definitive reason. Could you provide some explanations as to what experiments you have conducted to reach that conclusion and how this second point about chaperone eluding with your protein relevant to the first and the last section of your question?


Codon alignment via Python? I have pairs of coding DNA sequences which I wish to perform pairwise codon alignments via Python, I have "half completed" the process.

So far..

I retrive pairs of orthologous DNA sequences from genbank using Biopython package.
I translate the orthologous pairs into peptide sequences and then align them using EMBOSS Needle program.

I wish to..

Transfer the gaps from the peptide sequences into the original DNA sequences.

Question

I would appreciate suggestions for programs/code (called from Python) that can transfer gaps from aligned peptide sequence pairs onto codons of the corresponding nucleotide sequence pairs. Or programs/code that can carry out the pairwise codon alignment from scratch.

The basic process would be (in pseudocode, I don't know python well enough, I'm a Perl geek):

$seq1=ATGCCAGGCTGA
$seq2=ATGGGACCATAA;
for ($i=0;$i<length($seq1);$i++){
   codons1[$i]=amino_acid
}
for ($i=0;$i<length($seq2);$i++){
       codons2[$i]=amino_acid
}

At this point you will have two arrays or hashes or tuples or dicts or whatever holding the amino acid that corresponds to each codon position of the input seqs. You go and do your translation and dS/dN thing and you can then use these lists to map back to the original nucleotides:

for ($i=0;$i<length($ProteinSseq1);$i++){
  print codons1[$i]
}

You will need to adapt this to deal with codons correctly (i++ will only increment by one, you need to extract the triplets) and then to read the gaps but these are all programming issues that have nothing to do with the biological side of things.


How to induce a steady increase in cyctoplasmic [Ca2+] in HEK293T cells? And is there any simple marker/method to confirm it? We are trying to find out whether increase or decrease of cytoplasmic calcium concentration affects the interaction of two proteins, using co-IP in HEK293T cells as a readout.

In different forums and papers I have found that to increase cytoplasmic Ca2+ levels in non-exciteable cells, there are three major categories of compounds. Ionophores (A23187, Ionomycin), Agonists of InsP3-PKC signalling (carbachol, ATP) and SERCA inhibitors(Thapsigargin, CPA).

However, different papers and different people on use  different concentrations and durations of treatments. Since a lot of the drugs generate rather transient spikes, I realize that the timing is crucial here. Since, we do not have the resources for the optimisation of [Ca2+]-sensing dye imaging, I am also wondering whether there is a simpler way of roughly assessing [Ca2+], perhaps by by analyzing a marker protein/RNA using Western Blot or qPCR?

Thanks a lot!

As far as I know, microscopy (be it with dyes like fluor or with genome-encoded calcium indicators) is really your only good bet, especially for getting quantitative sensitivity, which I think is what you're looking for. Changes in cytosolic calcium are incredibly dynamic both in time and space, which is something to consider when asking how calcium affects your two proteins.

I do know of an example where investigators transferred cells to buffers with different Ca2+ concentrations and permeablized them with a mild detergent to raise calcium levels (Borges-Pereira et al 2015). I'm not sure if that would work for your system, but it's worth taking a look, as I think it raises the levels pretty gently and steadily, and you have a better idea of what your intracellular concentration is going to be without directly visualizing it. Considering you won't be able to tell the Ca2+ concentration at any given time without microscopy, things like SOCE and intracellular chelation rates might be important, so you'll want to watch out for when after treatment you start your assay, perhaps trying a few different time points

Hope that was of some help!


What are the response frequencies of sensory neurons? Both visual and auditory stimuli are sent to the brain via ganglion cells (retinal resp. spiral). Both are the first cells along their resp. pathways that produce action potentials.

My question concerns typical frequencies of action potentials sent along the axons of the visual vs. auditory ganglion cells as a reaction to a "typical stimulus", i.e. a medium long, medium strong signal of some fixed frequency (e.g. light: red, sound: 440Hz) against a white resp. silent background.

Are these frequencies of comparable range, or does one type of ganglion cell (retinal vs. spiral) fire with a significantly higher or lower rate than the other?

(The question would not make sense, if the physical frequencies of light and sound - which trigger the receptor cells - would be coded by frequencies of action potentials. But I assume that this is not the case, is it?)

The auditory brainstem shows "phase-locking" typically up to 1-3Khz at most; 3000Hz is an incredibly high firing rate for a single neuron, but this phase-locking is achieved not by individual cells firing in-phase with an auditory stimulus, but rather with a population of cells that tend to fire in-phase, such that if you average across the population you get a phase-locked population volley.

In some cases, in some animals, this phase locking can even get to the higher frequencies (see here for example).

However, this phase locking seems primarily important for sound localization via interaural time differences. Frequency itself is encoded by which population of hair cells is activated, according to the properties of the basilar membrane. Firing rates of individual spiral ganglion cells are only faster than 100 Hz at very high stimulus intensities.

Similar to the spiral ganglion cells, retinal ganglion cells primary encode intensity information in their firing rates.

However, in both cases, it's important to recognize how crucial adaptation is in sensory systems. RGCs in particular fire primarily to transients, so it is typical to use light flashes, drifting gratings, or other dynamic stimuli. The response to a "medium long, medium strong signal of some fixed (wavelength)" is going to be brief, followed by silence, not a constant response like you imply.


Why would a flower evolve such that a particular pollinator cannot pollinate it? I went on an interpretive trail today and came across a wild flower sign. It said that some flower species evolved such that they can not be pollinated by humming birds as they are shaped such that only an insect proboscis could get into it. Why would a flower evolve in such a way? Wouldn't it be advantageous to take any pollinator?

An interpreter in the visitor center suggested it might be that the flower wants to save it's limited pollen for pollinators most likely to visit other families of its species. I'm not completely sure I buy this, as a pollinator willing to visit one flower of a species is likely to visit another flower of the same species. That said, I think he might have been on to something. Alternatively, this link made me think perhaps certain pollinators might damage the flower and it would want to discourage them.

This question goes beyond a flower co-evolving such that a particular organism could specialize in pollinating it; I'm curious why a flower would specifically evolve such that it could not be pollinated by a particular organism.

I think the explanation by the interpreter is most appropriate. The definition of species is a particular category of organisms capable of reproduction among themselves. Thus pollen of a particular species must fall on the stigma of the same species. But pollinators visit all species of flowers (as they never visit Biology Stock Exchange, thus ignorant of the definition of species) which bears nectar and the entrance is big enough to let them in.

The flowers in your question increase their chance of pollination by reducing the varieties of flowers a particular pollinator can visit. Lets make it simpler (or even more difficult for those who don't like mathematics!)...

Suppose there lives 4 humming birds and 4 bees in a oasis...both are too lazy to visit other oasis in search of nectar. One morning 4 flowers bloom in that oasis...2 wild flowers you mentioned and 2 wide mouthed flower of some other species.  Now 1 flower of the wild species can be visited by 4 bees (as humming birds can't enter the flower). One flower of the other species can be visited by 4 bees and 4 humming birds. This large number of pollinators for the second type of flower reduces its chance to be visited by a pollinator that visited a flower of the same species. Whereas for the wild type flower the possible number of pollinators are very few (only 4)...so the chance of one bee visiting two flowers of the same species is very common and so is the chance of it getting pollinated.

In this way these flowers increase their chance of pollination by modification of their shape.


Is there a fundamental reason that plants cannot fix their own nitrogen? Plants must have nitrogen to grow. According to the answer to this question, there are no plants that can fix their own nitrogen (without the help of bacteria).

Plants get their nitrogen in the form of nitrates (NO3-) or ammonia (NH4+). Nitrates and ammonia get into the soil through

lightning (causing N2 and O2 to combine to form NO which then reacts with atmospheric water and is brought to earth by rain)
nitrogen-fixing bacteria associated with leguminous plants
fixed nitrogen from dead plants/animals (ammonification), urine, etc.
ammonifying and other bacteria

The answer also states that it seems to be possible to engineer plants to be able to fix nitrogen.

So one could think plants could have evolved to be able to fix nitrogen, but did not.  Maybe it just did not happen based on it's probability to happen.
Is there any other explanation?

Maybe the ability to fix nitrogen would have a harmful effect on plants? Or fixation requires a complex set of related mutations? Are there enough areas with soil depleted of nitrates to exert a selection pressure for nitrogen-fixing plants?

That is an interesting question. But rises some line of thought by analogy, e.g. why people won't evolve to produce their own ATP without mitochondria? (I mean of course Eukaryotas in general). I don't see any reason why multicellular organism cannot incorporate bacterial functionality either as happened with mitochondria, or as just separate cell type, that will provide desirable enzymatic reactions.

The answer, no matter how unsatisfactory, might be simple: because it so happened. We definitely can create experimental conditions lacking N-fixing bacteria as well as varying amounts of nitrates, nitrites etc. And then produce and screen line of mutants for ability to fix nitrogen without symbiotic partners.


How do kidney cells excrete their own wastes? The kidney is composed of tissues, and those tissues are made up of numerous cells - so how do these cells excrete their wastes?

Lastly, are there any wastes in the venous blood (renal vein), what makes the renal artery and vein different? - what substances do they each carry?

I checked my anatomy notes and online figures about the kidney. There is no mention about dedicated arteries for feeding kidney cells. So it does not work the same way as the heart does, where there is a dedicated coronary artery. The kidneys use the same blood vessels for filtering and for nutrition/waste transport purposes too.

Figure 1 - kidney anatomy - source

Figure 2 - nephron anatomy - source

The urea is created from NH4+ and HCO3- in the liver (mostly) and the kidney because of blood pH regulation purposes. It neutralizes the HCO3- created by the lungs from CO2 and OH-.

  The urea cycle (also known as the Ornithine cycle) is a cycle of
  biochemical reactions occurring in many animals that produces urea
  ((NH2)2CO) from ammonia (NH3). This cycle was the first metabolic
  cycle discovered (Hans Krebs and Kurt Henseleit, 1932), five years
  before the discovery of the TCA cycle. In mammals, the urea cycle
  takes place primarily in the liver, and to a lesser extent in the
  kidney.

  In chemical terms, urea synthesis is an irreversible, energy driven
  neutralization of the strong base HCO3- by the weak acid NH4+, and the
  average daily excretion of 30 g of urea is equivalent to the disposal
  of about 1 mol of HCO3- per day. Thus, a major function of hepatic
  urea synthesis is to effect this neutralization, without which the
  body would otherwise be confronted by a major load of alkali.

  Urea is excreted by the kidney, and is normally present in plasma and
  body fluids at a concentration of 3.0–6.5 mmol/L.

wikipedia - Ornithine cycle
Textbook of Hepatology - Ammonia, urea production and pH regulation - Dieter Häussinger
1984 - The role of ureagenesis in pH homeostasis

The kidney reabsorbs urea in order to concentrate the urine:

Figure 3 - nephron with material transports - urea resorption at the end of the urine creation process - source

  About 40% of the urea filtered is normally found in the final
  urine, since there is more reabsorption than secretion along the
  nephron.

wikipedia - Renal urea handling:
2007 - Critical Role of Urea in the Urine-Concentrating Mechanism

The kidney secretes the urea to the urine, but it absorbs more by the reabsorption than it secreted.

  The kidney freely filters urea at the glomerulus, and then it both
  reabsorbs and secretes it. Because the tubules reabsorb more urea than
  they secrete, the amount of urea excreted in the urine is less than
  the quantity filtered. In the example shown in Figure 36-1A (i.e.,
  average urine flow), the kidneys excrete ∼40% of the filtered urea.
  The primary sites for urea reabsorption are the proximal tubule and
  the medullary collecting duct, whereas the primary sites for secretion
  are the thin limbs of the loop of Henle.

Medical Physiology by Walter F. Boron and Emile L.

So if we are talking about urea, then it is secreted to the urine. If we are talking about other waste products, then e.g. CO2 is certainly handled by the veins.


Would somebody born 'reversed' (e.g. heart on their right side, etc.) be completely healthy? By reversed I mean their body is a complete mirror image of a normal human's.

Yes, such a conditions exists. It is called "situs inversus" (literally "inverted sites"). All major organs are placed on the opposite site, the condition is relatively rare with an incidence rate of 1:10.000. There are some even rarer forms occuring, when the organs are flipped, but the heart is still on the left side (levocardia) as opposed to the case when it is also on the other side (dextrocardia).

While some  of the patients are phenotypically normal (besides having their organs on the "wrong" side), congenital heart disease and ciliary disorders (also known as Kartagener syndrome) can occur. See the linked paper below for an overview.

For more information see here and here and the article:

Situs inversus and ciliary abnormalities: 20 years later, what is the
connection?


Microtiter Dish Biofilm Formation Assay- Pseudomonas and Crystal Violet If Pseudomonas is a gram negative bacteria, it does not retain crystal violet but why is it that so many people are using crystal violet staining in theri Microtiter Dish Biofilm Formation Assay?

Using the Gram stain for differentiation between G- and + requires the addition of alcohol, the critical step in Gram staining. Actually the first step, simple staining, goes the same for all types of bacteria. All bacteria gain the stain, but addition of alcohol makes the lipid in bacteria like Pseudomonas to lose it.


Does the new virus tree of life change their position between living and non-living things? Viruses still do not fit the criteria of living or it's simplest form (the living cell), why would some say that the new virus tree of life makes it more closer to life? Aren't mitochondria in a point of view closer to life than viruses?

The definition of life is a question of philosophy

The definition of life is a question of philosophy and not of biology. However, because discussing it often require some knowledge of biology and because it is so common for the general public to misunderstand that the definition of life is not of biological interest, the question has already been addressed on this biology.SE. Please have a look at:

why-are-viruses-considered-microbes and why-isnt-a-virus-alive.

Why would the tree of viruses affect our definition of life?

It is impossible to say much without a link to the original claim. I will need to speculate on what the authors of this claim first meant.

A tree of viruses gives a visual representation of a feature that we tend to associate to living things only, that is they evolve and speciate. Of course, we did not need to build a tree of viruses to understand that they evolve and speciate but a visual representation can sometimes offer an emotional response that will push some to prefer considering viruses as living things. In consequences, it is possible that the vision of this tree affect the emotional aspect of what we define as "living things" and might push the community to expand their standard definition to include viruses. Again, it is important to understand that the definition of life really has absolutely no impact on Biology.


Insect identification, Bangalore India Can anyone identify this insect? It was sitting on my refrigerator.

Size: approximately 1 cm height, 1 inch across

My location: Bangalore, India

So i did some more research and found some canon photos of two moth species both found in india and super similar to this

both of them have brown spots around them
both of them are found in india
 So it was hard for me to eliminate one of them
here are both the insects
Sphenarches Anisodactylus

Sphenarches caffer

So now its up to you to decide which one it is???


Would a human survive eating only living ants? After reading an admittedly foolish question about 1 googol ants vs. 1000 humans, I had a question. Could a human survive solely on eating ants (common ants, not the stinging kind, or leafcutters etc.)

This study in 1984 suggests it's a bad idea and other sites have said eating ants is for weight loss.

The abstract says that it goes into detail about the problems associated with eating ants as well as their low nutritional value.

So I believe the answer is no. You could not survive long term on a diet of only ants.


How are Maggots Sterilized (Disinfected)? For maggot therapy, how are maggots disinfected? I'd imagine there's a limited scope of measurements that can be taken to sterilize the maggots - i.e. we don't want to sterilize them and kill them too.

History
Ambroise Paré is credited with being the first to note his observations on Maggot Debridement Therapy (MDT) in the 1500 though it is a technology that has been used for centuries (reference). It wasn't until the 1920's that therapeutic experimentation with maggots was instigated by William Baer, a clinical professor in orthopaedic surgery at the Johns Hopkins University in Baltimore, Maryland, whose unorthodox methods were successful in the treatment of osteomyelitis and pyogenic wounds. He is also considered the father of modern MDT since he was the first to devise a way to sterilize maggots (reference).
Procedure
In addition to removing necrotic tissue from the wound (a procedure known as debridement) maggots have also been proven to disinfect wounds, promote healing, and inhibit a pesky substance known as biofilm from forming on the wound bed. Maggots are nature’s cleansers, showing up to remove dead tissue and promote healing (reference).
Currently Lucilia sericata, or the greenbottle blowfly larvae is preferred for MDT because

Firstly, larvae have been shown to debride wounds with extremely low
probability of myiasis upon clinical application. Larval secretions
have been shown to help in tissue regeneration. L. sericata have also
been shown to lower bacteremia levels in patients infected with MRSA (reference).

Sterilizing maggots
In early applications, sterilizing the larvae was a major problem. Doctors had to first bathe the eggs in bleach and then soak them in mercuric chloride or formaldehyde. The bandages, gaudy and cumbersome for the patients, were held in place with either surgical tape or Unna’s paste—made of zinc oxide, gelatin, glycerine, and water. Other problems that doctors faced included the maggots escaping during the application process and the leakage of toxic waste secreted by the maggots into the wound, which led to infections such as tetanus. Today, commercial and research laboratories produce sterile larvae. And instead of the bulky gauze bandage, a form-fitting cast with a nylon net to corral the larvae is placed over the wound. An absorbent pad put on top of the netting soaks up the larvae’s toxic waste products. The number of larvae used has also changed. Early prescriptions ranged from 5–6 maggots for a fingertip injury to 500–600 for a more serious wound. Today, the scientific standard of 10 larvae/cm2 is used (reference).
William Baer proposed a method to produce sterilized maggots and it is understood that sterilization has to start from the egg stage in itself (reference). The sterilization solution that he proposed was.

Stock Solution of bichloride of mercury, strength one in 1,000 parts.
Stock Solution of fifty per cent. ethyl alcohol. Take equal volume of
each Solution, mix, and add one-half of one per cent. chemically pure
hydrochloric acid. The final Solution will contain bichloride of
mercury, strength one in 2,000 parts, twenty-five per cent. alcohol,
and one-half of one per cent. hydrochloric acid.

He did not sterilize the maggots as such but took care to feed it sterile food. His work can be read here. Another solution used for sterilization was  5 per cent solution of formalin plus 1 per cent sodium hydroxide (reference).  Sterilization of maggot larvae in itself was found to be hard with some success being reported (reference). Current maggot sterilization techniques include.

UV Sterilization
Rapid washer sterilization
Egg to maggot sterilization (reference)

There is no first generation that has been detailed as such. Mostly sterilization starts from the egg stage. As far as bacteria in the gut is concerned, if sterilization is carried out well, it has been found that there is a significant decrease in any harmful bacteria present (reference). Most details of sterilizing maggot larvae is given in this paper. Consider reading this paper as well.


DNA replacement: new species This is a hypothetical question

What would happen if the DNA of a prokaryote was replaced with the one of a prokaryote of another species, would the cell structures change and adapt to the new DNA and would the cell survive?

(Would the result be similar if we did the same with two eukaryotic zygotes of different species?)

Such genome transplantation was performed between two Mycoplasma species in Craig Venter institute Genome transplantation in bacteria: changing one species to another. They found that the donor genome completely changes the recipient cell to accept the identity of the original donor cell.

Note of caution: the above experiment was conducted between two highly similar species, and as of yet it is unclear what is going to happen if the exchange is performed between two distantly related bacteria species.

As for eukaryotes -- the transplants may be not viable at all, because naked DNA is going to lack epigenetic information (histone modifications, DNA methylation) that is preset during gametogenesis.


What is this plant with some seeds around its leaf? I am in India, This plant is growing on floor with very less soil
on it. I took 3 pictures of the same plant, It just rained yesterday.
I didn't see any insects around this plant. here is it:

It is Andrographis paniculata also know as Kalmegh or Kalamegha

It has close resemblance to Mexican Tea Plant also.


Is synesthesia caused by crossing the circuitry of different sensory inputs? I have a question about human perception. After reading the book "Sensory Perceptual Issues in Autism and Asperger Syndrome" and knowing about synesthesia (https://en.wikipedia.org/wiki/Synesthesia) something occurred to me.

If unique circuits of neurons are responsible for each of our senses, and the circuits can cross with each other (synesthesia), and given that autistic people can switch off a sense or may have problems filtering inputs, and all impulses are of one kind, how can the brain know where these inputs are coming from? For example if input is coming only from the eye, can a person think that it is coming from the ear? Can we see with our ears, or hear with our eyes, through some sort of circuit-crossing?

Short Answer
Synesthesia happens at a point during processing where we are not dealing with "raw visual input" or "raw auditory input" anymore, but already with more abstract constructs such as "colors" or "sounds".
Full Answer
Your question seems to consider sensory perception as a matter of "inputs" and the brain detecting those inputs, such that for example the only difference, from the brain's point of view, between visual inputs and auditory inputs is that one comes from the ear and the other from the eye.
A more accurate way of seeing it is that our sensory perceptions are really the brain constructing a coherent reality from the information it got from our senses. And I do mean "information" in the most abstract, computer-sciency sense possible. It's not like our eye is a photographic plate that contains "what we see", and the brain just has to reconstruct that. The processing of visual information, by which I mean picking out various features from the light received and deriving meaning from them, starts right in the retina. Some examples from the "14.5 Visual Processing in the Retina" section in this page:
http://nba.uth.tmc.edu/neuroscience/s2/chapter14.html
On bipolar cells:

The two bipolar cell types have different functional properties.

The off bipolar cells function to detect dark objects in a lighter background.

The on bipolar cells function to detect light objects in a darker background.

On horizontal cells:

The surround effect, produced by the horizontal cells, enhances brightness contrasts to produce sharper images, to make an object appear brighter or darker depending on the background and to maintain these contrasts under different illumination levels.

On the retinal ganglion cells:

The retinal ganglion cells provide information important for detecting the shape and movement of objects.
Type P retinal ganglion cells are color-sensitive object detectors.
Type M retinal ganglion cells are color-insensitive motion detectors.

On amacrine cells:

There are 20 or more types of amacrine cells based on their morphology and neurochemistry. The roles of three types have been identified. One type

is responsible for producing the movement sensitive (rapidly adapting) response of the Type M ganglion cells.

enhances the center-surround effect in ganglion cell receptive fields.

connects rod bipolar cells to cone bipolar cells, thus allowing ganglion cells to respond to the entire range of light levels, from scotopic to photopic.

Similarly in our ears, the cilia cells that vibrate in response to sound are frequency-dependent, and it is information about those frequencies that gets transmitted to the rest of the brain for processing. In other words the very organ that detects sound also performs a kind of Fourier transform on the sound waves it detects before anything else.
See for example:
https://psychology.stackexchange.com/questions/15274/how-does-the-inner-ear-encode-sound-intensity
This parsing, combining and interpreting of information continues throughout the perceptual circuits of the brain, and not in a straightforward way either - it is hypothesized that there are two independent or semi-independent processing streams for visual information, the ventral and dorsal streams, one which is for identifying objects and the other for guiding actions:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4678292/
There is also information flowing the other way, where more "advanced" brain regions draw conclusions about what's actually there and feed those conclusions back into the more "basic perception" parts to ensure that that's what we see. I.e. perception has both "feedforward" and "feedback" processes, or "bottom-up" and "top-down".
All of this is to say, there is absolutely no way for the brain to confuse information from the retina and information from the ear; the early processing in both of those is too tightly linked to the organ itself, and perception as a whole is inextricably linked to cognition. It's not like a mouse and keyboard that you can plug into different sockets; the retina technically is part of the brain in the first place!
This is not to say visual and auditory senses cannot be confused, obviously synesthesia happens, but it likely happens at a point in the processing where we're not dealing with "raw visual input" or "raw auditory input" anymore, but already more abstract constructs such as "colors" or "sounds".
For example this paper (gotten from the Wikipedia page https://en.wikipedia.org/wiki/Neural_basis_of_synesthesia) :
https://web.archive.org/web/20060527085838/http://psy.ucsd.edu/~edhubbard/papers/JCS.pdf
Hypothesizes that the synaesthetic association of letters with colors is caused by cross-wiring between the area of the visual cortex that processes letters and the one that processes colors.
This paper from the same source:
https://academic.oup.com/brain/article-abstract/118/3/661/321747?redirectedFrom=fulltext
Finds that color-word synaesthetes had, when told words the associated with colors, activation in the language and "advanced" visual processing areas but not in more basic visual processing areas.
Similarly for autism, given that sensory perception happens at every level in the brain, including conscious thought, those perceptions can be blocked or filtered (or not) by the brain at any stage. No need to assume it is at the "raw input" stage.


Are there oligocellular organisms in nature and, if so, what are they like? I'd think protozoans can be oligocellular, but I haven't found any examples, and I'm curious to know what is the minimum number of cells an organism can have other than a single cell.

Various colonial and multicellular forms of cyanobacterial species are reviewed in:

Beardall, J et al. (2009) Allometry and stoichiometry of unicellular, colonial and multicellular phytoplankton. New Phytologist 181: 295-309

Nostoc and Volvox are some of the simplest true multicellular organisms known (usually 3-4 cell types), but in both cases the differentiated colonies (filaments in Nostoc, spheres in Volvox) typically consist of hundreds of cells.
The paper below reports the emergence of a colonial form of a unicellular organism. Since there is no evidence that the individual cells within a colony have specialised functions this doesn't really count as 'oligocellular' but it is an interesting angle on the question nevertheless.

Boraas, ME et al. (1998)Phagotrophy by a flagellate selects for colonial prey: A possible origin of multicellularity. Evolutionary Ecology 12: 153-164
Abstract: Predation was a powerful selective force promoting increased morphological complexity in a unicellular prey held in constant environmental conditions. The green alga, Chlorella vulgaris, is a well-studied eukaryote, which has retained its normal unicellular form in cultures in our laboratories for thousands of generations. For the experiments reported here, steady-state unicellular C. vulgaris continuous cultures were inoculated with the predator Ochromonas vallescia, a phagotrophic flagellated protist (`flagellate'). Within less than 100 generations of the prey, a multicellular Chlorella growth form became dominant in the culture (subsequently repeated in other cultures). The prey Chlorella first formed globose clusters of tens to hundreds of cells. After about 10-20 generations in the presence of the phagotroph, eight-celled colonies predominated. These colonies retained the eight-celled form indefinitely in continuous culture and when plated onto agar. These self-replicating, stable colonies were virtually immune to predation by the flagellate, but small enough that each Chlorella cell was exposed directly to the nutrient medium.


Are there examples of the green beard effect in humans? Green-beard effects are genes that:

Produce an effect that can be detected
Produce preference to others with the same effect

Are there any examples of this in humans?

Your examples are way too broad. A green-beard effect only applies to the effects of a single gene or group of linked genes, not to just any trait. Racism and your Mongol war example are too complex to be explained by this effect. In reality examples will mostly be found in single-celled organisms where expression of a single protein can have whole-organism effects such as causing aggregation, or in larger organisms where some highly visible effect is possible such as a colour change.

There are very few real known examples of the green-beard effect, but four are listed on the Wikipedia page:

The killing of red ant queens carrying a particular allele by workers with a different allele (Keller & Ross, 1998)
Altruism in social amoeba resulting from homophilic adhesion of a protein (Queller et al., 2003)
A multi-locus example in which similarly-coloured male lizards protect one another (Sinervo et al., 2006)
A neat example in yeast whereby individuals sharing an allele for a particular locus selectively aggregate, preventing those without the allele from benefiting by proxy from their trait (Smukalla et al., 2008)

References

 Keller L, Ross KG. 1998. Selfish genes: a green beard in the red fire ant. Nature 394: 573–575.
 Queller DC, Ponte E, Bozzaro S, Strassmann JE. 2003. Single-Gene Greenbeard Effects in the Social Amoeba Dictyostelium Discoideum. Science 299: 105–106.
 Sinervo B, Chaine A, Clobert J, Calsbeek R, Hazard L, Lancaster L, McAdam AG, Alonzo S, Corrigan G, Hochberg ME. 2006. Self-recognition, color signals, and cycles of greenbeard mutualism and altruism. Proc Natl Acad Sci U S A 103: 7372–7377.
 Smukalla S, Caldara M, Pochet N, Beauvais A, Guadagnini S, Yan C, Vinces MD, Jansen A, Prevost MC, Latgé J-P, et al.. 2008. FLO1 Is a Variable Green Beard Gene that Drives Biofilm-like Cooperation in Budding Yeast. Cell 135: 726–737.


How are Mono and Diglycerides metabolized without the Free Fatty Acids of Triglycerides? Having difficulty figuring out what the body does with ingested mono and diglycerides if the usual process of TAG metabolism includes the FFA released from the TAG returning to the MAG to recreate a TAG in the enterocyte, whereas with MAG and DAG consumption, those FFA don't exist. There are many studies (Nagao, 2000, Takatoshi, 2002 and others) confirming that DAG oil consumption leads to weight loss, which is seemingly obvious as the fat cannot be stored without the FFA getting repackaged into TAGs for storage in the adipose tissue. I have not found any studies on what actually happens to the MAGs in lieu of its normal course. I would much appreciate if someone could direct me to literature discussing this process or help me better understand it. Many thanks! Anyone?

Inside the intestinal lumen, di- and triacylglycerol are hydrolysed to free fatty acid and monoglyceride by lipase.

These diffuse through the plasma membrane of enterocyte where they will   used to resynthetize triacylglycerol, and ultimately the lipoprotein chylomicron for transport into the general circulation.

Contrary to what your question seems to imply, the glycerol to which the free fatty acid are affixed is not necessarily coming from the food: glycerol is routinely produced by glycolysis. (This notably also happens in the adypocytes). There is no requirement that food contain a ratio three fatty acid to one glycerol to be fully absorbed - if the weight loss property of DAG are true, it may be through  a different mechanism.


Enzymes and Reversibility of Reactions Richard Feynman mentions in the third chapter of The Feynman Lectures:

  So the real system is in the GDP-GTP transformation; in the dark the GTP which has been stored up during the day is used to run the whole cycle around the other way. An enzyme you see, does not care in which direction the reaction goes, for if it did it would violate one of the laws of physics. 1

Which law of physics is Feynman referring to and how would it "caring" violate it?

Chapter 3 Vol. I of The Feynman Lectures, just search for "violate"

I think Feynman is referring to the second law of thermodynamics.

The entire statement is this:

  The most important feature of the cycle of Fig. 3–1 is the transformation from GDP to GTP (guanosine-di-phosphate to guanosine-tri-phosphate) because the one substance has much more energy in it than the other. Just as there is a “box” in certain enzymes for carrying hydrogen atoms around, there are special energy-carrying “boxes” which involve the triphosphate group. So, GTP has more energy than GDP and if the cycle is going one way, we are producing molecules which have extra energy and which can go drive some other cycle which requires energy, for example the contraction of muscle. The muscle will not contract unless there is GTP. We can take muscle fiber, put it in water, and add GTP, and the fibers contract, changing GTP to GDP if the right enzymes are present. So the real system is in the GDP-GTP transformation; in the dark the GTP which has been stored up during the day is used to run the whole cycle around the other way. An enzyme, you see, does not care in which direction the reaction goes, for if it did it would violate one of the laws of physics.

Now, there are some mistakes here. For instance, GTP is not used in the muscle contraction but ATP. Perhaps this was not quite known during Feynman's times. Coming to the point, I think what Feynman means is that external work has to be done by the enzyme (that catalyses the GTP-GTP exchange) if it is actually moving the chemical equilibrium towards one side (against what would happen in an uncatalyzed condition). Some enzymes can actually do that (shift equilibria and catalyse one sided reactions), by using energy from ATP hydrolysis or other energetic transformations but since they are performing work by using energy from an external source, they are also not violating the second law.

That's the essence of the second law of thermodynamics: you cannot move heat from a cold reservoir to a hot reservoir unless external work is done. We don't have "heat" here but there concept is the same for chemical energy and reaction rates.


On stochastic Lotka-Volterra predator-prey model I am currently working (as a mathematician) on some estimations involving an stochastic predator-prey type model in which some of the coefficients have been perturbed by a Brownian Motion yielding to a system of stochastic differential equations.

The basic formulation of this problem can be found for instance in this article.

We have the following model

\begin{equation}\label{0}
    \begin{cases}
    dX(t)=X(t)\left(a-bX(t)-\frac{sY(t)}{\beta+Y(t)}\right)dt\\
    X(0)=x>0,\\
    dY(t)=Y(t)\left(\frac{h X(t)}{\beta+Y(t)}-c-fY(t)\right)dt\\
    Y(0)=y>0.
\end{cases}
\end{equation}

where we use Holling II response function.

In the literature (mostly mathematics literature) the authors propose to perturb the birth rate of the preys $a\mapsto a+\dot{B}_1(t)$ and the mortality rate of predators $c\mapsto c+\dot{B}_2(t)$.

This yields to the following (stochastic) system

\begin{equation}\label{1}
    \begin{cases}
    dX(t)=X(t)\left(a-bX(t)-\frac{sY(t)}{\beta+Y(t)}\right)dt+\sigma_1 X(t)dB_1(t),\\
    X(0)=x>0,\\
    dY(t)=Y(t)\left(\frac{h X(t)}{\beta+Y(t)}-c-fY(t)\right)dt+\sigma_2 Y(t)dB_2(t),\\
    Y(0)=y>0
\end{cases}
\end{equation}

I know nothing about biology but I am concerned about a couple of things regarding this particular formulation:

If we assume that the Brownian motions are perturbing the birth/mortality rates, how can I interpret the fact that this new "perturbed" rates can become negative (due to the effect of the BM). Does it have any sense (in the framework of this particular model) to talk about "negative birth rate" or "negative mortality rate"?
What if the "perturbed" mortality rate goes beyond $100 \%$? Mathematically nothing "wrong" will happen, but what about the interpretation?

Notice that the "noise"  and the model as a whole can be interpreted differently (ignoring the fact that we are actually modelling the dynamics of two species) but my main issue is that if I(together with many authors) am stating that we perturb a certain parameter I believe that we must respect the basic assumptions of the model!

I hope everything's clear and I thank you all in advance, any opinion or suggestion will be welcome!

To interpret $a$ and $c$ as a birth and mortality rates is somewhat inaccurate, as $a$ and $c$, as written are density-independent rates that grow or shrink populations exponentially. If $a$ were negative, the prey population would shrink and most people would find a problem like that unexciting unless it was, say, a sink population maintained by immigration from another population. This is true of $c$ being negative, where the predator population would grow independent of the prey population. More accurately, $a$ can be interpreted as the difference between birth, $b$, and deaths, $\delta$; i.e., $a = b - \delta$. In this case, depending on the kinds of stochasticity being added to the model, negative $a$ is not just normal, but expected. The same is true for $c$. Ultimately, a perturbations like the white noise in this equation is simultaneously perturbing the difference between birth and death rates, which explains the negative difference.
The value of the rates seem to have the same interpretation if they are constant or are perturbed to an arbitrary magnitude.

I hope this helps!


Consensus symbols in multiple sequence alignment I was using multAlin for multiple aligning a set of sequences. The output I and came across included the following documentation (English corrected):

  Consensus symbols:  ! is any of IV  $ is any of LM
  % is any of FY  # is any of NDQEBZ

I understand what it says but I don't know how to interpret it further. What impact does this have on the sequence alignment?

The use of these symbols in output of the type shown below is purely presentational, to help you inspect the alignment and identify regions of partial conservation.

                  51                                                 100
          CCPC50  SEEGFK.YGE GILEVAEKNP DLTWTEADLI EYVTDPKPWL VKMTDDKGAK
          CCRF2C  TYPEFK.YKD SIVALGASG. .FAWTEEDIA TYVKDPGAFL KEKLDDKKAK
          CCRF2S  TQADFKGYGE GMKEAGAKG. .LAWDEEHFV QYVQDPTKFL KEYTGDAKAK
          CCQF2R  HKDNYA.YSE SYTEMKAKG. .LTWTEANLA AYVKNPKAFV LEKSGDPKAK
          CCQF2P  TFAGYS.YSP GYTVMGQKG. .HTWDDNALK AYLLDPKGYV QAKSGDPKAN
       Consensus  t...%k.Y.e g..e.gakg. .ltWt#..l. .Yv.#Pk.fl .ek.gD.kAk

This is quite independent of the logic (algorithm) of the program, which is indicated by the documentational comments:

  Symbol comparison table: blosum62
  Gap weight: 12
  Gap length weight: 2

This also gives a reference to the original paper you should read to find more information about the program.

You would also be advised to read the Wikipedia entry on Multiple Sequence Alignment and on Sequence Alignment in general. I would mention that this is an old method (as the appearance of the site also indicates). If it gives useful results, fine. Otherwise you might try the more popular and more frequently updated Clustal, which is available online or as a standalone program.


Why isn't the sticky bud plant more widespread Why isn't the sticky bud plant (Galium aparine) everywhere around the world? Because to me it seems that it has the best method of seed dispersion/transportation (wiki link: https://en.wikipedia.org/wiki/Galium_aparine)

As already pointed out in comments, Galium aparine is actually very widespread, according to wikipedia it occurs in "a wide region of Europe, North Africa and Asia from Britain and the Canary Islands to Japan. It is now naturalized throughout most of the United States, Canada, Mexico, Central America, South America, Australia, New Zealand, some oceanic islands and scattered locations in Africa."
Because it occurs on moist and rich soils, it doesn't occur everywhere. It is unable to grow on dry and nutrient-poor soils (like deserts and steppes). But it is also absent in frequently mown grassland.


What is the germ layer origin of human lung fibroblasts? What is the germ layer origin of human lung-derived fibroblasts?

All normal fibroblasts are mesenchymal in origin, including lung fibroblasts. In certain situations, usually injury related, epithelial cells can undergo an epithelial to mesenchymal transition (EMT).


Why do carrots spoil so fast? The carrots we buy from a supermarkets spoil very fast, albeit giving many consumers a false sense of preservability due to their structural rigidity. The answer extends to many other vegetables many of us eat:

 Larsinio (2006)- wikimedia, public domain, DOR 27/09/2012

The question is, why do well aerated carrots spoil in the matter of days, at room temperature?

Things to consider: a tuberous rhizome with rough and segmented skin / oxygen levels / levels of aeration / relatively high sugar content / differences in immediate microbiome / lack of possible synergies which the earth provides...the majority of antibiotics is extracted from soil microorganisms {1},{2}....

First we will take a look at the lines of resistance of a carrot. There are three

  The skin - The first line of resistance is the outer membrane or skin of the carrot and chemical compounds that are normally present
  there. Two antifungal polyacetylenes, falcarinol and falcarindiol, and
  an isocoumarin, 6-methoxymellein, are present in small amounts in a
  normal carrot and present the first barrier in undamaged carrots.

  Post Harvest - If during harvest or post harvest handling this barrier is broken, the surface is punctured, scraped or sliced,
  microorganisms may begin to grow. The carrot at this point begins a
  wound healing process by accumulating suberin, a complex
  polysaccharide, at the wound site. Along with suberin, lignin is also
  accumulated. Suberisation is complete within 48 hours after wounding,
  and lignification is complete within 168 hours of wounding..

  Phytoalexin barrier - The last and most important line of resistance is the phytoalexin barrier. Phytoalexins are chemicals
  produced by plants that impart disease resistance in response to
  mechanical injury, physiological stimuli or infection. Scopoletin, a
  coumarin,and para-hydroxy benzoic acid, a phenol, are apparently early
  arrivals on the scene but later disappear (reference).

There are three enemies of carrot storage: wilt, re-growth and rot.

Some reasons for carrots rotting faster:

Many fruits and vegetables start to produce ethylene gas when they start to ripen. Some foods are extremely sensitive to ethylene gas which makes them rot faster (reference). I am guessing that you keep different vegetables close together. Maybe if you stored carrots separately, it might make them last a bit longer.

  Major post-harvest losses in carrots are due to Sclerotinia rot,
  Botrytis rot, Bacterial soft rot (Erwinia) and Sour rot (Geotrichum).
  Of these, Sclerotinia rot is the most prevalent.The Sclerotinia fungus
  infects the carrot roots in the field through the crown. During
  storage, the Sclerotinia fungus produces a white, cottony mycelium
  which covers the roots. Infected roots are usually soft and watery (reference).

There would definitely be more reasons but I am guessing that these are the major contributors to it rotting faster.


Differences between right and left handed people Are there any articles reporting any significant differences in behavior, attitudes, intelligence, appearance, etc., between right and left handed people?

According to this Psychology Today article: 3 Myths and 3 Facts about Left-Handers (with numerous links to many papers throughout the article), there are no particular difference between left and right handed people in terms of intelligence, personality, creativity or mortality.

There seems to be a noticeable difference in the number of people having the language centre being in the left hemisphere of the brain (95% for right handed people vs 70% for left handed people).


Are there any creatures that will eat their own limbs or body parts to survive? I'm curious if there are any insects, bacteria or perhaps even large animals who would bite off their own limbs or body pieces to chew on in the desperate times of hunger.

What you're describing is actually a well-documented occurrence in individual cells and single-celled organisms. The phenomenon is called autophagy, and Wikipedia has a page about it here. The basic gist is that when cellular components stop functioning or need to be removed for some other reason, the cell essentially digests those components and reuses their parts to make something else. Cells can also consume themselves to prevent the spread of disease or in the case of extreme starvation, when the extra energy might be needed to keep the organism alive.

Self-cannibalism on the macro scale (larger than single cells) is significantly rarer, but it can and does happen. For example, leopard geckos (and maybe some other lizard species? I'm not sure) regularly eat their own shed skin pieces to conserve energy and nutrients. Sea squirts (a type of marine invertebrates) literally digest their own brains as a part of their life cycle, and apparently, some crickets have been known to consume their own wings. Generally, though, unless the limb in question is already damaged and/or rendered unusable, it would be a waste of energy for its owner to consume it, as the energy spent repairing the damage would likely outweigh the energy gained from its consumption in the first place. That is why it's a relatively rare behavior in multicellular organisms.


Chemical reactions at the synapse For my course project, I am thinking of listing out major chemical reactions that occur at synapses, along with their temporal characteristics.

I could not find any textbooks to use as a starting point, and Google did not help me either. I was hoping to receive help in finding a review paper or textbook about chemical computations at the synapse.

If you are interested it from the point of view of "chemical computations", you probably want literature which looks at signal transduction in detail. I would suggest Marks' et al textbook on signal transduction. I have not yet read it through (it is on my list), but I liked the clear writing style of the introduction, and, as you can see from the table of contents, it does have chapters which address synapses and their neurotransmitters specifically.

I doubt that it will contain a complete list (there are several hundreds of compounds which can be considered to be neurotransmitters), but as an introductory textbook, it is likely to contain the major ones.


Speciation and Phylogeny of Lactobacillus The lactobacillus, also called Döderlein's bacillus is a genus of facultative aerobic bacteria. There are several species such as Lactobacillus acidophillus and Lactobacillus reuteri.

I have several questions, all linked, for the concern of speciation of bacteria species used for lactic fermentation by humans.

Are all species that are used for cheese and yoghurt fermentation part of the genus Lactobacillus?
Do all species used for cheese and yoghurt fermentation form a monophyletic clade?
Did the speciation of this clade occurr before or after the use of these bacteria by humans?
What was the ecological niche of the ancestor(s) before humans used them for cheese and yoghurt?

generally, lactic acid bacteria (LAB) are the ones you should be looking at for milk-based fermentation products. although sometimes species like bifidobacterium are added, which is of a completely different phylum. also, for cheese production, or the Dutch variety I am familiar with anyway, you would need fungi as well.

the lactobacillales order is not monophyletic, as you can see on the wiki page there are at least two different clades.

the wikipedia page 'Yogurt' speculates on the ecological niche of LAB: "Analysis of the L. delbrueckii subsp. bulgaricus genome indicates that the bacterium may have originated on the surface of a plant. Milk may have become spontaneously and unintentionally infected through contact with plants, or bacteria may have been transferred via the udder of domestic milk-producing animals." (source)

EDIT: the LAB are an order, they have been around for quite some time before the humans showed up.


Algae or Lichen identification. Coastal BC, Canada I have tried all books and internet resources I know of, but I still have no idea what this might be — a lichen or something else.

At first glimpse, I thought it was something man-made and unnatural, but then I looked closer and saw how it appears to be attached and growing. It grows on exposed rocks well above the high tide. The photo is taken in late March, on northern Vancouver Island. It's loosely attached to the rock.

It was somewhat abundant around the general area (within of a few km), but I haven't seen it elsewhere - although I'm not from BC so there might be a lot of this around.

The water droplet in the lower right corner give a rough sense of scale.

Edit:
Adding another photo in which I just noticed a streak of white, which I included in original resolution.

I want to propose you expand your search to a broader taxonomic scope. Specifically, I think you might be looking at a species of "red" green algae (family: Trentepohliaceae).

From Nelson et al. (2011):

All Trentepohliaceae have filamentous growth forms and often contain large amounts of carotenoid pigments (ß-carotene and hematochrome), causing the algae to appear yellow orange in color (Thompson and Wujek 1997, Lo´pez-Bautista et al. 2002).

The Trentepohliaceae contains five genera: (Trentepohlia, Printzina, Phycopeltis, Cephaleuros and Stomatochroon) and 70+ species worldwide.

For example, the following algae (picture from England) looks fairly similar to your specimen:
Trentepohlia aurea

 Source: David Fenwick
If your specimen is a species in this family of algae, it is most likely in the Trentepohlia genus (or possibly Printzina genus).
Trentepohlia is a genus of filamentous chlorophyte green algae in the family Trentepohliaceae.

Typically orange or yellow in color.
Live on tree trunks and wet rocks or symbiotically in lichens.

Here's a picture of a free-living Trentepohlia species from coastal Oregon, USA:

 Source: Richard C. Hoyer (2015)

The source notes that the specimen was simply ID'd as "Trentepohlia sp." by Tim Rodenkirk (Botanist with the Coos Bay BLM in North Bend, Oregon).


Why lab technicians use indirect (antibody reaction) method for diagnosing? In microbiology we have two types of microbial diagnosis. The direct method is where we detect the invader's DNA, Antigens or culture to see the exact pathogen while the second, indirect, method is the reacting the antibodies of patient's serum with different reagents.

If we use the indirect method (antibody reaction) and find that they are producing antibodies against a specific disease (let's say streptococcus A) what is the benefit of having found that they are fighting Strep A since the body is already clearly fighting it and putting up the best defence to fight the disease?

Would a doctor really prescribe antibiotics even though here is already an immune reaction against the infection?

If diagnosis and treatment are useless then why do we waste the time to do it?

Short answer: Antibiotic treatment is important because the body can't always keep up with the infection even if it has launched a response.

Background:

First, let's look at what the antibody reaction method is actually doing.

Taking a sample of blood or body fluid
Testing the sample with known pathogens - viruses, bacteria, fungi, etc.
Identifying which infection causes a reaction.

This allows us to determine which infection we are dealing with. This can be especially useful when the infection is hidden in a place we are unable to easily swab - the stomach, heart, a small wound that has already healed. Sometimes this test is just used to monitor how well you are fighting the infection, but it also allows them to evaluate what the best course of treatment is for you. (Reference 1)

Just because the body has an immune reaction doesn't mean that the body's immune system can actually finish the battle against a disease. In the example case of Strep A, you may be able to get over the infection yourself but it will take longer than if you are prescribed antibiotics against it.

See this question on the CDC:

  Q: How common is invasive group A streptococcal disease?

  A: Approximately 9,000-11,500 cases of invasive GAS (Group A Streptococcus) disease occur each
  year in the United States, resulting in 1,000-1,800 deaths annually.

Note that invasive Strep A usually infects children, elderly, and  immunocompromised people (anyone with a weaker immune system typically).

Unless you have absolutely no immune system at all, there will be an antibody response put out by your body. The NHS goes into detail about different parts of your immune system.

Recall also that Strep A (our example) could divide faster than the body can keep up with. So we would need antibiotic help to fight the disease. Using the "indirect" method we can find a hidden infection.

According to the NHS the antibiotics put a stop to growth and spread which allows the body to come in and finally finish them all off, or they disrupt a process the bacteria needs to survive and kill the infection for the body. Thereby helping the immune system (the body's best line of defence) finish off the infection when it couldn't do it on its own.


Heterozygosity under genetic drift The wright-Fisher model of genetic drift is:

$$p_{ij} = \binom{2N}{j}\left(\frac{i}{2N}\right)^j \left(1- \frac{i}{2N}\right)^{2N-j} $$

,where $\binom{2N}{j}$ is a binomial coefficient.

From this equation one can infer that the expected heterozygostiy should decrease by $1-\frac{1}{2N}$ at each time step because:

$$E[x_{t+1}(1-x_{t+1}) \space|\space x_t] = (1-\frac{1}{2N})x_t(1-x_t)$$

I don't understand this equality. That might be very simple though! Can you help me making sense of it?

source

The notation at this site resembles that in your question but preserves the $\frac{x_t}{2N}$ notation for probability of selecting an allele.

$$E[\frac{x_{t+1}}{2N})(1 - \frac{x_{t+1}}{2N} )|x_t] = (\frac{x_{t}}{2N})(1 - \frac{x_{t}}{2N}) (1 - \frac{1}{2N})  $$

The expression $(\frac{x_{t}}{2N})(1 - \frac{x_{t}}{2N}) $ is the probability of heterozygosity at step $t.$

Your expression says that the expected heterozygosity at step $(t+1)$ is equal to the heterozygosity at step at $t$ multiplied by $(1-\frac{1}{2N}).$

For a population of size $2N,~(1-\frac{1}{2N})^{2N}\approx 1/e,$ so large populations are insulated from this effect and small ones may lose genetic diversity rapidly.

A typical explanation can be found here. The notation at this site condenses the expression $(\frac{x_{t}}{2N})(1 - \frac{x_{t}}{2N}) $ to $H_n$ and explicitly says it is $1 - F_n, $ in which $F_n$ is the probability of homozygous at step $n.$


Why are diseases generally specific to a particular species "Zoonosis" is the process of transmitting a disease from an infected animal to a human. This suggests that animal-to-human transmission is not common. HIV is believed to have first spread to humans zoonotically, but has since mutated to a human-only strain.

This all raises the question: Why do diseases mostly just target a particular species? Aren't most metabolic processes very similar across species, especially within the same order and class? Dogs and cats can't catch the common cold, but they have similar diseases of their own.

There are obviously enough similarities that mice can be used in preliminary tests of human drugs, but the results are very tentative until human trials are done.

The pathogens which are responsible for certain diseases have adapted to their hosts. Viruses need to attach to structures on their cells they invade to replicate. These structures usually consist of proteins and are unique for the respective species (e.g. the ACE2 receptor in the case of Covid-19). During an infection, there will be billions of viruses released and some carry mutations, which are just mishaps in the replication process. In most cases, these errors are leading to a virus that is not viable or cannot infect, i.e. the mutated virus can't replicate and the mutation gets lost, but sometimes it can infect the host better and thus will have a higher chance to propagate.
If this happens with a zoonotic pathogen after it has spread to a human, a new disease has emerged.


What does it mean for a hormone to be "active" In my textbook it is stated that the T3 hormone produced at the thyroid gland is 3-5 times more biologically active than T4.

How is being active defined and how can this effect be measured?

Biological activity has a range of definitions, but in this case I believe it to mean that the T3 hormone is produced at a rate 3-5x that of T4. This can be measured with fluorescent tags. Typically, fluorescent tagging uses a reactive derivative of a fluorescent molecule, called a fluorophore. The fluorophore selectively binds to a specific region or functional group on the target molecule and can be attached chemically or biologically. Using technologies, such as microscopes, fluorescence can be viewed/imaged; this allows scientists to count, track, and/or monitor molecules over time.


Are there venomous plants? There certainly are poisonous plants, but I was wondering, whether there are venomous specimen, too?

First, I thought the stinging nettle could be one such. After all, it's common knowledge it "applies a toxin upon touch". However, reading about the mechanics it seems that the injection is actually a much more passive procedure, which would render the plant poisonous, wouldn't it?

So what are some venomous plants?

By definition, the word "venomous" can only technically be applied to animals.  The most "poisonous" plant would be the gympie gympie tree, but if you want something "venomous", you might be able to find something similar within some species of carnivorous plants.


Can plants feel pain? I was wondering whether plants could feel pain, for example, does grass feel pain when you mow the lawn? Or do the plants and trees that grow vegetables and fruits feel pain when you harvest them?

The internet is very vague about it. There are several articles on the internet, but they just say that plants do not feel pain, they only send out a chemical substance. Others say that almost all multicellular organisms feel pain, because pain is defined as any signal of having impaired tissue.

I think that plants can't feel pain because they have no nerves or central nervous system. However I'm not sure whether this means that plants can't feel pain.

Since the question is clear when pain is defined as any signal of having impaired tissue, I think it would be more interesting in the case that pain is defined as actual discomfort, like humans and animals (maybe it should be restricted to Eumetazoa) feel it.

I think before discussing "pain", we'd probably have to discuss whether plants actually can "feel".

This is also down to how one wants to define this (hence "opinion based"), but I assume most people (?) would equal the lack of a brain/neurons with the lack of the capability to feel. And I presume so do you, as you show by using the tag "neuroscience".

In which case the answer to your question "Can plants feel pain?" is "no", regardless of whether plants react to damage through the release of chemicals or not, and whether one would like to classify this as "pain" or not.


Is there a distinction between the fisherian runaway theory and Fisher's sexy son theory? In many websites/books they are referred to as part of the same process whereby:

"runaway" describing that the process continues even after traits become maladaptive
the "sexy son theory" explains the mechanism that underlies this.

However many sites (like wikipedia) describe them as two alternative processes.

What am I missing?

The Fisherian runaway is the observed phenomenon of an "arms race" of features and traits in sexual dimorphism, the Sexy sons hypothesis is the theory of why it happens. One is factual/known data and the other is a hypothetical explanation as to why we see that data.


Can foxes move their ears independently? I've read that dogs can do move their ears independently, i.e., point one ear in the direction of a sound without having to point the other one at the same time. Is this a common trait with other canids, such as foxes? Can most eared mammals do this, with humans being an exception (except for a few exceptional humans)?

Yes, they can. Here are a couple pics I found of foxes moving their ears independently:

This is something all canids can do (1)(2) Btw, I can move my ears independantly. It's all in the finding the right muscles.


How to determine the actual flux in the human metabolic model of a cell line? The problem to be solved is to determine what the flux values are for the different reactions in the human metabolic model.

As far as I understand, a good way to do that would be to use gene expression data to calculate a flux, but I am not sure that is a good idea or if it is even possible.  I am not very sure of what is the correct process to do this.

Thanks for any help or suggestions!

I am no expert on the field, but quantifying gene expression isn't a simple problem, although it is a possibility.

A solution I know to be used is using radioactive markers. See for example this review and particularly "The cell-cell lactate shuttle" section, which might give some insights.

This can include radioactive tracers (such as [14C]lactate), non-radioactive tracers (with [13C] or [2H]), "net exchange measurements" (I don't really know what this means here, perhaps the kind of exchange calculations they present here), and muscle biopsies (it is then possible to measure the metabolite concentration by enzymatic reaction or spectrophotometry for example).


Why does glomerulus don't allow white blood cells to leave? The glomerulus in nephrons are just a ball of capillaries, so why can't it allow the white blood cells to squeeze though the epithelial cells into Bowman's capsule just like the formation of tissue fluid in other capillaries by filtration?

Red blood cells, White blood cells, platelets and proteins with large molecular weight cannot pass through the podocyte and fenestrations in glomerular capillary, but small molecules like water, salts and sugars are filtered out as part of urine.

As these cells and proteins are large to cross through this filter, they remain in the capillary and create osmotic pressure within the capillary. Bowman’s space has osmotic pressure approximately zero. So, only hydrostatic pressure works in this state and help in movement of fluid across the capillary wall.

Via:  https://opentextbc.ca/anatomyandphysiology/chapter/25-5-physiology-of-urine-formation/


What is the sequence of pPROLar.A plasmid? I've been looking for the sequence of pPROLar.A122 plasmid but I haven't found it. Where could I find the sequence?

The first link (addgene) on googling reports a plasmid which is reported to have the pPROLar.A backbone. However, this is a modified version with Ampicillin and LuxR. I'm trying to reconstruct it from it and another plasmid.

The plasmid map looks like this:

Thanks!

The pPROLar.A112 sequence is:

  CCATGGGTGA ACAGAAACTG ATCAGCGAAG AGGATCTGGG TGGAGATGAC GATGACAAGG
  TGGTCGACAA GCTTGGATCC CTGCAGGCCT CAGGGCCCGA TCGATGCGGC CGCTTAATTA
  ATTAATCTAG AGGCATCAAA TAAAACGAAA GGCTCAGTCG AAAGACTGGG CCTTTCGTTT
  TATCTGTTGT TTGTCGGTGA ACGCTCTCCT GAGTAGGACA AATCCGCCGC CCTAGACCTA
  GGGGATATAT TCCGCTTCCT CGCTCACTGA CTCGCTACGC TCGGTCGTTC GACTGCGGCG
  AGCGGAAATG GCTTACGAAC GGGGCGGAGA TTTCCTGGAA GATGCCAGGA AGATACTTAA
  CAGGGAAGTG AGAGGGCCGC GGCAAAGCCG TTTTTCCATA GGCTCCGCCC CCCTGACAAG
  CATCACGAAA TCTGACGCTC AAATCAGTGG TGGCGAAACC CGACAGGACT ATAAAGATAC
  CAGGCGTTTC CCCCTGGCGG CTCCCTCGTG CGCTCTCCTG TTCCTGCCTT TCGGTTTACC
  GGTGTCATTC CGCTGTTATG GCCGCGTTTG TCTCATTCCA CGCCTGACAC TCAGTTCCGG
  GTAGGCAGTT CGCTCCAAGC TGGACTGTAT GCACGAACCC CCCGTTCAGT CCGACCGCTG
  CGCCTTATCC GGTAACTATC GTCTTGAGTC CAACCCGGAA AGACATGCAA AAGCACCACT
  GGCAGCAGCC ACTGGTAATT GATTTAGAGG AGTTAGTCTT GAAGTCATGC GCCGGTTAAG
  GCTAAACTGA AAGGACAAGT TTTGGTGACT GCGCTCCTCC AAGCCAGTTA CCTCGGTTCA
  AAGAGTTGGT AGCTCAGAGA ACCTTCGAAA AACCGCCCTG CAAGGCGGTT TTTTCGTTTT
  CAGAGCAAGA GATTACGCGC AGACCAAAAC GATCTCAAGA AGATCATCTT ATTAATCAGA
  TAAAATATTA CTAGATTTCA GTGCAATTTA TCTCTTCAAA TGTAGCACCT GAAGTCAGCC
  CCATACGATA TAAGTTGTTA CTAGTGCTTG GATTCTCACC AATAAAAAAC GCCCGGCGGC
  AACCGAGCGT TCTGAACAAA TCCAGATGGA GTTCTGAGGT CATTACTGGA TCTATCAACA
  GGAGTCCAAG CGAGCTCTCG AACCCCAGAG TCCCGCTCAG AAGAACTCGT CAAGAAGGCG
  ATAGAAGGCG ATGCGCTGCG AATCGGGAGC GGCGATACCG TAAAGCACGA GGAAGCGGTC
  AGCCCATTCG CCGCCAAGCT CTTCAGCAAT ATCACGGGTA GCCAACGCTA TGTCCTGATA
  GCGGTCCGCC ACACCCAGCC GGCCACAGTC GATGAATCCA GAAAAGCGGC CATTTTCCAC
  CATGATATTC GGCAAGCAGG CATCGCCATG GGTCACGACG AGATCCTCGC CGTCGGGCAT
  GCGCGCCTTG AGCCTGGCGA ACAGTTCGGC TGGCGCGAGC CCCTGATGCT CTTCGTCCAG
  ATCATCCTGA TCGACAAGAC CGGCTTCCAT CCGAGTACGT GCTCGCTCGA TGCGATGTTT
  CGCTTGGTGG TCGAATGGGC AGGTAGCCGG ATCAAGCGTA TGCAGCCGCC GCATTGCATC
  AGCCATGATG GATACTTTCT CGGCAGGAGC AAGGTGAGAT GACAGGAGAT CCTGCCCCGG
  CACTTCGCCC AATAGCAGCC AGTCCCTTCC CGCTTCAGTG ACAACGTCGA GCACAGCTGC
  GCAAGGAACG CCCGTCGTGG CCAGCCACGA TAGCCGCGCT GCCTCGTCCT GCAGTTCATT
  CAGGGCACCG GACAGGTCGG TCTTGACAAA AAGAACCGGG CGCCCCTGCG CTGACAGCCG
  GAACACGGCG GCATCAGAGC AGCCGATTGT CTGTTGTGCC CAGTCATAGC CGAATAGCCT
  CTCCACCCAA GCGGCCGGAG AACCTGCGTG CAATCCATCT TGTTCAATCA TGCGAAACGA
  TCCTCATCCT GTCTCTTGAT CAGATCTTGA TCCCCTGCGC CATCAGATCC TTGGCGGCAA
  GAAAGCCATC CAGTTTACTT TGCAGGGCTT CCCAACCTTA CCAGAGGGCG CCCCAGCTGG
  CAATTCCGAC GTCTGTGTGG AATTGTGAGC GGATAACAAT TTCACACAGG GCCCTCGGAC
  ACCGAGGAGA ATGTCAAGAG GCGAACACAC AACGTCTTGG AGCGCCAGAG GAGGAACGAG
  CTAAAACGGA GCTTTTTTGC CCTGCGTGAC CAGATCCCGG AGTTGGAAAA CAATGAAAAG
  GCCCCCAAGG TAGTTATCCT TAAAAAAGCC ACAGCATACA TCCTGTCCGT CCAAGCAGAG
  GAGCAAAAGC TCATTTCTGA AGAGGACTTG TTGCGGAAAC GACGAGAACA GTTGAAACAC
  AAACTTGAAC AGCTACGGAA CTCTTGTGCG TAAGGAAAAG TAAGGAAAAC GATTCCTTCT
  AACAGAAATG TCCTGAGCAA TCACCTATGA ACTGTCGACT CGAGCATAGC ATTTTTATCC
  ATAAGATTAG CGGATCTAAC CTTTACAATT GTGAGCGCTC ACAATTATGA TAGATTCAAT
  TGTGAGCGGA TAACAATTTC ACACAGAATT CATTAAAGAG GAGAAAGGTA C

It was sent to me directly from Takara Bio.


In plants why are potassium and nitrate ions absorbed faster than any others? Quoting my A-level biology textbook:

  $\ce{K^+,  NO3^-}$ are absorbed by plants faster than any other ions. Whereas, $\ce{Ca^2+, SO4^2-}$ are absorbed with the slowest speed.

What is the reason?

My reasoning: I first though the size of ions would matter in this case. Obviously, $\ce{K^+}$ is smaller than $\ce{Ca^2+}$,  then it 'seemed to me' that smaller ions would be absorbed faster. The same reasoning can be applied to $\ce{NO3^-,  SO4^2-}$. But, there are smaller ions than $\ce{K^+}$ which are absorbed slower eg. $\ce{Na+}$. So, obviously size only does not matter here. There are other factors.

Since plants absorb minerals, like potassium, calcium, sulfur, etc. in their ionic form, like K+, NO3-, SO42-, Ca2+, they need to absorb them actively. Since these ions are charged, they have difficulty while passing through the plasma membrane. Hence, plants need to expend energy in order to transport them. For this, they use ATP and membrane transporter proteins. These transporters transport ions across cell membrane with an accompanying ion (H+) so as to maintain electrochemical gradient. As a result (partly), these transporters are highly selective for the ions they carry. For example, a K+ transporter will not transport SO42- or another ion. See this answer to see how transporters achieve this selectivity.

The above part explains how ions are transported in plants. Now, lets come to the main question i.e. why some ions are transported faster than others. Well, there is no definitive answer to this (at least none that I know of). But I can think of two possible reasons for this (using only the examples of K+, Ca2+, NO3- and SO42-):

Magnitude of Charge: one fact here is that both K+ and NO3- have a charge of $\pm$1, whereas Ca2+ and SO42- have a charge of $\pm$2. So what? This makes their transport a bit more difficult. For example, to transport K+ across the membrane, the transporter would antiport 1 H+ for 1 K+, whereas a similar antiporter would transport 2 H+ out to bring 1 Ca2+ in. Obviously, this does not explain the difference between ions with same charge, which the following point seems to do.
Requirement: one of the most important points to keep in mind here is the difference in requirements of different ions by the plant. This is why plant macronutrients (i.e. required in large quantities) have been divided into primary macronutrients (N, P, K) and secondary macronutrients (all others, including Ca, S, Na). As you see, nitrogen and potassium are mostly the limiting factors of crop production. This is why plants require them in large quantities, and hence try to absorb them as fast as possible. This, partly again, explains why K+ and NO3- (the only artificial nitrogen source other than NH4+) are absorbed faster by plants while Ca2+ and SO42- are absorbed slowly.

References:

Mineral Absorption - Wikipedia
Secondary Plant Nutrients: Calcium, Magnesium, and Sulfur - Mississippi State University


Why don't anti-viral drugs like "Acyclovir" work against coronaviruses? I've always used Acyclovir to treat cold sores, why doesn't it work on other viruses?

How do coronaviruses differ from herpesviruses?

Aciclovir specifically targets HSV-family viruses.

It is metabolized by a viral-specific enzyme into an inhibitor of the specific DNA polymerase expressed by the virus:

  in infected cells, HSV or VZV coded thymidine kinase facilitates
  the conversion of aciclovir to aciclovir monophosphate, which is then converted to aciclovir triphosphate by cellular enzymes. Aciclovir triphosphate acts as an inhibitor of and substrate for the herpes specified DNA polymerase, preventing further viral DNA synthesis.

https://www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/pdf?OpenAgent&id=CP-2009-PI-00595-3

Other viruses don't express these specific enzymes, and even if they have similar enzymes they may not interact the same way with the drug. Even within the herpesvirus family, the drug is not equally effective against every virus.

Coronaviruses are RNA viruses, so even though the drug is not effective for DNA viruses outside the herpesvirus family, coronaviruses are definitely not going to be affected because they don't even have a DNA polymerase to inhibit.


Optical Density conversion to cfu / ml I am having troubles understanding the correlation between OD measurements and CFU/ml. What is the conversion factor between the two units, and does this conversion factor somehow compensate for dead cells OD might be reading? (Also lets say the OD is set at the standard 600nm).

The optical density measurement is the quantity of living and non-living cells in a sample. The colony forming unit measures only the viable cells in a sample. An OD 600nm is equivalent to approximately 8 x 10^8 CFU/ml. However, this is only an approximation and cannot fully take into account the dead cells the OD may be reading, it also depends on the microorganism that is being researched. A standard curve can be calculated from data, but it is quite difficult to attain an exact result.
A very useful article on the correlation between the two measurements can be found here (from the Brazilian Journal of Microbiology).


What are hyphal compartments? The hyphae are the branching filaments that make up the mycelium of a fungus. Hyphal compartments are part of the hyphae. What are they exactly?

I did a quick lookup on google for "hyphal compartments" and the number of online texts/books/citations using this term is quite meagre to say the least. One of the images that I found was this-

And I have reached to the conclusion that--
Hyphae cells (only in septate species) are known as hyphal compartments.
Quoting from wikipedia (read if you don't know about septate and coenocytic varieties of hyphae)

A hypha (plural hyphae, from Greek ὑφή, huphḗ, “web”) is a long, branching filamentous structure of a fungus, oomycete, or actinobacterium.In most fungi, hyphae are the main mode of vegetative growth, and are collectively called a mycelium.
A hypha consists of one or more cells surrounded by a tubular cell
wall. In most fungi, hyphae are divided into cells by internal
cross-walls called "septa" (singular septum). Septa are usually
perforated by pores large enough for ribosomes, mitochondria and
sometimes nuclei to flow between cells. The major structural polymer
in fungal cell walls is typically chitin, in contrast to plants and
oomycetes that have cellulosic cell walls. Some fungi have aseptate
hyphae, meaning their hyphae are not partitioned by septa.
Hyphae have an average diameter of 4-6 µm.


Actively Harmful mutations Usually harmful mutations are those which disrupt a vital function, what you might call "passively" harmful. What about a mutation that makes a protein, which is not just useless, but actually toxic to its host?  Are there any known examples?

There are definitely examples! For one, you might consider sickle-cell anemia to fall into this category.

The mutation that causes this disease leads to abnormal strands of hemoglobin that distort the shape of red blood cells, to the point that those cells can directly disrupt blood flow.

Interestingly, carriers of the sickle-cell trait actually have some protection against malaria, which explains the high incidence of the allele despite the dangerous consequences of the disease.

You can find many other examples in the category of autosomal dominant disorders (though note that sickle-cell is considered recessive, though carriers can still have some negative effects). Because these disorders only require one copy of a gene to cause illness, there is often some toxicity of the mutated protein, whereas in what you refer to as "passively" harmful mutations, one healthy copy can often compensate, fully or partially. Of course these are general statements and there will always be exceptions, but I hope thinking about it this way can guide your curiousity!


Do acetyl-CoA, acetyl-CoA carboxylase and acetyl-glutamate carry any charge? Do the following compounds have any charge? If not, then why? If yes, is there any database that would give me this information if the compound is negatively or positively charged?

The compounds are as follows:
Acetyl-CoA
Acetyl-CoA carboxylase
Acetyl-glutamate

I have searched and somehow I am getting more confused.

The first compound you mention is acetyl-co-enzyme A (acetyl-CoA) (first picture, left panel). The acetyl group is uncharged, but the co-enzyme A (CoA) group (Fig. 1, right panel) does carry charge through its phosphate groups. In normal physiologic environments these phosphate groups will donate one or more protons, leaving the molecule negatively charged, as shown in Fig. 1, right panel below:

Fig. 1 Acetyl-CoA (left) and the co-enzyme A group (right).

The second compound is an enzyme, namely acetyl-CoA carboxylase. Consisting of many, many amino-acids it will carry many, many charges under physiological conditions. Some of these will be negative, some positive.

The third compound you mention is acetyl-glutamate:

Acetyl-Glutamate

This compound carries two carboxyl groups, which makes the compound acidic and negatively charged under physiological conditions, as it will donate one or two protons to the environment, dependent on the pH.

PS: For an in-depth answer on the basic chemistry and pKa values I would ask this at Chemistry.SE :)


Why do carnivores evolve? If humans can live without consuming other animals, then why do we do it? From a biological point of view, why do we eat meat? I would also extend the question to other animals because many animals are carnivorous: why did carnivory evolve and why do animals eat meat?

I'm going to focus on the why do carnivores exist part of this question, which should be extendible to answer why humans eat meat.

Let's start a thought experiment in which we only allow the consumption of vegetation (plants). In the simple system, we have our plants (lettuce) and our herbivores (rabbits). The lettuces have a constant population size and can support a limited population of rabbits. The rabbits satisfy their energetic and nutritional requirements by eating lettuces.

We then introduce a new species (humans) which are capable of eating both lettuce and rabbits (omnivores). If the humans limited themselves to only the lettuces as a food source they would have to compete with the rabbits in order to survive. Alternatively, the humans could hunt rabbits, as rabbits are also a potential source of energy and nutrition. The point being that, if a strategy has the potential to satisfy the energetic and nutritional requirements of a species, then that strategy has the potential to evolve. Because both plants and animals carry energetic and nutritional value, herbivory and carnivory/omnivory can evolve.

  "All behaviour takes time. All behaviour consumes energy." [1]

Now consider the nutritional and energetic value of two the two food sources, plants and meat. Meat is typically richer in calories than vegetation, particularly those coming from fat and protein. 100 grams of lettuce contains around 14 calories, while 100 grams of beef contains about 200 calories. Protein is used by the body for growth, to repair tissues, produce hormones and enzymes and much more. Fat has a high energy content per gram (roughly twice as many calories per gram than protein or carbohydrate), is essential for the digestion of some vitamins,  and is an effective insulator. Given that behaviour takes time and energy, it is perhaps not hard to see that consuming meat can help to satisfy the energy requirements more quickly than consuming plants, allowing meat eaters more time for other essential activity like sleep and reproduction. Consider the activity of two large mammals, elephants and lions. Elephants spend a lot of time eating, some 12-18 hours per day (fortunately for them are quite able to eat on the move). Lions on the other hand typically hunt for short periods of the day (dawn and dusk), allowing them to avoid the heat (reducing water requirements), to rest, and reproduce.

Consider also that vegetation is often hard to digest — it is often is rich in cellulose. Many herbivorous species have complex adaptations to help digestion. Therefore, it's not necessarily easy, or easier, to evolve to eat only vegetation. Improved energy acquisition can evolve by both eating more energy rich foods and by more efficiently extracting energy.

Carnivory is also present in plants. According to this paper [2], such plants may be an adaptation to nutrient-poor conditions, where the ability to digest insects (and other small animals) would be a massive benefit, allowing carnivory to evolve rapidly.

  Botanical carnivory is thought to have evolved in nutrient-poor and
  well-lit habitats such as bogs because the marginal benefits accruing
  from carnivory exceed the marginal photosynthetic costs associated
  with the maintenance of carnivorous organs.

The Egyptian mongoose is an omnivore. This species varies its diet across the year, according to what is available. For example, insects are the major component of its diet in spring, while no fish are eaten during summer (because of dry canals in the summer) and fish are a major component in the winter. This illustrates that allowing omnivory/carnivory can increase the resources available, potentially allowing better survival and reproduction relative to a herbivorous/narrow foraging strategy in the same species. Consider this problem in, for example, boreal or temperate climates, where winter can cover ground vegetation in snow and tree's will reduce foliage. Consuming animals would allow the acquisition of energy and nutrients through the winter.

In summary, carnivory can evolve because animals are a good and plentiful source of energy and nutrition, and may allow diversification of strategies, improving survival and reproduction. If animals were bad food sources then carnivory would be less common as it would be a more difficult/problematic behaviour to evolve.

While many people & organisations (including PETA) try to claim that we are not well adapted to being carnivores, many of the claimed adaptations to herbivory/lack of adaptations to omnivory are overstated, misleadingly presented, and even false, and are used in order to promote their own agenda. It's also worth noting that we are not well adapted to being herbivores (e.g. gut flora) and chimpanzees, one of our closest ancestors, are also omnivores.

[1] Krebs & Davies Behavioural Ecology, An evolutionary approach.* ISBN-10: 0865427313.

[2] Ellison, Aaron M., and Nicholas J. Gotelli. "Nitrogen availability alters the expression of carnivory in the northern pitcher plant, Sarracenia purpurea." Proc Natl Acad Sci, USA 99.7 (2002): 4409-4412.


Vitamin and mineral contents of common fruits I'm looking for nutritional data, mostly vitamin and mineral contents of common fruits, such as apples, bananas, oranges, kiwis etc.

Are there scientific (published and peer-reviewed) sources that list or compare those? I spent an hour on Google Scholar but most of the sources there discuss only a small aspect (e.g. vitamin C content) or compare different states of fruits (frozen, fresh, canned). I'm not well educated in human nutritional aspects so I may overlook this one keyword to search for.

I'm aware of tables on the Internet discussing these aspects but I need a solid scientific basis.

I know two databases for such information: The "National Nutrient Database for Standard Reference" (reference 1) from the United States Department of Agriculture (which you list yourself) and the "Nutrition Data" (reference 2) Database. Both allow searching for specific foods and give the values back. I like the second more, since it gives you the complete output it has and you don't have to choose three single nutrients like for the USDA database.

References:

USDA National Nutrient Database for Standard Reference
Nutrition Data


How do cancers eventually lead to death / other debilitating symptoms? With regards to people I know or have read about who live with cancer, most of their symptoms are results of chemotherapy, surgical interventions, etc., which have the goal of eradicating the cancer. Assuming the cancer went untreated,* what kinds of symptoms would the cancer itself lead to, and by what mechanism would it cause death (in most cases)?

Please excuse my ignorance. I know that every cancer is different, and even different cases of a single type of cancer can present differently; so there may be many different answers to this question, but I'm not sure if they eventually lead to the same thing.

*I'm asking purely out of curiosity – I'm not "opposed" to chemotherapy or anything like that.

This is a very general answer to a very general question.

So, in general, cancer occurs when cells stop behaving as they are supposed to.
Your body is made by something like 200 different kinds of cells (epithelial cells, neuronal cells, blood cells and so on) working together to maintain the body's functions. If many of those cells stop doing what they are supposed to do then your body will start malfunctioning. Different kinds of malfunctioning will occur depending on what kind and on how many cancer cells will spread throughout your body. This can eventually cause system failures.
If your lung cells are malfunctioning, for example, you may expect respiration problems.
Often cancerous cells spread all around your body (metastasis) and several tissues and organs will be compromised simultaneously leading to a complex pattern of symptoms.
Fatigue, pain, inflammations, and bleeding are common symptoms in many advanced stages of cancer since tissues and organs start to get seriously damaged.


Anatomy of joints of human hand Q) A girl slipped and is falling. She puts out her arms to prevent falling. Which joints are most affected by her fall?

Fibrous and Synovial joints.
Cartilagenous and Synovial joints.
Fibrous and Cartilaginous joints.

The answer is 1.

Attempt:
Since it is the arms that will be affected, Synovial joints will be affected. But I don't remember there being any fibrous or cartilaginous in hands.

Are there any fibrous or cartilaginous joints in hand?

The intermediate radio-ulnar joint is fibrous in arms.

[Source: Slideshare.net]

You can see the the interosseus membrane between radius and ulna which is composed of white collagen fibres.

Furthermore, there is a cartilaginous joint between epiphysis and diaphysis of humerus which is made up of hyaline cartilage. But it is lost during development and is absent in adults.


Humans genetic/phylogenetic "next relative" in central Europe? What species in central Europe in the phylogenetic tree shows the closest difference in time to the most recent common ancestor with Homo sapiens?

I am not sure I understood the question. Is the following your question?

  Among all species living in central Europe, which one is the most closely related to homo sapiens?

Source of information

opentreeoflife.org (nice vizualisation on OneZoom.org) is one of the most update synthesis of existing research inn phylogenetic reconstruction. I base my answer in consideration of the tree on OneZoom.org.

Answer

Outside Homo sapiens, there is no living primates (or any other Euarchonta) in Central Europe. The sister branch of primates include Lagomorpha (Hares and Rabbits) and Rodents (mice, rats, squirrels, prairie dogs, porcupines, beavers, guinea pigs, hamsters, and capybaras). In other words, any Lagomorpha and any Rodents are all equally related to any Primate (incl. Homo sapiens). Their Most Recent Common Ancestor (MRCA) lived about 75 millions years ago.

Examples of species of lagormorpha and rodents that live in Europe include Mus musculus, Rattus norvegicus, Lepus europeanus and Sciurus vulgaris.

How about Hedgehogs?

Hedghogs are Insectivora and they are a sister group to all primates, lagomorpha and rodents. Their MRCA lived about 80 million years ago. So, no there are species currently living in Europe that are more closely related to us than hedgehogs.

Note

The term "next relative" does not mean anything! You might want to understand your understanding of phylogeny with an introductory course.


Plant identification in Turkey What species is this ? It is a stinky, hairy plant. I have found it nearby a river. It had reached a height of 1 meter. Bloomed three weeks ago. Found in Turkey.

Looks like a Hyoscyamus niger also called stinking nightshade.


Why would it be beneficial for cortisol and corticosterone to exhibit pronounced anti-inflammatory activity? These questions are always a little silly (as we will never truly know), but it always struck me as odd that corticosterone and cortisol exhibit pronounced anti-inflammatory activity.

Because these compounds are released during fight-or-flight episodes, it seems almost counter-intuitive for an organism to promote "anti-inflammatory activity" during an event that is most likely coincident with injury (i.e. wounds from fighting / escaping).

Anti-inflammatory activity, I believe, is fairly synonymous with anti-coagulation activity. If wounds are most likely to occur during periods of fight-or-flight (which is a reasonable intuition), why would organisms select for a glucocorticoid that has additional effects such as reducing acute clotting capacity?

The only thing that I can think of is there is an energetic cost to initiating the coagulation cascade, which would siphon energy away from skeletal muscle. Any thoughts / hypotheses?

Cheers~

Interesting question. It's easy to imagine why you would want to suppress inflammation in a fight-or-flight situation. Inflammation can cause painful swelling, fever, and it can dull mental acuity, all of which might hurt your chances of a win or escape.

After a little PubMed search, it looks like sympathetic adrenal responses (like cortisol) can actually induce a net hypercoagulability of the blood (1). So, even though inflammation does induce coagulation, it looks like the sympathetic anti-inflammatory response is not necessarily synonymous with anti-coagulation. This also makes sense in the context of Cushing's Syndrome, where hypercoagulation is associate with elevate cortisol levels, among other factors (2).