When is voltage generated across a membrane? I'm very confused so bear with me please.

Electrogenic pumps are carrier proteins that generate voltage through the movement of ions, right ?

When is a voltage generated ? When there's a net movement of ions ?

Doesn't that mean that when any ion passes through a channel protein, voltage is generated ? And energy is released ? Doesn't that make them electrogenic too ?

We need energy to move ions against their concentration gradient but if energy is released when ions move then why do we need energy ?

Is it that a voltage is generated when an ion moves towards the env with the same charge ? So when the movement enhances the overall seperation of charge , a voltage is generated ? And energy is released ?

In other words, the movement of Na+ through the Na+ channel protein down a concentration gradient doesn't release energy because the Na+ is moving towards the -ve environment but it being pumped outside does ? See that doesn't make sense either, because we need energy to pump and ion.

I'm very very confused

The main thing the sodium/potassium pump does is to move sodium and potassium ions, Na+ and K+. It technically generates a bit of charge separation in doing this, but you can ignore it for now.

What is important is that because of the operation of this pump, you now have two sides of membrane with different ion concentrations. One side is high in sodium ions (outside the cell), the other side is high in potassium ions (inside the cell).

So far, that doesn't really do anything electrical, but it does take a lot of energy to get this arrangement: the whole time, the pump is moving sodium ions to where sodium ions are high, and moving potassium ions to where potassium ions are high. Moving things against their concentration gradient costs energy. The sodium/potassium pump gets this energy from ATP.

Now, imagine you open some pores in the membrane (we call them leak channels), that are a particular size that only lets potassium ions through. The sodium ions can't move, but the potassium ions can. A few potassium ions move over to the high sodium side, down the concentration gradient for potassium. This doesn't take any energy, it just happens passively. It also doesn't involve very many ions, just a few, so the concentrations don't change much.

However, potassium ions have charge! These are positive charges, flowing out of the cell: that makes the inside more negative.

Also, because they are positively charged, potassium ions would tend to move towards more negatively charged spaces. So, as the inside of the cell gets more negative, potassium won't leave as quickly. There is an equilibrium, where the forces pulling potassium ions out to where potassium concentration is low equals the forces pulling potassium ions in to where the voltage is negative.

The voltage where this equilibrium occurs is called the resting membrane potential, and for many cells is somewhere between -100 and -40 millivolts: that's the voltage generated across the membrane, indirectly, by the sodium/potassium pump.

Purves' Neuroscience is a good general reference textbook for this sort of thing. The Goldman equation is a mathematical way to figure out what the voltage will be if you know the concentrations and permeability.

Voltage is not generated through the charge movement as such, it the magnetic field that is generated directly through movement of charges, although such movement contributes to voltage generation.

Voltage by definition is a potential to do work (to move charges), it always involves 2 points the difference in electric potential between which is voltage. If you want to measure voltage in a selected area, you always measure it relative to another reference area (like, there always is a "reference electrode"), because you measure the difference in electric potential between these 2 areas.

So, voltage is generated through separation of opposite charges. Like, a negative -80-60 mV resting potential inside a cell is maintained relative to an area of positive charges outside.

"The Na+/K+-ATPase enzyme is active (i.e. it uses energy from ATP). For every ATP molecule that the pump uses, three sodium ions are exported and two potassium ions are imported; there is hence a net export of a single positive charge per pump cycle." (wiki) Thus it can be supposed that energy is consumed by Na+/K+ ion propagation, though the definition of "energy" varies by context, voltage means potential energy.


What is a reflex pathway? I know that the pathway of nerve impulses during a reflex action is called a reflex arc. However, I want to know whether the term reflex arc can be called either a reflex path or simple reflex?

A reflex arc is sometimes called the reflex pathway. While there is no involvement of the brain in the output/response to stimulus, it does receive signals via the spinal cord informing it of the action. In other words, the reflex action is registered in the brain as soon as it occurs.


Can you please identify these yellow dot parasites which grow on non-living surface? Little yellow dot parasites have screwed me for years and I still don't know how to fight back as I don't know what they are. I just know that they are living beings because they grow in number.
Images:

(Click the images to enlarge)
Location: North India
Size: Visible to naked eyes (one dot is approx 0.25 mm in diameter; their colony is upto 5 mm in length or diameter; their colonies aren't perfect circles as seen in the images)
Behavior: They grow on any plastic, metal and glass surfaces (but not on clothes, walls or wood) if they are stored in open (the surface is in contact with oxygen)
Can you please identify it?

This looks like the work of an insect, perhaps a fly.
You can check by experimentation.
Try covering part of one surface with a fly-proof covering.
Take photos at weekly intervals of exactly the same area, compare images.
black-and-white images below from
Forensic Science International 137 (2003) 152–159
"Distinction of bloodstain patterns from fly artifacts"
Mark Beneckea, Larry Barksdale
DOI: 10.1016/j.forsciint.2003.07.012
Bar on images is 1cm


Evolution of sexual reproduction from asexual How exactly did asexually reproducing organisms evolve into sexually reproducing ones? Why was it considered more favourable?

Sexual reproduction is a process where two cells fuse to form a diploid cell. Unicellular organisms (or even multicellular lower organisms like alga, fungi and protists) prefers to reproduce by asexual means under favourable conditions. But when the conditions become unfavourable, they opt to follow sexual reproduction. This suggests, sexual reproduction evolved to increase the chances of survival under unfavourable condition.

So how does sexual reproduction helps in increasing survival rate? By fusion of cells i.e., sexual reproduction a cell now becomes diploid and hence have two copies of its genome. This increased copy of genome is beneficial in repairing any breaks or alteration in genome, as the other copy will act as a template for repair (via homologous recombination).

To get a better hold of this, let us take an example. Let there be a population of haploid cells. This population was exposed to conditions which would cause damage to genome, specifically would cause breaks in DNA. There were two cells "Fella A" and "Fella B". They both knew that their genome has suffered damages, but neither was successful in repairing the DNA as they required an intact DNA template for repair. Suddenly "Fella B" came up with this great idea to fuse with "Fella A". This would work, reasoned "Fella B", as the position of damage in the DNA in his genome is different from the position in "Fella A". Fusion of cells was the first step towards evolution of sexual reproduction.

Later on the biological system realised importance of variation generated by sexual reproduction and hence this mode of reproduction caught on with various lineages.

No, you've got the wrong end of the stick... asexual reproduction came from sexual reproduction, not the other way around! Asexual reproduction is a degenerate state that has benefits but is an evolutionary dead end because sexual combination is necessary to promote beneficial alleles and build new genes.  See:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231362/

The answer that says "Sexual vs asexual is not a binary condition" is misleading; yes, that is true.  Sexual species will start to experiment with asexual forms if they can because that confers advantages.  The ability to be parthenogenic is very useful, but since it is a dead end, the ability to reproduce sexually should not be lost.

Although sex was quite tricky to evolve in the first place, it was necessary from the very beginning.  It evolved from simpler systems of gene swapping and building that were needed from the beginning.


Why can humans feel electricity? What evolutionary process has provided humans with the ability of feeling electric current? Besides lightning and electric eel, what natural hazards include electricity that poses a threat to humans?

Electrical currents stimulate neurons aspecifically. For example, the BrainPort artificial vision device conveys visual information through electrical stimulation of mechanoreceptors in the tongue. Similarly, cochlear implants and retinal implants convey acoustic and visual information through electrical stimulation of the inner ear and retina, respectively. The list goes on. Bottom line is, none of these organs (tongue, ear or eye) evolved to process electrical stimuli. And in fact, there are no specific current or voltage sensors in man. Electric currents aspecifically stimulate neurons, causing them to fire. When sensory afferents are activated in this way, sensory perceptions are generated.

In case of lightning (electrical shock to the skin) it is mainly pain and heat receptors that mediate the sensation. In the case of the BrainPort, it is the tactile receptors on the tongue that are mainly stimulated (taste perceptions are rare). In case of cochlear implants it is auditory nerve fibers and in retinal implants it is optic nerve fibers that are stimulated. Hence, various, and in fact all, neurons can be stimulated by electric current.

Note that sharks feature Ampullae of Lorenzini. These sensory organs are electroreceptors, which allow sharks to sense the bio-electrical fields of prey under water.

Electricity is essential in order to control and coordinate neurons and skeletal muscles activities. You should imagine a neuron as a very complicated logic port of an electronic circuit, that receives information through its dendrits from other neuronal cells and then integrate this information in its body. If the spatial and temporal summation of inhibiting and stimulating signals is overthreshold, then at level of the first part of the axon, there is the creation of the all-or-null response of the neuronal cell: the action potential. In general, there is the simultaneous activation of the voltage-gated sodium channels that elicit spikes spreading them along the whole axon that is connected to other neuronal dendrits or skeletal muscle cells. These ones, receive and integrate in the same manner the stimuli sent to them. As you can easily imagine, external electric stimuli, like electrostimulators or instrument used by neurologist to analyze neuronal and muscle activities in diagnostic tasks are able to alterate the natural electric potential present across the cell membranes of these excitable cell types and response to this  electric field. Indeed, cells possess and actively keep an electric potential among the two sides of the phospholipidic bilayer of the cell membrane of about -70mV. This one is due to the asimmetric distribution of ionic species (sodium, potassium and chloride mainly) sustained using chemical energy obtained from exogenous sources. Thus, in general, our cells are not able to feel electricity directly but every phenomena, either phisical or chemical, able to alterate the electrical equilibium (homeostasis) of the cell membranes induce a response at inner cellular level leading, for example, to neuronal cell response or skeletal muscle contraction. You can think to the use of defibrilator to treat cardiac arithmias that send to the hearth strong current pulse-wave, that in case of fibrillation or ventricular tachycardia is frequently capable to restore normal cardiac activity and save life. Also pacemaker acts in a similar manner. Some pathologies like ALS, Alzheimer's, Parkinson, Myotonia involve also alteration of this electric mechanism leading to modified capacity of the cells to handle and interpret these electric message. In electrophysiology research, external stimulation of cells by electrodes (see patch clamp technique) is used to test the effect of drugs to treat these pathologic conditions.
Finally, I can say that evolution didn't give us the ability to feel electricity, instead it has been adapted as a cellular-level instrument handled by cells to communicate and integrate (or store in brain) stimuli and information.


Are (muscle) satellite cells the same as muscle stem cells? In terms of muscle: are the terms 'satellite cell' and 'muscle stem cell' interchangeable? That is, are there muscle stem cells that are not satellite cells, or vice versa?

Based on this review, satellite cells can replenish injured muscles, but among satellite cells there are satellite stem cells to maintain the pool of satellite cells.


Can one talk about deacetylation of a promoter rather than associated histone? I am confused on a detail in a paper I am reading and am not sure whether I am misunderstanding the wording or misunderstanding the concept.  I am including the whole abstract of this paper for background:

Epigenetic regulation of uterine biology by transcription factor KLF11 via posttranslational histone deacetylation of cytochrome p450 metabolic enzymes.
Zheng Y, Tabbaa ZM, Khan Z, Schoolmeester JK, El-Nashar S, Famuyide A, Keeney GL, Daftary GS.
Abstract:
Endocrine regulation of uterine biology is critical for embryo
receptivity and human reproduction. Uterine endometrium depends on
extrinsic sex steroid input and hence likely has mechanisms that
enable adaptation to hormonal variation. Emerging evidence suggests
that sex steroid bioavailability in the endometrium is determined by
adjusting their metabolic rate and fate via regulation of cytochrome
(CYP) p450 enzymes. The CYP enzymes are targeted by ubiquitously
expressed Sp/Krüppel-like (Sp/KLF) transcription factors.
Specifically, KLF11 is highly expressed in reproductive tissues,
regulates an array of endocrine/metabolic pathways via epigenetic
histone-based mechanisms and, when aberrantly expressed, is associated
with diabetes and reproductive tract diseases, such as leiomyoma and
endometriosis. Using KLF11 as a model to investigate epigenetic
regulation of endometrial first-pass metabolism, we evaluated the
expression of a comprehensive array of metabolic enzymes in Ishikawa
cells. KLF11 repressed most endometrial CYP enzymes. To characterize
KLF11-recruited epigenetic regulatory mechanisms, we focused on the
estrogen-metabolizing enzyme CYP3A4. KLF11 expression declined in
secretory phase endometrial epithelium associated with increased
CYP3A4 expression. Additionally, KLF11 bound to CYP3A4 promoter GC
elements and thereby repressed promoter, message, protein as well as
enzymatic function. This repression was epigenetically mediated,
because KLF11 colocalized with and recruited the corepressor
SIN3A/histone deacetylase resulting in selective deacetylation of the
CYP3A4 promoter. Repression was reversed by a mutation in KLF11 that
abrogated cofactor recruitment and binding. This repression was also
pharmacologically reversible with an histone deacetylase inhibitor.
Pharmacological alteration of endometrial metabolism could have
long-term translational implications on human reproduction and uterine
disease.
Citation:
Zheng Y, Tabbaa ZM, Khan Z, Schoolmeester JK, El-Nashar S, Famuyide A, et al. Epigenetic regulation of uterine biology by transcription factor KLF11 via posttranslational histone deacetylation of cytochrome p450 metabolic enzymes. Endocrinology. 2014;155:4507–20.

My question is on the fourth-to-last sentence of this abstract specifically:
"This repression was epigenetically mediated, because KLF11 colocalized with and recruited the corepressor SIN3A/histone deacetylase resulting in selective deacetylation of the CYP3A4 promoter."
This sentence seems to say that SIN3A/histone deacetylase is deacetylating the CYP3A4 promoter itself (i.e. it is deacetylating a region of DNA directly).  However, shouldn't a histone deacetylase be deacetylating a histone, not a region of DNA?  Am I misunderstanding the mechanism?  Or is "deacetylation of the CYP3A4 promoter" really a short-hand way of saying "deacetylation of a histone that is associated with the CYP3A4 promoter"?
Thanks in advance for your help!

The authors obviously meant to write that the histones associated with the promoter become deacetylated. They cannot mean the promoter itself as that is DNA.

What they wrote is not shorthand or acceptable alternative usage, but just a mistake — published papers often contain typos and mistakes of this sort. Probably the authors meant to write the technically correct form of words but lost a phrase. Or perhaps they had exceeded the limit to the number of words allowed in the summary, and so they went through trimming, but trimmed too much.

Why didn’t the referees pick this up? Of course they should have, but they were probably more concerned with the contents of the paper and whether the experiments described by the authors justified their conclusions. They are busy scientists and probably doing the job voluntarily.

In conclusion, scientists are human, scientific writing is difficult, and everyone makes mistakes. But we should still try to convey our ideas as clearly as possible, and certainly not copy something that is technically incorrect or ambiguous, just because it has made it into print.

This is all about DNA-Protein interactions.
The promoter region of the DNA is interacting with the Histone modifications, which are controlled by other proteins.


What is the name of the smallest self-replicating thing? Some time last year, I found an article on Wikipedia about the smallest something to be able to reproduce.

I don't remember exactly what it was, but I am fairly certain that after the initial discovery another of the previous organism (this one slightly smaller) was discovered.

I think that the smallest something might have been the smallest self-replicating protein, or smallest self-replicating molecule, or something like that.

It was not mentioned in this thread: Which organism has the smallest genome length?

It had a strange, stand-out name and I believe it was discovered in the 90s.

You're probably thinking of the Spiegelman Monster. It was actually discovered in 1965, but it was discovered that it became shorter over time in 1997.

It also wasn't included in that thread, and it has a strange name.

http://en.wikipedia.org/wiki/Spiegelman_Monster

A research team (Lee et al.) has discovered what maybe the smallest known self replicating RNA molecule - actually a 32-unit-long "a-helical peptide" whatever that is. It is based on the yeast transcription factor GCN4. The 32 peptide sequence is so small, that one could describe it in text form simply as:

ArCONH--RMKQLEEKVYELLSKVA-CLEYEVARLKKLVGE--CONH2
ArCONH--RMKQLEEKVYELLSKVA-COSBn
H2N--CLEYEVARLKKLVGE--CONH2

Two of those lines are likely to be pre-cursor molecules required (the food), and one is likely to be the RNA sequence, I think the final line.

This is a lot smaller than the smallest known or simplest genome, which could be Carsonella ruddii, which lives off sap-feeding insects, has taken the record for smallest genome with just 159,662 'letters' (or base pairs) of DNA and 182 protein-coding genes.
Source: https://www.nature.com/news/2006/061009/full/news061009-10.html

Also, it's likely you should checkout this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4187685/ "Systems Biology Perspectives on Minimal and Simpler Cells
"


Is it possible for virus infected cells to continue to present a self-antigen on the MHC1? Forgive my ignorance, as I'm new to immunology, however it seems like there would be some amount of positive selective pressure for viruses to develop the ability to continue to present the host's self-antigen on the MHC1 of a newly infected cell, thereby disguising the infection from the body's immune system (or at least from the cytotoxic T cells).

Is this in theory possible? Or is there a reason it cannot occur.

Self antigen is presented throughout viral infections.  You seem to think that cytotoxic T lymphocytes respond to absence of self. That’s backward. CTL respond to their specific peptide target no matter how much self antigen there is. In a typical response, there may be 100,000 self peptide/MHC complexes and 100 viral peptide/MHC complexes, and that’s enough for a CTL response.

One trigger for NK cells is absence of self, so perhaps that’s the source of your confusion.

From what I know, the cell does not actively choose to display viral antigens on its MHC 1 receptors. As proteins within the cell are inevitably degraded as a part of garbage disposal, these peptides are transported to the ER, where they bind to MHC 1 and display on the cell surface. When a virus infects a cell, some of its proteins are similarly degraded, either by the cell's own defenses or as a part of their normal life cycle.

So, there will inevitably come a time when a viral antigen will make its way to a cell's surface. The only way to stop it would be to stop protein degradation in the cell entirely, which is not a good idea. What viruses do try is downregulating MHC 1 molecules themselves, so there are less receptors to display antigens, but a reduced MCH 1 expression attracts the attention of NK cells.


What are the "minimum requirements" for a single cell? I saw a description of the "minimum requirements" for a cell at http://creation.com/origin-of-life in the section called "What are the minimum requirements for a cell to live?" and I'm wondering if this is scientifically accurate - and if not - what are the real requirements?

[note/warning - the link above is to a creationist site - I'm only quoting this source because I'm trying find the science involved and I didn't find other sources talking about all the necessary pieces. I'm not trying to promote creationism with this question so please don't attack the source or me for bringing it.  If you can find a non-creationist source which outlines these requirements, I'll be happy to update the question and remove this source.)

In summary it lists the requirements as follows:

cell membrane
way of storing information (DNA)
way of reading 2. to make components needed

RNA polymerase
gyrases to untwist DNA
ribosomes to make proteins
(a few others I omitted b/c I don't know if they're really important)

means of creating fuel (ATP synthase)
a means of copying the information for reproduction

The context of the question is similar to Can scientists create totally synthetic life? and a question I wrote What is the most complex biological organism (or precursors) that we have been able to synthesize from raw materials?.

I'm trying to understand what would be involved in making a cell from scratch. Somehow I found this source but I don't know if it's accurate.

So, to make cells from scratch you would need: amphiphilic molecules to form a membrane, a decent mix of simple molecules (sugars, nucleic acids, peptides) that serve as reactant and building blocks for more complex things, some simple catalyzer (metals, minerals, pepetides, aptamers, etc..) to run the reactions, enough energy to maintain lots of reactions running and keep them far from the equilibrium. Of course, lots of time...

An even more minimalistic approach would use a single molecule to do the enzymatic job while storing evolvable informations. In this case RNA alone has been proposed as substitute for proteins and DNA in a very minimal cell. In theory also DNA alone could do the same. However the minimal tasks needed to be done: maintain the self (to be compartimentalized), to grow (to have a flux of molecule not in equilibrium), to divide, to maintain the information stably enough to be useful for the next generation and at the same time prone too mutability to evolve.

One more point. Life itself doesn't strictly require to be compartmentalized.
You can think of a network of chemical reactions that have the ability to grow, to replicate its components etc but without a cell membrane. However I think that a cell-like form of life is somewhat more likely to happen.

Cell is the structural and functional unit of life, made up of a small mass of protoplasm delimited by a semi permeable membrane and capable of self reproduction without any living medium. This is a proper definition of cell and the minimal requirements would be all these mentioned here.
You can also see cell theory by M.J. Schleiden and Theodor Schwann.
But most importantly not only genetic information and membrane are required, most required part will be Cell should be capable of self reproduction without any living medium

Like for example RBC is not called cell cause they can't reproduce themselves. But nerve cell is called cell cause though they are not divisible but in embryonic condition the cell division occurred. Also in case of virus, as they can't reproduce without a host,they can't be called cell.
Red blood corpuscles aren't cells have a good proof in this article (check blood trivia part)
red blood corpuscle


Can somebody be deaf to voices of some people only? The voice of females is generally of high frequency, while that of males is generally of low frequency.

Also, as we age, we gradually keep losing the ability of hearing sounds of high frequencies.

So, can such a situation occur when a person is not able to hear voices of females, or maybe of certain people, while he can hear the voices of other people? I tried searching about it, but found nothing.

Although you loose the high frequencies in your hearing with age (20kHz and below), this is highly unlikely. The frequency spectrum of our voice is pretty much limited, which is also shown by the fact the for normal telephone, the spectrum transmitted is located between 300 and 3400Hz and the spectrum band between 300 and 3000Hz is named the "voice band". See here for some details.

According to reference 1 the "voice fundamental frequency" for men is between 85 and 180Hz (depending on the reference) and for women between 165 and 255Hz. These frequencies are close enough together to rule out specific hearing of male or female voices. Furthermore the frequencies even overlap.

What happens in age-related pathological hearing loss (also termed Presbycusis) is that voices generally get muffled due to losses in the spectrum and hearing intensity. See the Wikipedia link and also reference 2 for more details.

Reference:

The frequency range of the voice fundamental in the speech of  male
and female adults
Presbycusis

Sensorineural Hearing Loss (SNHL) can reduce the ability to hear faint sounds even when the sounds are clear and audible. Tone deafness in contrast affects a person's ability to learn music, but not the ability to perceive or recognize speech.


Osmotic pressure and turgor pressure details I am a high school student and I am very confused in how we define osmotic pressure?
Osmotic pressure is defined as the pressure required to stop the diffusion of solvent into a solution by applying external pressure over solution, which means that when the pure solvent is diffusing into the solution then it will apply pressure on the semi permeable membrane and when we have applied the same external pressure over the solution then there is no net movement of solvent occurs across the membrane and mathematically it is equal to P=cRT, where c is the concentration of solution , T is temperature in kelvin and R is the universal gas constant, if we go by this equation and calculate the osmotic pressure of 1 molar concentrated solution at room temperature it comes out to be almost 2495Pa which means 2495Newton/m^2 which is very high pressure and it doesn't seem to be true as osmosis is very slow process it surely cannot generate that much of pressure( just to imagine how large is that pressure assume an area of 1m^2 and place Mass of 249.5kg on it), so I think that it should not be that higher, so ,I am unable to understand what is actually osmotic pressure ,on which does it actually act and how do we actually calculate it?
we say that when a cell is placed in hypotonic solution then osmotic pressure is greater than Turgor pressure and water will flow inside the cell, but I have a confusion that like turgor pressure acts on the wall of cell ,osmotic pressure should also act on the wall and in opposite direction of turgor pressure, so by this logic wall should compress more as osmotic pressure on it will cause it to compress and turgor pressure will cause it to expand but Osmotic pressure is greater than turgor pressure it should compress, but it doesn't happen? we only talk of turgor pressure to explain the expansion but not osmotic pressure why? I know I am going wrong somewhere if Osmotic pressure would really leads the cell to compress then an animal cell would have never burst in hypotonic solution. and if osmotic pressure is also acting on the wall or membrane then net pressure on the wall is O.P-T.P (in inward direction) , and not only T.P (outward) so the wall pressure here also should not be same as turgor pressure?
If anyone will explain me this by giving as many examples as possible than it would be very helpful for me to understand because its my first time I came to know about these things.

when we talk about external force applied in this case we talk about a setup that is made by us. like a U tube experiment that is filled with water and separates both the hands of the tube via semipermiable membrane and we add solute one side and due to this water starts to rise in that hand of the tube to avoid this rise in water level an external pressure is applied tht prevents this water rise and this pressure is termed as osmotic pressure. THIS IS THE CASE OF A ENVIROMENT WHERE EXTERNALFORCES CAN BE APPLIED BY US AND IT IS VERY MUCH DIFFERENT FROM THAT OF THE CELL WORLD.
in case of cells osmotic pressure is directly proportional to the concentration of the solution i.e more the solute more the OP and visa versa. in cells osmotic pressure are internal force that is caused due to  difference in concentration of the solutions.
and as we know water move from low osmotic pressure to high osmotic pressure
{ from less concentrated to more concentrated solution} thus cell swells up because of entering of water when cell is placed in pure water or hypotonic solution.
CONCLUSION : CELL DO NOT SHRINK BECAUSE NO EXTERNAL FORCE IS APPLIED BY US THE DEFINATION U GAVE IS CORRECT BUT IT IS NOT APPLIED IN CELL WORLD. IN CELL WORLD OP IS A PRESSURE DEVELOPED DUE TO DIFFERENCE IN CONCENTRATION OF SOLUTIONS AND THIS PRESSURE IS CREATED INORDER TO EQUAL THE CONCENTRATION OF SOLVENT (WATER) IN BOTH THE SOLUTIONS.


Why are things conscious? I've been referred to here from https://philosophy.stackexchange.com/questions/8052/why-are-things-conscious. Could you guys help out? Here's the question:

What is the reason for animals or more general entities being conscious? How did this evolve? What is the advantage?

I'm aware of ideas that consciousness is merely a illusion, however I find them less than convincing. The counter-argument would follow the line "if consciousness is an illusion, who has the illusion and more importantly why?". Additionally I believe that consciousness is a bare empirical fact. Even more, it is the basis for empirical thought. That "consciousness is an illusion" is not a good idea has been discussed by e.g. Searle (a video can be found here http://www.youtube.com/watch?v=yCii726A4Jc)

So what are good explanatory models for consciousness?

Disclaimer: there is a very large amount of literature on the subject and I am in no way expert enough to properly review it here.

In any case, here's a few papers that review the issue and may serve as a basis to look up other references

Evolution of consciousness: phylogeny, ontogeny, and emergence from general anesthesia - Mashour and Alkire, PNAS 2013

  We propose that the stepwise emergence from general anesthesia can serve as a reproducible model to study the evolution of consciousness across various species and use current data from anesthesiology to shed light on the phylogeny of consciousness. Ultimately, we conclude that the neurobiological structure of the vertebrate central nervous system is evolutionarily ancient and highly conserved across species and that the basic neurophysiologic mechanisms supporting consciousness in humans are found at the earliest points of vertebrate brain evolution.
  [...]
  The distinction between phenomenal and access consciousness was noted, but phenomenal consciousness itself reflects the dissociable neurobiologica processes of awareness and arousal. Awareness refers to the content of consciousness (red apple vs. blue sky), whereas arousal refers to brain activation and level-of-consciousness (alert vs. drowsy vs. asleep vs. anesthetized). A number of current theories about consciousness propose that the cortex is the primary site containing the neural correlates of awareness, whereas midline subcortical brain structures provide ascending arousal influences to the cortex

This is also reviewed in this paper:

Subjective experience is probably not limited to humans: the evidence from neurobiology and behavior. - Baars, Conscious Cogn., 2005

  Thus consciousness is not a metaphysical absolute, but a scientific construct like any other. In humans, the standard behavioral index of conscious cognition is accurate or verifiable report. It has been used scientifically since the beginning of psychophysics in the 1820s. Accurate report is highly reliable, but of course it is subject to limitations like any other empirical measure (Baars, 1988).
  [...]
  In humans the thalamus and cortex are crucial for supporting the contents of consciousness (Edelman & Tononi, 2000). Thalamus is often considered to be an extension of cortex, an added sandwich of interacting layers that controls most traffic to and from cortex. Local damage to cortical sensory regions, like the fusiform gyrus for face perception, results in a loss of conscious knowledge about faces but not about other visual features like color, location, or size. If the intralaminar nuclei of the thalamus are lesioned bilaterally, the conscious state is lost. By comparison, large lesions to cerebellum, basal ganglia, and spinal cord do not impair either conscious contents or state. Cerebellar damage can cause paralysis but not loss of consciousness. Lesion evidence on these points is supported by stimulation experiments using electrodes, transcranial magnetic stimulation (TMS), and microdialysis. It is also reflected in functional brain imaging. The evidence is therefore very strong that the T-C system supports consciousness. That is why many neuroscientists consider the T-C system to be the “seat” of conscious experience, and have done so for at least a century.

Again, citing from the first paper:

  The recent experiments with general anesthesia in humans suggest that phylogenetically ancient structures in the brainstem and diencephalon—with only limited neocortical involvement—are sufficient to support primitive consciousness. Where, then, does consciousness arise on the evolutionary timeline? One might be tempted to conclude that consciousness commenced as our mammalian ancestors evolved just beyond reptiles and their predominantly subcortical brains. However, paleontological findings suggest that the synapsid line that gave rise to mammals and the sauropsid line that gave rise to reptiles and birds both diverged from the primitive anapsid line at a single point ~315 million years ago. Furthermore, there is significant evidence that avian species are capable of higher cognition and even consciousness itself. For example, birds demonstrate evidence of explicit episodic recall (i.e., conscious memory of an event) and theory of mind (i.e., attribution of subjective mental events to another being). Thus, it would be misguided to try to identify a single point at which consciousness emerged because evidence suggests that consciousness evolved along two independent lineages.

Neuroscience is my specialty.  What we call consciousness is thought to be an evolutionary elaboration of a property of cells called "irritability", which is the cell's ability to respond to signals from its environment.  There are many manifestations of this: chemicals binding to protein receptors, light interacting with proteins (as in photosynthesis), mechanical forces causing cell movement, bacterial chemo-taxis, and the list goes on.

The analogy is like this.  What we call eating and elimination are analogous to cell metabolism.  As a whole organism we must eat to replenish the body, and eliminate the waste produced. A single cell must also absorb nutrients to maintain itself and eliminate the waste products.

So, it is like a fractal.  The same functions displayed by individual cells also manifest at the level of the whole organism. So, as the GI tract is the organ analogous to cell metabolism, the nervous system is the organ analogous to cell irritability.  One could imagine that what we experience as our personal consciousness is in fact like taking an integral over the irritability of all the cells in our nervous system.  Many people focus on the neurons, but all the cells in the brain contribute to the brain's function.

Now, this form of explanation is not really an explanation as much as it is a description of our biology.  The obvious question arises: why are cells irritable? Because, irritability is basically the individual consciousness of an individual cell.  Well, one then realizes that the response properties of cells to stimuli come from the action of the molecules and forces that make up the cell. The immediate forces are non-covalent interactions, mainly poorly understood even in terms of physics, such as forms of adhesion (consider Velcro or glue). These are emergent properties that stem from the assemblage of molecules of which cells are composed.

But let us grant that physicists eventually come to understand such "derived" forces in terms of the elementary four forces of the universe: electromagnetism, gravity, strong and weak nuclear.  Then, it is clear that there is a potential contained in these forces to combine in ways that cause complex molecular assemblies that self-organize and display irritability.

Thus, the issue of consciousness presumably links back to somehow being an inherent emergent property of the forces of nature.

Again, this is all relatively uncontroversial, but building such a chain of explanation is not really an explanation as much as just being a description of how things are organized in the world.  And I think it is clear to any thinking person that a description of something is not the same as an explanation of something.

So, if you follow this far, then you can appreciate why the Greeks thought that Atlas, who held up the world, stood on the back of a tortoise, and this tortoise was on top of another tortoise who was on top of another tortoise, all the way to infinity.

We have simply replaced Atlas and the tortoises with language of modern science.  It is still an infinite regress.  The short answer to "why are things conscious" is that it seems to be a property of the universe to display consciousness.

Now, there is one great man who thought about this problem and constructed what I consider the best explanation.  This was Gottfried Leibniz, the man who invented calculus.  Leibniz invented the idea of a "monad", and he considered monads as the basic units, the atoms, in the sense of being the indivisible units of reality.  The monad, as an atom, is pure consciousness.  So, Leibniz came to the conclusion that the reason there is consciousness is because consciousness is the fundamental building block of reality.

Monads are what everything is made of: us, cells, atoms, quarks, electrons, etc.  These are all different forms of monads.  According to Leibniz, they are all different forms of consciousness, and they combine in fractal patterns to make forms of consciousness within forms of consciousness within forms of consciousness.  And this pattern goes in both directions from the infinitely small to the infinitely large.  According to this idea, just because something does not seem to be conscious in the same form we are conscious does not mean it is not conscious.

This is how Leibniz solved what is called the "mind body problem", which is really the heading under which your question falls.

If one wishes merely for intellectual understanding of the nature of our consciousness, it is my opinion that Leibniz' ideas are the best available.

If you wish to go beyond mere intellectual understand to a deeper level of awareness of these issues, then I suggest you look up and study the works of a writer named Patanjali.


What are the ploidy levels in major groups of organisms? If total number of chromosome in the cell is x, then for-example;

Are all animals diploid (x= 2n) ?

Are all fungi haploid (x= n) ?

Are all plants diploid (x= 2n) ?

Are all Protists diploid (x= 2n) ?

Also, what is the ploidy of archaea and bacteria?

Thank you very much.

Are all animals haploid (n=x) ?

No

  Are all fungi haploid (n=x) ?

No

  Are all plants diploid (2n=x) ?

No

  Are all Protists diploid (2n=x) ?

No

  Also, what is the ploidy of archaea and bacteria?

Generally speaking, Bacteria and Archaea don't have chromosomes (but have circular DNA). As such the question of ploidy does not really apply to them.

You might want to read about Biological life cycle to understand the terms haplontic, diplontic, haplodiplontic (and other similar terms).

Ploidy level can easily varies among species of the same family (typically in plants for which hybridization is common). There is no reason to expect that a taxon as big as "fungi" (for example) would all have the same level of ploidy.

Note that your question that all animals are haploids is surprising as you just described that humans are diploids.

In animal, reproductive cells are haploid for human

Male bees, wasps, and ants are haploid because of the way they develop: from unfertilized, haploid eggs

some fungi are also haploid


Does posture matter while drinking water? I have heard a lot of people (where I am from, India) say that one must drink water sitting, not standing. Recently, I also came across a video that said the same thing (link). The reason given is that when you drink water standing, it goes to the colon too quickly, whereas while sitting, the water is better absorbed by the organs. Is this true? Is there a biological basis for why I should drink water sitting?

I tried to find literature on this matter, but apparently there isn't a whole lot. I found this paper where they tried to see the water passage rate in the GI tract of rabbits, mentioning how the water goes from stomach to cecum to proximal large colon, but obviously did not study posture.

Note: I think this question belongs here better than Skeptics.SE as I am looking for a biological explanation

The stomach is equipped with the pyloric valve to regulate transpyloric flow to the duodenum.
Both cold and warm drinks stimulate a pattern of motility associated with retardation of transpyloric flow.

The pyloric valve is responsible for acidifying water that you drink, and if the body's guard against amoeba's and dysentery depended on body position, it would be low survival performance, given that sedentary posture is associated with poorer health outcomes, including an increased risk of type 2 diabetes. You will benefit from minimizing time spent sitting each day, and from breaking up periods of time spent being sedentary, as often as possible. It's aperture at rest is 3mm, so it's of minimal difficulty for the stomach to hold water as required for optimal health. It's highly likely that water is kept for enough time to expose it to stomach acids, regardless of body position, and then it's transmitted.
Water doesn't flow straight through the stomach like a straight tube when it's empty.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1382811/pdf/gut00528-0043.pdf

First off: pure, reverse osmosis treated, bottled water HAS NO NUTRIENTS. Secondly, of everything you swallow, nothing goes too fast on it's way to the colon. The small intestine is a network of twisted tubing, around 20 feet long. Nothing is going through there "Too fast".

Sources: https://carta.anthropogeny.org/moca/topics/smalllarge-intestine-length-ratio


In men, why do over 80% of sperm have abnormal form? Here is the percentage of normal forms among fertile mens according to the centile (Source: Cooper et al. 2010):

2.5: 3%
5 (below this is Teratozoospermia): 4%
10: 5.5%
25: 9%
50 (median): 15%
75: 24.5%
90: 36%
95: 44%
97.5: 48%

Men who have less than 4% of their sperm that have normal morphology are diagnosticated with Teratozoospermia (also called Teratospermia) and are likely to be infertile, though technically 5% of fertile men have Teratozoospermia.

I read on the internet that abnormally-shaped sperms are bad and useless because their abnormal shape prevents transport through the cervix and/or prevents them from adhering to the ovum.

But I think that if they were really that bad, Mother Nature would not have engineered the average men with 85% of their sperm abnormally-shaped.

And I also heard that even animals have a big fraction of their sperm that are abnormally-shaped.

So, in men, why do over 80% of sperm have abnormal form?

So I've dug a bit into how a 'normal morphological' form is defined and characterised, since assessing morphology into 'normal' and 'not normal' is always a very tricky thing.

Looking into the method section of the source you cited, we get:

  All laboratories generating the data analysed here used standardized
  methods for semen analysis [...] The various editions of the manual provided similar
  methods for assessing sperm concentration, motility and morphology but
  provided different criteria for categorising morphology.

So the  problem begins already with the fact that there is not one, but multiple different recommended practices.
(For anyone interested the different staining methods used were: Bryan–Leishman [B], DiffQuik [D], Haematoxylin and Eosin [H], Papanicolaou [P], Quickdip [Q] and Shorr [S]. Of thses H, S and P were used for generation of the 'normal morphology' reference set).

Clearly this problem was also obvious to the authors, so they tried to restrict the data they used:

  Although all centres reported using WHO procedures, the recommended
  methodologies have changed over time, and many centres have
  experienced difficulties with the subjective assessments of
  morphology. Data on normal sperm morphology were only included if
  results were reported as determined according to the so-called
  ‘strict’ (Tygerberg) method (WHO, 1992, 1999).

Fortunately these WHO guidelines are available on Google Books and they require the following points to met (most of which were defined by 95% confidence intervals of control samples):

head length 4.0-5.0µm
head width 2.5-3.5µm
head length-to-width ratio 1.5-1.75
well defined microsomal region compromising 40-70% of the head area
mid piece should be slender, <1µm
[mid piece should be] 1.5x size of the head
[mid piece should be] axially attached to the head
Cytoplasmic droplets should be less than half size of the head
Tail should be [...] approximately 45µm long

Plus one very important sentence:

  This classification scheme requires that all 'borderline' forms be considered abnormal

This sentence is important, because it means that each criterion stated has to be fulfilled for a single sperm to classified as morphological normal.
If we take only the numeric requirements (which should cover ~95% of the normal value distribution for a healthy population) and assume that they are not correlated, this means that for any given single healthy sperm we have a $0.95^9 = 0.63 = 63\%$ chance that it is within the 95% interval of all defined parameters.
This means that applying this strict categorisation scheme should even for a 100% healthy population only result around 63% sperm cells categorised as morphologically normal (ignoring that the parameters are probably not interdependent which would make it a bit better).

If we now take into account that the analysed samples were probably not 100% healthy cells and remember that the (reported) difficulties of assessing morphology, I think that the reported values for 'morphological normal' are not as quite as unexpected as they might seem.

Note: all bold highlighting in the quote blocks was added by me.

Biological evolution occurs when there is a change in gene frequencies over time (as I recall).  There are two components, or elements, required for this process:

genetic variation, which provides the raw material
natural selection, which results in the genes from the most successful reproducers being transferred to subsequent generations

The data you present support the hypothesis that “normal” sperm morphology in human males is not a strongly selected trait (because otherwise “normal” sperm would be more prevalent). Period. Full stop.

Any attempt to answer the “Why” part of this would have to be a conjecture, and ultimately untestable on an evolutionary scale.


Does the testicle's temperature increases with the body temperature during a high fever? The testes is the male sexual organ. It is positioned outside the abdomen along with the scrotum. I would like to know if its temperature is independent from the body temperature due to its location.

The question is quite vague. Please specify for clear answer.
However, although testicles are out of the body, but a part for sure. Due to pyrogen attack when the body temperature increases, literally the temperature of the testicles should be increased but clear research has not been found yet.
Please specify your question.


Evolution - The ability to control ear muscles Among animals the ability to control ear muscles is pretty common, but only a few humans have the ability. Is it because we in general lost this ability ?

Yes, humans have lost the ability to move their ears toward sounds like many other animals such as cats and rabbits.

It is thought that our ancestors lost the ability to move their ears around 30 million years ago when

  Ear size decreased and the associated musculature changed 1 (Steven Hackley).

A review from Steven Hackley outlines the evidence that the neural circuit remains in modern human brains. Apparently, the neural circuit still responds to directional sounds and may cause our ears to curl slightly (2 - 3 mm).

This adaptation would have very little pressure on gene pool selection, as it provides little to no advantage other than slight, likely negligible, hearing improvement.

As survival fitness in terms of hunter-gatherer qualities, such as those of keen hearing and sight, are today meaningless in terms of reproductive viability, this phenotype would not persist over time, in my opinion.


Will moth larvae pupate in response to food deprivation Context: Trying to exterminate a clothes moth infestation.

Supposing you have a room with clothes moths, or rather, with clothes moth eggs and larvae.

Suppose then, that you remove all of the soft furnishings, all of the clothes, all of the carpet, and you thoroughly clean and vaccuum to remove as much dust and hair as possible.

Would one predict that the remaining larvae would then immediately pupate into moths, in response to this food deprivation?

I know that lots of plants will suddenly flower or fruit if they perceive that they are at risk of dying, in order to reproduce before they die. I believe the moths are essentially just a reproductive phase of the moth, so I'd be unsurprised if they did pupate.

On the other hand, I imagine pupation takes a lot of energy and food reserves (not to mention needing material for the cocoon), so I can imagine that they might be unable to do this?

Which way do it go?

Will moth larvae pupate in response to food deprivation

Not officially an expert, but I have been watching clothes moths for years and haven't noticed any small ones, so dont expect early pupation. I would expect small pupae to give small moths (like with houseflies). I do see the hormone traps reduce population, but only with lots of them (2 per small room).


Are there differences in cell membrane cholesterol levels between cell types? With different cell types, and cell functions, are there distinct levels of cholesterol in each cell type's cell membrane, or do all cell types have a similar amount of cholesterol?

I am assuming certain cell types require different levels of cell membrane stability, and as such, different levels of cholesterol in that cell membrane.

Yes, there are differences in cell membrane's cholesterol levels among different human cell types.

This table from Alberts (2002) shows the difference in cholesterol composition in a liver cell, a red blood cell and a Schwann cell/oligodendrocyte (myelin):

Table: Approximate Lipid Compositions of Different Cell Membranes

Besides that, the table shows that there is difference in the cholesterol composition among different membranes in the same cell (compare plasma membrane, mitochondrion and ER). Actually, that's a more famous difference, depicted in this figure from Lehninger (2000):

Figure: Lipid composition of the plasma membrane and organelle membranes of a rat hepatocyte. The functional specialization of each membrane type is reflected in its unique lipid composition. Cholesterol is prominent in plasma membranes but barely detectable in mitochondrial membranes.

Sources:

Alberts, B. (2002). Molecular biology of the cell. New York: Garland Science.
Lehninger, A., Nelson, D., Cox, M. (2000). Principles of biochemistry. New York: Worth.

You're right, different cells have different quantities of cholesterol within the membrane. For example a red blood cell will have more cholesterol in it's membrane compared to an epithelial cell in the small intestine. This would be because the blood cell is free floating within the body rather than being physically adhered to something, so a greater level of stability is needed. It is solely dependent on the cells function.


How do people measure how many calories or proteins/fats/сarbohydrates are in some food? How is the composition (in fats, proteins or carbohydrates) of a certain food estimated and how is the amount of calories provided by the food calculated?

Messured by the amount of energy it will take to raise 1 degree celsius in 1 kg of water. You really can never go by what the packaging says either. All depending on how food is prepared, even your digestion differs the count person to person.


Why magnesium ion is needed for activity of G-proteins? I was studying about G-protein coupled signaling sysytem, somewhere they have mentioned about need of Mg$^{2+}$ for acticty of G-protein and related it to increase of cyclic AMP production. On further reading I came to know that the said ion is related to GTPase activity of G-protein, but how does it relate to incresed cyclic AMP production?

Ion can change secondary structure of an enzyme. Magnesium ion is coordinated within certain domains (for example, EF-hand motif) and makes them more ordered. Usually it happens via hydrophilic shell of residues embedded into a hydrophobic one (https://www.pnas.org/content/87/15/5648).

You can reverse it by adding a chelator (EDTA, for example) and protein is more disordered which can affect it's activity.


What is the pathogenuc mechanism of brown pigment lipofuscin in muscle atrophy? I think it is autophagy. Lysosomal degradation. Autophagocytosis.

Example of the brown pigment (lipofuscin) here:

I am not sure if autophagy is the right answer to the "pathogenic" mechanism of atrophy.

Is autophagy the pathogenic mechanism of atrophy?
Or what pathogenic mechanism is involved if you see lipofuscin in the histologic slide?

Simple answer: Atrophy through autophagy.


Can elephants trumpet when they have water in their trunks? I am writing a fun story about elephants and want to know if elephants can trumpet or at least, make noises when they have water in their trunks, like when they are drinking water. Thanks for your help!

I think no. Because the elephant uses its trunk to make noise and if the trunk is filled with water then there is no chance the voice would come out.


Why some tissues like small intestine epithelium are able to be replaced so often, yet they are not one of the most common cancers? My small intestine epithelium cells are replaced thousands times more than my prostate. Yet I'm much more likely of getting a prostate cancer than cancer on my intestine epithelium. Is there a known cause for this?

Does our body have better DNA-repairing mechanisms or something like that for those tissues ?

The human prostate has two main epithelial cell types, basal and luminal, as well as a minor population of neuroendocrine cells. Primary prostate cancer nearly always has a luminal phenotype characterized by atypical glands, strong androgen receptor (AR) signaling, and an absence of basal cells .                  Intestinal epithelium. The intestinal epithelium is the single cell layer that form the luminal surface (lining) of both the small and large intestine (colon) of the gastrointestinal tract.


What happens between two nodes in an evolutionary tree? Hey guys can you help me with this one!?

What happens between two nodes (in an evolutionary tree) or a between a node and a tip?

A) at least one character changes

B) all organisms die

C) Nothing can happen between two nodes

D) Monophyly, Paraphyly, Polyphyly

E) None of the above

I came down to E) and C). Since B) doesnt even make sense, organisms don't die among two nodes- they evolve. D) it is irrelevant to the question asked A) I think that probably is wrong as well, since among a node and a tip, the organism stays the same and finally I thought C) could be the answer, but at the same time a new trait could be formed,

Your answer is A. for one simple reason, two different nodes represent at least one notable/measurable difference between groups, so between any two nodes there must be at least one difference.

Look at this example, whether A and B represents Mammals and Birds or two subspecies of chimp, or two strains of virus the fact they are two separate nodes means there is some difference between them. When constructing a tree there has to be at least one character difference to have more than one node. A tree with no differences is just a dot by itself.

Also an organisms does not stay the same between a node an the tip (the tip is a node) to use the below example the starred node between A and B is the most recent common ancestor of A and B which is not the same thing as A or B.

The question does not make much sense and I think you've gone about as far as anyone can go.

  A) at least one character changes

It depends what it means by character and it depends the detail semantic of the tree. In general, an evolutionary tree, usually called a phylogenetic tree attempts at representing time by the length of the edges in between two nodes. The goal is, in general, not to represent anything else.

In the comments, @John has argued that time can be consider as a character.  Personally, when I read the term "character" I think of a phenotypic character. While it will pretty much always be true that among two nodes some difference will exist in the phenotypic character, it is not a fundamental consequence of the concept of evolutionary tree. This is why I argued that A is false. @John takes the opposite stance in his answer. Note also, that sometimes (although quite rarely today) phenotypic states are used to build a tree and hence, in such case, it would be a direct consequence of the methodology that two nodes must necessarily differ by the value of at least one phenotypic character.

This disagreement between @John and I highlights that the question is poorly phrased and actually makes little sense.

  B) all organisms die

Well, most likely enough time separate the two nodes that all organisms that were represented in the ancestral node are dead but of course they have reproduced, so that we actually have another node that descend from it.

  C) Nothing can happen between two nodes

As you said, they evolve. So, things happen!

  D) Monophyly, Paraphyly, Polyphyly

As you said, those terms make no sense here!

  E) None of the above

If there is any intuitive answer to the question what has happened between two nodes is time has passed. I think the answer your teacher was expecting here is E but it is also possible (s)he was expecting A. Really that's a pretty poorly written question.


What does the root "phyllum" mean used botanical binomial nomenclature I often encounter the root "phyllum" in binomial names in botany, but I've had trouble finding an actual definition for this root in any Latin dictionary outside of its taxonomic meaning. From context it seems to mean "leaf":

Acer macrophyllum - Bigleaf Maple
Tsuga heterophylla - A Hemlock with distinct two-ranked needles

But the Latin for leaf should be folium. Is there any real rhyme or reason to this? I don't know if this is a question better directed towards the Latin stackexchange, but I thought a botanist might have some insight on the subject.

Binomial names often use of greek words. Phyllum means -- as you correctly stated -- "leaf", but is not derived from latin but from the greek φύλλον, 'phyllon'.

By the way, there are also lots of examples where the latin word 'folium' is used. To stick with the genus Acer from your example, there is another species named Acer gracilifolium. So don't be confused by the linguistic chaos in binomial nomenclature.

Phyllum is used to refer leaf in Botanical nomenclature. How the word "Phyllum" is derived is not known.


Why is it that guttation is most commonly observed in the morning? Knowing that guttation occurs through a plant's hydathodes due to root pressure forcing liquid water out of the leaves, I am curious as to why so many small drops of water are observable on plants in the morning. Could this potentially have to do with the moisture in the air at night vs day? Since humidity tends to increase at night?

Thanks in advance!

Guttation is commonly seen at night and early morning. Plants release excess of water via the guttation. During day time as the transpiration rate increases, excess of water is released via transpiration and hence guttation decreases. Also due to high temperature these small droplets are quickly evaporated during day time.

The stomata are mostly closed at night and early morning. Early morning rising temperatures cause efflux of H2O from the hydathodes while stomata are still closed, and by the time the stomata are opened, the efflux switches to the shorter route through the stomata.


What is the silencing mechanism of AGO1,AGO3 and AGO4? I read that this proteins lack of slicer activity, so what mechanism do they use to perform gene regulation?

Paper by Zinovyev and colleagues in the paper "Mathematical modeling of microRNA‐mediated mechanisms of translation repression" find that there are reports to 9 different mechanisms of miRNA-regulation.

Here we are reviewing available experimental data on all reported mechanisms of microRNA action, grouping them in a way which elucidates the main details supporting each of these proposed mechanisms.

Here is a list of the mentioned mechanisms:

M1: Cap-40S Initiation Inhibition
M2: 60S Ribosomal Unit Joining Inhibition
M3: Elongation Inhibition
M4: Ribosome Drop-Off
M5: Co-translational Nascent Protein Degradation
M6: Sequestration in P-Bodies
M7: mRNA Decay
M8:  mRNA Cleavage
M9: Transcriptional Inhibition Through microRNA-Mediated Chromatin Reorganization Following by Gene Silencing

Also here is a link to the Pubmed entry of the article:


What is a concussion? When I was a kid and someone got a concussion, I seem to remember people telling me that it was when your brain impacts the side of your skull, accelerating fast enough to do so despite the cerebrospinal fluid buffer.

But wikipedia doesn't mention this explicitly. Is this just one possible cause for concussions? Is it possible to generalize about them? How much don't we know?

Concussion generally refers to the set of clinical symptoms that are secondary to the head injury and are characteristic by altered state of consciousness like instant onset of transient neurologic dysfunction, lack of consciousness or temporary respiratory arrest and loss of reflexes.

Since it's connected to the head trauma by definition, there is in principium no other cause of it.

The patophysiologic mechanism of concussion is not well understood yet, it's thought it results from two main sources:

the acceleration of brain causes increase of pressure
the impact of brain on the hard shell causes deformation and sheer stress in brain tissue (probably stronger cause of cytologic changes discussed later on)

These two mechanisms might lead to changes in the tissue structure and also trigger cytologic changes in the astrocytes and neurons such as:

  Astrocytes respond to a focal mechanical stimulation by propagating intercellular waves through their network. Mechanically stimulated astrocyte networks show changes in the cytoskeleton, organelle function, and biochemical cascades over time.

The changes in neurons detected in vitro include microstructural changes, direct membrane permeability change and change in the receptor abundance, structure of subunits and

  Early evidence showed that these physical insults can affect the properties of important synaptic glutamate receptors that can regulate neurotransmission and plasticity in networks. Moreover, inhibitory synaptic receptor functions can be altered with a physical force, showing that the balance of excitation/inhibition coupling is important to consider when assessing the effects of these physical forces. Perhaps equally important is the alteration in the receptor composition and intracellular signaling that occurs after a microinjury.

Microinjury is also linked to triggering of cell death pathways in brain cells.

The importance of these mechanisms are not yet clearly understood though and there probably are many more playing their role.

Sources:

Overview study
Robbins and Cotran pathologic basis of disease

The CDC has a nice webpage about concussions and traumatic brain injury, as does the Mayo Clinic. The brain and head move rapidly back and forth due to impact or sudden acceleration or deceleration, in spite of the cerebral spinal fluid bathing the brain cavity. This causes chemical changes in the brain and/or damage to brain cells, affecting brain function.

Symptoms are not always instantaneous; sometimes it can take hours or days for symptoms to arise. There are multiple diagnostic tools that exist, including graded symptom checklists, the Standardized Assessment of Concussion, neuropsychological assessments, and the Balance Error Scoring System. These are summarized in this American Academy of Neurology (AAN) article from 2013.


Why do humans not have a powerful sense of smell? It seems like a useful ability to be able to detect many different things about, say, another organism. A lot of mammals have this ability. Why not humans? Did we evolve it out or never develop it?

Humans' poor sense of smell is a myth, borne of 19th century speculation rather than actual data. This is described in an excellent recent paper in Science , "Poor human olfaction is a 19th-century myth" by John P. McGann. Quoting from a recent blog post of mine,

  The myth dates to the work of the pioneering and hugely influential
  anatomist and anthropologist Paul Broca, who concluded that the
  relatively small olfactory bulbs in humans and other primates enabled
  the occupancy of this space by facilities of intelligence and even
  free will: “…it is no longer the sense of smell that guides the
  animal: it’s intelligence enlightened by all the senses… This is the
  cause of the atrophy of the olfactory apparatus of primates." This
  presumed “atrophy” and poor sense of smell however, were not based on
  any actual data on primates’ sense of smell! The myth propagated and
  expanded in the 20th century, becoming dogma. Back in the 19th, even
  Freud weighed in, noting that the lack of a strong sense of smell
  contributed, in humans compared to other animals, to sexual repression
  and mental disorders.

Humans, when trained, smell quite well, and can for example follow scent trails through grassy fields. Interestingly, the number of olfactory neurons is very similar in humans and other mammals (plotted in the aforementioned post).

This is a question relegated to evolutionary biology.  Our sense of smell is as it is because that is part of our evolution and it is what works best for us. Also consider that you used the word "powerful" The word is arbitrary when comparing the sense to other animals. The more sensitive sense of smell in dogs for example is tied to their survival


How does LCR compare to Assembly PCR The question pretty much explains itself. How do the two methods compare? I've always used Assembly PCR but the method is prone to mistakes and I'm curious how it compares to Ligase Chain Reaction (LCR).

I have used both Gibson assembly (what you mean by assembly?) and LCR as replacements for blunt or sticky ended cloning. LCR has, for me, worked better in that a higher proportion of constructs that come out have been assembled correctly and I have noticed no mutations after LCR while I have seen them somewhat often with Gibson.


Why don't we hear all the processes in our body and what prevents us from doing so? Why don't we hear all the processes in our body (like the rushing of our bloodcells through our arteries, the pumping of our heart, the electricity of neurotransmitters or our brain cells, etc.)

Is it only because the sound is too low for us to hear?

The issue here is with the definition of the word "hear". We do hear most of this, that is our ears actually pick up and transmit this sound. But we don't hear it in the sense that our brain ignores it and filters it out of what we are aware of. Only a very small fraction of all the sensory data that comes into the brain ever gets processed. The brain does something called sensory modulation it filters through all the sensory data and decides what is worth paying attention too.

This happens at several levels, not surprising since we see these same levels of filtering in animals, as soon as you evolve sensory organs the ability to filter sensory information is an advantage. Some happens directly at the sensory organ, many have a threshold before a signal is sent. In the brain the reticular formation is responsible for much of it. But each sensory processing area also does some of its own filtering. Basically each portion of the brain contributes in some way. Attention and how it is controlled is greatly studied as it is central to how consciousness functions. A complete rundown of all sensory processing is tricky since some senses (like smell) skip some parts of the process, and there are so many ways it can be filtered. you can find a more detailed breakdown here.

The sound is mostly drowned out by all the other sounds in your environment. The environment is just too noisy. However you can hear it if you are place in sensory deprivation chamber. You can hear stuff like your heart beat, the eyelids moving, joints creaking, muscles tensing and even the movement of blood in the arteries within your ear.

You cannot hear neurotransmitter diffusion because it is a movement of chemicals, which do not generate a pressure wave and is thus soundless.

But there are sounds that you hear. You can hear yourself breathing and chewing your food.


What purpose does the wax coating on blueberries serve? What purpose does the wax coating on blueberries serve? Is it some sort of protective layer?

A search on the web reveals that it is called "bloom". But the source is not a credible, scientific source. And it doesn't explain in detail what the coating does.

My uneducated guess is that the wax is called Epicuticular wax.

  The main functions of the epicuticular wax are to decrease surface
  wetting and moisture loss. Other functions include reflection of
  ultraviolet light, assisting in the formation of an ultrahydrophobic
  and self-cleaning surface and acting as an anti-climb surface.

Years ago my wife and I made  grape juice that turned to wine. This happened because the bloom on the grapes harbors yeast cells. The same situation occurs with other berries including blueberries.  Organisms living on the surface of other organisms are usually symbionts


Is it possible to become pregnant indirectly? Is it possible to become pregnant indirectly? For instance, if there is some wet semen left behind inside tight clothing, jeans for example, and a woman tries them on for a couple of minutes? What is sperm's motility after it's deposited on cloth in room temperature? Can sperm still swim inside from outside if it's near the vaginal opening in the cloth? What are the chances of pregnancy if the woman is/is not wearing any underwear?

yes this is possible, as long as the sperm make it onto the mucus membrane of the vagina. the LIKELYHOOD depends on the fabric and how much semen is in the fabric, if it's still clotted or not, and environmental factors.


I am trying to identify this plant I am trying to identify this medium arching shrub growing to about 1.5m high x 2m wide in the subtropical climate of the Mt Coot-tha Botanic Gardens in Brisbane, Australia. Unfortunately there was no label with it. The inflorescence is about 3cm across, a greenish yellow, and made up of many tentacle-like florets.  I don't think it is an Australian native plant.

It looks like combretaceae, or a species related to it.


Have humans evolved to live longer? Do people live longer only because of better hygiene, medicine, society etc or also because they're slowly evolving to live longer under same circumstances?

Yes and no.

According to this paper, great apes and our ancestors had a life expectancy at birth of about 13 years (chimpanzees). Over a few million years of evolution, human life expectancy rose to >30 years in the 18th century. Industrialization and improved nutrition, hygiene and medicine resulted in a jump to >60 and now around 80 years in developed countries in just 200 years. The paper compares data from Sweden, but if you look at the data from gapminder.org, you see that this trend holds true for all nations (especially developing countries like India and China, who doubled their life expectancy in just 50 years).

So, while humans have evolved to live longer (as you asked in the title), due to a lower mortality and resulting increase in the age of maturity as well as the likely benefit of "grandmothers" (older, infertile females helping to feed their grandchildren) (discussed in this source), the recent increase in life expectancy in just a few generations is unlikely due to evolution.

While humans are still evolving, we have reduced the selective pressure. There is no benefit to the survival of the offspring when we live past 80-100 years. And comparing countries with lower standards in hygiene and medicine (I totally recommend playing with the gapminder tools), their life expectancy was still pretty low in recent years, only increasing with access to clean water, food and medicine. Comments on extending the lifespan usually refer to medical interventions to cope with the effects of aging.

I would say that humans have not developed to live longer. There have been many harmful changes. One is that humans have lost the ability to produce their own Vitamin C.
Vitamin C

Hygeine has been a huge factor in humans living longer, especially drinking water being clean. For instance the American Public Health Association campaigned since the 1870's for antibiotics, clean water separate from potable water, immunisation and other health measures to be freely available. Their positive effects are discussed at causes of longer life


What is the difference between the evolution of fins in whales and fish? For a homework assignment I received the following question:

Which statement best explains the evolution of fins in whales and fish?

a. The common ancestor of whales and fish possessed genes for fins.

b. Whales and fish possess the same mutations in their genomes.

c. Fins evolved in whales and fish because they both use them to swim in water.

d. Fins evolved in whales and fish because of different mutations that occurred
in their genomes.

e. Fins evolved in whales and fish because their most recent common ancestor swam in water.

My answer is (c). Of the given options, it seems most accurate. I feel that the language is unclear as many organisms who do not have fins swim in water. That can be a logic against the option. But, the given answer is (d). That seems too bizarre as even humans and fishes have different mutations in their genomes. (c) seems more appropriate as it can exemplify convergent evolution.

I agree with you that the question is ambiguous, and also that the most sensible answer would be C.  However, one could make a more or less reasonable argument in favor of several other answers, too.

  a. The common ancestor of whales and fish possessed genes for fins.

Technically, this statement is true.  At least some of the fins of whales and fish are even distantly homologous, even though the lineages leading to tetrapods (including whales) and to ray-finned fishes diverged quite early in their evolutionary history.

(Specifically, the flippers of whales are modified tetrapod forelimbs, which are homologous to the pectoral fins of ray-finned fishes.  Whether one should also consider the tails fins of whales and fish to be homologous is a bit more debatable: the actual fin structures are very different, and presumably share few if any developmental pathways, but the tail and the spinal column which they attach to and are powered by is clearly a shared feature of both groups.)

However, while shared evolutionary history may explain why fish and whales have similarly placed flippers / pectoral fins, and why they both have a flexible spine that supports undulatory swimming with the help of a tail fin, it does not explain the convergent evolution of whales' forelimbs (which were formerly adapted for walking on land) into fin-like flippers.  So in that sense, while perhaps partially correct, this answer is also quite incomplete.

  b. Whales and fish possess the same mutations in their genomes.

It's hard to even tell what this statement means.  Insofar as it's a restatement of the fact that whales and fish share some of their evolutionary history (up to the divergence of the bone-finned and ray-finned fishes), it's no more or less correct than statement A above.

However, I suspect that the intended meaning of this statement is that whales and (ray-finned) fish would've separately evolved the same "fin-making" mutations after their lineages diverges, which is both clearly incorrect and also, even prima facie, statistically very unlikely.  So I would rule this one out.

  c. Fins evolved in whales and fish because they both use them to swim in water.

This statement is written using teleological language, which some may consider misleading, as it could be misinterpreted as implying that evolution was a directed process: it could be interpreted as saying that whales needed to be able to swim, so they chose to evolve fins (or that some guiding consciousness granted them fins).  This is, of course, incorrect — or, at least, we have no scientific evidence of there being any such conscious force guiding evolution, or of any organism (with the arguable exception of humans) being able to deliberately direct their own evolution.

However, it's quite possible to interpret this statement in a way that makes it perfectly correct: as both whales and fish move around by swimming, possessing fins (or something similar to fins) is an advantageous trait for them, and has thus been favored by natural selection.  If pressed, I would thus choose this one as the most correct answer out of the given options.

In particular, note that the argument made by AliceD that "they have to develop fins first before they can use them" is not really true: the ancestors of both whales and fish were swimming long before they evolved fins, and thus the selection pressure in favor of having fins (or fin-like structures) was already present before the fins themselves evolved.

In particular, the first aquatic ancestors of whales are believed to have swum much like modern-day otters and seals, using their flipper-like limbs as makeshift fins.  While there's no discrete transition point where one could definitely say that whale limbs turned into proper fins, it is clear that the fins, and their direct evolutionary predecessors, were being actively used for swimming, and that this fact directly drove their evolution into the actual fins that modern whales have.

  d. Fins evolved in whales and fish because of different mutations that occurred in their genomes.

While technically correct, this statement is so vague that it's all but meaningless.  All evolution is driven by mutations, and those mutations, being basically random, are rarely if ever the same in any two lineages.

Certainly, it would be silly to claim that "different mutations occurring in their genomes" is an explanation of why whales and fish evolved fins: humans also constantly have different mutations occurring in our genomes, but we clearly don't seem to be evolving fins.  Neither are pigs or bumblebees or sunflowers, even though all of those species (and, of course, all others too) are also constantly experiencing different mutations in their genomes.

Really, this answer reminds me of the story about a person in a car who gets lost and stops to ask a passerby where they are; the passerby, after a moment's thought, replies "you're in your car."  While technically correct, that answer is absolutely useless — and so is this one, too.

  e. Fins evolved in whales and fish because their most recent common ancestor swam in water.

Again, this answer could be interpreted as basically a restatement of answer A, and thus as being partially correct.  However, it completely ignores the convergent selection pressure described in answer C, which is responsible for the more recent evolution of whale flippers into something resembling fish fins more than, say, human hands or the feet of hippopotamuses (currently believed to be the closest living relatives of whales and other cetaceans).  Thus, I would not pick this answer, for the same reason that I wouldn't pick answer A.

This was a question on the 2016 Toronto Biology Exam, precisely question 42.

Though the question was asked vaguely, d is the best answer. It's quite obvious that if animals are in water, fins will eventually evolve to improve fitness, that's pretty obvious.

However, if they are both in water, why are their fins different? This touches on the more complex concept of analogous structures; structures that perform similar functions but are anatomically different.

Well, why are they anatomically different? Different mutations in their genomes resulted in those differences.

Therefore, d is the better answer. It does ask which "best" explains.


Are there any theories using thermodynamics/statistical mechanics or information theory principles to modelling in ecology? So far, I've only known one: the MaxEnt theory. It uses the maximum information entropy developed by information theorist, which in turn inspired by the thermodynamics from physics, to predict the number of organism in an area. This theory is developed by John Harte.
You can read about this theory in Quanta Magazine.

I also know the book Towards the Thermodynamics Theory for Ecological Systems, written by Jørgensen and Svirezhev.

I find it hard to find another theory similar with the two theories above. Do you know any theories using the thermodynamics or information principles to modelling in ecology?

I have opened a reddit discussion about this.

John Harte's work on applying the mathematical theory of maximum entropy to ecology is certainly one of the better known examples of the application of this area of mathematics to science, in part because he literally wrote the textbook: Maximum Entropy and Ecology: A Theory of Abundance, Distribution, and Energetics (Oxford Series in Ecology and Evolution)

To be clear, maximum entropy (also known as MaxEnt in some of the literature, though most/all researchers use the longer form in publications) is a mathematical tool stemming from the fields of probability theory, statistics, and information theory.  Its use is classically most often seen in thermodynamics, statistical thermodynamics, physics, and information theory, primarily because these were the areas in which E.T. Jaynes was working when he posited the idea. Wikipedia has links to his two seminal papers.But because of it's mathematical form, it can be applied in a multitude of areas, typically where one can utilize probabilistic methods.

If you're looking for additional areas of application, simply google the phrase "applied maximum entropy" and you'll find a wealth of areas including: econometrics, natural language processing, nuclear medicine, queuing systems, mass spectrometry, image processing, machine learning, and many others.

For ecology related work, a cross search on maximum entropy and "genetics", "evolution", "species", and similar words will provide a wealth of papers like "A maximum entropy approach to species distribution modeling".

Given the generic nature of your question, I might suggest that you'll find E.T. Jaynes' paper "On the Rationale of Maximum-Entropy Methods" (IEEE, 1982) useful.

Those generally interested in the broader applications of information theoretic methods to biology will likely appreciate some of the work that came out of last year's NIMBioS Workshop on Information and Entropy in Biological Systems (which Harte both attended and presented at), the BIRS Workshop Biological and Bio-Inspired Information Theory, and the 2014 CECAM Entropy in Biomolecular Systems. The NIMBios Workshop was organized by John Baez, a physicist, who has worked with MaxEnt methods and explored them on his blog "Azimuth".

Those with a more sophisticated mathematical background (including measure theory, functional analysis, etc.) may appreciate Henryk Gzyl's text The Method of Maximum Entropy (World Scientific: Series on Advances in Mathematics for Applied Sciences, Vol 29, 1995).

-- Additional thoughts after the question was edited --

First for those who don't have the background, I highly recommend reading the two seminal papers on information theory and statistical mechanics by ET Jaynes and the standard text on information theory Elements of Information Theory by Thomas M. Cover and Joy A. Thomas.

In addition to the information theoretic related areas, you might want to take a look at the discipline of complexity theory, which has primarily grown out of the Santa Fe Institute over the past several decades and which includes information theory as part of its disciplines. If you're unfamiliar with the broader topic, Melanie Mitchell has an excellent overview with her book Complexity: A Guided Tour. Also related to complexity is the area of cellular automata which one could view as a very base model of more complex ecological systems. Here, perhaps Stephen Wolfram's A New Kind of Science or Cellular Automata and Complexity will be enlightening. The broader theories coming out of these primarily mathematical areas may be useful to you.

In particular, given the types of models in ecosystems, I might suggest taking a look at some of the mathematical modeling going on at the intersection of complexity and economics. For a relatively simple introduction to this area, one could look at the relatively introductory text Complexity and the Economy by W. Brian Arthur which is very interesting. The economy is essentially a very specific type of ecology dealing with human beings, assets, and the monetary system.

Another area which I've seen a lot of literature over the last few years is applicable to the ideas of resiliency and complexity in cities, for assisting in designing more robust city planning. This really isn't that far from the naturally evolving systems being looked at in ecology settings.

For those looking for researchers in the area of complexity, I have a list of many who are on twitter in a variety of sub-areas. In addition to individuals, it also includes a number of institutes and related organizations as well.

I'd also suggest, that for the broadest theoretical setting, one could actually start with the topic known as "Big History" which takes the broadest approach of looking at history and the evolution of the cosmos over 13.7 billion years since the big bang. This conceptualization includes ideas like evolution, complexity, and emergence on the biggest scales, a set of theories that could be similarly applied to ecologies both large and small. For this viewpoint, I would suggest two works by David Christian including Maps of Time: An Introduction to Big History and Big History: The Big Bang, Life on Earth, and the Rise of Humanity.

In essence, with many of these topics and viewpoints, one is treating individual animals or even entire species as elementary particles and then using the mathematical models of statistical thermodynamics to tease out specific types of data or trends. As layers of overlapping "particles" interact with each other, they cause emergent types properties, and then these resultant emergent properties combine to create further layers of emergent properties, none of which might have been necessarily deduced from the initial conditions. Within Big History, these types of emergence go from the big bang and basic particles in the early universe to the ultimate evolution of humankind by way of a variety of stages.

An alternative way to understand this issue has been ultimately named (in its more recent publications) as Organic Biophysics of Ecosystems. Some of their publications (several of them are available either on ResearchGate or on https://interdisciplinaryscience.es/publications) are (If you are interested, I would advise reading the articles in the exact reverse order of time to that shown below).
This approach uses equations whose mathematical structure is simpler than other models in this field, and which are equivalent in structure to those equations used by conventional physics.
Rodríguez, R.A., Riera, R., Herrera, A.M., Duncan, J.M., Vanni, M.J., Delgado, J.D., González, M.J. 2019. Degrees of freedom: Definitions and their minimum and most meaningful combination for the modelling of ecosystem dynamics with the help of physical principles. Ecological Modelling 392: 226−235.
Rodríguez, R.A., Duncan. J.M., Delgado, J.D., Vanni, M.J., Riera, R., González, M.J. 2018. Additional empirical evidence on the intrinsic trend to stationarity in the long run and the nested relationship between abiotic, biotic and anthropogenic factors starting from the organic biophysics of ecosystems (OBEC). Ecological Modelling 383: 23-30.
Riera, R., Rodríguez, R.A. Herrera, A.M., Delgado, J.D., Fath, B.D. 2018. Endorheic currents in ecology: an example of the effects from scientific specialization and interdisciplinary isolation. Interdisciplinary Science Reviews 43(2): 175-191.
Rodríguez, R.A., Riera, R., Delgado, J.D. 2017d. Ecology: Science or philately? An interdisciplinary analysis of sustainability by exploring if it is possible to get more and more information by reducing collateral environmental damages. Science of the Total Environment 596/597: 43−52.
Rodríguez, R.A., Duncan, J.M., Vanni , M.J., Melkikh , A.V., Delgado, J.D., Riera, R., Herrera, A.M., Camarena Luhrs , T., Quirós , A., Fernández Palacios, J.M., Miranda, J.V., Perdomo , M.E., Fernández Rodríguez, M.J., Jiménez Rodríguez , A., Otto, R., Escudero, C.G., Navarro Cerrillo , R.M., González , M.J. 2017c. Exploring the analytical consequences of ecological subjects unwittingly neglected by the mainstream of evolutionary thought. Ecological Modelling 355: 70-83.
Rodríguez, R.A., Duncan, J.M., Delgado, J.D., Vanni, M.J., Riera, R., Herrera, A.M., González, M.J. 2017b Assessment of ecosystem trophodynamic power: A model based on the power equation for an oscillating string. Ecological Modelling 362: 80-86.
Rodríguez, R.A., Duncan, J.M., Riera, R., Delgado, J.D., Quirós, A., Vanni, M.J., Camarena, T., Miranda, J.V., Perdomo, M.A., Herrera, A.M., González, M.J. 2017a. Thermostatistical distribution of a trophic energy proxy: Extension for modelling energy pyramids at the inter taxocene scale and under non stationary conditions. Ecological Modelling 361: 113−121.
Rodríguez, R.A., Herrera, A.M., Duncan, J.M., Riera, R., Quirós, A., Perdomo, M.E., Jiménez-Rodríguez, A., Fernández-Palacios, J.M., Vanni, M.J., Otto, R., Escudero, C.G., Camarena, T., Navarro-Cerrillo, R.M., Delgado, J.D., González, M.J. 2016c. Response to comments on “Uncertainty principle in niche assessment: A solution to the dilemma redundancy vs. competitive exclusion, and some analytical consequences”. Ecological Modelling 341: 1‒4.
Rodríguez, R.A., Herrera, A.M., Quirós, A., Fernández-Rodríguez, M.J., Delgado, J.D., Jiménez-Rodríguez, A., Fernández-Palacios, J.M., Otto, R., Escudero, C.G., Camarena Luhrs, T., Miranda, J.V., Navarro-Cerrillo, R.M., Perdomo, M.E., Riera, R. 2016b. Exploring the spontaneous contribution of Claude E. Shannon to eco-evolutionary theory. Ecological Modelling 327: 57–64.
Rodríguez, R.A., Herrera, A.M., Santander, J., Miranda, J.V., Perdomo, M.E., Quirós, A., Riera, R., Fath, B.D. 2016a. From a stationary to a non-stationary ecological state equation: adding a tool for ecological monitoring. Ecological Modelling 320: 44–51.
Rodríguez, R.A., Herrera, A.M., Riera, R., Escudero C.G., Delgado, J.D. 2015b. Empirical clues about the fulfillment of quantum principles in ecology: potential meaning and theoretical challenges. Ecological Modelling 301: 90–97.
Rodríguez, R.A., Herrera, A.M., Riera, R., Delgado, J.D., Quirós, A., Perdomo, M.E. Santander, J., Miranda, J.V., Fernández-Rodríguez, M.J., Jiménez-Rodríguez, A., Fernández-Palacios, J.M., Otto, R., Escudero, C.G., Navarro-Cerrillo, R.M. 2015a. Thermostatistical distribution of a trophic energy proxy with analytical consequences for evolutionary ecology, species coexistence and the maximum entropy formalism. Ecological Modelling 296: 24–35.
Rodríguez, R.A., Delgado, J.D., Herrera, A.M., Riera, R., Navarro, R.M., Melián, C., Dieguez, L., Quirós, A. 2013b. Effects of two traits of the ecological state equation on our current understanding of species coexistence and ecosystem services. Ecological Modelling 265: 1–13.
Rodríguez, R.A., Herrera, A.M., Delgado, J.D., Otto, R., Quirós, A., Santander, J., Miranda, J.V., Fernández, M., Jiménez-Rodríguez, A., Riera, R., Navarro, R.M., Perdomo, M.E., Fernández-Palacios, J.M., Escudero, C.G., Arévalo, J.R., Diéguez, L. 2013a. Biomass-dispersal trade-off and the functional meaning of species diversity. Ecological Modelling 261/262: 8–18.
Rodríguez, R.A., Herrera, A.M., Otto, R., Delgado, J.D., Fernández-Palacios, J.M., Arévalo, J.R. 2012. Ecological state equation. Ecological Modelling 224: 18–24.


Neutralizing TCA washes Trichloroacetic Acid (TCA) is commonly used for protein precipitation but the wash waste needs to be neutralized prior to disposal. What exactly is required to effectively neutralize TCA waste? Do I just add caustic?

A neutralization reaction occurs between Brönsted acids and bases to form a salt.

In this case, you have to add a Brönsted base to neutralize your acid. If the final pH is important, you should work out the exact quantity of base to add. Otherwise, just use litmus paper to check the pH of your solution, and add base until it's neutral.

EDIT

In view of the other answer proposed, I want to stress the following:

Do NOT dispose of your solution in the sink/sewer. Leave it in its plastic bin until a lab technician takes it to the furnace.

If the base you use is sodium bicarbonate (NaHCO3), there will be bubbling, caused by the decomposition of carbonic acid (H2CO3) into water (H2O) and carbon dioxide (CO2). You've successfully neutralized the TCA once there's no bubbling upon addition of NaHCO3.

It is indeed best to proceed slowly while adding your base.

I've been fortunate to find a protocol hidden away in my lab archives.

The acid waste can be accumulated for 10 days before it needs to be neutralized. The waste should be kept in a carboy in a fume hood.
50 mL 50% w/v Sodium Bicarbonate slurry should be added per liter of TCA waste. During neutralization fumes will be generated which may include chlorine gas.
When the pH reaches 6-8, dispose the waste into the sewer.