Ions in Stomatal Opening Mechanism When a stoma’s guard cells try to swell and open the stomata, they actively pump out protons outside of the cell. This causes a membrane potential, where the inside of the cell is negative with respect to the outside. This then causes potassium ions, which are positive, to rush into the cell, mitigating that potential. However, my texts say that anions such as chloride and malate ions follow potassium into the cell as well; their rationale is that positive ions must be balanced by the presence of negative ions. I do not understand why this is the case. If you extruded positive ions (protons) out of the cell and allowed positive ions (potassium) back in, there would be no ionic imbalance to draw the anions from where they’re idling. Could someone clear this up for me?

The ion concentrations are different inside and outside of the cell, allowing a potential.  The cell becomes even more polarized by the pumping out of H+ ions, making the cell even more negative (potential difference). Then this negative potential happens to cause voltage-gated channels to open and the uptake of potassium occurs. This will depolarize the cell (return it to the base potential difference).  It is usually very important for the cell to maintain the negative potential after it recovers. To combat the uptake of potassium, negative charges can be used to balance the increased positive ion influx so the resting potential is stabilized.

These mechanisms are usually mediated by special proteins that are regulated by actual electrical changes in the membrane.


How does sex differentiation work in Paracerceis sculpta, the sexually tetramorphic isopod? Paracerceis sculpta is a marine isopod species known for its unusual reproductive strategy:

female: medium-sized; lives in harems run by an α male
α male: large; keeps a harem of females
β male: medium; mimics a female in order to enter a harem and mate
γ male: small; mimics a juvenile in order to slip into a harem and mate

.

How does this 4-way sex differentiation occur? That is, what determines which of the morphs an individual develops into?

Shuster, SM & C Sassaman (1997)
  Genetic interaction between male mating strategy and sex ratio in a marine isopod. Nature 388: 373-377

As described in this paper, the chromosomal system of sex determination in Paracerceis sculpta is ZW=females, ZZ=males. Genetic evidence indicates that the morph of a ZZ male is determined by a second locus, Ams (alternative mating strategy) which exists in three allelic forms whose dominance relationship is Amsβ > Amsγ > Amsα. So for example, to be an α type male, an individual must be ZZ Amsα / Amsα.

That's the end of the answer, what follows is supplementary information.

The paper also describes an additional layer of complexity in the sex-determining system of P. sculpta involving sex changes in both directions. This is explained by a model in terms of two other factors: an autosomal locus Tfr (transformer) and a cytoplasmic factor ECF (extra-chromosomal factor) which interact as shown in the Table below (taken from the paper). However, this doesn't really add anything to the Ams story as far as male morphs are concerned, except that some of them start as females.


Are all genes transcribed in differentiated cells? My textbook tells me that it’s specific transcription factors that allow for a different set of genes to be expressed in different cells (differential gene expression). My book gives the example of liver and lens cells—liver cells contain the specific transcription factors (STFs) to activate the enhancer for the albumin gene, while lens cells contain the STFs to activate the enhancer for the crystallin gene. Liver cells do not have the STFs to activate the crystallin gene, and lens cells cannot activate the album gene.

However, my book also tells me that there is a basal level of transcription that arises from the binding of general transcription factors. Enhancers only increase the rate of transcription on top of that basal rate. Does this mean that in differentiated cells, all genes are indeed transcribed? I.e. a lens cell does transcribe the gene for albumin and the liver cell does transcribe the gene for crystallin?

(The wording of my book dissuades me: "Liver cell: The albumin gene is expressed, and the crystallin gene is not. Lens cell: The crystallin gene is expressed, and the albumin gene is not.”)

No
Not all genes are transcribed, repressor proteins and nuclear receptors can bind the DNA preventing transcription of particular genes. Even things like histone regulation can prevent transcription. There may even be epigenetic regulation of transcription.

Source 1

Source 2


Where are interneurons in Autonomic Nervous System? According to  the following, it implies that preganglionic neurons are interneurons.

  Interneuron called preganglionic neuron whose cell body is situated in the "intermediolateral" column of spinal cord( also called 'lateral column').1

From this:

  The interneuron (connector neuron) of somatic system has cell body in the dorsal horn and terminates in the ventral horn, while that of ANS has cell body in the intermediolateral horn and terminates in the autonomic ganglia....In the ANS, there are two efferent neuron chains between CNS and the effector organ: first efferent neuron (pre-ganglionic neuron) has its cell body in CNS while the second efferent neuron (post-ganglionic neuron) has its cell body out-side the CNS in the ganglion.

But this source implies quite opposite:

  The spinal sympathetic interneurons that most directly influence the activity of sympathetic preganglionic neurons after spinal cord injury....

So which one is correct?

It sort of depends on your definition of interneuron. Many school-level textbooks suggest that any neuron that has neurons both pre and post synaptically are interneurons. Therefore both the preganglionic neuron and the spinal sympathetic interneurons could be considered interneurons. This means that all neurons in the brain are interneurons and vastly oversimplifies the CNS.

I would argue that it's probably more helpful to think of the preganglionic neurons as "projecting" neurons, as they come down the spinal cord. The post-ganglionic neuron is more like a motor neuron.

Edit: I answered a similar question in more detail here: Is the bipolar neuron of the retina considered a sensory neuron?


What is the impact of stress on the human body? Can stress trigger any changes in the human body? I'd like to know more about things less commonly known than, for example: sweating and tiredness. What are the long term risks of chronic stress? Do stressful people have higher chance of having heart-diseases or affected by hair-loss, for example?
I'm also interested in how can an emotion induce physiological changes in our body?

Stress is the reaction, which our body reacts against the pressure or tension. There are many impact of stress on the human body, which includes

Emotional:  Moodiness, short temper, agitation, inability to relax, feeling lonely and always depressed.
Cognitive:  Memory problems, unable to concentrate, very poor judgment, negative thoughts, always anxious and worrying
Physical: Frequently suffering from pains and aches
Behavior: Addiction toward drugs, alcohol or cigarettes for relief, nervous, being alone, insomnia.
Other problems like headache, muscle pain, chest pain, fatigue, etc.


A question about dna triplex Short DNA triplex strands have been identified in various organsims. But, would injecting a single strand of DNA or RNA (with its bases complementary to the bases of DNA found in the major groove of a certain gene ) cause it to form a DNA triplex   at that gene?

Possibly, yes, but there are complications.

There are other conditions that help create the energetically-favorable conditions for bases to bind in a way to form a triplex, including acidity and presence of magnesium ions.

The region of DNA where your gene of interest lies (or its regulatory regions, depending on what you're trying to do) would need to be unpacked, as well. DNA is usually packaged into chromatin. Histone complexes, which wrap up DNA, provide some measure of protection of the major groove. To make a triplex, you'd need biochemical conditions that unwrap histones and support triplex formation, generally.

Use of RNA, specifically, could be complicated if it is or could be processed into a short- or microRNA element, which could be consumed in downregulating the population of mRNA molecules (which, in turn, ultimately regulates gene expression). It isn't helpful if it gets used up before it binds to your triplex of interest.

There is some pharmaceutical interest in TFOs (triplex-forming oligonucleotides) as a drug-delivery mechanism.

If some gene is broken and implicated in a genetic disease, say, and its DNA or nearby regulatory regions can be made accessible, perhaps a TFO can be administered that would help turn up or down the expression of that gene's protein product.

Papers on TFOs could probably point you to other engineering problems that researchers have encountered and would need to overcome in order to create an effective medicine.


Lizards are sometimes called cold-blooded because they depend on their surrounding temperatures to keep them warm. Predict how the composition of the cell membrane of a lizard might change from winter to summer. Justify predictions.

Can someone please help me figure this out. Does it have to do with fluidity?

Just going to follow up on your thought here.

The fluidity of the cell membrane does vary with composition.  Off the top of my head there are four main components of the animal cell membrane:

1) proteins.  membrane proteins are responsible for the import and export of nutrients, waste, information etc from the cell, so lets assume that this needs to be fairly constant part of the composition while the seasons change.

2) cholesterol and similar compounds.  These are flat an inflexible compounds which will tend to lower the fluidity of the membrane.

3) unsaturated fatty acids and lipids.  These are long carbon chained compounds with some double bonds in them.  Because the double bonds cause the chains to be less mobile, but they don't pack well as they are not as flexible, so tend to make the membrane a bit more fluid.  Think about how butter (mostly saturated fats) is solid at room temperature while olive oil (monounsaturated oil) is liquid.

4) saturated fatty acids and lipids.  These are completely mobile carbon chains.  Without any double bonds, these tend to be the more flexible and can create a more tightly packed membrane, resulting in a stiffer membraine.

You can imagine for the cell to maintain the same flexibility at the lower winter temperatures (4) and (2) would tend to decrease and (3) might tend to decrease.

Does this make sense?


Recycling and storage of nitrogen from breakdown of macromolecules? If nitrogen is so important (it's a constituent of both proteins and nucleic acids), why are animals still throwing them out, and needing to eat it again? Is it true that in almost a billion years of evolution, life still haven't found a way to recycle nitrogen inside the cells or inside the body of multi-cellular organisms? Why does this seem so hard to achieve? Or are there animals that don't need to excrete nitrogen compounds (like ammonia, urea and uric acid), and instead reuse them?

Short answer: This is because the most common form of nitrogen found in multicellular organisms (not incorporated into any other compound) i.e. ammonia is too toxic to be stored or recycled.

Background: Ammonia, the product of deamination of amino acids, is basic in nature ($NH_3~+~H_2O \rightarrow NH_4OH \rightleftharpoons NH_4^+ + OH^-$) and thus disturbs intracellular pH (Ohmori et al, 1986). Though the mechanisms through which ammonia exerts its toxic effects are not known, hyperammonemia is known to alter several amino acid pathways and neurotransmitter systems, cerebral energy metabolism, nitric oxide synthesis, oxidative stress and signal transduction pathways, leading to irreversible damage to the developing central nervous system: cortical atrophy, ventricular enlargement and demyelination; causing cognitive impairment, seizures and cerebral palsy (Braissant et al, 2013).

Talking about how it is produced (just for information, skip this part if you are aware of urea cycle): Amino acids are deaminated for storage since the carbon skeleton of these amino acids can be easily converted to glucose or fatty acids for storage. This reaction yields ammonia which, in liver, is converted to urea (via urea cycle) which is not only less toxic, but also requires lesser water for excretion. See this page for more information and the diagram below.

Talking about why it is not recycled, there has always been a constant supply of amino acids to organisms (through nitrogen fixation or food). Indeed, amino acids are deaminated for storage i.e. we already have more than enough of it. Also, storing urea is also not easy since it is toxic too (it is just less toxic than ammonia). And since these products are so much harmful, it seems difficult for an organism to evolve itself so that it can store toxins rather than just throwing it away so that it can later be ingested in a useful form (amino acids from plants or herbivores). Finally, evolution works as decent with modification, meaning if something is a better alternative of current situation, it is not necessary that organisms will evolve towards that (unless there is strong selection pressure for it). In short, evolving to recycle nitrogen is (most likely) just not worth it.

P.S. you might be interested in this question to know more about evolution. Another answer here talks about storing excess nitrogen by adding ammonia into amino acids, yielding glutamate and glutamine. However, this process can be used only to a limited extent due to limited amount of substrate ($\alpha$-keto glutaric acid and glutamate) in the body. Also, excess glutamine in the body can have many major and minor side effects like skin rash, vomiting, etc. (see here for full list). Also, excess glutamate has much more pronounced effects. Since glutamate is a neurotransmitter, its excess causes cellular damage. This is what makes it an excitotoxin (see this for more details). Apart from this, the substrate ($\alpha$-keto glutaric acid) is an intermediate of Krebs cycle and is important in many other cellular activities (see here for details). So, its deficiency (caused due to conversion into glutamate) can easily affect many crucial metabolic activities. Thus, though this process seems an effective way of recycling nitrogen, it has many side-effects and is not much reliable i.e. can only be seen as an immediate solution. This is why when glutamate and glutamine build up in body, they are converted back to $\alpha$-keto glutaric acid and glutamate and the ammonia released via urea cycle.


How does geography affect morphological features of the human body I've seen many times how a person born in one place, goes to another country for a long time, and then they start looking more like the people there, but I never found out how it works.
This report claims that second generation Japanese, born in the US are taller and heavier than those living in their native lands (there had been no intermingling of races).

To what extent do the genetic/environmental factors control human morphology ?
What factors apart from the diet can bring about such morphological differences ?

Geography does not typically affect the morphology of the human body.
In certain special cases, there are physiological adaptations, the most obvious being tanning and acclimatization to high altitude, but these aren't changes in body morphology.
So why the difference in children of immigrants?  This is because diet, nutrition, and disease have quite strong effects on children's growth. Kids growing up in a healthier environment with more food get bigger, and those are linked to the wealth of the community where you live.


What is peptide mapping? After searching online for peptide mapping to my understanding it can be treated as the fingerprint of the protein. It is obtained at the end of several chemical processes and it helps to understand the protein being analyzed.

Does this method operate in "sequence space" then? If so, what exactly is the relation of the two?

Shimadzu explains peptide mapping as follows:

  Peptide mapping involves selectively cleaving the individual target [proteins] using an appropriate enzyme or chemical and analyzing the peptide fragments obtained using HPLC [high-performance liquid chromatography] or another suitable method. [... I]dentification of the peptide fragments separated by LC [...] [can be done] using amino acid composition analysis, N-terminal amino acid sequence analysis, or mass spectrometry.

As such, it does not provide a sequence of amino acids. Instead, you get a specific set of peptides of different sizes, dependent on the method used, that in turn can be used for protein fingerprinting.


What information does the nociceptor relay to the brain about stimuli below threshold? A. The duration of the stimulation

B. The location of the stimulation

C. The membrane potential at the site of stimulation

D. None of the above

I think the answer is B, because when the nociceptor is stimulated it relays information to the brain regarding location. Is this also true about stimuli below threshold?

Short answer
D.

Background
Nociceptors are free nerve endings, and usually consist of bundles of unmyelinated fibers (Messlinger, 1997).

So nociceptors are basically axonal fibers. Below threshold, activation of these fibers do not cause action potentials to occur. Since action potentials are, basically, all-or-nothing events no signals will be sent to the brain. Hence, the brain will not receive information on either duration (A), or location (B) of the pain stimulus. The membrane potential (C) is a non-sense answer. Membrane potential, although it may affect receptor response properties, is never the primary message of a receptor signal. It is about the sensation of physical stimuli (in this case painful mechanical, heat or chemical stimuli).

So the answer is -D- as we have disputed A, B and C.

Note
When receptors convey graded potentials, the term 'below-threshold' doesn't really apply anymore. Graded potentials can, in principle, convey the smallest stimulus difference as they operate on an analogue scale. Therefore, this question targets your understanding of the binary nature of action potentials and their threshold, and what that means for the detection of below-threshold stimuli.

Reference
- Messlinger, Anaesthesist (1997); 46(2): 142-53


If an ethnic group holds nearly 100% of a particular haplogroup, does it means that people who have this haplogroup are their descendants? Let me give you a hypothetical example. If the Egyptians were 100% E3b1, and the Levantines 50%, and the Anatolians 25%. Does this indicate that the Levantines and Anatolians are descended from Egyptians?

But what if instead of Egyptians, it was a distant people like Vietnamites who were 100% E3b1?

Short answer:
No.

If populations A and B share a haplogroup it does not imply that population A is B's ancestor, or population B is A's ancestor. No present-day population is the descendant of any present-day population, though both populations may share common ancestors. The common haplogroup is probably inherited from common ancestors.

Long answer:
No.

When you say "Egyptians" or "Vietnamese", in genomic studies you generally mean present-day people. People living in present-day Egypt or Vietnam may be related to each other, but they cannot as groups be each others' descendants. It is more likely that there is some ancestral population that is the common ancestor of both groups that carried the genetic variant. The only exception I can imagine is a VERY recent colonization (assuming there were no indigenous people in the colonized country, which is effectively never the case).

To take this specific example, it would be most likely that at some point in ancient human history the expanding human population (from e.g. out of Africa) had people carrying a haplogroup that settled Egypt, Anatolia, and Vietnam in independent events.

Therefore none of those groups would be descended from one another. Each population was founded by the people who stayed in that region, not the related people who left and colonized other regions.

Sampling of ancient DNA makes the question more interesting, if you for example found 20,000 year old bones sharing the haplogroup. Maybe that is a descendant of one or both populations. But again the relationship of that ancient individual to present-day geopolitical borders would still be fairly meaningless without a lot of supporting data.

It is additionally possible that the haplogroup arose independently in two different populations. This is sometimes called parallel evolution or convergent evolution. In this case there is actually no relationship at all between the populations. While this is much less likely than common descent, it is nonetheless a hypothesis that you need to reject before you claim that one group are the descendants of another group.

I hope that this helps!


What is the difference between "dikaryotic" and "heterokaryotic" states in the sexual lifecyles of fungi? Many fungi undergo a reproductive phase in which more than one genetically distinct nuclei (from 2 separate mating types) is present within the same cytoplasm. In the Ascomycota and Basidiomycota, this phase is termed "dikaryotic", whereas in other fungal phyla the phase is "heterokaryotic." What is the difference here? Is it purely number of nuclei per cell, or does the difference depend on how many genetically distinct nuclei are present (2 or >2)?

A heterokaryon is a fungal cell which has two or more genetically-distinct but allelically-compatible nuclei, as suggested by this resource, as well as this Wikipedia article.

A dikaryon is a fungal cell which has precisely two genetically-distinct but allelically-compatible nuclei, as shown here and here.

In this sense,  a heterokaryon is a general term, whereas a dikaryon is a specific term. A dikaryon and a trikaryon (although not often seen in literature) are both heterokaryons.


Following DNA replication during S-phase of the cell-cycle, are all genomic regions subjected to the same stringent level of DNA-Repair? To my (limited) understanding, there are 2 main ways that mutations can occur in DNA: Environmental (UV, etc) and mistakes during cell division.

I was wondering if there is a mechanism that can give priority to certain genes to be accurately duplicated. Some sort of trigger that says "double-check this specific gene before continuing with the duplication".

And if there is such a mechanism, then I wonder if there is some sort of dependency system for genes that control groups of other genes. So that if a certain gene "activates" the double-check trigger, it would automatically add that trigger to the group of genes which are affected by it.

Thanks.

So far, the known mechanism of DNA repair is to recognize mismatches or damaged nucleotides by enzymes surrounding DNA rather than by scanning along DNA. Therefore double check could not happen under such conditions.


Is this ladybird larva secreting a protective fluid? I know that adult ladybird beetles can secrete a fluid to keep predators from eating them. Can the larvae do that too? Or are these yellow droplets something else?

In larvae stage Ladybird beetles secretes yellow gooey alkaloids from its abdomen.

Ladybird beetles oozes hemolymph(in other word its blood), which is toxic and very smelly, when threatened. It's a mixture of various alkaloids and repulse the predators.

Good Job, There might be no picture more clearer than you provided

source:

[1]: Ladybird defence alkaloids: Structural, chemotaxonomic and biosynthetic aspects (Col.: Coccinellidae), Désiré Daloze, Jean-Claude Braekman, Jacques M. Pasteels

[2]: 10 Fascinating Facts About Ladybugs


How to prove that pork meat has parasites I suspect that the pork sold at a certain shop is infected with the parasite pork tapeworm (Taenia solium).

Is there a way I can prove this without special equipment? Would it work to leave the raw meat in the fridge (at 4 degrees Celcius, or higher?) for a week or so and the worms will come out of their eggs and grow big enough for the eye?

Short answer
T. solium infection can be identified in pork meat by visual inspection.

Background
The stage of the life cycle of the tape worm T. solium in pigs is characterized by cysticerci, which is the larval stage consisting of a protoscolex (head) of the tapeworm. Humans are the definitive host, which means they are the species in which the parasite completes its life cycle, reaches adulthood and is able to produce eggs.

The larvae are observable in pork meat, and cysticercosis is generally identified during slaughter when cysts can be seen in muscle or organs (Fig. 1).

Fig. 1. T. solium cysticerci. (A): as seen in infected pork. (B): excised into a Petri dish. The white dot in each cyst corresponds to the scolex. Source: Garcia et al. (2011)

It is not until these cysticerci are ingested by humans that the tape worm starts to develop fully into a meters-long tape worm, as it enters the next and final stage of its life cycle (Fig. 2).

Fig. 2. Taenia life cycle. Source: CDC

Hence, leaving the meat in the fridge will not induce growth, as a human is needed to induce outgrowth of the protoscolex into the mature tape worm.

Reference
Garcia et al., Lancet (2011): 362 (9383): 547–56


What are the programming languages important to learn for a geneticist or bioinformatician? I am interested in learning more about both genomics and bioinformatics, with emphasis on genomics. I was told after taking an introductory course of genomics that the programming language "R" and "python" are widely used. However having asked about learning genomics before on this fourm, I was suggested alot of books for learning genomics with "Perl". I was also told anecdotally that "perl" is falling "out of favor" and "Python" and "R" are desired.

To give background on my coding skills, I flunked out of computer science due to poor coding skills and poor math skills. I still had an interest in the field and therefore started studying genomics and biology instead.
I would categorize my self as a beginner in java and python in terms of skills.

I was also told anecdotally that the best way to learn coding is by having a project. But I feel incompetent in my coding skills to even attempt anything.
I tried to learn Python via "Codecademy" and their 13 hour course for python. Having completed it I felt lost enough to make this post, looking for further guidance. I tried to read a bioinformatics book based in Python, but I missed the handholding and directed exercises that Codecademy gave me.

Should one interested in genomics learn the coding language, R or Perl? Also what would be the best ways to learn these for one who does "not excel" in coding?

If this post seems opinion based mods feel free to delete it or move it, I just was not sure how to phrase my concerns adequately.

Comparing some commonly used languages in bioinformatics

I think that indeed Perl is losing users but there are still quite a lot of people using it. Bash (or other shell) is essential. While one can replace Python with C or Java and eventually replace R by Python or Julia, I find Bash to be really necessary. To compare Python to R, Python is much faster. If you are a purist, you'll like Python much more than R. R is a weird language, I use it a lot but you always have to deal with very special kind of objects. The big advantage of R is its community; There are tons and tons of functions. Typically, for any task you you want to do and related to statistics or to phylogenetics, you'll find an already existing package that will do the job for you. C is nice and very popular. It is super fast but it is not super handy for most tasks. Moreover, C doesn't have an interpreter which is always kinda annoying when you're use to high level languages such as R typically. I know nobody who uses Ruby and I don't code in Ruby but it is an important language. Some may use it for bioinformatics and it is very much used in many other disciplines (unlike R, which only statisticians know).

What I personally use

Personally, I use mostly R, Python, C/C++ and Bash. Bash to organize stuff, modify files and manage processes on my machine and on remote machines. R for data analysis. Python when R is too slow (to analyze more data such as sequence data for example) and C/C++ to run individual based simulation. I happen to use some other languages for my work but not as often.

How to learn

Nobody excels at coding to start with. Actually, after my first class of programming I had in mind that programming was not meant for me. Now, I don't excel, I am just a biologist who codes a bit and not a computer scientist but I spend the majority of time coding and I love that. I learn a lot everyday but ever since I started to feel a bit confident, I found that I could do much with this knowledge. You'll probably realize after some time that few people are really good at coding and you can already do much with only a few days of training. Don't be afraid. I think that indeed one of the best way to learn a language is to use it for a project. Here are a bunch of things you could do:

Go on Dryad.com, get some data and analyze them. You can redo the analysis they did on the original paper for example. Or, better you could try to discover something by yourself by combining some existing data.
individual-based (OOP) simulations in population genetics

simulate genetic drift in populations. Try to estimate the probability of a new mutation to fix and the time it takes to get fixed.
Simulate the process of selective sweep with defining chromosomes.
You'd basically have to have a function that creates a list of objects of type individuals. Each individual has two objects called chromosomes. You have a function that simulate reproduction (without selection, recombination nor mutations to start with). And you need a function to print the statistics you need on a file. I think you could do a simple individual-based simulation in a few days only and then you'd feel more comfortable with the language and you would also have a better grasp on how one can numerically simulate a population through time.


Is there any study to find the plant with the absolute minimum light need? Is there any study to find plants with absolute minimum light need?

Consider a bathroom without windows that you have occasional artificial light (e.g. white LED light).

Another question is there any numeric system assigning a number to each plant representing its minimum and maximum light tolerance?

Let's at first take a set of SHORT DAY PLANTS which are distinguished from the other plants using the photoperiodism parameters. Taking one plant at a time and performing starch detection test by keeping the plant under sunlight may be the only possible way to determine which plant is the most efficient at producing maximum amount of food when kept under sunlight for a particular time.
If we go deeper into the molecular level, maybe a cross section of the chloroplasts could provide us with the data of number of Photosystem 2 that are present which get activated at 680nm of light and also the number of electron carries like Ubiquinone. Their abundance can determine the quickness of carrying out photosynthesis.
There are even a separate variety of C4 plants that undergo Crassulacean Acid Metabolism also known as CAM plants found in deserts that undergo photosynthesis at night.

Thus such an experiment would require diverse plants with several parameters to keep in mind and is quite difficult.


Can bacteria or other microorganisms be killed by applying pressure? Can you smash a bacteria (or any microorganism) and kill it?
Let's say there is millions of microorganisms on a table. When you put your finger on the table, will or can you kill at least some of them ?

Yes, you can kill bacteria using pressure. The devised used is called a French press

https://en.wikipedia.org/wiki/French_pressure_cell_press

http://www.glenmills.com/cell-disruption/high-pressure-homogenizer/french-press-gm/

However the pressure use is about 40k psi.... which is a lot higher pressure than anything a human body can generate.

Other methods to kill bacteria include,
heat, gamma radiation, oxidative chemicals, antibiotics, dehydration, salt, oxygen exclusion, freezing.

However bacteria are a very diverse group, so it might take one or more methods in combination to kill all bacteria (and their spores) in a sample.


How does tearing work? I found the question about tear gas very interesting. Shigeta says there that crying helps the cells of the eye to wash themselves clear of the toxic components in the tear gas.

Does non-emotional tearing always work this way? Is tearing not caused by cells in the tear duct working as receptors? If not, why we have tear duct (the first in-eye part of it)?
What is the cause of tear-production associated with crying during strong emotions? Is it due to hormones or nerve activation?

The regulation of tear production (lacrimation) involves reflexes initiated by sensory neurons in the cornea. Corneal pain receptors (nociceptors) and mechanoreceptors detect damaging stimuli and induce tearing to cleanse the ocular surface (and, hence, Shigeta is right as tear gas stimulates pain receptors). Corneal neurons sensitive to drying of the ocular surface also appear to increase tearing. These neurons also respond to cooling and hyperosmotic stimuli (Kurose & Meng, 2013). The tear duct is necessary to drain the tears away from the eye into the nasal cavity (Fig. 1).

Fig. 1. Tear glands and tear ducts. Source: Mayo Foundation for Medical Education and Research.

Strong emotional responses like crying can result in an overflow of tears (epiphora). Epiphora is mediated by the limbic system (the emotional center of the brain), especially the hypothalamus. Such strong parasympathetic stimulation is accompanied by other symptoms, like reddening of the face and convulsive breathing (University of Minnesota, Duluth).

Reference
- Kurose & Meng, J Neurophysiol (2013); 109(10): 2517-22


Why does the wavelength in curly hair differ? Different people and animals have different wavelengths in the curls in their hair. I understand what purposes hair serves in protecting the skin from light and bugs. I am wondering about the eventual physiological consequences of curly vs straight hairs.

Do the curls help in cooling, blocking light or catching wind over flat hair? Does the wavelength in curly hair have intrinsic properties that physically would give an animal advantages in climates where straight hair would not?

I will be happy to accept another answer.

My hypothesis when the curls are left ungroomed they will form knots. These knots form a barrier that works similar to woven wool. Unlike strait hair the mat of knots (dreadlocks) collect dirt and form denser material that insulates against direct light and mosquitoes better than strait material. The wave length does play a part as well. The smaller the wavelength the tighter the knot. The tightest knots are commonly found in places that have the most sun light per year.

Strait hair tends to keep heat in more and ice builds up less on it.


Is my RNA-seq experimental design correct to use it for SNP calling? I am a newbie here and would highly appreciate your advice about one particular experimental design.

We have data from RNAseq experiment which was originally designed to assess differential expression. The details of experiment are as follows:

2 modalities of the phenotype

Each phenotype is represented by 4 samples. 1 sample = 60 individuals pooled together at the stage of RNA isolation.

Molecule – polyadenylated mRNA

Sequencing chemistry – Illumina paired-end, read length - 2*100 bp

My question is whether it is correct to use this RNAseq data to call for SNPs? I made previous search and found that most of people calling SNP from RNAseq use 40-1000 samples (= individuals). But they initially designed RNAseq experiment for further GWAS. I see that this analysis cannot be applied to my data (at least because in my case individual flies were pooled without barcoding – 60 flies per a sample). However, can I still call for SNPs and upload the list to database as a list of potential targets for GWAS with, for example, estimation of functional impact upon protein structure? Will they be “true” SNPs, or our experimental design makes even this step invalid?

I found this paper https://www.ncbi.nlm.nih.gov/pubmed/27458203 where people used 2 phenotypes each represented by 2 samples what is almost like our experiment, but still have doubts.

Using RNAseq for SNP analysis is not the best tool available for several reasons. First, you will only find SNP in genes that are expressed (you need more than 120 reads per SNP in your experiment). Second, you will only find SNP in coding regions of the genes. For your particular experiment, where you have a pool of 60 individuals per sample, it's another drawback because you'll have 120 alleles in your sample (without knowing the allele combinations of the individuals).

Of course you can still try to find SNPs that are present in your phenotypes, but real GWAS kind of analysis is in my opinion not possible.


What does "fit" mean in "survival of the fittest"? What does "fit" mean in "survival of the fittest"?

'Survival of the fittest' has never really made sense, because it confuses the scientific (evo. biological) and colloquial definitions of the word - which some of the previous posters have also done.

Biological fitness simply refers to an individuals genetic contribution to the following generation. That is, a 'fitter' individual, in an evolutionary sense, is one whose genetic material is proportionally overrepresented in the next generation.

The mechanism by which an individual achieves this may include out-surviving competitors, but it's certainly not the only way to increase fitness. Two individuals may live for the same length of time, but one may successfully court more females, or out-compete the other for food resources, for example. So when we refer to a 'fitter' individual (or individuals), we're saying nothing about why they are so. It's not a comment on their 'fitness' in the human sense of the word (bigger, stronger, longer-living), it simply refers to how well they pass on their genetic material.

So you can see why the phrase is nonsense. If we're being precise, then 'survival of the fittest' translates to 'survival of the individual who is better able to pass on their genetic material to the next generation' - which is meaningless because it tangles up these different concepts.


What bacteria do unborn babies contain? This Scientific American article states that "[human] infestation [by bacteria] begins at birth". This would suggest that unborn babies are free from any bacteria. However, if the mother catches a bacterial infection, her unborn baby risks catching it, too. This would seem to contradict the Scientific American article.

Presumably, when a human egg is fertilized by a sperm, the resulting cell may be free of any bacteria. At some point, bacteria begin to colonize the growing human body. Which bacteria are the earliest to colonize, and at what point in the development cycle does this occur?

In particular: does the health of the foetus depend on the presence of certain bacteria?

Babies are bacteria-free at birth. The meconium (the first stool) contains no bacteria if secured early enough.

  Meconium is a sterile mucilaginous material that accumulates in the fetal intestine and is expelled soon after birth. It contains secretions of intestinal glands, gut constituents (proteins, bile acids, fatty acids, and steroids), and components of amniotic fluid and vernix caseosa.

Bacterial colonization of infants begins at birth - literally. They pick up bacteria from the mother's vaginal canal in passing, which they swallow. This is not seen in infants delivered by C-section. The importance of colonization picked up through normal birth is such, that some hospitals are swabbing the vagina of mothers delivering by CS and colonizing the oropharynx that way.  Breast-milk also contains lactobacilli and bifidobacteria that probably contribute to the initial establishment of the gut flora of newborns.

And, yes, an infection the mother has while delivering must be taken into account. Herpes and Group B strep are both dangerous for a neonate.

  The first microbes to colonize the intestines of newborn babies are the aerobic bacteria Escherichia coli and Streptococci. Later, the gut is colonized with anaerobic bacteria, e.g. Bacteroides, Bifidobacteria, and Clostridia. In 1–2 y, the gastrointestinal tract of infants has developed a natural microflora, which resembles the microflora of adults.

The infant continues to pick up bacteria from all people they come into regular contact with, including nurses.

  The effect of the maternal flora on the initial gut colonization may be less than expected as the fecal flora of infants started to resemble both the fecal flora of the mother as well as that of the first nurse.
  Breast milk may contain bacteria which colonizes the gut as well

Infants aren't overwhelmed by infection due to the presence of  antimicrobial peptides found on their skin, GI tract, and immunity is conferred via breast milk.

  Several AMP have been characterized in vernix and skin of the newborn, indicating a well-developed innate immune system, which may play a pivotal role at the time of postnatal colonization.

Antimicrobial Components of the Neonatal Gut Affected Upon Colonization
Dynamics of gut colonization and source of intestinal flora in healthy newborn infants
Protection of the Neonate by the Innate Immune System of Developing Gut and of Human Milk
Establishment and development of lactic acid bacteria and bifidobacteria microbiota in breast-milk and the infant gut


How do polygyne Carebara affinis or C. diversus (a.k.a. Pheidologeton affinis and P. diversus) colonies work? I live in Hong Kong. Typhoon Hato hit yesterday and a whole bunch of Carebara queens decided to take their nuptial flight. I caught close to 20 of them within 15 minutes.

I'm pretty sure they are Carebara affinis, though they can also be Carebara diversa. They are also known by their old names Pheidologeton affinis and P. diversus, respectively.

In any case, I have read from multiple places that both Carebara affinis and Carebara diversa are polygyne, which means they can found a large colony with multiple egg-laying queens.

So I decided to temporarily put them into the same lunch-box-sized plastic container.

However, soon after I put them into the same container, I discover that some of them would get their legs and even their antennae bitten off. I thought maybe it's because they found the container too crowded and wanted to eliminate some competitors, so I added two layers of toilet paper to give them more surface to crawl around. That didn't really help. Tonight, after coming home from work, I found most of them have been completely amputated. They aren't dead yet though; they are just left there wiggling around without legs. A few of the queens come out intact so I suppose they are somehow dominant. The ones who get amputated tend to end up in a pile. I'm not sure if the "dominant" queens decided to drag them and pile them together.

Is that at all normal? Is that how Carebara ants start a polygyne colony? Basically one or a few dominant queens amputating their sisters to turn them into egg-laying slaves of some sort? If the dominant queens wanted to kill the weaker ones, why not bite their heads off? I'm pretty sure they had the jaw strength if they wanted to. So, supposing that the amputated queens do survive, I'm not sure I see how that helps in the evolutionary sense. Unless that's actually how it works: one or a few dominant ones amputating weaker ones to force them to lay eggs together?

Does anybody know how to properly start a polygyne Carebara diversa or affinis colony from scratch?

I don't know about their polygyne nature, but carebara diversa queens are between 20-25mm and carebara affinis queens are between 14-16mm and are slightly lighter in colour. Hopefully that should help you identify them.


What is this thorny plant with cute leaves? I found this thorny plant with cute leaves growing in my garden in India,

I took a risk by plucking it to get photos of the front & back side of the leaves.

Front side of the leaf:

Back side of leaf:

Full plant:

Any Idea what this plant is?

https://en.wikipedia.org/wiki/Dalbergia_melanoxylon

The Mpingo looks quite similar to this plant. However, more information is needed like the approximate size of the leaves and the number of leaves on a branch.


Why isn't there 1' to 2' direction or something else except 5' to 3' in dna replication? I hope i would get logical answers. I  request to post it as soon as possible.

[Source]

DNA is a polynucleotide. The above structure is of a nucleotide which has three components, a nitrogenous base(yellow), a pentose sugar(purple) and a phosphate group. These nucleotides form phosphodiester linkages to form a polynucleotide.

[Source]

These phosphodiester linkages are formed between 3' and 5' carbons of the pentose sugar which is shown in the above image.

[Source]

The end of DNA having a free phosphate group at 5' of pentose sugar is known as the 5'-end of DNA, and the end of DNA having a free hydroxyl group at 3' of pentose sugar is called the 3'-end of DNA.

Here, you can play with the DNA.


When does a jalapeño begin to produce heat/capsaicin? I have a small Jalapeno plant in my apartment. About two weeks ago, it started producing a few flowers. In the last few days, many of them have started to turn into fruit; however, a few of the flowers have fallen off. The flowers do contain some seeds. They look rather like this:

Note this is not a picture of my plant (my flowers are white) but apart from the color it looks quite similar.

I tried munching on the seeds to see if they were hot. They weren't at all. I believe it is a common misconception that the seeds are where capsaicin concentrates, but should there have been any heat? Is there none in the seeds at all? Or was it too early in development?

Related questions: Do you think these seeds were viable at this point, or would they need to develop in an actual pepper fruit?

The reason the 'seeds' you ate weren't hot is because they're not seeds. What you thought are the seeds in the pepper flower are its anthers. The anthers are the pollen bearing parts of a flower. The unfertilized, and therefore undeveloped, seeds would be found in the flower's ovary which is at the base of the petals. The parts of a flower are labeled in this diagram.

I've tried both the seeds and the flesh of jalapeño peppers and noted the 'heat' in both but personally, I found the seeds a little hotter.


Why doesn't blood remain on a mosquito's proboscis in quantities that could spread blood-borne diseases? We know that HIV can't be transmitted by mosquitos, and nor can other highly virulent viruses that are transmitted through blood and bodily fluid exchanges, such as Ebola (thankfully!).

Marcus Junius Brutus asked an interesting question in a comment on that above-linked question's answer:

  [Why can't] tiny droplets of blood remain on the proboscis of the mosquito long enough for said mosquito to inject its proboscis into the bloodstream of another person? In particular, in what physical aspects is the proboscis different than a needle or razor? I am not talking about blood sucked into the gut of the mosquito, I am talking about blood remaining on the proboscis

There's no doubt that dirty mosquito proboscises aren't a vector for blood-based viruses (if they were, Ebola would be completely uncontainable in West Africa), and I understand the explanation on the above linked answer that there's no route from the mosquito's stomach to its proboscis other than via saliva production, but given how tiny the amounts of blood are that are required for transmission of such highly virulent viruses, why does it never happen in a similar way to transmission from a dirty needle or razor?

I've never seen a mosquito put its proboscis in sterilising fluid or an autoclave between feedings...

My best guess would be that mosquitoes are very efficient at taking up all available fluid, and that surface tension means that at this scale it is possible to take up every last droplet - but that's just a guess.

A mosquito's proboscis isn't like that of a butterfly, which could easily have nectar clinging to it when it is coiled up; instead, consider that the part of the mosquito's proboscis that enters a blood vessle is probably wiped clean when it is retracts outward through the epithelium. A a dirty needle or razor is many, many times larger than the sucking parts of a mosquito, and a razor is an unlikely vector of HIV.

Epithelial tissue consists of cells very tightly bound together; it has to be to prevent constant invasion by bacteria, fungi, etc. It takes some considerable force or sharpness to penetrate. If you've ever watched someone give you an injection (a vaccine, for example), the needle is never bloody upon withdrawal. You might get a bead of blood from the wound, but the needle itself will be quite clean. The reverse is also true due to essentially the same reasons: the likelihood of introducing a pathogen by dragging it from the surface into the subcutaneous area is so low that there is no absolute need to swab visibly clean skin before giving a subcutaneous injection:

  Although skin that is visibly soiled or dirty must be washed, swabbing the clean skin of a patient before giving an injection is unnecessary. Studies suggest that there is no increased risk of infection when injections were given in the absence of skin preparation. (WHO Bulletin)

HIV is the most serious virus (aside from Ebola, about which much is still unknown) which can be transmitted by needlestick. Sharps injuries - needles, suture needles, scalpels, lancets, etc. - are very common in the medical field, estimated to be much higher than 350,000/year due to underreporting and occurrence in non-hospital settings, e.g. nursing homes, etc. Of course, in the majority of sharps injuries, the sharp wasn't likely to have been used on someone with HIV. Still. HIV is not rare.

Even with a potential half-million exposures a year to sharps, as of December 31, 2013, only 58 confirmed occupational transmissions of HIV and 150 possible transmissions had been reported in the United States. Of these, the vast majority follow hollow needle sticks (88%), where blood drawn from a patient still remains in the bore of the needle which can be reinjected into the unfortunate recipient. If the patient is terminally ill with AIDS, the incidence of transmission by hollow needlestick is increased, meaning the viral load in the blood is important. A solid needle, even a bloody one, presents a very low risk (the risk is, in fact, unknown*.) Getting blood splashed in the eye is a higher risk than a sharp solid (i.e. suture or lancet) needle.

The piercing mouthparts (The mandibles and the maxillae) are solid, akin to a solid sharp. Only the twin tubes (the hypopharynx and the labrum) actually reach blood.

So, given the combined factors of limited survival of HIV on exposed surfaces, the small size of the proboscis (compared to a suturing needle or a lancet, both of which have a higher surface area, yet not known for certain ever to have transmitted HIV), the low probability that the mouth parts have HIV-laden droplets of blood on it, the fact that only the tip of the hypopharynx and labrum encounter blood (the fluid most likely to contain virus) and the extremely low probability that there are enough actual HIV viruses to cause an infection anywhere on the proboscis, I hope this answers your question.

Edited to add: I've focused on HIV here, because it's not known to infect mosquitoes. Mosquitoes are considered by many to be the most dangerous animal in the world. They transmit a significant number of viruses and parasites (like dog heartworm, elephantiasis, dengue fever, equine encephalitis, etc.), but (hypothesized from those diseases that have been studied in mosquitoes) only after being infected by the pathogens themselves. Some die of the infection; some die before the infection spreads through the mosquito's body, some don't harm the mosquito. But transmission is from infected saliva injected into or onto the bite site, not virus particles on the proboscis, as evidenced by the need for adequate incubation time between the bite that takes up the virus to the bite that transmits the virus. If there was sufficient virus on the surface of the proboscis, that incubation time would not be necessary.

Best infection control practices for intradermal, subcutaneous, and intramuscular needle injections
Workbook for Designing, Implementing and Evaluating a Sharps Injury Prevention Program
Occupational HIV infection among health care workers exposed to blood and body fluids in Brazil
Needlesticks: What you must know


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

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

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

Reference

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


Why do we use different micropipette tips for different volumes? Isn’t it easier to use a 1000 µl micropipette tip for all volumes? I don’t understand why there are different tips for smaller volumes. Does it affect the accuracy of the pipette for very small (<5µl) samples?

The short answer is yes, the accuracy is affected.

Automatic pipettes are most accurate in the middle of their range. The average error on a pipettes is already about 2%, but this is worse at the top end or bottom end of the pipettes minimal and maximal volume.

More subtly, have you ever tried to pipette 1 uL with a 1 mL pipette? Or even 5 uL. The bore of the pipette is too wide for starters, and the expulsion force/pressure to eject the fluid wouldn’t work very well.

On top of that, the surface tension would seriously hamper any ability to actually manipulate the fluid.


How would a medication cause a one to maintain a different weight? This isn’t really a medical question, I’m just really curious about this.

I was maintaining weight A and then started taking a medication that brought me to weight B. While on the medication, I maintain weight B. When I stop taking it, my weight goes down presumably to weight A.

The increase or decrease of weight in changing medications doesn’t puzzle me. It’s the maintaining of the weight.

Would the medication be affecting metabolism or what?

Based on my reading, weight gain, as in resetting your maintenance set-point, which is what it sounds like you are describing, is a very well-known side-effect of the serotonin selective reuptake inhibitors (SSRI).  In some cases, patients may even discontinue the medication.  As far as I know, the underlying physiology behind this specific example is not well-understood.

In recent years, the use of next-generation sequencing (NGS) of DNA has been used to characterize the so-called microbiome in the gut of individual humans (sequencing faeces).  Some studies have reported that thin, or skinny people have somewhat different microbiomes than fat, or obese people, leading to the hypothesis that some overweight people might have bacteria that are more efficient at breaking down their food such that more of the calories are available for absorption.  Some evidence supporting this interpretation comes from experiments with fecal transplants.

If a medication also affects a patient’s microbiome (in addition to the drug’s intended therapeutic effects) then that could be another, less obvious(?) mechanism for weight changes.


Does rainwater contain many fewer micro-organisms than river water? From watching many documentaries on micro-organisms, I can tell water typically contains quite a lot of them.

But what about rainwater? (before it hits the ground). I know nothing about any micro-organisms that live in the sky or clouds. Does rainwater contain fewer, and less dangerous, micro-organisms?

According to a number of citations listed on Kenyon College's MicrobeWiki, rain can contain microorganisms via a process called "bioprecipitation."

Essentially, microorganisms, dust and other small particles get swept up into the atmosphere, and cold temperatures cause atmospheric water vapor to freeze around the organism/particle. Once the ice-covered particle picks up enough mass, it falls from the sky and reaches earth as precipitation (likely rain if temperature is warm enough).

Here is a schematic from Wright et al. (2104) of how an increase in relative humidity, due to a cold-frontal passage, can trigger biological ice nuclei release followed by seeding of the frontal cloud band with the lofted ice nuclei:

 So How Many (and Which) Bacteria Are in Rain?

Which Bacteria?

According to Wikipedia:

  The ice-nucleating bacteria currently known are mostly plant pathogens

According to MicrobeWiki, these include:

  Exserohilum turcicum, Pseudomonas viridiflava, Pseudomonas fluorescens, Pantoea agglomerans and Xanthomonas campestris.

  The most well described organism that demonstrates ice nucleation is Pseudomonas syringae, which was determined to specifically supply a source of ice nucleators by Leroy Maki in the 1970’s.

According to work by Natasha DeLeon-Rodriguez, Athanasios Nenes, et al. (full paper here and NPR story here), 100s of species of bacteria exist in the clouds and it's not uncommon to find almost 20 species in any given sample (60% of which on average were still living).

Here's a graph showing the relative amounts of various taxa found in their samples:

How Many Bacteria?

DeLeon-Rodriguez et al's (2013) results revealed an average bacterial concentration of somewhere between $5.1 × 10^3 cells /  m^3$ to $1.5 × 10^5 cells /  m^3$ of cloud (depending on method of counting).

Quickly doing some math (1 m$^3$ = 1000000 mL), their results suggest that, on average across a cubic meter of cloud, there is <1 bacteria / mL of moisture.

According to research by Joly et al (2014) that specifically examined ice nuclei (or "IN"):

  there were 0 to ~220 biological IN/mL of cloud water (i.e. 0-22 per m$^3$ of cloudy air based on cloud liquid water content estimates) and these represented 65% to 100% of the total IN.

Comparatively, river water (and drinking water) can contain a lot more bacteria (i.e., 80,000 bacteria / mL) and other microorganisms.

However, this disparity is not always so great, especially if we focus at comparing counts of only one or a few species (and not total bacterial counts).

Based on research of a tropical reservoir by Kaushik et al (2014):

  Levels of E. coli were found to be in the range of 0 CFU/100 mL – 75 CFU/100 mL for the rainwater, and were 10–94 CFU/100 mL for the reservoir water.

Note: CFU = colony forming units. (estimation of microbial numbers by CFU will, in most cases, undercount the number of living cells. [wikipedia]).

Citations

 DeLeon-Rodriguez, N., Lathem, T. L., Rodriguez-R, L. M., Barazesh, J. M., Anderson, B. E., Beyersdorf, A. J., ... & Konstantinidis, K. T. (2013). Microbiome of the upper troposphere: species composition and prevalence, effects of tropical storms, and atmospheric implications. Proceedings of the National Academy of Sciences 110(7), 2575-2580.
 Joly, M., Amato, P., Deguillaume, L., Monier, M., Hoose, C., and Delort, A. (2014). Direct Quantification of Total and Biological Ice Nuclei in Cloud Water. Atmos. Chem. Phys. Discuss 14(3):3707–3731.
 Kaushik R, Balasubramanian R, Dunstan H (2014) Microbial Quality and Phylogenetic Diversity of Fresh Rainwater and Tropical Freshwater Reservoir. PLoS ONE 9(6): e100737. doi:10.1371/journal.pone.0100737
 Wright, T. P., Hader, J. D., McMeeking, G. R., & Petters, M. D. (2014). High relative humidity as a trigger for widespread release of ice nuclei. Aerosol Science and Technology 48(11), i-v.
For further reading, also see the associated citations from MicrobeWiki.
I think you would also benefit by perusing the works of Pierre Amato.


If you didn't have an utricule or saccule would you still know if you are accelerating and going up or down? In the vestibular system the utricule and saccule makes you that you know whether you are going up or down (saccule) or backwards/forwards (urticule).

But imagine you don't have them anymore or they are damaged, would you still be able to know if you are accelerating or in an elevator? I thought it still would be possible because you would feel the pressure in you back when accelerating or on your feet when going up. But is it true that you still know what is going on by registrating the pressures in you body, or is it not possible any more? If it is still possible what would the surplus value of the urticule and saccule?

Your semicircular canals are concerned with balance (or spatial orientation). Proprioception, on the other hand, deals with where the body parts are with respect to each other and the physical world. (Some people lump the two; it's easier to think of them independently, because they really do quite different things.)

Proprioception (and closely associated kinesthetics) is possible because of nerve signals from skin, tendons, muscles, and joints. This gives us the senses of limb position and movement, the sense of tension or force, the sense of effort, the sense of gravity.[1] Propioception alone cannot compensate for serious balance problems.

The vestibular system exists through input from three semicircular canals located in the inner ear on each side. The canals are oriented at (basically) 90° angles to each other so that we can maintain our balance no matter which position our head is in. These are also connected to one's ocular reflexes. Together they're called the vestibolo-occular system, which functions as a reflex (VOR).

  Three sensory systems, vestibular, visual, and somatosensory/proprioceptive, serve our sense of balance. Each of these systems provides unique sensory information to the brain where it is integrated (often in complex ways) to produce a final motor output to muscle groups for maintaining gaze, head and body posture, and controlling static and dynamic balance.[3]

Without these systems, we would be completely unable to get or stay in a standing position. We certainly could not walk.

An analogy would be to get strapped into one of those spinning seats, in this case, one that rapidly spins inverting you, alternating between forwards and backwards (which would kind of include up and down) but not sideways. You would be unable to focus your eyes on anything. You would see your world spinning, and you would have lost your sense of balance. You would immediately go to the ground, even though your proprioceptors were working perfectly.

However, once you did "go to ground", say, in an elevator, you probably could tell if you were accelerating upwards or downwards. Closing your eyes would help to drown out the more unpleasant 'noise' (input).

So, long story short, the answer is yes. Likewise, you would probably still be able to touch your nose, etc. But it would not be possible to do more complex things, like walk, or even sit unless your back and sides were supported.

[1] Proprioception From a Spinocerebellar Perspective
[2] mpairments of reaching movements in patients without proprioception. I. Spatial errors
[3] Anatomical and Physiological Considerations in Vestibular Dysfunction and Compensation


Are fish and reptilian scales homologous? Wikipedia:

  Fish scales are dermally derived, specifically in the mesoderm. This
  fact distinguishes them from reptile scales paleontologically.

So aren't reptilia scales also dermally derived?

No, fish scales are dermal (= formed in derma) bones like skull roof bones. Scales in reptiles are formed by epidermis and are made primarily of protein (from keratinocytes), being similar in derivation to hair, feather and nails.

On the other hand, in reptiles one must differentiate between scales and osteoderms (= scutes). Scutes are widespread among reptiles and they are similar to fish scales in that they are produced in derma and are ossified. Similar structures are found in some amphibians and in armadillo. Nevertheless, different types of osteoderms are currently considered as converges: "it is essential to recognize that osteoderms represent non-homologous structures that have been independently evolved a number of times" and have no direct homology with fish scales.


Carotenoid biosynthesis in yeast Does Budding Yeast Sacchromyces cerevisiae produces significant amount of carotenoids?
Have anybody estimated the ratio of flux going in branches 1. Cholesterol synthesis(via squalene)
2. Coenzyme Q6 and 3. Dolichols Glycoprotein and others from the branch point of Farnesyl diphosphate.

Here is the kegg pathway

http://www.genome.jp/kegg-bin/show_pathway?map00900
I also have pathway formatted but couldn't upload.

The enzyme phytoene synthase is the first committed step in carotenoid biosynthesis. Saccharomyces cerevisiae doesn't have this enzyme, nor does it have the rest of the relevant pathway. Other yeasts such as Rhodotorula spp and Phaffia rhodozyma can make carotenoids.

However, carotenoid biosynthesis has been engineered into S. cerevisiae.


Overcoming Inbreeding Depression When inbreeding depression occurs, a genetically unrelated individual is mated with the animal to introduce genetic variability and remove homozygosity. In this case either outbreeding or crossbreeding may be carried out. Is there any preference for either technique over the other?
Out-breeding here refers to mating between two individuals in the same breed, but no recent common ancestors.
Cross-breeding refers to mating between two individuals of different breeds entirely.

Inbreeding depression can be overcome by the following ways :
1. Out breeding- the breeding of animals which are unrelated to each other and do not have come ancestors for 4-6 generations
2. Out crossing- mating done with the animals osf same breed but after 4-6 generations
3. Cross breeding- superior male mated with superior female of another breed
4. Interspecific hybridisations- male and female  animal  of two different related species


Does the human eye’s field of view shrink when focusing on far away objects? It seems like the lenses of the eye is like a fisheye lens that flattens out to a normal lens when looking at far away objects. Does that also mean that the field of view gets narrowed down as well? Or is that not how light works?

The lens does flatten when contracted to look at far objects. This is however still a regular cylindrical lens. It's not perfect (even when corrected), but close to it. Straight lines project to straight lines on the image plane (for your eye the retina).

A fisheye lens is different because it creates strong geometrical distortions. A straight line will appear curved on the image plane. You can see that on the images taken below (from some random source). Left is a regular lens, right is a fisheye lens.

The human eye actually introduces some so-called barrel distortions (so it's a little bit like a fisheye lens). You can demonstrate that by looking at this checkerboard pattern (from Helmholtz's treatise on physiological optics). If your eye is close enough you'll see the checkerboard straight, because the barrel distortion introduced by your eye will "straightens" the distorted checkerboard.

Focusing at different distances will make objects appear sharp. Because all light rays coming from this object will project at the same point on your retina. Objects at a different distance will appear blurred because light rays will project at different points causing a "spread" (defocus blur, see image from wikipedia "circle of confusion" article). This is however totally independent from the field of view. Test it yourself: take a pen, place it close to your eye. Pay attention to an object far in your periphery, nearly outside your field of view. Now focus to the sky behind the pen (~infinite focus distance), then your pen. In both cases you can still see the object in periphery because your fov hasn't changed.


Why is blood removed from meat? Blood is removed from meat before it is consumed. Below is, for example, how chickens are processed from Wikipedia.

Removed from transport cages
Hung by the legs on a shackle, mounted on a conveyor chain.
Stunned using an electrically charged water bath
Killed by cutting the blood vessels in the neck
Bled so that most blood has left the carcass
Scalded to soften the attachment of the feathers
Plucked to remove the feathers
Head removed
Hock cutting to remove the feet
Rehung in the evisceration room
Gutted or eviscerated to remove the internal organs
Washed to remove blood and soiling from the carcass
Chilled to prevent bacterial spoiling

Why is the blood removed? Does it just simply taste bad? This might be a stupid question but being vegetarian, I may not know.

Blood finds use in many different dishes as well as biotechnological applications. Research-grade BSA (bovine serum albumin) is derived from cow's blood, there are not special facilities, same cows go for steaks and car seats. So part answer is economical: blood can be processed further. Also it is just easier not trying to preserve liquid inside vessel already opened by slitting the throat. It also seems that blood can rot faster than other tissues, maybe, because in dead animal immune responses are deteriorated and every infection in blood will activate.


What are the various types of protein-protein interactions I understand there are a number of protein-protein interactions, but what types of interactions exist? and what are the characteristics of them?

There are so many types of protein-protein interactions via various domains, such as SH2 binding (in RTK signaling), Pleckstrin Homology domain (involved in signaling) among others. This site gives a nice list: http://pawsonlab.mshri.on.ca/index.php?option=com_content&task=view&id=30&Itemid=63

Of course, protein-protein interactions rely on the premises of basic biochemistry:

van-der waals interactions (at the most basic level)
Electrostatic interactions
"Lock and Key" model: Some proteins have specific binding pockets for domains of other proteins
Induced fit

There are many ways to study protein-protein interactions, including, but not limited to

Pull-down assays
2D SDS-PAGE / MS
Yeast two-hybrid
Immunoprecipitation


How can i count my E. coli colonies? I did a test which involved growing e. coli on a petri dish. I did not dilute the sample, and this resulted in growing hundreds of small, overlapping colonies. However, they still can be counted, but it has been tedious work. Does anyone have tricks for counting small colonies? Also, I've read people will just write >300 if their colony count is too large. Is this data sufficient? I need to compare the colony count for several petri dishes and they all have quite a lot. If i just write ">300" for 80% of my data, it won't be a very good comparison. Can anyone help me out here?

Divide the plate into equal sectors. Count one sector as accurately as you can then multiply that number by the number of sectors. This assumes the colonies are roughly equally distributed.


Polarized epithelium and localization of ion channels I'm trying to learn more about polarized epithelial cells of the gut. I am familiar with classic brush border transporters localized to the apical memebrane to facilitate nutrient absorption. I am wondering though, where are ion channels located? I would guess basolaterally since they would be exposed to the extracellular space. I would appreciate a primary reference showing the location of voltage-gated channels in particular as I could not find them myself.

Well, that's a first for me. I wouldn't have guessed gut cells would have voltage-gated channels.
This article describes voltage-gated sodium channels on both the luminal and basolateral membranes:

Barshack, I., Levite, M., Lang, A., Fudim, E., Picard, O., Ben Horin, S., & Chowers, Y. (2008). Functional voltage-gated sodium channels are expressed in human intestinal epithelial cells. Digestion, 77(2), 108-117.
http://www.ncbi.nlm.nih.gov/pubmed/18391489


How is the GenBank used in typical biological research? How is the GenBank used in typical biological research? According to the GenBank statistics, the database contains about 100 million sequences. I find it difficult to understand why is all that data needed. To make the question less broad, what are the most common use-cases? Check if someone already sequenced DNA of some plant or animal?

Go to Google Scholar. Enter "Genbank" into the search field and press return. Limit the results to 2013 and later (left side of the results).  Skip the few entries that say only "GenBank." Browse through the pages and pages of search results to get a feel for the many ways that GenBank is used in scientific research. It's used from everything for phylogenetic analysis (relationships among organisms) to determining protein structure and so much more.


Who is organizing the heartbeat and its roles in the body? Throughout the decades we heard that the heart is the only muscle whose nervous system is not acting. So who is he responsible for organising the heartbeat and its roles?

The Sinoatrial Node is a ganglion (clump of nerves) attached to the heart, which regulates heartbeat independently from the brain (http://en.wikipedia.org/wiki/Sinoatrial_node).

Heart rate can also be influenced by hormonal responses produced by the autonomic nervous system. To quote Wikipedia:

  While heart rhythm is regulated entirely by the sinoatrial node under
  normal conditions, heart rate is regulated by sympathetic and
  parasympathetic input to the sinoatrial node. The accelerans nerve
  provides sympathetic input to the heart by releasing norepinephrine
  onto the cells of the sinoatrial node, and the vagus nerve provides
  parasympathetic input to the heart by releasing acetylcholine onto
  sinoatrial node cells.

Source: en.wikipedia.org/wiki/Heart_rate#Physiology


What is this creepy little thing that I found sticking on my bathroom wall? I found this creepy looking thing hanging on my bathroom wall. This is actually the 2nd time I have seen it. The first one I saw looked kind of dried up already stuck in between the walls. But this looks fresh and new. It's scary and gives me goosebumps just looking at it. Can somebody pls help

This is the pupal stage of a lepidopteran (i.e. a butterfly/moth). The pupa is encased in the brown silken cocoon in the centre of the 'net'. The 'net' itself is built from the setae (hairs) of the caterpillar, which it sheds prior to cocoon formation.
Here's some photos of similar formations:

http://www.richard-seaman.com/Insects/Vietnam/Highlights/index.html#Chrysalis
https://www.nhm.ac.uk/wpy/gallery/2019-the-hairnet-cocoon?tags=ed.current
https://besgroup.org/2015/11/05/a-parasitic-fly-emerged-from-the-cocoon-of-a-footman-moth/


What generates variation in a species? What is the biological mechanism behind the variation within sexually reproducing species? Obviously, the children are combinations, to differing degrees, of their parents. But how does the variation originate in the parents to begin with?

I'm not referring to evolution or mutations rather I have in mind things like facial structure and personality in humans, or fur coloring in dogs. I just thought I vaguely remembered there was some kind of driver of variation... For example, does the parent produce a variety of germ cells that purposely differ from the parent's geneome?

I just think I'm missing something here.

(I'm familiar with DNA and genetics having taken a biology class in college and remembering much of it, I just can't seem to put my finger on this point...)

After mutations, which probably is the source of most variation.  The classic biological model of variation comes from accidents of history and environment.

Many mutations disappear over time because they aren't helpful (advantageous).  The reasons variations persist for more than a few generations is that our differences have helped us to live successful lives and (in biological terms of success) have offspring.  In europe the lactate dehydrogenase gene and others like it that help people digest milk is active through adult life as the result of domestication of milk producing animals,  in asia, this trait is rarer or non existent as agriculture does not produce milk there (in most cases).

This is a broad difference, but its true in smaller ways for all of our individual traits, or so the theory goes.  Individual family traits are helpful to create stronger family bonds, so even something like distinctive dimples or foreheads have claim to being an advantageous trait.  Its possible that blonde hair is the product of such an advantage - its a strong signal to paternity if the father is blonde for instance.

Another answer to your question I think, is that there are probably mechanisms in the cell or in mate selection that increase or decrease variation in the community at given times of stress.  For instance, snakes are among the animals who have a particular ability to select gender depending upon the conditions the female is experiencing.  more males may increase variation in the community - fewer males and more females will decrease it.  (not by a lot mind you, but a bit).

Additional response added as requested:

I see what you are getting at - why do children seem like such individual and unique things sometimes?

In sexual reproduction, the offspring are the product of the shuffling of the parent's genomes through meiosis, where the pairs of chromosomes we have are combined to make a single chromosome that will be half of the children genome.

This process can result in completely novel combinations of genes while conveying many likenesses from the parent.  I would guesstimate that this is the major cause of the uniqueness of offspring/children.

Also in mammals there are some cell lines which splice families of genes which will cause offspring to be potentially quite different from either parent.  Immune genes for instance are created from scratch from a bunch of genes that the parents give.  Making each offspring unique but also the product of the parent's genetic repertoire.  This can be significant as it affects health and also to some extent attraction - studies have shown that people who smell attractive to us are immunologically distinct from us.

@David mentions epigenetic variation, which is a more recent significant development.  During our life, the germline (sperm/egg) DNA may be chemically labelled depending upon environmental conditions we experience.  A famous example is experiencing famine conditions, which caused the children to be born on the small side amongst other effects.   More recent studies have shown that this is a widespread mechanism to control cells in our body during our lifetime as well as communicate to our offspring how life is.  It is expected that this labeling does not affect us forever - the epigenetic labels change over the course of a generation quite often (we believe).


Why is one phase of a plant dominant (Alternation of generation)? In plants, there is the alternation of generation.

In nearly all land plants, one phase of the two possible phases is dominant--namely the sporophyte.

The "dominance" over the other phase can be seen in the following ways:

The gametophyte organism depends on its sporophyte progenitor, while the sporophyte organism is fine without the other.
The sporophytes are more structurally complex, larger and longer lived.
The sporophytes carry out more activities/functions and receives more subjective attention.

I want to know if there is an evolutionary reason why alternation of generation, one phase is dominant. Here are some guesses:

Zipf's law: as one of the two phases got more complex (start doing more complex jobs) It became more convenient and more likely for that phase to acquire other functions, causing the complexity of that phase to increase with a sort of positive-feed-back-loop, while it became more beneficial for the other phase to depend on the other more and more, to reduce its complexity.
Chromosomal difference: the sporophytes of plants are diploid while the gametophytes are haploid, perhaps one of the two configurations is more efficient?
The sporophyte generation "reproduce" asexually, perhaps this allows it to have a little "head-start" in accumulating non-sexually reproductive functions and became more complex as explained in 1.

Short answer:

Many of the evolutionary developments in plants developed in the sporophyte life stage. Because increased fitness of these increasingly sporophyte-"dominant" plants would result in a greater survival and reproductive success, these plants became more dominant than the more-limited gametophyte-dominant early plants.

In other words, natural selection of the fittest plants (which happen to have sporophyte traits increasingly adapated for living on land) likely led to the dominance in the sporophyte life stage.

Long Answer:

I would suspect this is due to the evolutionary advantages that are associated with the sporophyte life stage in land plants. Multiple advantages developed in the sporophyte stage of plants as they evolved from simple gametophyte-dominant bryophyte ancestors to the vast array of much more successful and dominant ferns, gymnosperms, and angiosperms.

 Shift from gametophyte-dominated life cycle (in bryophytes) to sporophyte-dominated life cycle. Source: Cengage Learning (2016)

Evolutionary developments that have occurred across almost 500 million years in land plants include the development of stomata, true leaves, pollen and seeds, and flowers and fruits. Each of these developments occurred in the sporophyte life stage.

Each of these evolutionary traits had significant effect on the success of the various plant types that possess them, as can be inferred from the increasing success and dominance of increasingly more evolved plant Divisions.

Each of these sporophyte-focused evolutionary traits increased the reproductive success of plants (therefore swaying increasing advantage toward plants possessing increasingly sporophyte-dominant life cycles) due to their ability to increase plant size, growth, and success living in arid (i.e., terrestrial) environments.

stomata allow for increased gas exchange with more limited water loss (note: these were necessary with the development of cuticles in sporophytes of early bryophytes as well)
vascular tissue2 allow plants to grow taller/bigger/more complex while still receiving water and nutrients from the soil
true leaves allow for greater energy capture and growth (and therefore increased competitive advantages)
pollen and seeds allow for greater dispersal and removes/limits the constraints of aridity on fertilization
flowers and fruits increase pollination and seed dispersal

Reducing the gametophyte stage to small cells within larger sporophyte plants allows this otherwise water-necessary process to occur in the dry conditions of living on land. As such, the pollen-bearing plants (i.e., gymnosperms and angiosperms) have been very successful in colonizing vast terrestrial ecosystems.

Another evolutionary advantage proposed, (e.g., see Bernstein et al. (1981)1 and Michod & Gayley (1992)3) is that the diploidy of the sporophyte stage allows masking of the expression of deleterious mutations through genetic complementation. From Wikipedia:

  Thus if one of the parental genomes in the diploid cells contains mutations leading to defects in one or more gene products, these deficiencies could be compensated for by the other parental genome (which nevertheless may have its own defects in other genes). As the diploid phase was becoming predominant, the masking effect likely allowed genome size, and hence information content, to increase without the constraint of having to improve accuracy of replication. The opportunity to increase information content at low cost is advantageous because it permits new adaptations to be encoded.

However, this proposal has been more recently challenged by Szövényi *et al. (2013)4 because evidence suggests that selection isn't more effective in haploid vs. diploid lifecycle phases of mosses and angiosperms.

For further reading:

"Evolutionary history of plants" [Wikipedia]
"Evolution of Seed Plants" [Lumen Learning]
"Evolution of Seed Plants" [OpenStaxCollege]

 Citations

1  Bernstein, H; Byers, GS; Michod, RE (1981). Evolution of sexual reproduction: Importance of DNA repair, complementation, and variation. The American Naturalist. 117 (4):537–549. doi:10.1086/283734

2  Lucas, W.J., Groover, A., Lichtenberger, R., Furuta, K., Yadav, S.R., Helariutta, Y., He, X.Q., Fukuda, H., Kang, J., Brady, S.M. and Patrick, J.W., 2013. The plant vascular system: evolution, development and functions F. Journal of integrative plant biology, 55(4):294-388.

3  Michod, RE; Gayley, TW (1992). Masking of mutations and the evolution of sex. The American Naturalist. 139 (4):706–734. doi:10.1086/285354

4  Szövényi, Péter; Ricca, Mariana; Hock, Zsófia; Shaw, Jonathan A.; Shimizu, Kentaro K. & Wagner, Andreas (2013). Selection is no more efficient in haploid than in diploid life stages of an angiosperm and a moss. Molecular Biology and Evolution. 30 (8): 1929–39. doi:10.1093/molbev/mst095


methods for targetted deletion of genomic regions? I would like to know what are currently used methods for targeted deletion of genomic regions in mammalian organisms or cell lines. I have heard of Zinc-Finger nucleases as a recent genetic engineering method, but I don't know if there are other methods, more efficient or better tailored, for the deletion of specific regions.

I can only provide you with a few pointers from memory, as an ad hoc search for "review of dna cutting techniques" was not prolific.

Please consider the provided information with precaution and only for pointers to help you do literature research.

cre/lox system and variants (best known), belong to SSRs (Site specific recombinases)
various Restriction enzyme based systems (see Homing Endonucleases)
meganuclease based tools
aptamer based
based on hybridizing n-mer probes which yields a reactive species nicking the DNA at the probe's-site when introduced to certain chemicals such as oxoacids
light twizzers and lasers /purely proof of concept (perhaps already commercialized?)
ZFNs and variants / protein based-probes . http://en.wikipedia.org/wiki/Zinc_finger_nuclease

There are definitely published reviews on this exhaustive topic, notwithstanding the dozens of books.
I would estimate that there are at least 10 commercial methods, and almost 100 methods in total when theoretical and proof-of concepts are included.

Naturally (literally!), the vast majority of methods will be based on the noncovalent interaction of an n-mer "homing construct"/probe a)attached to an nuclease or b)an
attachment site for a nuclease or c)participate in the reaction for the formation of a reactive chemical species to break the sugar-phosphate backbone.

I would speculate that most other methods are likely not practical in terms of either efficiency and/or affordability.

To learn about the applicability of the respective methods relating to your field of research, and be provided with an overview of the pros and cons of the methods, you will still need to find a good review paper.


What is the point of a runny nose during a cold? What is the biological purpose of having a runny nose during a cold?

Note, this is a different question than "What causes a runny nose" and other similar questions. Those question are about the cause, what starts the nose running. This question is about why? What is the body trying to do by making the nose run.

For example a cough, I'm guessing, is to help remove or loosen gunk in the lungs. Tears seem to have a point of cleaning the eyes. Diarrhea seems to have a point of clearing the bowels. Fevers have a point of killing viruses. Vomiting seems to have a point of getting rid of bad things in the stomach. Sweating seems to have a point of cooling the body down.

During a cold though, while reasons like inflammation etc cause a runny nose, what's the point? Why did we evolve to have runny noses during colds? What's the body trying to achieve by giving us a runny nose, specifically during a cold.

Edited by request for clarity

The biological purpose of a runny nose is to clear pathogens and allergens trapped in the mucus out of the nasal cavity and sinuses as a result of rhinitis or sinusitis.

Mucus is considered to be part of the innate immune system and provides mechanical and chemical defenses against pathogens.

Mucus acts as a barrier protection that is difficult for pathogens to breach.
Mucus is capable of trapping pathogens in it and when that mucus is swept out of your upper respiratory track through your nose or down your esophagus, the pathogens are removed from those areas as well.
Defensive proteins called Mucins, Lysozymes, and Immunoglobulins are secreted into the mucus and provide additional protection, as they can lyse or opsonize pathogens.

Mucus keeps epithelial cells moist so that they do not dehydrate as air passes over them. This in turn keeps epithelial cells healthy so that they maintain a tight cell layer in order to protect the underlying tissue.

As part of the mechanical defenses against pathogens, epithelial cells are ciliated and they rhythmically sweep mucus from the sinuses and nasal cavity mainly into your esophagus and digestive system, but can also move mucus into your nose. Most of the time we aren't even aware this clearance of mucus is happening and it travels down our esophagus into our stomach's and intestines where it can be excreted from the body. This is the case when you do not have an infection and your mucus is not viscous.

When you have an infection the inflammatory response is triggered by cytokines from macrophages. Those cytokines induce cells in the area to do many things. One is to increase mucus production. This may cause epithelial cells in your nostrils and nasal cavity and sinuses to secrete more mucus as well, and this will be swept away through your nose, where you will notice it as a runny nose.

Usually your nose is runnier with rhinovirus infections or with allergens than it is when you have a bacterial infection where mucous tends to be thicker and more viscous. The ciliated epithelial cells have an easier time moving the thinner mucous of a viral infection or allergy than the thicker mucus of a bacterial infection, so you notice a runny nose more when you have a cold or hay fever.

So in short, the biological purpose of a runny nose is that it is part of the immune response to clear pathogens away and protect your uninfected epithelial cells from being infected. It also clears out much of the debris and inflammatory proteins that are found at the site of the infection so that they do not remain in the area to further inflame tissue that is trying to heal. When you have allergies your immune system reacts inappropriately to a benign substance, and if the allergen finds its way into your nasal cavity, it will generate rhinitis and cause your nose to run.


What Freshwater Fish Are Affected By Magnetic Fields I am interested in knowing which freshwater fish are affected by magnetic fields.  I've heard that Lake Sturgeon are, but would like more references. This is for a project that will have buried 3 phase power cables.

Sockeye salmon species definitely do, although admittedly the interesting salmon are those that spend significant time in the ocean.
Here's some evidence that carp can.
Raindbow trout are also capable.
Zebrafish are also able.
Japanese eels too, of which some are freshwater.


Multiplication to formalize Microbiological Processes I am not from the field, but have a question regarding modeling in biology:

I know that some processes can be modeled with the mathematical multiplication operation, and wondered if anyone could give me an example (or examples).
Especially with regards to axonal growth and the chemical (de-)stabilization taking place which involve microtubuli and actin, I was wondering if these processes again could be formalized mathematically as multiplication of (several) variables.

I have looked through the internet but did not find anything so far,
any help is appreciated

Here's the quick answer you asked for, too big for comments so sorry if this is not a full answer either.

This paper is an example of cytoskeletal modelling.  the equations are not simple products (that is to say they have exponentials, derivatives and other non- multiplication operations in them).

This example reference is a simple axonal growth model.  You will see derivatives being modeled as products.  Not sure if this is what you are looking for.


Nutrition mineral intake method I always wonder if rather than getting minerals from food, can I directly eat them and will they have same effect as in food,
e.g. can I eat iron filings for iron, magnesium and drink hard water for calcium?

Is there any difference between having minerals through food or directly eating metals?

To absorb essential elements, body must get them in form of stable ions.
So for calcium and magnesium, our body absorbs them from the hard water in the same way it obtains from other sources and uses them identically.
For iron, we cannot obtain iron from iron fillings because iron reacts with water and other chemicals in our body which can produce harmful effects.
For further information on absorbtion of calcium from hard water visit http://goaskalice.columbia.edu/answered-questions/calcium-hard-water