How and why did mouth and nasal cavity evolve separate? My initial objection is that nose filters air, mouth is for eating but is used for breathing also, plus they both are used to create sounds. What is the cause and reason in this case, why do we need two "holes" and one is not good enough?

Neither the nostrils nor the mouth originally evolved for breathing.  Fish have (two pairs of) nostrils which they use to smell and mouths which they use to eat, but they breathe through their gills.  Some lobe-finned fishes (the ancestors to tetrapods) evolved a connection between the posterior nostrils and the oral cavity called choanae.  A fossil called Kenichthys is a transitional form in this development.  The evolutionary reasons behind this development are not particularly well understood.  (This should not be surprising when discussing something that happened in the Devonian.  It's only recently that the discovery of Kenichthys ended the controversy of whether chonae in tetrapods are homologous to posterior nostrils in fish.)

Basal reptiles have nostrils and mouths and can breathe through both of them, but do not have a separation between the oral and nasal cavities.  The next important development is a secondary palate (which separates the nasal and oral cavities).  This allows animals to continue breathing while swallowing food.  Animals without such a separation must hold their breath while swallowing.  This ability is certainly useful in many situations, and unsurprisingly several solutions to this problem have evolved in different lineages.


Can Meiosis 2 be called as mitosis? I know Meoisis involves a reductional division and an equational division.Say if I am asked a question to find the no. of divisions an egg mother cell undergoes in a Polygonum type division to form the 7 celled 8 nucleate stage, would the Meoisis2 be counted as a mitosis?
Then would it be said to have undergone 1 reduction division and 2 equational division(1Meoisis +2Mitosis).
Or is it just 1Meoisis +1Mitosis ?

Meiosis 2 can not be called mitosis.

You correctly recognized there are similarities between Meiosis 2 and mitosis. In other contexts, however, there are further differences. For instance Mitosis usually does not recombine genetic material (https://en.wikipedia.org/wiki/Meiosis), and the molecules that regulate Meiosis 2 and Mitosis are different. Calling "Meiosis 2" "mitosis" could lead to miscommunication.


What is the mechanism of reflex arcs? When a reflex arc occurs the signal from the receptor passes straight to the motor neuron instead of being passed onto the brain.

This is a rather simplistic explanation, I was hoping to make it more detailed. How does the body know when a threshold, heat for example, has been crossed and what mechanism is able to activate the reflex?

Also where does this occur, in the receptor or the spine?

Withdrawal reflex

You asked specifically about the withdrawal reflex and the receptors that trigger this. The initiation of the reflex arc is determined at the level of the nociceptors (pain-transducing receptors) in the epidermis. For the most part, these are part of “free” (not encapsulated) nerve endings of sensory fibers. These fibers course within spinal nerves whose cell bodies are located in the dorsal root ganglia adjacent to the spinal cord. There are two types of nociceptive endings:

mechanical: with parent fibers Aδ

transduce severe mechanical deformation

polymodal: with parent C-fiber units

transduce heat, cold, irritant signals

This picture shows free nerve endings in the epidermis. The boxed portion of the big picture is expanded in the bottom right.

The withdrawal reflex initiated by these receptors is mediated by a polysnaptic (multiple neurons) arc. The sensory neuron synapses with interneurons in the spinal cord.1 Some of these use glutamatergic connections to activate appropriate muscle groups mediating withdrawal. Others inhibit the reciprocal muscle groups (reciprocal inhibition) to allow this movement to be unimpeded.

Here is a cartoon diagram showing the spinal components of the reflex arc in a cross-sectional level of the spinal cord. Notice the interneuron between the sensory and motor neurons (although it's not labeled as such here):

Stretch reflex

In order to provide a broader picture of the basic principles involved in spinal reflexes, it's helpful to also mention the stretch reflex. This is perhaps the quintessential reflex arc because it is monosynaptic, exemplified by the patellar tendon reflex. The stretch reflex is fast, with a latency (stimulus–response interval) of about 15–25 ms (contrast the polysynaptic withdrawal reflex with latency ~70-100 ms.)

The stretch is initiated at the Golgi tendon organs. These are found at the junction between muscle and tendon. The (Ib) nerve fiber splays out and intertwines with tendon fiber bundles. The  nerve endings are activated by the tension of muscle contraction (either passive (as when the patellar tendon is tapped), or active (as during voluntary movement). The afferent sensory neurons directly excite homonymous motor neurons  (i.e. motor neurons supplying the same muscles), and inhibit (via interposed “Ia internuncials”) the antagonist muscles.

I have limited the discussion here to the withdrawal reflex you asked about and another basic spinal reflex arc as an illustration of principle. There are many other, mostly more complex reflex arcs that are beyond the scope of this answer, but I highly recommend checking out a neuroanatomy or neurophysiology textbook such as the one I've listed below if you'd like more information.

Note

1. Although the discussion here is limited to the anatomy of the reflex arc, there are additional synapses within the spinal cord that connect with ascending circuits, as described in the section about afferent neurons of spinal nerves in another answer. Some of these tracts end up at the cortex and are the basis for conscious perception. However, note that this process is multisynaptic and takes longer. The beauty of the spinal reflex arc is that it does not require information to travel all the way up to the brain and back down, which would slow down the response considerably. Practically, this means that you will pull your hand away from a hot stove before you have conscious sensory awareness of the burn.

Reference

Apart from linked article and images with sources below, all information is summarized from:

MJ Turlough FitzGerald,  Gregory Gruener, Estomih Mtui. Clinical Neuroanatomy & Neuroscience © 2012, Elsevier Limited.

Image 1 from: http://en.wikipedia.org/wiki/Free_nerve_ending

Image 2 from: http://www.tutorvista.com/content/biology/biology-iv/nervous-coordination/natural-reflex.php


Can Listeria monocytogenes endotoxin act as an A-B toxin? I think no, but I am not sure since Listeria is Gram-positive and probably has lipopolysaccharide (exception among Gram positive bacteria).

Can Listeria monocytogenes' endotoxin act like exotoxin A-B?
(In which component B lets component A inside the cell and component A causes the toxicity.)

Considering great research we did after the answer was accepted, I should add important information about the topic. The old (and accepted) answer follows in "" marks for the sake of clarity.

We found that in spite of the earlier reports, the newest ones failed to find endotoxin-like structure in the Listeria born material. Most academic discussions about the issue say there is no such thing called "listeric endotoxin", thus I gave a right answer to a "compromised" question.

I should say that question is still brilliant because it promoted great research and should be an important source for everyone looking for information about listeric "endotoxin"

  Listeria endotoxin is not a protein. Thus, is lacks enzymatic activity
  and acts indirectly by binding to sensitive receptors on macrophages.
  Thus, it can not cause lysis itself.

  Considering AB-exotoxins, A-subunit is a protein that has enzymatic
  activity (responsible for toxin action)  and subunit B has no
  enzymatic activity (protein responsible for binding to receptors).

  Thus, the answer to your brilliant question is NO, Listeria endotoxin
  cannot act as AB-exotoxin being nonprotein and non enzymatic
  substance.

  Also, don't be confused with Listeriolysin O, which is listeria's
  eXotoxin protein which is pore-creating protein.


Are microwaves harmful to us? They closed my question on the Physics Stack Exchange because it wasn't a purely physics question, so I'm trying here.

Recently I've come across the topic of scrapping microwaves, and the various warnings about the potential dangers. I've found out that generally speaking higher frequency radiation is more harmful, also that frequency itself is not the sole factor of harmfulness; as one question on the Physics site remarks the fact that microwaves and Wi-Fi use the same 2.4 GHz range, yet Wi-Fi doesn't cook. Anyway, I saw on a website:

  Don’t take apart the magnetron or play with it for several good
  reasons! First, there is the obvious danger of 2.45 GHz microwave
  radiation.

There are two problems I see with this warning. First of all isn't 2.45 GHz well into the radio wave category? And also radiation of 2.45 GHz wouldn't be harmful in and of itself, right?

Also a comment from the Physics site:

  wifi would be dangerous because of the microwaves, but it is limited
  to very low powers

This seems to imply that microwaves in and of themselves are harmful.

$2.45~\rm GHz$ is well into the microwave region, which is usually defined as radio waves with a frequency of greater than $1~\rm GHz$.

Microwaves can be harmful. If you stood in front of a $1~\rm MW$ microwave dish, you would be cooked basically instantly. But that doesn't mean they are harmful in small doses: if you stand in front of a $1~\rm MW$ visible light source, you would also be cooked. You can hold your hands in front of a fire, but sticking your hands in would be bad. Like heat and visible light, microwaves aren't intrinsically harmful in moderation, but they can be deadly if you have enough of them.


Creating animal models I was wondering how a scientist in a lab may know which type of animal model to use. I have been looking at the effect of a protein on a disease. And have thought about the ways that’s i know this has been done in other research-
- deletion of gene which encodes for protein
- insert GFP by Gene for protein leaving gene intact
- or insert gfp by gene for protein deleting the gene
However I cannot seem to understand how a scientist decides to choose a certain model?

If you look at the definition of a model organism as this can be found on the Nature Homepage, this clarifies quite a lot:

  An organism suitable for studying a specific trait, disease, or
  phenomenon, due to its short generation time, characterized genome, or
  similarity to humans; examples are a fly, fish, rodent or pig, whose
  biology is well known and accessible for laboratory studies.

So you want an organism, that:

can be bred in large numbers
has a sufficiently short generation time, so you can analyze several generations of it
is well characterized
sufficiently close to the organism you want to learn more about (mostly: Humans), so the findings can be transfered
can be mutated and has your gene/protein/etc. of interest
has been sequenced completely

Besides this general considerations, practical ones also play a role. If you don't have a fish facility on hand, you will most likely not start using zebrafish as your animal model.

There are certainly more requirements, see one of the references.

References:

Requirements and selection of an animal model.
Selecting appropriate animal models and strains: Making the best use
of research, information and outreach
Basic Principles in Selecting Animal Species for Research Projects


What is meant by Gene Expression Level? I am new to BioInformatics, I want to know what is gene expression level and how it is determined.. Anyone who can answer this silly question.

“Gene expression level” is an imprecise and partially ambiguous term
  that should be avoided.

Many (but not all) genes have the information to produce proteins†, but there is no need for this information to be used at any given time — it depends on the requirements of the organism or cell. For example the DNA of lung cells contains the information to produce the protein chains of haemoglobin, but it is never used in those cells. We can say that “the gene is not expressed”.

So the absence of expression is fairly easy. However, for a protein-coding gene the meaning and quantitation of expression is more difficult. That is because in expressing the information in the gene the DNA is first transcribed into mRNA by RNA polymerase, and then that information that encodes a protein can be translated into protein on the ribosome.

The word level refers to quantification, and is a sloppy substitute for quantity or perhaps rate (quantity produced in unit time) or perhaps relative quantity.

But the main difficulty is whether in quantifying gene expression you measure the quantity of mRNA synthesised under standard conditions or the quantity of protein produced.

If you are a bioinformatician encountering this term, my bet is that it is in relation to the currently (2018) popular RNA-Seq technique, which in fact provides relative measurements of the quantity of RNAs of different types produced under standard conditions. This is generally expressed in units called FPKM — Fragments Per Kilobase of transcript per Million mapped reads. The difference between this technique and the northern blotting mentioned by @Hawkeye, is that the latter is used to detect a single mRNA, whereas RNA-Seq applies to all the mRNAs that are present in a sample.

In the field of proteomics, it is possible that the term is being used in relation to the amount of protein produced, which may be roughly quantified by two-dimensional gel electrophoresis.

†Some genes encode RNAs that do not encode proteins (ribosomal RNAs, transfer RNAs, RNAs involved in splicing and in modification of rRNA, microRNAs etc.). The expression of the genes for these will end with the synthesis of the RNA.


Why are organs not harvested from deceased cancer patients? From my understanding, cancer is not contagious, and if a cancerous cell from a patient is introduced to a healthy person, then the immune system of the latter can destroy this cell. In such a case, why are internal organs from cancer patients not used for donation? Is this because there is a small probability of the immune system failing? Isn't there any other way to make these organs usable again?

There are different reasons why cancer patients are mostly excluded from donating organs.

Although the probability of transmitting cancer is small, it is not zero. Also tumors tend to form metastases over time, which spread throughout the body. It is possible that a cancer has formed metastases in other, distant organs, which are too small to detect. Since recipients of organs have to take strong immune suppressing medication to prevent the rejection of the transplant, the immune system might not be able to fight the cancer cells anymore. Because of this medication, transplant patients already have a higher chance of getting cancer, because their immune system does not capture cells when they go rogue. See reference 1 for a more general description and 2 for the detailed report, reference 3 for the higher cancer risk of transplant patients.
Tumors can go dormant when they are treated with chemotherapeutics to evade destruction, but these dormant cells can re-wake. If this happens after the transplantation of an organ, this is obviously bad for the recipient. See reference 4 for details on mechanisms.
Cancer patients who died from the disease have often been treated with agressive drugs like chemotherapeutics. While these attack mostly the fast dividing cells of the tumor, they also have more or less strong side effects on the body. A lot of organs are simply not in the state (or have a strong chance of being in this state) anymore to be transplanted. Nobody wants to transplant a dysfunctional organ. See reference 5 for details.

References:

Cancer Spreads from Organ Donor to 4 People in 'Extraordinary' Case
Transmission of breast cancer by a single multiorgan donor to 4
transplant recipients
Cancer in the Transplant Recipient
Tumor dormancy as an alternative step in the development of
chemoresistance and metastasis - clinical implications
Long-Term Side Effects of Cancer Treatment


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

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

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

So what are good explanatory models for consciousness?

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

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

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

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

This is also reviewed in this paper:

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

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

Again, citing from the first paper:

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


Influence of artificial sunlight on the human body In a hypothetical scenario, where a large, permanently manned craft is in a continual orbit, and natural sunlight cannot be used as the craft may keep moving and turning, artificial sunlight is used in the form of LED panels.

My question is this: Will the LEDs have any adverse effect on the human body? The LEDs are of the SoLED variety which have very low IR levels and almost nil UV light levels, have any adverse effects on the body? I suppose the lack of UV may cause some disturbance in Vitamin D and melanin levels. Is this valid? Would there be any other problems?

Yes. Natural sunlight doesn't have a good substituent.

Melatonin levels and circardian rhythms are directly affected by natural sunlight.

As far as LEDs goes, a french study concluded that blue light may have photochemical risks and affect our retina.

Source

http://www.ledinside.com/knowledge/2014/4/effect_of_artificual_and_natural_light_on_the_human_body


Can mRNA vaccine have flaws and generate the wrong spike protein? Someone asked me if SARS-COV2 mRNA vaccine could create the wrong spike protein and have a negative effect on our immune system. Since I know too little about biology I couldn't answer that and started doing some deeper research than I did before on mRNA. But I can't seem to find anything to answer my question (it most probably is because I lack the knowledge in this field).
So here are the two main questions of this problem:

When created, can the mRNA vaccine have flaws and when injected generate a different spike protein than the SARS-COV2 one ?
If so can the spike protein be harmful to our system in any way ?

I am sorry for any term not correct in this context.

The mRNA won't be entirely perfect, but the imperfections will not matter.
The spike protein is big, encoded by thousands of base pairs in the virus. In the virus itself, it's not entirely homogeneous: there are always going to be small mutations that cause different variants to be produced, but nearly all of those are nearly identical.
The mRNA in a vaccine may also have some degree of copying errors introduced during amplification, which will produce some distribution of variants. Though the specifics are different, random copying errors in a synthetic process and random copying errors in natural viral replications will produce qualitatively similar types of distributions (more serious errors producing truncations and recombinations can occur in both as well, but similar arguments apply and they're even less likely to be functional).
Moreover, since only the spike protein is there, it can't actually produce a damaging infection, only teach your immune system what an infection looks like. Finally, since it's easy to validate a batch of mRNA via sequencing, ordinary quality control procedures should be fine to make sure what goes into the vial is what was planned (modulo the variances described above, when they are at a low enough frequency to fall below the threshold of discrimination).
In short: don't worry about the mRNA varying. If you're going to worry about something, worry about the virus varying enough that our nice, tightly controlled mRNA doesn't match it any more.


What are sources for learning bioinformatics for self-learning? What are the sources for learning bioinformatics(books, websites/MOOCs)? Does it require prior knowledge of programming language because I am a complete noob when it comes to programming language.

Learning a language such as python or perl is almost necessary.

You might have a look at coursera.

There are quite some bioinformatics-oriented courses:

https://www.coursera.org/courses?query=bioinformatics&languages=en

University of California San Diego has a series of bioinformatics courses, with one that seems made for beginners in programming:

https://www.coursera.org/course/algobioprogramming

I haven't had a detailed look at this one, but I liked their more advanced courses.

In coursera, the courses are often organized in so-called "specializations" which give you a certificate, but are not free. However, you can normally enroll to individual courses without paying.

I would also advise learning how to use a UNIX-like command-line environment, and tools such as sed, awk, grep.

The following sites might be good for this:

http://www.grymoire.com/Unix/

http://software-carpentry.org/lessons/

The scope of the latter is broader, and the things they teach could be valuable if you want to do scientific programming in general.


Does gray/white hair turn gray/white from a normal hair? or does a gray/white hair actually grow gray/white originally? I am really curious if hair actually tuns white/gray from default color, or does it have a defect as it is made and grows out of your head a different color?

It can actually be for both reasons and it more or less depends on the age what happens. The pigment of the hair is produced by pigment cells (the melanocytes) in the hair bulge and is then integrated into the growing hair (image from here).

The pigment melanin produced by these cells can be destroyed by reactive oxigen species which then leads to grey hair which can still be pigmented at the tip.

The other possibility is connected to the hair cycle. After growing for a while the growth stops, the hair falls out and the hair follicle goes into a resting state. In this phase the pigment cells die. When the hair follicle starts a new hair cycle, the pigment cell population in the hair bulb is renewed from the melanocyte stem cells in the hair bulge. Over time the number of the melanocyte stem cells gets lower until there are none left eventually. At this point new hairs will grow without pigment and be grey/white.

There are two interesting publications about this topic:

Oxidative Stress in Ageing of Hair
Melanocyte Stem Cell Maintenance and Hair Graying


Difference between Medical and Airport scanner radiation What is the difference between radiation doses of a medical scanner and airport security scanner (X-Ray full body scan)? Is it the same kind of radiation? Does it pose any danger for people who fly often?

The type of radiation is quite different in a medical X-ray vs. an airport scanner.

Medical X-rays are high frequency (beyond ultraviolet) radiation, typically on a wavelength of a few angstroms.  While I would emphasize that @Ram is right to point out that there is not very much radiation in a medical X-ray since electronic detectors have been in place over film, the radiation itself is capable of penetrating the entire body and causes ionization.  The body can tolerate a certain amount of this, but that's why we use X-rays - they go through just about anything but bone/minerals and metals.

Airport security scanners emit terahertz radiation, which has a wavelength between microwave and infrared.  This is a very low level of energy per photon.  Terahertz radiation will not penetrate more than a centimeter of light material, which is more suitable to find hidden metal objects (which reflect terawaves).  Relative to X-rays it causes practically no radiation damage.  The intensity of the radiation is also pretty low since these scans are also detected by digital cameras, which are quite sensitive.

Compare the machinery.  X-ray technicians, who might have to take dozens of X-ray exposures a day, usually go behind a protective screen to take a medical x-ray.  The airport body scanners are open to the air and the terahertz radiation spills out into the crowd and the workers stand by it every day.  It has practically no expectation of being hazardous.  This device is pretty good as frequent fliers can have as many scans per year as are needed and health concerns are not significant.

Its always possible we might find some issues with Terahertz radiation in the future, but its hard to imagine it - its safer than standing 2 feet away from a working, closed oven.


For humans, why is red the color of distinction rather than green? The human eye is most sensitive to the color green. However, for some reason red is often selected as the color of distinction or alert. For example, in Renaissance times, painters would outline their figures in a thin red line. In manuscripts, a "red letter" (or "rubric") was used to emphasize an initial capital. Today, we routinely use red for emergency lights or whenever we want to call attention to something. Considering that red is the color our eyes are least sensitive to -- and green the most --  it seems counter-intuitive that we would use red when we want to draw attention to something. Why is this?

The reason is more historical than biological.

Our own eyes are more sensitive to green light, and ambient light is mostly green (we are a diurnal being). If you start doing real botany, you will notice that you can distinguish a lot of species just from the shade of green (and for trees, this also from far away).

Red is a difficult colour to produce, and often not very stable over time, and in nature is not so frequent. But it was used because it was also not very common in constructed environments. For example, for the Romans it was a symbol of power (and richness) because it was very expensive to produce red dyes. So red is visible because of the contrast with other colours.

The most visible colour is yellow: the "red" cones are really centred on yellow, and the "green" cones are still very sensitive to yellow. A good yellow appears brighter than any other colours because it stimulates both  the medium-wavelength cones and the long-wavelength cones in the human eye. Now emergency services tend to use yellow.

Note: red is not so special (but having a third type of eye cone is very special). Blood is red, but one rarely sees it as red: it quickly turns dark. Fruit? I think blue, green, yellow, orangeish, and dark brown were more common than red (and I recognize a tree by its leaves, from far away, so I'll know what fruit there are).

Traffic light: lights were already very yellowish, and blue, purple, and violets are not that visible, so green, orange, yellow, red, and also white are the most logical colours. I think yellow and white were too similar (especially in cities), because they were the colour of illumination and headlights. Note: in maritime traffic, red, green, yellow, and white are used (not orange).


Mutate from non-GM to GM? Would non-GM crops such as Grains, Fruits, & Vegitables retain their non-GM make up if they were to be re-planted in soils that have been made entirely of composted GM plants and GM plant matter?
Or would the GM plant matter still retain those properties enough mutate the transplanted or planted crop?

The process of genetically modifying crops is performed in a lab. Genes would not leak into planted organic crops from compost any more than they would move from decomposing soil nematodes, earthworms, or manure. So no, organic plants would not be genetically modified. However, the labeling of a crop as "organic" is not always standardized, so it could be a cause of concern for some people who do not understand the process.


Why is extracellular measurement of action potentials so different from intracellular? I had read in a paper that present a low noise amplifier the following:

"...This level of input signal is larger than both typical action potentials (<500μV) and local field potentials (<5 mV). If a larger input signal is expected, the amplifier’s supply voltage can be increased at the expense of higher power consumption.We verified that our neural amplifier works in a real recording environment by using it to record action potentials in the robust nucleus of the arcopallium (RA) of the anesthesized zebra finch. Data were taken with a carbon fiber electrode (Kation Scientific, Inc.) electrode that had an impedance of approximately 800kHz at 1 KHz. A long extracellular trace and a short extracellular trace recorded from our amplifier (normalized by its gain) are shown in Figure 2. They were found to be identical to that recorded by a commercial neural amplifier (A-M Systems, Model 1800)."

Link:

  http://www.rle.mit.edu/acbs/pdfpublications/journal_papers/woradorn_tbcas_neural_amp.pdf

Please, can someone help me to understand how we can measure an action potential as shown in figure 2? We know that action potential amplitude is approximately 70mV as shown in figure 1 but figure 2 shows that is approximately 70μV.Is this possible?

Figure 1

Figure 2

I'm going to mostly duplicate my answer to another question Neural signals amplitude since it's exactly the same as this one, but it has no upvotes so I can't vote as duplicate. Once I get an upvote either place I'll vote to close the other.

In the first figure, those voltages refer to the difference between the inside and outside of the cell (i.e., -70mV means the cell is 70mV more negative than the outside).

You can't possibly measure that potential difference from outside of a cell. When you do extracellular recording, like in the second figure, you are measuring spatial differences in ion concentrations that occur due to ions flowing in and out of cells. For example, when a cell fires an action potential, lots of positive ions flow into the cell; this makes the area just around the cell slightly more negative than an area further away. The magnitude of this potential as measured depends greatly on your recording configuration, the type of signal you are recording (i.e., population activity or just a single cell; synaptic currents versus action potentials), how close your electrode is to the signal you are recording, and where your ground is (or position of both of your electrodes if you are doing a bipolar recording).

Also, in this second recording, either the voltage is reversed (i.e., the electrode near the cell is taken as ground), or it is actually measuring return currents in the dendrites of the cell; otherwise, the action potential would be in the opposite polarity (downward first, then upward) compared to inside the cell.

Although it varies, in most cases the signals you record extracellularly are on the order of microvolts to a couple of volts.

Lastly, in the quote you reference, the line before it was:

  The total harmonic distortion (THD) of our amplifier stays
  below 1% for input signals smaller than 7.3 mV peak-to-peak.

That article is describing an amplifier system for recording extracellularly (potentially for a brain-machine interface). They are saying that one type of distorting noise is not a problem in their amplifier at the input voltages you would expect in an extracellular recording of spikes or local field potentials, which indeed would usually be less than 5 mV. This amplifier would not be suitable for recording intracellularly.


What would happen if most the fat in your body was rapidly converted into energy in 2 minutes? It all started out as an argument I had with my friend.He said that "it would be the equivalent of catching a fire and burning"

But all I thought would happen is that you would now be very hyper because you have a lot of energy in you body.

Please scientific answers only.

I also happen to be in the 11th grade and I dont do bio, but I knew this would be the best place to post the question.Please dont use scientific concepts I would not understand.

You guys are probably going to ask me to give an example of a way through which it might happen. So here is one way I have come up with:
Lets say the AMPK protein malfunctions and causes all the cells to release all this energy.

It depends, but you're going to die.

Specifically, it depends on how fat you are. Even Andreas Munzer is going to die. At only 3% body fat, burning all his fat (9kcal/g) would "only" increase his internal body temperature by 270 degrees C. Factoring in the energy required to boil off his body moisture and adding in body heat leaves Andreas at  ~200 C or so (pretty unevenly distributed) minus whatever heat he could give off through his skin in two minutes. He's definitely dead, but probably not on fire. The flash point of animal fat oil is about 300 C, so most of his body probably isn't going to be hot enough to burn on its own. There will probably be some smoking, though.

The average body fat percentage is more like 22%(for males), and the numbers there are unequivocal. That person is going to catch on fire, as their body temperature is going to go up about ~1800 C after boiling off all the water. That's enough to melt your titanium hip implants.

In short: you'll die pretty quickly, and then you might catch on fire before your two minutes are up, unless you're Andreas Munzer or another professional bodybuilder.


Constant or variable number of chiasmata during recombination? During recombination, is the number of chiasmata consistent for each gamete and are the chiasmata regions consistent within a single organism?

There is a large amount of variation in the distribution and number of chiasmata or crossing overs (COs). The total number of chiasmata per cell can vary within the same organism.
Where chiasmata occur along the chromosome is also not consistent cell to cell. Hotspots are 1-2kb regions that experience elevated recombination compared to neighboring genomic regions. A way to think of the distribution of COs is that ~80% of recombination happens in hotspots which comprise ~10% of the genome.

Recombination depends on the chromatin context, so chiasmata are rare near the centromere and positive interference results in chiasmata being spaced out along the chromosome. A good prediction of total chiasmata number per cell is at least 1 per chromosome. Some researchers argue that one CO per chromosome arm is more accurate.

Below is a link to a good article that expands on some of the ways recombination varies in humans.
http://www.nature.com/nrg/journal/v8/n1/abs/nrg1947.html


How do poiklotherms survive at different temperatures even though enzymes work at specific temperature? Since enzymes have an optimum temperature at which they are able to catalyze the reaction best and increasing the temperature above optimum can even damage them, how do poikilotherms survive as they change their body temperature according to environment unlike homeotherms. Also wouldn't their metabolism stop with increased temperature?

Instead of viewing poikilotherms as having the same temperature as the environment, view them as lacking an internal thermoregulatory system. Poikilotherms indeed suffer from not having the ability to regulate their internal temperature.

Homeothermy is ecologically advantageous, allowing optimal functioning at a range of temperature. Poikilotherms, therefore, are more restricted in their habitat range, have to depend on external mechanisms for maintaining temperature (eg: Hibernation, Shade-loving lizards, burrowing in desert animals) or simply die due to environmental change (eg: poikilothermic fish are the earliest to die from a thermal runoff into a water body).


How to calculate Fst from AMOVA I calculated an AMOVA from a genind object, with one hierarchical factor. In the table I obtain there are SSD values (for my grouping factor,"Error" and total) and sigma2 values (for my grouping factor and "Error")

I have two questions:

What does "error" stand for?
How do I calculate Fst? Which values do I have to use?

I have never performed an AMOVA myself and I don't know what a genind object is. But ...

Error

Typically, "error" can also be called "residuals". In other words, it is the sum of squared deviation between the data and the regression line (just like in any regression model). You might want to learn a little bit about regression and ANOVA to understand your AMOVA.

Fst definition

From Nei 1973 (very good paper, I recommend reading it),

$$F_{ST} = \frac{H_S-H_T}{H_T}$$

, where $H_S$ is the average subpopulation variance in allele frequency and $H_T$ is the total variance in allele frequency.

What you probably got from the AMOVA output

You should have these info in your AMOVA output. If it only give you the total variance and the between group variance (which is what is used for the F-test), then just remember that the among variance is the total variance minus the between group variance.


Does avoiding medication that alleviates symptoms shorten the length of a cold? People use over the counter (OTC) medications to relieve symptoms of the common cold.

However, these symptoms are part of the immune response, right? They are driven by the body responding to the virus and attempting to make the body less habitable and thus easier to kill it off.

Do OTC medications that reduce cold symptoms cause the cold to persist longer? Should such medications be avoided if the goal is to reduce cold duration rather than symptoms?

It is plausible but by no means established that antipyretics (fever suppressors) in particular could increase the duration of infection/symptoms, because fever is part of a functional immune response.

From Graham et al 1990 (a small [n=56] randomized trial of the use of antipyretic pain relievers in volunteers experimentally infected with rhinovirus):

  Use of aspirin and acetaminophen was associated with suppression of serum neutralizing antibody response (P less than .05 vs. placebo) and increased nasal symptoms and signs (P less than .05 vs. placebo) ... There were no significant differences in viral shedding among the four groups, but a trend toward longer duration of virus shedding was observed in the aspirin and acetaminophen groups.

In other words, it looked like the people who took aspirin or acetaminophen had weaker immune responses and more cold symptoms. They might have been infectious for slightly longer, but it's hard to tell (also, duration of infectiousness is not the same as the duration of symptoms ...)

However, a review (Kim et al 2013) concluded that NSAIDs (non-steroidal anti-inflammatory drugs) slightly (but non-significantly) reduced the duration of illness.

  In a pooled analysis, NSAIDs did not significantly reduce the total symptom score (SMD -0.40, 95% CI -1.03 to 0.24, three studies, random-effects model), or duration of colds ([mean difference] -0.23 [days], 95% CI -1.75 to 1.29, two studies, random-effects model) [emphasis added]

Here is the figure from that analysis:

"Common cold" is often considered synonymous with rhinovirus infection, but may also include mild influenza infections. An observational study on influenza A and two other infections (Graham et al 2000) found

  There was a striking correlation between antipyretic therapy and duration of illness in subjects infected with influenza A and S. sonnei, but not R. rickettsii ... Multivariate analysis suggested that antipyretic therapy prolonged illness in subjects infected with influenza A, but its use was the result of prolonged illness in those infected with S. sonnei.

In other words, to the extent that one can really distinguish causality in an observational study, it seemed that taking antipyretics made influenza illness longer, but that causality went in the other direction for S. sonnei (i.e., people took more antipyretics when they were sick for longer).

The usual caveats associated with small studies and researcher degrees of freedom apply when interpreting the results of these studies ...

J Infect Dis. 1990 Dec;162(6):1277-82
Adverse effects of aspirin, acetaminophen, and ibuprofen on immune function, viral shedding, and clinical status in rhinovirus-infected volunteers.
Pharmacotherapy 2000 (20), 1417–1422.
(doi:10.1592/phco.20.19.1417.34865)  Effect of antipyretic
therapy on the duration of illness in experimental
influenza A, Shigella sonnei, and Rickettsia rickettsii
infections.
Cochrane Database Syst Rev. 2013 Jun 4;(6):CD006362. doi: 10.1002/14651858.CD006362.pub3.
Non-steroidal anti-inflammatory drugs for the common cold. Kim SY, Chang YJ, Cho HM, Hwang YW, Moon YS.


How far is stem cell research from being to generate a new organ? How far are we from being able to use stem cell research to generate a sperm, a heart, a liver, and a kidney?

In stem cell research, my understanding is that you must start off with some cell to initiate the process. Can this be any cell, or must it be an embryonic cell made out of a sperm and an egg?

Sperm can already be generated using stem cells http://blogs.discovermagazine.com/d-brief/2016/02/25/scientists-grow-working-sperm-from-stem-cells/#.V-UADBV94o8
Also, heart, liver and kidney cells as well.
http://www.popsci.com/scientists-grow-transplantable-hearts-with-stem-cells
http://www.ncbi.nlm.nih.gov/pubmed/26458176

Full organs are still far. The main problems are to grow them separately from the rest of the body (embryonic development) and to vascularize them.
One solution is to grow them in other animals http://www.dailymail.co.uk/sciencetech/article-3442818/Growing-human-organs-farm-creatures-takes-step-closer-New-guidelines-allow-research-human-animal-hybrids.html

There are experiments done with some success in using "decellularized" kidneys as a scaffold to "grow" a new kidney by perfusing stem cells into it. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4927010/

There are the so-called organoids, very little agglomerates of different organ-specific cells differentiated from stem cells. They are far from being functional organs but it's definitely a start. http://hub4organoids.eu/organoid-technology/

Some labs are experimenting with 3D printing. They use stem cells to derive all the organ-specific cells needed and then they try to rebuild a functional organ by printing cell by cell, layer after layer. http://www.nature.com/nbt/journal/v32/n8/full/nbt.2958.html

Lastly, embryonic stem cells are not strictly needed anymore, they can be substituted (in most of the cases) by iPS that can be derived from many different adult cells (i.e. no embryo is needed).


Name of dsRNA (or dsDNA) where all strands are identical What is the name of dsRNA (or DNA) where all component strands are identical (i.e. where the complex consists of multiple copies of the same ssRNA)?

Example: 2 identical ssRNAs forming a dsRNA

C C G C G G C G G
| | | | . | | | |
G G C G G C G C C

Furthermore, is there a different name for it depending on the degree of complementarity (full Watson-Crick complementarity vs. full complementarity with non-Watson-Crick basepairs vs. lower complementarity due to bulges etc)?

My thoughts

You probably wouldn't say "RNA homo n-mer" (for the example above "homo dimer/2-mer") since I assume that would be referring to a 2-nucleotide long ssRNA?

Can you use the terms dimer, trimer, tetramer, 5-mer, 6-mer etc in multiple ways; (a) referring to the binding of nucleotides to each other to form a polymer/n-mer of nucleotides i.e. polyribonucleic acid, and (b) to whole ssRNA or dsRNA binding to each other to form a "dimer"?

You also probably wouldn't refer to it as a "homo duplex" since that refers to  something related to chromosomal crossover.

Such a nucleic acid sequence is described as a palindrome or palindromic.

Wikipedia has an entry for palindromic sequence in which it is defined as:

  A palindromic sequence is a nucleic acid sequence on double-stranded DNA or RNA wherein reading 5′ (five-prime) to 3′ (three prime) forward on one strand matches the sequence reading 5′ to 3′ on the complementary strand with which it forms a double helix. This definition of palindrome thus depends on complementary strands being palindromic of each other.

It should be noted that this is a description (rather than a name) that is usually applied to segments of larger nucleic acid molecules or to synthetic constructs. I am not aware of a generic name for short dsRNA (or dsDNA) like the one in the question as they are not, to my knowledge, found in Nature and so there has been no reason to devise a name for them. Thus, there are no names for variants either. If you wish to write an article about such things you would need to invent your own terms, but keep well clear of ‘-mers’ (see use of e.g. tetramer).

The sequence presented in the question does not conform to the Wikipedia definition, above, as it has a central mismatch and is therefore not a perfect double-helix. However, as the use of the term palindrome for nucleic acids is a somewhat cavalier extension of the general use of the English word palindrome (an example of which is “ABLE WAS I ERE I SAW ELBA”), I would regard a further minor modification of the Wikipedia author’s definition as unexceptionable.


How quickly is antibiotic resistance lost? I would imagine the bacterial genome is highly conserved and limited in its space, but maybe I am wrong.

If you were to take a strain of antibiotic resistant bacteria and kept them isolated, but fed well and so forth, how long would it take for them to lose their resistance? A year? A decade? 100 years? 1000 years? At some point it seems like that trait would disappear, but I have no feeling for how long. Please support your answer with a relevant citation.

EDIT:

My purpose is simple: I am thinking about a strategy for dealing with antibiotic resistance. If we were to ban them across the entire world (could be impossible) how long would we need to wait before they would be usable again. If it was a matter of years, then we could almost do a rotation of existing antibiotics (if we had enough) because I would rather not live in post-antiobitic world.

Antibiotic resistances in bacteria is commonly encoded by extrachromosomal DNA, the plasmids. These are circular pieces of DNA, which are much smaller than the hosts genome and which replicate independently from it. See the image from the Wikipedia:

These plasmids can be transfered between different bacterial cells, which then also get resistant. Plasmids are divided between daughter cells, when the parent cell divides. One of the few exceptions seems to be Mycobacterium tuberculosis, which does not seem to carry plasmids but also develops resistances. It has been hypothesized that they contain extrachromosomal single-stranded DNA ("Does Mycobacterium tuberculosis have plasmids?")

Regarding your question: Plasmids which carry antibiotic resistances will only disappear, when the antibiotic is not seen for a while, since the cells, which don't carry it, have a growth advantage over cells who are still carriers (since they save the energy of forming the plasmid). However, these resistance plasmids are nothing new, evolutionary speaking. They appeared as a countermeasure against fungal toxins.

In the lab, bacterial strains loose plasmids within a few days, when not kept under selection pressure according to my experience. There are a few paper who looked into it:

Natural selection, infectious transfer and the existence conditions
for bacterial plasmids.
The persistence of parasitic plasmids.
The evolution of plasmid-carried antibiotic resistance


Why does the DNA of Bacillus subtilis not contain DNA families of 20-37 members? I am reading the book "Molecular biology of the Cell, 6th edition" and in chapter one page 18 the following figure is included

I am presuming this figure represents all genes within the Bacillus subtilis, which makes me wonder: why are there no families with 20-37 genes? There is a group for 4-19, and one for 38-77. What happened to all sizes in between?

Based on the paper (open access) from which this figure was adapted, the 38-77 group consists of 5 gene families with 38, 47, 57, 64 or 77 members. In contrast, there are 284 “families” with 2 members, 91 with 3 members, 42 with 4 members, 25 with 5 members, etc. This is clearer in the original figure:

Thus the larger gene families are outliers and there simply exists no gene families in B. subtilis with 20-37 genes (at least by the methodology of this paper).


What happens to the absorbed blue and red light in the chlorophyll molecule? If the chlorophyll molecule (its chromophore) absorbs red and blue light and reflects green light, shouldn't the absorbed blue and red light be emitted back when its excited electrons relax?

It is glad to say that we can enter to this question due to having of valuable theorem of 1st law of thermodynamics. Energy cannot be destroy but it can convert in to another type of energy.The chlorophyll molecule decide it to, become photo energy to chemical energy.

while happening the electron transport chain electrons are going through the primary receptors. This is not happening as the electrons traveling on a trip, this is really a complicated procedure.While they are passing through the primary receptors some reactions are happening. So from which should be contribute to have energy for this reactions. By the energy of absorbed blue and red lights. So it turns it to chemical energy. It store as ATP, and NADPH. So there is no more way for emit that light away. This scenario  is firm by the following.

Reference
- The Light Reactions of Photosynthesis. In: Biochemistry. 5th ed.


When does the first "random mutation" of DNA (have to) occur? When reading about how evolution happens, "random mutations" are often spoken of.

As far as I understand, "random mutation" refers to the unsuccessful self-replication of DNA (the new version of which is then passed on correctly). But when does this change happen? During fertilization? Shortly before (in the sperm or egg itself) or shortly thereafter? And what is the last possible time for that to happen so that it gets passed onto every cell in the body and eventually brings forth a new physical trait?

I hope the questions make sense, I don't have a lot of background in biology.

Edit for completeness: When is the earliest possible moment for a mutation to take place? (A mutation that will ultimately make it to the offspring and eventually cause a new trait.) Is it in the ovaries/testicles or even before that?

Random mutations happen everywhere in the body all the time. Most are harmless, some cause problems, some cause cancer. Some are beneficial. If a beneficial mutation occurs in the germ cell line, it will be passed on to the offspring. Depending on how beneficial it is, it can spread like wildfire (the mutation allowing lactase to continue to be expressed after infancy is a good example of this, as is sickle cell trait); if it is harmful, the carrier may die before birth, in infancy, etc. If it causes a later onset disease (e.g. early Parkinson's)1, the carrier has time to mate, reproduce and pass the disease on to their offspring. More and more diseases are being found to be genetic in nature now that genetic studies are so much easier to perform.

Again, for a mutation to be passed on, it must occur anywhere in the germ cell line of a parent, right up to the last stage before being released as an ova or a sperm cell, during fertilization, or during the very early stages of embryonic development in cells genetically programmed to become germ cells. If it occurs after fertilization, it will not affect that person, but its offspring. Depending on how early the mutation occurs, it may affect other parts of the reproductive system as well.

If a mutation happens in an embryo in a non-germ cell line, it may affect that person mildly, profoundly, not at all, or the embryo may die if it is a deleterious mutation in a critical organ system, say the heart.

But you need not put random mutations in scare quotes. I'm pretty sure you don't trust me, but they happen all the time, in every tissue, in you yourself as well as in everyone you know and everyone you don't know. And, by the grace of God, many of them can be repaired, and we don't ever have any ill effects from them. Alas, not all are repaired, and some lead to cancer.

Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1


What is the human species divergence time How far back along the evolutionary tree do we have to go to find divergence to a completely different species to Hom. sapiens? I don't count Neanderthals because it seems that part of our genome contains fragments of Neanderthal DNA, and therefore, according to the species definition, Humans and Neanderthals could not have been an entirely different species. What about Denisovans? Is enough known about their DNA to consider them a completely different species? In fact, is it even possible to distinguish 'a species' from the DNA alone?

The erectus line that gives rise to antecessor is your best bet, at about 1.2 MYA. http://www.nature.com/nature/journal/v485/n7396/full/485033a.html
part of the problem is you are hitting the limit of where the term species is useful, once you get really close to the speciation event the term breaks down becasue everything is a ring species once time is included. Erectus includes both our ancestors and populations wholly isolated from us. Its like trying to draw a line between yellow and orange on a spectrum.


Why are sugars in whole fruits not digested the same way sugars in juice are? In this paper of the WHO, it is claimed that we should limit our consumption of free sugars:

  WHO recommends a reduced intake of free sugars throughout the
  lifecourse. [...]  Free sugars include monosaccharides and
  disaccharides added to foods and beverages by the manufacturer, cook
  or consumer, and sugars naturally present in honey, syrups, fruit
  juices and fruit juice concentrates.

At first, I was wondering if the sugars in a fruit can be different from sugars in a juice. According to the answer to my question here, the sugar molecules are exactly the same in both (in the case of a 100% pure juice).

So, why this recommendation? Why doesn't our body digest sugars from fresh fruit the same way as sugars from juice? To make it simple, my question only concerns 100% pure juice with no added sugars.

I tried to find an answer and, according to the answers of this question, because our body is slow to digest sugars from a fruit, it assimilates it better. Is it right? And, if it is the case, if we eat fiber and starch with our fruit juice, it should be the same as a fresh fruit, right?

Sugars in 100% natural fruit juices are chemically the same as in whole fruits. They mainly include glucose, fructose and sucrose:

Apple nutrition data (expand the carbohydrate section)
Apple juice nutrition data

Sugars in whole fruits are "incorporated" into the fruit, which means the digestive system first needs to physically decompose the fruit and then extract and absorb sugars, which takes some time. In fruit juices, sugars are "free," so they are absorbed quicker than from whole fruits, which results in higher blood glucose levels, which is a risk factor for diabetes type 2 (Defeatdiabetes, Diabetes.co.uk).

Also, fruit juices are liquid, so they pass through the stomach quicker than whole fruits, so they fill the stomach for a shorter time and may be therefore less satiating. This can make you drink more juice than you intended, which can result in unwanted weight gain.

If you eat foods high in fiber along with juice, the fiber will slow down the absorption of sugars from the juice (Nutrients). If you eat foods that contain mainly plain starch (white bread, cookies or rice, or potatoes) along with juice, the starch will be quickly digested and absorbed as glucose and will raise the blood glucose even quicker than the sugar from the juice.

The effect of nutrients from foods on blood glucose level after meals is expressed as glycemic index (GI): the higher the GI, the higher blood glucose (Harvard):

Glucose = 100
Cornflakes (mainly plain starch) = 81
Potato, boiled (mainly plain starch) = 78
White bread (mainly plain starch) = 75
White rice (mainly plain starch) = 73
Sucrose = 65
Honey = 61
Apple juice = 41
Apple: = 36
Kidney beans (high in fiber) = 24
Fructose = 15

In conclusion, natural sugars from whole fruits, fruit juices and artificially added sugars are all digested in the same way, but sugars from juices are absorbed quicker, which can result in higher blood glucose levels. Foods that contain mainly plain starch can raise the blood glucose levels much more than fruits and fruit juices.


Can someone help me analyze this article? I need to read this article — "Beyond the rainbow" by
Marie-Claire Koschowitz et al., for an exam.

Following are some questions for which I could not figure the answer out after reading.

1) Why does this miniaturization necessitates insulation ? Following is quote from article: "For fast-growing, presumably warm- blooded animals , such miniaturization would only have been possible with sufficient body insulation. "

2) Dinosaurs suppose to have tetrachromacy. The article mentions "dinosaurs were endowed with the highly differentiated color vision of birds". Does this mean Dinosaur's "inherited" their tetrachromacy from birds ? Why does the article mention reptiles before that ? Are birds reptiles ?

3) The article starts talking about how mammals develop fur and lost their highly differentiated color vision because they gave up structural color signaling. What is the direct connection between mammals and the dinosaurs ? I don't see the parallel here....why bring the mammals into the discussion ?

4) What is the connection between pennaceous feather and planar feathers ?

Any or all questions answered is welcome ! Thanks !

I will answer the questions one by one-

Why does this miniaturization necessitates insulation ?
An organism's volume determines the total amount of heat that can be stored. The loss (exchange) of heat between the body and external environment mainly occurs on the skin's surface. Hence, body volume determines how much heat is stored, while body surface determines how fast that heat is dissipated to the environment. Volume increases with a power of three with radius, while surface increases with a power of two. Hence, smaller animals have large surface-to-volume ratios, which decreases rapidly with body size. Hence, small animals will dissipate relatively more heat per unit of time.
Dinosaurs suppose to have tetrachromacy. The article mentions "dinosaurs were endowed with the highly differentiated color vision of birds". Does this mean Dinosaur's "inherited" their tetrachromacy from birds ?
No, birds are the closest living relatives to dinosaurs, and birds can be said to have inherited tetrachromacy from dinosaurs - see the cladogram below.

Why does the article mention reptiles before that ? Are birds reptiles ?
Birds are not reptiles, they are separate classes within the animal kingdom.
What is the direct connection between mammals and the dinosaurs ? ... why bring the mammals into the discussion ?
Here below is another cladogram; there is no obvious, direct (evolutionary) connection between dinosaurs and mammals. The thing is that dinosaurs ruled the world before the last mass extinction, thereafter it were the mammals. That's why the authors discuss them both, I guess. Especially since we are mammals it may make sense to draw parallels.

What is the connection between pennaceous feather and planar feathers
As far as I could track the two down, they are the same (Prum, 2006)

Lastly, in response to your original question, before edits: Here is a link with a plain-English popular-scientific web article published online by the first author.


Why does an increased heart rate mean increased blood pressure? Say a person starts exercising. If their cardiac volume remains the same but their heart rate increases so that the overall result is an increase in cardiac output, will their blood pressure increase during the exercise ? If it does, why ?

In good approximation, the arterial blood pressure PA depends with

PA = PV + R x dv/dt,

on central venous pressure PV, total peripheral resistance R (also referred to as TPR or PVR) and cardiac output dv/dt (aka CO) – the usually cited equation MAP = CO * PVR is an over-simplification. Since cardiac output is defined with

dv/dt = RH * VS

as a result of heart rate (RH) and stroke volume (VS) the blood pressure should increase if heart rate increases.

However, in reality, the conditions are more complex. In exercise body temperature increases, which leads (via the thermoregulatory system) to vasodilation, so that the total peripheral resistance R decreases, which is able to reduce the blood pressure again.

Decreasing PV in exercise should occur on a very slow time-scale and only be relevant in long-time endurance training.

Concentrations of some hormones change in exercise. Levels of some stress hormones (catecholamines) rise and therefore increase cardiac output, but their action on peripheral resistance is heterogeneous. It goes up, if alpha receptors are stimulated, but decreases after stimulation of beta receptors. Similar to (and partly mediated by) beta adrenergic action classic thyroid hormones (e.g. T4, T3 and 3,5-T2) increase heart rate but decrease total peripheral resistance. It depends on the type of exercise if thyroid hormones rise or drop. They are increased in short-term or endurance exercise (representing type 2 allostasis) but decrease in exhausting exercise (leading to type 1 allostasis).

In summary, it depends on many factors, if blood pressure increases during exercise. In ergometry the blood pressure usually slightly rises.

References

1: GREENE BA. Cardiac output and total peripheral resistance in anesthesiology;
clinical applications. J Am Med Assoc. 1958 Mar 1;166(9):1003-10. PMID
13502096. https://www.ncbi.nlm.nih.gov/pubmed/13502096 https://doi.org/10.1001/jama.1958.02990090011003

2: Mayet J, Hughes A. Cardiac and vascular pathophysiology in hypertension.
Heart. 2003 Sep;89(9):1104-9. PMID 12923045. https://www.ncbi.nlm.nih.gov/pubmed/12923045/ https://doi.org/10.1136/heart.89.9.1104

3: Silva AS, Zanesco A. Physical exercise, β-adrenergic receptors, and vascular response. Jornal Vascular Brasileiro. 2010 9(2). https://doi.org/10.1590/S1677-54492010000200007

4: Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood
A, Klein HH, Dietrich JW. Thyroid Allostasis-Adaptive Responses of Thyrotropic
Feedback Control to Conditions of Strain, Stress, and Developmental Programming.
Front Endocrinol (Lausanne). 2017 Jul 20;8:163. doi: 10.3389/fendo.2017.00163.. PMID 28775711. https://www.ncbi.nlm.nih.gov/pubmed/28775711 https://doi.org/10.3389/fendo.2017.00163


Why don't animals produce alcohol As I understand during anaerobic respiration, the electrons received from the decomposition of glucose are transferred to nicotinamide adenine dinucleotide and flavin adenine dinucleotide. As there is no oxygen the electrons are then transferred to something else, either Lactic Acid or Ethanol (in the case of yeast).

So why do animals produce Lactic Acid and not Ethanol?

Also, (I know this is silly, but) what would happen if they did?

Consider this from the point of view of integrating whole body metabolism.

The body operates on a fuel economy built around glucose. Active muscle produces lactate (C3) which is exported to the liver through the bloodstream. Liver converts lactate to glucose (C6) which is then exported to the tissues.

What if muscle produced ethanol (C2)? Liver metabolises this to acetate. This could be converted to acetyl CoA and so on to fatty acids, but there is no way to achieve net synthesis of glucose from acetate. Muscle can of course use fatty acids, so you could conceive of an alternative system based upon this. It may be that this is less efficent from the point of view of energy useage - I haven't checked this because there is a more compelling argument against using ethanol.

According to this paper, lactate levels in the bloodstream can reach 15 - 25 mM during exercise. If muscle exported ethanol instead of lactate then blood alcohol content (BAC) would reach the same levels.

The middle of that range, 20 mM ethanol, is equivalent to a BAC of 0.076% which is just below the legal limit for driving in the USA and the UK, and above the legal limit in many European countries. This BAC is associated with effects upon reasoning, depth perception and peripheral vision. So, from an evolutionary position it really wouldn't make sense to have a metabolic system based around sending this much ethanol through the blood.


Why is the start of my coding sequence ATG and not TAC? I am engineering a set of genetic sequences and have come across a surprisingly basic point of confusion that seems to have fallen through the cracks regarding coding sequences.
The standard start codon is AUG, and since this is an RNA sequence, I would thus expect that the start of the coding sequence would then be TAC, since DNA is complementary to the mRNA transcript taken from it. Wikipedia and various introductory texts confirm this expectation, e.g., in wikipedia's article on the central dogma:

The ribosome reads the mRNA triplet codons, usually beginning with an AUG

Here's another example: in the Khan academy introduction to the genetic code, the codon illustration clearly shows an AUG in the mRNA sequence.
The coding sequences that I am composing into my design, however, are all listed as starting with ATG, rather than TAC, which would be the complement of AUG. I am certain the coding sequences are not wrong, since some are very well established parts like BBa_E0040.
Something seems to have gotten confused or elided in many standard explanations, then. Why do coding sequences start with ATG and not TAC?

This image from the Kahn Academy article 'Overview of transcription' might help:

Essentially, the sense/coding strand of the DNA encodes the sequence that is transcribed. The RNA polymerase binds to the antisense/template strand, for which the code is indeed TAC, but when it then transcribes this strand it is again complemented, giving us the AUG that is recognised by initiator tRNAMet (also known as tRNAfmet), as shown in this diagram from the Kahn academy article on 'tRNA and Ribosomes'.

(Note that this diagram is actually showing Met in the middle of a sequence, rather than the start. fMET binding looks slightly different.


How to safely sterilize urea-containing growth medium? I'm using urea-containing growth medium for experiments with bacteria (1-2 l/day). After the experiment, the growth medium has to be sterilized and disposed. I did this so far by autoclaving, but our technician complained about the ammonia smell that develops (urea breaks down when heated, releasing ammonia).

I'm pretty sure the amount released into the air is not dangerous (I've emptied the autoclave several times), especially if you don't purposefully breathe in the first gust of air that comes out after opening, but I think it's useful to look into alternatives. Also I'm not sure if the autoclave might get damaged on the long run.

Does anyone have experience with this? Do you see a way to sterilize larger amounts of growth medium reliably without heating?

Autoclaving is the best way for sterilization. If your growth medium is large, how much chemical disinfectant do you think you would need to bring up to its working concentration?

Add some acid to your waste medium (so that it's only weakly acidic), not as disinfectant, but to suppress ammonia formation. Urea will still break down during autoclave, but ammonium ion (pKa~9) will generally stay in solution.


Mitochondrial Genetic code We know that the genetic code is universal. My query is why the mitochondrial genetic code is different from universal genetic code?

Your premise is incorrect, the genetic code is NOT universal. There is a 'standard' genetic code, which is found among higher animals and plants and most bacteria, but there is a variety of other genetic codes found in the main genome of more obscure organisms. These are listed at: http://www.ncbi.nlm.nih.gov/Taxonomy/Utils/wprintgc.cgi .

There is also no mitochondrial genetic code but a variety of mitochondrial (and plastid) genetic codes. One feature of genomes with non-standard genetic codes is small size, so that the number of proteins influenced by a change from a common precursor genetic code would have been small.

In the case of mammalian mitochondria there are fewer tRNAs and these have non-standard anticodon-codon interactions. Thus rationalization of these genetic codes may have been due to pressure to reduce the size of the genome.


What are the theoretical and actual (measured) minimum water potentials in plants? I'm a plant physiology researcher, but water potentials are not really my thing, so I don't have a great grasp on the literature. I'm dealing with water potential data right now though, and it seems questionable to me. Some of the measured water potential (solute + metric potentials, after lysing cells to break turgor) are as low as -48 bars (most in -10 to -35 range).

That would, if my math is correct, translate to a solute concentration in the 2000 mOsmol range, which seems extremely high to me. Consequently, I'm trying to determine if there is an analytic issue with the data collection. I've run through the equipment chain, checked calibrations, and everything seems ok. I've also been combing plant physiology lit. for comparable data, and I find some in that range, but I can't find any theoretical work that would help set a 'ceiling' for what constitutes a reasonable solute + metric potential.

So, my questions are these:

What is the theoretical maximum capacity for dissolved ion concentration in water, and what pressure potential would that represent, compared to pure water.
Is anyone aware of plant physiology research that has attempted to establish a minimum in vivo water potential in plants (either total potential, or S+M if it's broken out)?

Sodium Chloride (which I am here assuming to be the major salt in your solution) has a solubility of 6 Moles/L this corresponds to 12000 mOsmol, so the 2000 mOsmol you are measuring is not entirely implausible. However normally plant cells should have an osmolarity on the order of 300-400 mOsmol. In order to judge if your value was calculated correctly, it would be necessary for you to tell us exactly how you calculated and how you measured.
I am not aware of such literature but I am not a plant physiologist myself.


Remove RNAse from pipettes? Our lab uses old Gilson Pipetman pipettes. I've been using some for making mRNA by in vitro transcription and started running into RNAse issues. I'm trying to clean everything up, including the pipettes. I'm not sure these old pipettes can be autoclaved, at least not in one piece, I think I can take them apart and autoclave the parts that might touch the solutions. Is there some way to wash the pipettes out effectively and remove any RNAses?

I use boxes of RNAse free barrier tips, do all my work on new pieces of aluminum foil, use commercial RNAse free water, gloves, labcoat, facemask, etc. However yields from the in vitro transcription kit have been reduced, and yields from the tailing kit are even worse, sometimes losing 90% of the RNA. There's only so much I can do, our building is old and full of dust and the damn pipes above my work bench leak ( all the pipes leak, had 2 major pipe bursts in the last 6 months ).

I'll probably have to get new kits. Just have to prove to my advisor that the kits are contaminated.

According to the Gilson Pipettman User Guide you can autoclave the following parts: Tip ejector, Tip holder and the connecting nut (have a look into the PDF linked above if you are not sure about the parts). All other parts can not be autoclaved. Gilson says the following conditions can be used (page 17 in the user guide): Autoclave for 20 minutes at 121°C, 0.1 MPa.

However, when you really have a DNAse contamination, you will not get rid of it with autoclaving, since RNAses are too stable. You can either try the various solutions on the market which made for killing RNAses or simply get a new set of pipettes used only for RNA work (on a different bench in a different lab with a completely different and fresh set of chemicals and plastic ware). And I would recommend filter tips for this work. They are more expensive but in the long run it will save money since you don't have to repeat experiments.

Regarding your leaking pipettes: The pipettes contain rubber rings and teflon seals in the inside which have to be replaced from time to time. The image below shows how (parts C and D), the ring can be purchased from Gilson. If you don't know how to do this work (and have no technician who does) you can also send in the pipettes for service. This costs a bit of money, but is ways better than to use unreliable, leaky pipettes.

And don't worry, Gilson pipettes are pretty good. I have used now more or less all brands on the market and I still prefer them. They only need some service from time to time.


Cardiac pacemaker: how can different nodes have different frequencies? Primary SA node creates 70 beats per minute and secondary AV node 40-60 beats per minute. Is the AV node inactive (and other subsequent nodes) while the SA node is functional? If the primary, secondary and tertiary nodes are working simultaneously, wouldn't the difference in the beats per minute cause a mess?

The AV node and any other nodes are suppressed by the SA node because it is the fastest.  If the SA node is sick or slow or there is a conduction problem one of these other nodes can take over calling the beat.

http://www.cvphysiology.com/Arrhythmias/A018. bold emphasis mine.

  The higher frequency of SA nodal firing suppresses other pacemaker
  sites by a mechanism called overdrive suppression. If a latent
  pacemaker is being depolarized at a higher frequency than its
  intrinsic rate of automaticity by an adjacent cell that is driven by
  the primary pacemaker, then the increased frequency of depolarizations
  leads to an increase in intracellular sodium ions because more sodium
  ions enter the cell per unit time. This increased sodium stimulates the Na+-K+-ATPase (increases its activity) to expel more sodium from the cell in exchange for potassium (see figure). Because this pump is electrogenic, increased pump activity increases the amount of hyperpolarizing currents generated by the pump. This drives the membrane potential more negative, thereby offsetting the depolarizing pacemaker currents (If) being carried into the cell. This effectively prevents the pacemaker currents from depolarizing the cell to its threshold potential, and thereby prevents the spontaneous generation of action potentials. If the cell ceases to be driven by the SA node (e.g., because of AV block), then the additional hyperpolarizing currents will be lost and spontaneous depolarization and action potential generation can occur.


Database of cancer cells I am looking for a database(or any kind of information source) of cancer cells, which has information about the speed of reproduction of these cells, how fast they grow, etc.

So I could make my simulation as accurate as possible, as close to reality as possible (I am working on developing a software that simulates how cancerous cells spread).

Edit

  Are you interested in growth rates in culture or in vivo (e.g. tumours)

Okay, I am a noob in biology, so let me explain it like that.
I am using Voronoi graphs for simulation, so I think that I am interested in tumor level, how each cell interacts with each other, and thus how fast can cancerous cells overpopulate healthy(or other cancerous) cells.

The National Cancer Institute (NCI) has a list of doubling times for a variety of commonly used cell lines, see
https://dtp.cancer.gov/discovery_development/nci-60/cell_list.htm

I my experience, these doubling times are quite stable/reproducible, provided that cells are kept in standard culture conditions. While doubling times differ a lot between cell lines, they are also very different in size, and larger cells tend to have longer doubling times so that the biomass growth rate is actually rather similar between lines.

Note: these doubling times refer to cell culture conditions. Actual tumors in vivo grow much more slowly, due to lack of nutrients, suppression by immune cells, and what not. Estimating cell growth rates in tumors is a much more complicated business, and I don't know of any database for that.


E. coli not growing in liquid medium We are regularly doing bacterial transformation and subculture from plate to liquid media to extract DNA. This usually goes very well and is straightforward, but occasionally, the colonies that grew well on a plate, will not grow in liquid culture (with the same antibiotics that were in the plate). This has happened now to three persons on multiple plasmids.

For example, I was trying to ligate an ampicillin resistance gene (with its promoter) inside pENTR4 plasmid (already with Kanamycin resistance). My plate and LB both contained the two antibiotics, but the colonies only manage to get slightly turbid at a 16h timepoint.

Phage contamination is very unlikely, and the effect cannot be due to a toxicity of the inserted fragment, as both insert and vector have been grown in these same bacteria multiple times without problem.

Help?

EDIT1 - We use Carbenicillin in place of ampicillin in the plate, but not in the liquid media.

EDIT2 - After managing to grow some colonies in liquid, I managed to get a small amount of the plasmid (profile was good; concentration = 70ng/ul). The weird thing is that when I retransformed this DNA in Stbl3 bacteria, I had absolutely no trouble. Do you think the bacteria stock could be responsible?

I think there is more than one possibility for this.

Plates bearing colonies are stored for too long in 4C(as @mdperry suggested). This causes the colonies to lose the plasmid over-time as the antibiotic in the plate gets degraded over-time. There is a study on this and I've shared the link. (http://homepages.bw.edu/~mbumbuli/biotech/colin/index.html).
The insert is toxic to cells and promoter is not strong enough. There is a leaky expression causing cells to die.
Check the competent cells and their storage condition as it would greatly affect the efficiency of transformation. Do a mock transformation with plain plasmid without insert and spread them on an antibiotic plate.


What are the requirements for a spectrometer to be used in biological research? Suppose one would do spectrophotometry on biological materials. What would be the minimum requirements for the measuring device so that the results could be published in a reputable journal? I suppose that two important properties are

resolution of the spectrum (would e.g. 25 nm be enough? 15 nm? 5 nm?)
measurement error (10%, 5%, 1%, ..?)

What else (if anything) should be taken into consideration?

For all the common uses of a spectrophotometer in biology, any commercial one should be sufficient. For all the routine stuff, the quality of the spectrophotometer is usually of negligible importance.

There are no general rules on what errors and resolution are acceptable, that always depends on what you're measuring. The error should be significantly smaller than size of the effect you're looking at, otherwise you get no useable data.

There are many sources of error with biological systems, the spectrophotometer is really one of the last ones you would think of. Simply the error of pipetting is likely far larger than the error of the spectrophotometer, and differences in the preparation of your biological samples might introduce an even larger error. Unless you're doing something beyond the routine uses of UV/Vis spectrometry, you probably don't need to worry about this.


What prevent us from synthesizing a cell from "scratch"? In this recent article "Design and synthesis of a minimal bacterial genome", they created a minimal cell with only 473 genes. However, they didn't synthesize all of the necessary components of the cell to get going. How much of those extra stuff can we currently synthesize, and what are the ones that we can't synthesize in the lab to create a working cell from scratch?

Designing/engineering functional proteins from scratch is feasible but would take a ridiculous amount of work. Michael Hecht is one person I know of who has done this (example: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0015364). J Craig Venter wants to determine the minimal set of molecular machines required for life, regardless of their origin. This would begin to illuminate which protein functions are absolutely required for life. I believe we could design and engineer proteins de novo to perform all of those functions in theory, but in practice it would be unrealistic. I think the key point to glean from their synthetic cell is the set of functions, not specific genes, required for life. Those functions could be performed by evolved or synthetic molecules.

As a side note, while I believe that to be the overarching goal, they do note the surprising lack of functional characterization in the syn3.0 genome.


How would one describe the R-factor in crystallography? Yes, there is the wikipedia definition, but how would one explain this concept to a non structural biologist?

Crystallography requires the collection of many measurements (could be a few thousand to even millions depending on the size of the molecule and complexity of the crystal (technically speaking, the size of the crystal's unit cell is a major determining factor for the size of the data set).  I'm not going to assume this is a small molecule crystal like a salt or a large molecule like a protein.  its not necessary here.

I'll call this a set of intensity measurements, even though what is actually used is the square root of the intensities measured, called the structure factor.

The only way we really know that the molecular structure model is correct is that it generates as accurately as possible the intensities that were experimentally measured.

R, which I believe stands for residual, is a fractional difference between the measured intensities and what any proposed molecular model gives.

The residual is calculated as the absolute value of F(model)-F(measured).  This means that 0.0 is a perfect match while 1.0 is a perfectly awful fit that shows the model is perfectly awful.

In practice 0.60 is usually as bad as random model will give you (there's a statistical argument as to why it doesn't go higher).  Also the measurements are usually not perfect - they contain errors in measurements or artifacts from imperfect crystals or the detector, so an R value of < 0.20 (20%) is typically what you see in a reasonable paper.  I think its commonly less than 0.15 for most structures now in fact.


What is the smallest molecule that can present as an antigen to the immune system in the context of allergies? People often claim, in a colloquial sense, that they are "allergic to everything".

Is it possible to have a full-fledged IgE mediated allergic response to very small molecules?  I was always under the impression that the smallest antigen was a oligopeptide, but is it possible for someone to be allergic to something like isopropanol, glucose, or another small organic molecule?

How about allergies to metals, as I know those are fairly common, would they be mediated through a similar mechanism?

At one of my previous companies that raised antibodies to proteins and post-translational modifications, we found that 6-8 amino acids was generally the smallest peptide length required for an epitope. Anything much smaller than that won't induce the cross-linking or conformational changes required for signal transduction and an allergic response. As WYSIWYG notes, allergies to small molecules/atoms are formed via hapten-carrier interactions. These can be covalent, as in the nickel-transferrin example, or as a result of denaturation/chemical modification, as likely happens with people who are allergic to things like isopropanol or bleach.

I very much doubt that there can be such a thing as a glucose allergy, as it is so ubiquitous in the body that such antibodies/T-cells would be negatively selected long before they could do any damage.


Do plants refix some of the carbon dioxide in the Calvin cycle that they produce through cellular respiration? Plants do cellular respiration and release CO2 into the air, but does the plant also use some of this CO2 to do the Calvin cycle? Or does all the CO2 required for the Calvin cycle come in through the stomata?

Gases like CO2 move quite freely in biological systems, approximating the laws of diffusion (note: there are of course some exceptions, especially underwater, as well as with proteins that assist in bulk transport of CO2 like hemoglobin).

If you were to measure the net amount of CO2 coming into the stomata, it would indeed approximate the net CO2 use by the plant. From this, you could make a claim like "the CO2 a plant needs comes in through the stomata": this is true for the net, and that's usually what's most important to a biologist.

However, if you want to get picky about what really happens at a molecular level, the flux of CO2 coming through the stomata is not the same as the net: no one is keeping track of the individual gas molecules, they just float around back and forth. The only reason there is a net flow at all is due to a concentration gradient: because the plant uses some CO2, there is less inside than outside. When molecules move around randomly, that means that a few more end up coming inside than are leaving. When we talk about net diffusion we are talking about the averages of many many molecules over time.

Included in that random motion are not just the CO2 molecules present inside and outside the plant, but also those that the plant is producing through cellular respiration. By chance, certainly, some of these molecules could end up back in the Calvin cycle. Some could even exit through the stomata and come back in (my intuition is that this is quite improbable for an individual molecule but I haven't done the math...the important concept is that it's all one "pool").

If you really wanted to know, you could set up a Monte Carlo simulation (or use differential equations) and calculate probabilities of all sorts of event sequences for individual molecules. You could also tilt the scales a bit if you, say, put the equivalent of a 'plastic bag' over a leaf, either physically or in a model: if there's a limited amount of CO2 in the "outside" space it would be much more likely for individual molecules to be "reused".

From a biologists' perspective, though, and especially for ubiquitous, freely moving molecules like CO2, it's usually only important to think about net flow.


Are there animal species in which the females expend more energy attracting males than in their offspring? In general, males of a species expend a lot of energy attracting females.  There are many instances where males utilize much of their nutrient intake to produce antlers, tusks, horns, etc. to either attract females or compete with other males for potential mates.  Are their any instances in animals in which the females do this to attract males or to compete with other females?  If so, what features have the females evolved to win over potential mates and fight off competitors and what advantage is there for the species?

I'm aware of a few animals, such as the seahorse and jacana where the males invest more energy in the offspring, but I'm not sure that the females of these species expend some of the energy saved in the offpring and put it into attracting males or competition with other females.

The reason why, in most species, males are competing to access females and females are choosy is due to Bateman's principle.

  Bateman suggested that, since males are capable of producing millions of sperm cells with little effort, while females invest much higher levels of energy in order to nurture a relatively small number of eggs, the female plays a significantly larger role in their offspring's reproductive success. Bateman’s paradigm thus views females as the limiting factor of parental investment, over which males will compete in order to copulate successfully.

But there are exceptions to this general rule.

Fish

In many fish species (e.g. pipefish, scissortail sergeant and seahorses), males are choosy and females are competing. In these species, females deposit their eggs in a special brooding pouch that the male possesses. The male then has the energy cost of raising the offspring, while the female does not provide any parental care. As a result, males in these species must choose among competiting females for mates( Vincent et al., 1992)

Birds

In many bird species, there is bi-parental care, leading to competition among mates in both species. See the interesting case of Jacana jacana (Emlen and Wrege, 2004).

Frogs

In poison-arrow frogs (Dendrobates auratus), the male spend more energy for raising the offspring than the females and the males are therefore choosy (Wells, 1978).

Related: Why are female not competitive for reproduction like males?


Does the process of making a sourdough starter involve Darwinian selection? In essence - to make a sourdough starter:

Put flour and water in a jar, and leave it in a warm place overnight
Divide the remaining mixture in half, throw out half, add half as much flour and water again.
Repeat for 7 days.

I don't see why you couldn't just add all the ingredients required at the start, open it once a day to let more yeast drop in and give it a stir, and keep in a warm place every day.

The vague idea comes to me that throwing out half the mixture every day has a Darwinian element, but it doesn't involve any 'selection', you're simply casting out half, regardless of adaptability.

My question is: Does the process of making a sourdough starter involve Darwinian selection?

EDIT: There is no 'choice' involved in throwing out half the sourdough. It is entirely arbitrary - and both halves look equally the same.

Yes, continually diluting the mix like this encourages the organisms (bacteria, yeasts, fungi) to have more constant conditions (maximum nutrients, fewer waste products) and be in log phase growth. The mix selects for particular faster-growing organisms. if you did not dilute, the nutrient levels would change (lower) and waste products accumulate much faster. Then the conditions would be more different day-to-day.

Practically, the dilution adds more nutrients while still allowing the pH to fall. Without the dilution, particular bacteria tend to take over and lactic-acid producers dont get a chance.

refs
https://en.wikipedia.org/wiki/Bacterial_growth
https://en.wikipedia.org/wiki/Sourdough


What happens when cells in your body run out of telomeres? In my biology book I read about an experiment where the genes encoding telomerase were 'knocked out', but they could still live a normal life and no adverse effects were noticed until the 6th generation of offspring (although it did not say what the effects were).

I have often often heard how longer telomeres indicate longer life potential, but what happens when you run out of them? Would rapidly proliferating cells be affected before others? Do the cells then just stop dividing or would they continue to divide? If they continue to divide what would the effects be?

During mitosis the genetic material in the cell is replicated to produce a copy of the genome for each resulting daughter cell. Due to the nature of the process, the ends of the chromosomes are not completely replicated, resulting in a slightly shorter copy of each chromosome after each round of replication.

Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in 'normal'/somatic cells), which gives rise to a replicative lifespan; the number of times a cell can divide before permenantly leaving the cell cycle (known as cellular senescence).

This is generally viewed as an anti-cancer mechanism to protect against errors creeping in to the genome through many cell divisions. In order to become cancerous, a cell must first overcome its replicative lifespan [ref.]. This is achieved by activating the (normally inactive) telomerase enzyme that extends the telomeres - embryonic stem cells are one of the few cell types that normally express this enzyme, so they have unlimited replicative potential - a very important trait for stem cells.
So a rapidly proliferating cell would indeed 'use up' it's telomeres before a different cell type. The cell would then either enter a state of senscence (permenant cell-cycle arrest), or apoptose. There are a lot of factors governing which outcome is realized, but the senscent cell population increases with age, and is proposed to contribute to many aging phenotypes (there is a recent fascinating study published in Nature where the authors remove all the senscent cells from aging mice, and the mice actually get healthier! Can't wait for studies that relate to human aging and senescent cell clearance (ref.)).

I have elaborated on the function of telomeres in the context of organismal aging in my answer to this question.