text:
Can axons act as receptors?
In all histology books, it is stated that all sensory nerve endings (receptors) consist of dendrites that translate physical stimuli from the environment into neural signals. However, several sensory neurons seem to include axons, such as the merkel and olfactory cells shown below. They act as receptors, but feature axons as well. So is it the pictures, or the texts that are incorrect?

Axon is a kind of dendrite actually..

What exactly is your question? Whether 1) axons are part of sensory neurons, or whether 2) axons can have sensory function (given that dendrites typically act as receptor)? Please clarify.

@AliceD Sort of, technically they both are cytoplasmic processes.

@AliceD I just said axon is a kind of dendrite — a specialized one (both of them are grouped together as neurites, btw). So there is no argument here. Moreover, unlike apples and pears, dendrites and axons are the part of the same biological entity.

I removed the apples and the pears - bad analogy :) But I can't settle for an axon and dendrite being similar - http://biology.stackexchange.com/questions/9026/what-are-the-functions-and-differences-between-axons-and-dendrites there are a host of differences. No problem in having a different opinion here though. We are from different disciplines.

@AliceD When did I say that I do not acknowledge the differences? (Also I don't think I come across as an unreceptive person.) They have both similarity and differences. In bipolar neurons they look quite similar as well. In pseudounipolar neurons axons carry both afferent and efferent signals. Biology has several cases of non-absolute rules. You can always find domains of similarity and differences.

i mean can axons act as afferent nerve fibers (receptors)?

I slightly modified the question based on your comment above to clarify this question to the best of my understanding - I added an answer too. Feel free to roll back my changes if it doesn't reflect your ideas. +1 for this question. Very enlightening.

Short answer
The textbooks are right; the receptor part of sensory neurons is always considered to be the dendrite. Axons are nonetheless an integral part of some receptor types to send the signal to the brain. Other, more specialized sensory cells do not have an axon and therefore rely on secondary neurons to send the signal to the brain.
Background
There are three types of sensory cells, namely those with free nerve endings, those with specialized dendritic structures, and specialized receptor cells that synapse directly onto a secondary neuron (Fig. 1).

Fig. 1. Types of sensory neurons. Source: Premed HQ.

Sensory neurons with free nerve endings have an exposed dendrite that functions as receptor. Examples are nociceptors (pain receptors) and hair follicle receptors.
Other sensory neurons are complex cells that feature a dendritic region specialized for a particular receptor function. Examples are the Pacinian corpuscle and olfactory neurons.
The most common receptor type are specialized receptor neurons that have no axon and need a secondary sensory neuron to send the signal to the brain. Examples are the photoreceptor cells in the retina, the hair cells in the cochlea and Merkel cells.

In all histology books, it is stated that all sensory nerve endings
  (receptors) are made of dendrites which conduct sensation from
  environment to body but it doesn't seem to be true.

The phrase "nerve endings" (or "free nerve endings". See Wiki page) is typically associated with fine hairlike structures throughout the skin and organs that act as (one type of) touch, pain, or heat sensors. These are, yes, extensions of the dendrites of sensory neurons whose cell bodies live in the dorsal root ganglia of the spinal cord and who send the signal on via axons, either locally within the spinal cord or to brain structures.
But this is not the same as saying that all sensory structures of any sense modality are dendrites or extensions of them. Each sense has specialized cells to detect that sensory stimulus. The eye has photoreceptors (rods and cones), the ear has inner hair cells, the nose has olfactory receptor neurons, the tongue has taste cells, and the skin and organs have free nerve endings and specialized mechnoreceptors such as pacinian corpuscles. Most of these do the work of transducing the stimulus in a specialized receptor portion of the cell, such as the rod itself, or the cilia of a hair cell or ORN, etc., and then the signal is sent to the next cell in the sensory chain via a synapse, sometimes via a very short axon or just sort of axon "nub".


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Does a neuron ever generate an action potential without stimuli?
Most accounts I read involving action potentials and synapses and the like tend to focus mostly on the action potential as a mere automatic reaction to another similar event happening upstream.
From a more theoretical point of view, it would be nice to know if (and under what circumstances) a neuron would be able to generate an action potential, in the absence of an upstream neuron firing first.
I suspect that the nervous system, at least in higher animals, is not simply a relay system that processes and transmits information from senses to actuators like the limbs. The relay system picture is fine for short-timescale, reactionary behavior but it is hard to imagine any longer-timescale learning processes happening this way. This is what motivates my question.

Pacemaker cells in the heart might be an example for you

You might be interested in this quetions on neurons firing 'randomly'.

There are many spontaneously active neurons. This has been known for many years [1]. There are multiple sources that could make a neuron spontaneously fire. In cortical culture of neurons where there is no external input to the system, neurons are spontaneously active, for example [2]. Of course, there are spontaneous vesicle releases from synapses (miniature EPSC) in this case, so you might say there are still some "input" to each neuron. However, even if you block synaptic transmissions, and some neurons do fire spontaneously [3]. It could be ion channels, or some internal chemical process. If you include the network level spontaneous dynamics, there are even more possible ways to have active neural system without any stimulus.

Alving BO (1968) Spontaneous activity in isolated somata of Aplysia pacemaker neurons. J Gen Physiol 51: 29-45.
Potter, S. M. and Demarse, T. B. (2001). A new approach to neural cell culture for long-term studies. Journal of Neuroscience Methods, 110:17-24.
Häusser, M., Raman, I. M., Otis, T., Smith, S. L., Nelson, A., du Lac, S., Loewenstein, Y., Mahon, S., Pennartz, C., Cohen, I., and Yarom, Y. (2004). The beat goes on: Spontaneous firing in mammalian neuronal microcircuits. The Journal of Neuroscience, 24(42):9215-9219.

Neurones fire when they're sufficiently depolarised past their threshold. In the sensory system this is in response to an external stimuli which sets of a chain reaction. Then motor neurones may relay signals back and in this case the signal or initial depolarisation is occurring in the brain. However this is still caused by a stimuli even if indirectly. If we take an action it is generally because we thought which action we should take because of some sort of stimuli e.g. we are cold so we put a coat on.
But anything which depolarises neurones can set of an action potential. However there's always something which causes it to depolarise, perhaps a drug or a stimulus or another neurone. If any of these don't count as a stimuli depending on your definition, there's your answer.
Or perhaps if you consider cardiac muscle which can intrinsically depolarise. Not a neurone but there's an action potential. They just naturally depolarise over time and action potentials are set of regularly with no stimulus required.
As for learning, where the structure of neurones can change so they connect to new neurones or not to old neurones or vary in the strength of their connection.

There are spontaneously firing neurons known as intrinsically oscillatory neurons, or simply pacemaker neurons. Under the right conditions these can fire action potentials in a rhythmic pattern without neuronal input. Examples are the thalamocortical relay neurons in the thalamus and inferior olive neurons. The basic mechanism is that a low-threshold Ca2+ current generates a small depolarization that in turn activates full-blown action potentials. In the recovery phase after the burst of action potentials, a hyperpolarization-activated cation current is activated (Ih), which in turn depolarizes the neuron. This depolarization then initiates another Ca2+ current and the oscillation continues.

Thalamocortical cell with oscillatory behavior in vivo. Source: Steriade et al. (1993).
The thalamocortical oscillations are thought to be imprtant in the generation of the slow-wave EEG seen in the early phases of sleep, as well as during absence-epileptic seizures (petite mal).
Reference
- Steriade et al., Science (1993); 162: 679-85

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Does cat urine really fluoresce? If so, why?
I temporarily got caught in the Sad and Useless website, and found Science is Fun.
Most of the claims seem plausible, but I can't guess why cat urine would fluoresce.
Comments have directed me to Why Does Urine Glow Under a Black Light? which says:

You can use a black light to detect body fluids. It's actually a good way to look for pet urine or make sure a bathroom or hotel room is really clean. Cat urine, in particular, glows very brightly under ultraviolet light. Urine glows under a black light primarily because it contains the element phosphorus. Phosphorus glows yellowish green in the presence of oxygen, with or without black light, but the light imparts additional energy that make the chemiluminescence easier to see. Urine also contains broken down blood proteins that glow under a black light.

Certainly other mammals including humans have both phosphorus and broken down blood proteins in their urine, so is the proposed specificity to cat urine just an issue of concentration perhaps?

I don't find it implausible, but why cat urine specifically, and not of other animals?

I actually think thoughtco simplifies quite a bit. I don't think there is pure P in urine.

Could possibly be because of Urobilin. Also, diet also influences the urine composition. Some of the excreted products can be fluorescent (for e.g. riboflavin)

Cat is a carnivore. Myoglobin is also a heme protein and its breakdown would also produce the "bile pigments" and their downstream excretion metabolites. It is possible that a carnivore might produce more bile pigments because of their diet, compared to a herbivore. However, I am not sure about it.

@John Dvorak: In fact, other sorts of urine, including human, fluoresce under UV light.  Don't happen to have a cat, so I can't check relative intensity :-)

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Do SARS-CoV-2 virus particles really travel through filopodia and "emerge from the tips"?
Watching the new University of California San Francisco video Coronavirus forces cells to produce tentacle-like structures that infect neighboring cells I saw

The growths spread out, and coronaviruses emerge from the tips, ready to infect neighboring cells.

The caption on the video page includes the following:

When a cell is commandeered by SARS-CoV-2, however, these same kinases behave in ways that disrupt normal cell function and transform the host cell into a virus factory. Cell division comes to a halt, inflammation pathways are activated, and the cell even begins to produce tentacle-like structures known as filopodia, which protrude from the cell's surface and may serve as molecular highways that help the virus spread rapidly to neighboring cells.

Question: Do SARS-CoV-2 virus particles really travel through the induced filopodia and "emerge from the tips" of at least some kinds of human cells? Are they transported along the microfibers to the ends as part of this process? If so, how is this known? Images here and elsewhere seem to shown the virus particles dotted randomly along the filopodia and other areas of the cell surface as well.

It surely depends on the cell line, is it specific to vero E6 cells and maybe some models of epithelials (Caco-2, HAE, where filopodia are desired) ? There are some images where the virions budding vesicles seem to be exocytosed normally. You can try emailing the authors of 1 and  2.

@reuns I'm too shy


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Identify this dragonfly with orange body and orange wings?
The photo shows a red dragonfly on top (in front of some hot pink snail eggs) but an orange dragonfly with orange and perhaps translucent(?) wings near the bottom. This is the best resolution I could get. While the red one is easy to photograph (see Identify these two big, beautiful dragonflies in Taiwan?) this orange species is really jittery and difficult to approach.
I believe I have seen dozens of them in an isolated grassy patch in a parking lot, but they never landed and I could not capture a photo or see them clearly, but today this one was "available" for a photoshoot.
The orange dragonfly's body is about 4 to 5 cm long, the location is Hsinchu county Taiwan. That's all I've got, except that the last centimeter or so of the wings appear to be almost transparent.

These seem to both be Neurothemis taiwanensis.
On iNaturalist, if you search for dragonflies in Taiwan, it finds 104 species observed and submitted, and this Neurothemis taiwanensis is the most popularly-submitted species.
Browsing the gallery of photos in their database shows both red and orange varieties. If we filter the sex on just males, we see mainly deep-red ones:

...and filtering on just females yields mainly orange ones but also some red ones:
https://inaturalist.ca/taxa/503081-Neurothemis-taiwanensis/browse_photos?term_id=9&term_value_id=10&place_id=7887

Wow! Very nice, Yes I see that now. Okay I will now try to figure out how to use the inaturalist.ca site's features. Thank you very much!


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Colorblindness in females and random X chromosome inactivation
From Annenberg Learner:

Because the X is inactivated randomly in cells, one cell could have the maternal X inactivated, while the adjacent cell could have the paternal
  X inactivated. This causes a pattern of gene expression called mosaicism, which occurs when different alleles of X-linked genes are expressed in different cells.

However, this seems at odds with colorblindness being more likely in males.  From Wikipedia:

The genes that produce photopigments are carried on the X chromosome; if some of these genes are missing or damaged, color blindness will be expressed in males with a higher probability than in females because males only have one X chromosome, whereas females have two and a functional gene on only one of the X chromosomes is sufficient to yield the necessary photopigments.

Question: If X chromosomes are randomly inactivated cell by cell, shouldn't the fully functional photopigment-producing gene be inactivated approximately half the time?  In which case, wouldn't we instead see females with colorblindness with higher frequency as males, but experiencing colorblindness to a lesser extent?  (After all, two X chromosomes means two chances for a dysfunctional gene.)
I'm guessing I'm missing a piece of the puzzle here, e.g., perhaps the relevant cells "know" to inactivate the dysfunctional X chromosome, or perhaps it's to do with X chromosomes only being incompletely inactivated.

@Christiaan. I was thinking the exact same thing about the tags. But it had a part about sex determination in it, and while not what I would consider sex determination it was related to sex-linkage... I agree with your decision.

@AMR - I just posted in chat. Will ping

In heterozygote females with colour defect genes on the X-chromosome, even if approximately half of their photoreceptors are dysfunctional they usually have enough functional cone photoreceptors to have normal colour vision.
From Molecular genetics of colour vision deficiencies:

Due to X-chromosome inactivation during early development,
  heterozygotes are mosaics for two populations of cones, one expressing
  visual pigment genes encoded by an X-chromosome that would cause
  colour vision defects in males, and the other expressing genes that
  would confer normal colour vision on a male. In support of this,
  patches of defective colour perception were detected by shining a very
  narrow beam of red or green light into the retinas of female
  heterozygotes for X-linked colour vision defects. The majority of
  heterozygote women (carriers of colour vision defects) have normal
  colour vision.

This means that  – in most cases – for a female to be colourblind, her father must be colourblind and her mother must be either a heterozygote (carrier) or homozygote colourblind. In a male, only the mother's X-chromosome determines whether he inherits the defective genes, so he is more likely to have the colourblind trait.

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What kind of memory is "keyboard/keypad memory"?
I work in IT and I have observed many people who cannot remember their iPhone passwords or computer passwords off the top of their head. However, if presented with a keyboard or a phone with a functioning keypad, they can instantly remember exactly what their password or passcode is.
I'm curious to know what this kind of memory is called. Since it's somewhat related to visuals, but not necessarily (you don't need to look at your keyboard to type out your password.)

I came back from a week-long holiday about a year ago, and tried to pay for my airport parking and go home, only to discover that the debit card PIN I'd been using for the past 12 years had completely vanished from my existence. My memory of it had gone and my muscle memory was no longer working. I couldn't explain why this was and, after resorting to a credit card that I only happened to have on me (with its PIN; don't do this!) due to exceptionally unlikely circumstances, finally got home and spent the next few days re-learning my debit PIN. A wholly bizarre experience.

Short answer
Motor memory
Background
A striking personal example of your account pictured in the question was my experience where I had to type in my PIN at the bank counter on a keypad. It turned out I entered it incorrectly several times in a row, despite the fact that I had used that PIN a zillion times on ATM machines. Luckily, the bank employee had seen this phenomenon many times before, and she explained to me that the standard computer keypads have a different numerical layout than ATM machines. So to type in my PIN correctly I had to do it under visual guidance - an awkward experience. It showed quite strikingly that I had been entering my bank PIN using motor memory.
Much of our motor behavior is learned - think of learning to walk, cycle or ice skate. To achieve motor learning, the central nervous system is believed to use internal models that predict the mechanical dynamics necessary to execute a task. In theory, the internal model is an association from a desired trajectory for the hand to a pattern of muscle movements. This map is basically unique for the objects that we have learned to interact with. Because we routinely use our hands to interact with a remarkably diverse variety of mechanical systems, the ability to learn and recall internal memories is thought to be a fundamental property of the motor system (Shadmehr & Brashers-Krug, 1997).
Reference
Shadmehr & Brashers-Krug, J Neurosci (1997); 17(1): 409-19


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What do trans-fats do when in human body?
Trans fats cause health problems, especially to the heart.  https://en.wikipedia.org/wiki/Trans_fat#Health_risks
My guess is that all effects happen because trans-fats are inherently toxic as the body never evolved to process them. But then L-glucose has no harmful effects, even if it cannot be digested.
So how are trans-fats processed in the body differently, and where does all the harm happen?

The closure based on homework is a bit harsh - OP showed the parallel between L-glucose and I checked the wiki page and it is indeed unintelligible when one is interested in the mechanisms in which trans facts cause harm. I deem this a valid, interesting and sufficiently researched question.

In Ascherio & Willen (1997) it is mentioned that, and I quote:

[...] Trans fatty acids increase plasma concentrations of low-density lipoprotein (LDL)
  cholesterol and reduce concentrations of high-density lipoprotein (HDL) cholesterol relative to the parent natural fat. [...] [T]rans fatty acids increased the plasma ratio of total to HDL cholesterol nearly twofold compared with saturated fats. On the basis of these metabolic effects and the known relation of blood lipid concentrations to risk of coronary artery disease, we estimate conservatively that 30 000 premature deaths/y in the United States are attributable to consumption of trans fatty acids.

The US Heart Foundation explains in more layman's terms the same principles:

Trans fat is a type of unsaturated fat that behaves like a saturated fat because of its chemical structure. It increases our risk of heart disease by increasing the “bad” LDL cholesterol, while also lowering the “good” HDL cholesterol in our blood.

And from the Better Health Channel Australia we learn why LDL is 'bad':

Too much cholesterol circulating within LDL in our bloodstream leads to fatty deposits developing in the arteries. This causes the vessels to narrow and they can eventually become blocked. This can lead to heart disease and stroke.

Reference
Ascherio & Willen, Am J Clin Nutr 1997;66(suppl):1006S-lOS.


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How is information sent from the skin to the brain?
Say you have a needle, and you poke a very specific area on your left thumb.
A signal gets sent from that nerve up your spine and into your brain.
How does the brain know exactly where this signal has come from to such accuracy?

Does each nerve in every conceivable part of the body have a unique path that goes up the spine and into the brain, so that's how the brain knows where it came from?
Or does the nerve encode the signal as data which travels up a generic nerve, and the brain decodes the information, which contains the "address" of the particular spot that was stimulated? If this is the case, how are the data encoded? Binary?

For a quick primer, see http://en.wikipedia.org/wiki/Receptive_field#Somatosensory_system, but hopefully I (or someone else) can come along and fill in the gaps in a bit.

Ok so that explains the receptors and their surface area. How do these signals then reach the brain and how does the brain know exactly where the signal comes from?

Cross-posted on Cognitive Sciences...

@user2721465 I will try to address some of these questions in my answer.

In addition to what Spinoral has said, and in response to your comment above, I will add a bit more about the mechanisms.
Essentially, in some form or another it's receptive fields all the way up.
A brief outline of the anatomy:
The cells from the spinal cord are pseudounipolar and have their cell bodies in the dorsal root ganglia in the spinal cord.  The other "leg" of the sensory neuron projects to the medulla, which has cell bodies which send axons to the VPL thalamus, which then has cell bodies that project to the primary somatosensory cortex.  There are points of decussation (crossing over the midline), but I'll ignore those for now.
The receptive fields:

The receptive fields of somatosensory neurons share much in common with the receptive fields of visual neurons. As for visual neurons, the somatosensory receptive fields comprise a restricted 2-dimensional region of space where a stimulus can evoke a neuronal response. In somatosensory neurons, however, space refers to a region of the body and the stimulus can be touch, vibration, temperature or pain

(from Scholarpedia)
Essentially, the somatosensory input is "filtered" at all of those stops along the way and refined in terms of things such as whether the sensation came from the center or the edges of the receptive field, etc.
Cells in the cortex (the waypoint for the sensory information) are organized in microcolumns, which are representative of a particular location on the body (and arranged topographically into the "homunculus", as the other answer mentions).
All of this follows what is called the "labeled line" theory, which is getting a bit outmoded due to new knowledge about ensemble coding in neurons, but for purposes of the somatosensory system it still holds up pretty well.

This is a bit of a work in progress, but it should give you some terms to google, etc.

Great, thanks this is exactly what I was looking for. So there's 2×10^8 minicolumns in the cortex corresponding to places on the body. Does that mean that there's roughly an equal amount of sensory neuron pathways in the spinal cord correlating to these minicolumns?

@user2721465  It's not necessarily a 1-1 relationship between skin receptive field and column in the cortex (there are higher level "abstractions" in the cortex such as orientation of the stimulus, etc.).  Since the information is being "filtered", there are complex relationships between the thalamic cells, and there's some degree of consolidation that goes on.  The bundles of axons are converging on the cord at different levels (see a map of the dermatomes for the mapping), but the tracts are quite thick anatomically, so there's many thousands of axons in one nerve bundle.

(for example, the roots for the arms enter between the vertebrae of the cervical region -- http://en.wikipedia.org/wiki/Dermatome_%28anatomy%29, legs in the lumbar, etc.)

If this is something that you are interested in, the rat whisker system is the model used for decoding some of these pathways.  The earlier connections are different (it's a nerve that goes directly to the brainstem), but the cortical layout is similar.

The accuracy of sensation is actually quite variable depending on the region of our body. Highly innervated areas such as our fingers have a higher degree of accuracy than sparsely innervated areas such as our legs.
There is a simple experiment you can do to illustrate this. Close your eyes and then get a friend to lightly and slowly run their finger from your wrist, up towards the bend in your elbow on the inside of your arm. Try to guess at what point the reach the joint of your elbow.
In terms of how the brain knows where it came from,  there is part of your brain called the sensory cortex. This sensory cortex has a pattern that corresponds to areas of the body. This pattern is known as a the sensory homunculus (google images will find this). As signals pass up the various different spinal pathways and into the brain they are sent up to this sensory area and the appropriate region of the homunculus is stimulated thereby giving the sensation in the appropriate body area.
Interestingly in some brain surgery a patient may be kept conscious so that these areas can be directly stimulated by electric current and the patient will experience sensations.
There is also a matching area, called the motor cortex, which corresponds to movement rather than sensation.
The above is a simplified version of what goes on and there is lots more detail which would be covered in neuroanatomy books

Ok, so the signal from the nerves travels up the spinal pathways into the sensory homonculus.
Does the sensory homonculus know where the signal came from because a specific spinal pathway is used which is unique to each area of the body or is it because the signal is encoded in a particular and unique way?

Due to specific spinal pathways, but my point with the experiment and the arm is that this is not as accurate as you may perceive it to be.


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Hidden Markov Model
I read about the hidden markov model in bioinformatics. I amn't able to understand what it is.
Can anyone explain me in brief and in very very simple words what it is ?
I have NO background in bioinformatics or programming and wikipedia article on it is too scary .

Markov models are used in almost every scientific field. In short, it is a kind of stochastic (random) model and a hidden markov model is a statistical model where your system is assumed to follow a Markov property for which parameters are unknown. Because it is not specific to biology, I would recommend you to ask your question on crossValidated.SE

This question appears to be off-topic because it is about a statistical/computational concept

<this is about to get closed. I think it could be on topic if you edit it to make it specifically about the applications of HMMs to biology. For example in gene prediction or in the building of sequence profiles (e.g. hmmer)

@terdon.. I guess this problem comes from the way bioinformatics is taught.. When you start introductory bioinfo and read about the different tools and databases you often see some vague statement like- The sequences are discovered using HMM and then a non redundant database is made. The term is heavily used but not explained. Nobody usually uses or are even aware of tools like HMMER at this stage. I have also remained confused about this term called HMM for a while. This is still a relevant question but is out of scope of this forum- that's why closing it.

@WYSIWYG this is exactly the reason why i asked the question. But i understand why this is out of scope.

A Markov model is a description of a system that follows a Markov process. In a Markov process the next state of the system is a function of its current state and does not depend on where from and how it started. For example Brownian motion can be called a Markov process. The transition from current state to next state is described by probabilities.
So to conclude, a Markov model is a probabilistic model of a system that is assumed to have no memory.
In a Hidden Markov Model (HMM) the state(s) of the system are not known (therefore hidden). However, there are some functions that depend on the state and their outputs can be used to approximate the state of the system. There goes the definition- it is not that easy to explain how it is applied to different concepts (not just bioinformatics).
Strictly speaking this is off-topic. HMM is not a biological concept. It is a statistical/computational concept (it is like asking what is Dynamic Programming- which is the underlying concept behind BLAST algorithm).

Thank you for answering my question though I now understand that it is not strictly on topic.

I read about this in relation to protein domains and motifs. What does that have to do with HMM ?

Motif finding algorithms use HMM to predict the correct motif..

You can check this paper out to know about how HMM is applied in motif discovery. It is by Sean Eddy who has developed many popular HMM based tools


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Thymus and maternal microchimerism
I read in Bruce Alberts Molecular Biology of The Cell :

....If,however,cells from one strain of mouse are introduced into a neonatal mouse of another strain , some of these cells survive for most of the recipient animal's life, and the recipient will now accept a graft from the original donor, even though it rejects "third party" grafts.

As far as I understand , in this experiment,they got these results because thymus hadn't yet learned what was "own" and what was "foreign".
Is  the reason for why maternal microchimerism does not invoke immune response related to the above experiment ? Can we apply the same logic here ?

You are on the right track.  This is an example of microchimerism (the maternal part is a bit off), and the key issue at hand is central tolerance.
Background:
A good definition of microchimerism is:

Microchimerism is existence of an allogeneic DNA in a living creature. (1)

Scientist do this on purpose for all kinds of reasons, but mostly to ether is study the immune system directly or to get a near-transgenic model.  It should be noted that this isn't perfect, and that when you try to do this, you often can lead to auto-immune problems and often death of the mouse (30-50% survival in early work).  If you go back to one of (if not the) pioneers of immunology, Peter Medawar, you can see when how this was done:

Mice and chickens never develop, or develop to only a limited degree,
the power to react immunologically against foreign homologous tissue
cells with which they have been inoculated in fetal life. Animals so
treated are tolerant not only of the foreign cells of the original
inoculum, but also of skin grafts freshly transplanted in adult life
from the original donor or from a donor of the same antigenic
constitution. (2)

If you would prefer a visual layout of the experiment, Starlz put together one in his review of transplantation (Pubmed):

After looking over the section you quoted from Alberts, I'm pretty sure he was in fact referring back to these early experiments.  But that was all the way back in the 1950's, what have we learned as the mechanism in 60 years?
Possible Mechanism:
The truth is that we don't have an absolute grasp on how this works when it doesn't cause an autoimmune problem and abort the fetus or even neonate pup.  It's import to note that it probably does cause auto-immune problems and various other side effects (like sex differentiation) in mammals.
But when and how it is tolerated is likely mediated by central tolerance, and the ability to get the foreign MHC molecules tolerated by early lymphocytes.  Essentially, the cells have to get incorporated into the AIRE machinery at an early enough stage that the T-cells are selected against the foreign cells.
There is enough biology here that an in-depth answer could be a dissertation, so I only want to touch on a few more points.  You should note that this was done with relatively genetically similar animals, and most modern researchers use cells modified from genetically pure mouse breeds.   We also know a lot more on how the cells "recognize self" and the HLA types of the population.
You are most likely to succeed when the MHC molecules are very similar (ie from a direct family member).  This happens when the host and foreign cells have an HLA type match.
TLDR:
The lymphocytes, mostly T-cells in this case, of fetal mammals seem to be able to look at very similar MHC molecule on a foreign cell and decide "eh.. close enough," and build negative selection (part of β-selection) against lymphocytes that would kill the foreign cells.  This requires that the cell be in the right place at the right time, and of course, be "close enough."
Do let me know if something is not clear or needs to be expanded upon.  As someone who works in Immunology, I have difficulty determining where the detail line should be.

Thank you so much for such an awesome answer ! I never thought someone would give such a detailed explanation !

Have you come across papers showing evidence that maternal microchimerism in humans is tolerated because thymus of fetus thinks the maternal cells are its own cells ?

@biogirllajja No I don't and that's for a couple of reasons.  Cells going from the mother to the fetus are much more rare in humans than the reverse.  The only times we tend to find out about it tends to be when there is a problem and it isn't tolerated.  Your question would have to answered by a large, costly, study of the healthy population.  There's just not going to be the funding for it.


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Why bacteria produce light?
After seeing this video I am curious to know why the free living bacteria produce light. What advantage will they have ? Or is it just an "unintentional" result of one of their pathways ?

Go for the  link below, you will find an article on "How do marine bacteria produce light, why are they luminescent, and can we employ bacterial bioluminescence in aquatic biotechnology?"
www.biology-online.org/articles/marine_bacteria_produce_light/abstract.html
From this article :

The question remains whether quorum sensing regulation of bacterial
  luminescence is a kind of a ‘social behaviour’ in which cells
  ‘predict’ the possibility of increased mutagenesis where conditions
  allow for efficient metabolism leading to extensive bacterial growth.
  Such conditions may cause the appearance of large quantities of
  metabolites, including mutagenic agents. Thus, one could speculate
  that enhanced light emission at a high cell density may ensure more
  efficient DNA repair in response to potentially increased
  concentrations of mutagens. Alternatively, quorum sensing may be
  needed for another role of bacterial bioluminescence, besides
  stimulation of photoreactivation.


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Telomerase in tetrahymena
In this amazing video, at 26:03 we see this image
We now know that the telomerase contains a sequence complementary to the telomere sequence and so is able to do what it is capable of doing in this image.
My questions : What if we make a piece of dna with  five GGGGG at the 3' end ? Will the telomerase not work, as the RNA in telomerase has the sequence AACCCC and so won't be able to form complementary strand ? If so, has such a mutation been detected in any organism ie it's telomerase is unable to work just because it has a random insertion(maybe during replication) of one of the nucleotides in the telomere at the 3' end ?

Anyone who wishes to understand telomere and telomerase and want to know more about them from the discoverer of telomerase HERself please see the video I mentioned in the link! It's enlightening.

This is speculation, as I haven't done or read of the required experiment. However, I imagine that this would not be a problem.
You're right that the RNA template (TERC) would not hybridize with a poly-G sequence, and so the telomerase would not be able to add more telomere repeats. You can imagine that the poly-G sequence is a cap, preventing telomerase activity.
However, without the telomere repeats other proteins are likely to recognize the chromosome end as a DNA break. Exonucleases would likely chew at the end of the chromosome until they got to the actual telomere sequence, which is bound by protective proteins (namely Shelterin). With the poly-G region degraded, the end of the chromosome would now have the true telomere repeats, and telomerase would be able to add even more repeats.
Even if the poly-G region was bound by protective proteins, the telomeres naturally shorten with each replication cycle, due to the nature of 5' to 3' DNA replication. Therefore, the poly-G region would eventually be removed revealing the true telomere repeats and allowing telomerase to extend the chromosome once again.
In a worst case scenario, rather than degrade the poly-G region the cell undergoes recombination between poly-G regions on multiple chromosomes, leading to either massive chromosomes or circular chromosomes. However, I'm sure these cells would die with some kind of massive mitotic failure.


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Diffusion of FAD+
Why is NAD+ free to diffuse within the mitochondrion whereas FAD+ is not ? What biochemical properties cause this difference ?

As explained at the Wikipedia page for succinate dehydrogenase the FAD is covalently attached to one of the subunits of the protein. It is the first carrier in a short intramolecular redox chain involving Fe-S clusters, and possibly a haem, before the electrons derived from succinate are passed on to ubiquinone and on down the respiratory chain.
As you say, this contrasts with NAD which is a diffusible coenzyme.


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DNA ligase mechanism

I am unable to understand what happens to the phosphates from  ATP. What are they used for ?Charging 3' end or 5'end ?

When you ligate two strands of DNA you build up a phosphodiester bond. To do so, you need energy, and this energy for the DNA ligase comes from the ATP (in bacteria this energy can also come from NAD+.
The enzyme metabolizes ATP to AMP + PPi and binds the AMP in its active center. Then the AMP is involved in the reaction itself and released afterwards. This page has a few illustrations on this process.
If you want to dive really deep into the topic, have a look at this review:

Eukaryotic DNA Ligases: Structural and Functional Insights


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How exactly is glyceraldehyde 3-Phosphate reverted to ribulose 1,5-bisphosphate for the continuation of the calvin cycle?
Around 6 molecules of G3P is produced at the end of the Calvin Cycle (light independent reactions of photosynthesis), and 5 of which are reverted back to RuBp.
The general equation that I read is 5 G3P -----> 3 RuBp using 3 ATP.
It however doesn't seem to add up (regarding balancing of the atoms) as 5 phosphates would be converted to 6.
I would appreciate a link to any resource explaining this process in detail.
Thank you and have a nice day ^^

The detailed mechanism is available on http://en.wikipedia.org/wiki/Light-independent_reactions#Steps

You need to account for free phosphates (Pi) that derive from ATP and are released in phosphatase reactions. The regeneration of 3 ribulose-1,5-2P has the overall reaction
5 glyceraldehyde-3P + 3 ATP $\rightarrow$ 3 ribulose-1,5-2P + 3 ADP + 2 Pi
So in total eight phosphates (here counting ATP as 1) are redistributed, 6 of which end up in ribulose-1,5-2P, and two are released as free phosphates. (These Pi are then recaptured during ATP synthesis in the light-dependent reactions.)
The above is a summary reaction of course; the complete scheme involves 10 enzymatic reactions that rearrange carbons in various ways to form 5-carbon sugars from 3-carbon ones (which takes a bit of juggling of atoms). Release of free Pi occurs in the fructose biphosphatase and seduheptulose biphosphatase steps.
A detailed account can be found in any major biochemistry textbook, like Stryer's Biochemistry. Online resources like MetaCyc can also be helpful.


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Favored Conditions of Bacterial Growth
I have read that bacteria "thrive" in warm places. Naturally, I am very interested in why this is the case. Humans for instance thrive also in relatively warm conditions if it's too cold or too warm we die. However why would this also apply to bacteria?

The idea that bacteria thrive in warm places is mostly biased from a human perspective. Human researchers will tend to care more about bacteria that cause human disease. These pathogenic bacteria can replicate in/on humans at ~37 °C (which is warm). As Dexter points out, bacteria can grow at other temperatures.
But I'd go deeper and consider proteins (and other macromolecules) in the cell. For example, the enzymes that carry out many important processes for the bacteria (such as DNA polymerases that build the DNA) are most active at certain temperatures: in E. coli or humans or dogs that's ~37 °C; for a thermophile it's warmer. See below:

Actually it's not true. It depends on species of bacteria you are talking about. Bacteria can 'thrive*' in very wide range of temperature. They can be mainly categorized according to temperature,

Psychrophiles : live in very cold temperature. Reported lowest** temperature in which specific bacteria can 'thrive' is $-20^oC$ .
Mesophiles : live in moderate temperature
Thermophiles : live in very high temperature. These can 'thrive' at very high temperature like $+121^o C$

*By 'thrive' I mean they are actively dividing and metabolic process are not ceased.
**People store at bacteria at $-80^0C$ also but there they are not 'thriving' they are alive but freezed.


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Biological Evolution outside of Earth
What drives evolution forward? I heard that climate change drives species to evolve and adapt. Is there any other mechanism that is encoded in our DNA by which species can over abrupt changes, evolve and adapt?
Say for example Jupiter's moon Europa. If I find species of fishes here in Earth that could theoretically, barely survive on those oceans. If I come back in 5 million years will they look the same they did when I placed them there? or is the process of natural selection universal, and I would expect to see changes in the fishes due to their new environment which is not Earth. basically would foreign species also evolve and adapt.

The relationship and adaptations made to pathogens. As for your hypothetical situation, they would need a food source and a source of oxygen. It is hard to say whether they would even survive as they did not evolve there and we cannot be 100% sure that Europa will have all of the properties they need for survival. We see the effects on the astronauts who live at the space station. They experience bone density loss, develop vision problems, etc. all due to the fact that we did not evolve in free fall. It is difficult to make predictions about adaptation in places we did not evolve in.

You take a population of fish and put them in a new environment (another planet even). Will they evolve?
Yes they would evolve as long as they don't get extinct. It sounds very likely that they would very quickly get extinct though.
Note, however that they were already constantly evolving while being on earth whether or not their environment was stable or changing through time. Evolution is not a thing that occurs only when the environment is changing. Stabilizing selection, genetic drift and mutations affect the allele frequencies too, not only directional selection.
General comments on the post
I don't quite understand the relationship between the first paragraph and the second paragraph.
The first paragraph suggests a few misunderstanding of evolutionary processes. I recommend that you have a look at a free online introductory course of evolutionary biology such as Understanding Evolution by Berckeley University for example. Typically, if some concepts I used in the second paragraph above were unknown to you, then you definitely want to have a look at Understanding Evolution


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Enrichment of slow growing microbes: Large Test Tubes as an alternative?
Well, i would like to enrich bacterial and archaeal ammonia oxidisers from soil samples using Minimal Salt media. They are slow growing microbes. I would like to enrich them with the aim to produce pure cultures.
I have always used conical flasks for enrichment as they provide better aeration, surface area, better distribution of nutrients, etc. However, due to some unavoidable reason, i would like to find an alternative to conical flask. Is it fine to use large test tubes?

I can't think of any reason slant cultures wouldn't work. It's worth a try!

@jzx agar slants in the sense solid media? i would like to use broth (not solid media), may be i can keep the broth in a slant position?

Yes, that was my thought. Obviously not ideal since you'll have to be careful, but if that's all you have on hand it's what I would do.

You want to purify colonies by growing them and streaking? You can use larger test tubes with sufficient air volume (use around 5ml of broth in 20 ml test tube) and proper mixing.

@WYSIWYG, ya, i want to grow them in a selective broth and then get pure culture if possible. Many Literature from NCBI using 50 ml broth (minimal salt media) in a 150 ml Erlenmeyer flask. And since the Ammonia oxidizers grow real slow, the media is replaced (10% dispensed in fresh media) weekly.

@NokImchen can you not provide an enriching medium?


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Requirements for soil sample transportation over long distance
I need to collected soil sample from agricultural area far away from my lab. It would required about a week for the sample to arrive to lab. I need the soil sample for genomic DNA isolation (metagenomics) as well for isolation of certain species and culture them.
Therefore, the cells in the soil sample needs to be viable. What are the possible ways to long distance transportation of soils sample with intact viable cells?

I would say it depends on the cells you are looking for. Are you the first one in your lab doing this stuff or are there protocols available?

Yes, i am the first doing in my lab. I am targeting ammonia oxidizing bacteria and archaea.

Do what you have to do (extraction, culturing) on site?

I'm no expert, but it would seem to me that as long as the soil's approximate humidity level and temperature are maintained, you should be able to transport it for a week just fine. Think about it - the organisms in the soil are adapted to outdoor life, which (depending on their native climate) probably means varying amounts of water in the soil from time to time, and most likely temperature variations as well. It's not like you're trying to transport a viable human organ or something...

We did a soil sampling expedition around farms in the UK a few years ago.  We took with us some insulated plastic picnic drinks cool boxes, and a lot of pre-frozen camping freezer blocks.  We bagged up the soil samples, and put the bags in the drinks coolers with the frozen blocks.  This worked fine for our 48 hour trips.  If you were going for longer, you could try to arrange access to a rotation of frozen freezer blocks, or buy bags of supermarket ice along the way to top up the drinks coolers.  The idea for us was not to freeze the samples, but just to keep them cold enough that the organismal diversity was not changed too much during the transportation.


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Are there mechanisms that limit the amounts of time conjugation and F-plasmid transfer can happen? If yes, what are they?
Not all bacteria have acquired F-plasmids through conjugation. Some of the mechanisms for this are unsuccesful conjugation events (mechanical disruption), no transfer due to integration in bacterial chromosome, etc (See previous question and answer).
Now I am wondering if there are also mechanisms that self-limit the conjugation and transfer of F-plasmids. For instance that a bacterium can only transfer its F-plasmid once during its lifetime.

Yes there are many such mechanisms.
One of the simplest, but perhaps most easily overlooked, is metabolism.  Conjugation requires ATP.  In environments with low levels of nutrients, heterotrophs might not have enough "extra" ATP to fuel the conjugation process.  Note that both donor and recipient need to expend ATP in conjugation.  The donor needs to make the nicking enzyme, the pilus, and extrude the DNA into the recipient, and the recipient needs to synthesize DNA from the single-strand DNA that it has received.


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To what extent do fossils change over time?
Fossils are formed over millions of years. How do scientists quantify the extent to which a particular fossil has changed in shape/relative tissue density/etc. over geological timescales (if at all)? I ask this (as a non-biologist) because we are often presented with fossils as being exact copies of the original species, as it was when it was alive. I wondered if this is indeed the case and imagine that the answer will vary for fossils of soft versus harder tissue composition.
If organisms do indeed retain their shape almost entirely, what experiments are carried out to mimic geologic timescales and processes to demonstrate this?

There won't be a single answer to this question -- a skeleton will be different from an insect from a leaf. But taphonomy is study of the process of all the things that go into making a fossil a fossil. Start there and maybe refine your question.

Fossils typically are millions of years old, but they can form rather a lot quicker than that.


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Function of the 'double' leaf on a pomelo tree
What is the function of the 'double leaf' (I'm unsure what the technical name is...) on a pomelo tree leaf?
Furthermore, what evolutionary 'problem' is this structure solving?
See image with arrows that indicate the two parts to the leaf.

It's a lobed stem, i.e. the stem of the leaf has lobed mini leaves. It looks like the leaf originally was like this, and the stem developed lobes: https://upload.wikimedia.org/wikipedia/commons/thumb/2/24/Wild_Orange_underside_of_leaves_%2810868374834%29.jpg/1280px-Wild_Orange_underside_of_leaves_%2810868374834%29.jpg


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Is it possible to feel pain in some part of a body, but the pain "feeling" is introduced somewhere else?
Is it possible to feel pain in some part of a body, but that the cause of the pain is situated elsewhere in the body? For example, somebody feels pain in his toe, but it turns out that this pain is not signaled by nerves in his toe, but caused by a damaged nerve in the spinal cord, or somewhere in the brain.

Yes, this is pretty common.  Examples include

sciatica, pain felt down the back of a leg to the foot, from irritation to components of the sciatic nerve but commonly at the level of the sciatic nerve roots
angina pectoris, pain from myocardial ischaemia felt in the throat (Latin angina "infection of the throat"), arms, chest etc
shoulder tip pain from a subphrenic abscess

The clearest possible example of this is phantom limb pain, where pain is perceived to be arising from an amputated limb indicating that the pain is arising from central mechanisms.

An example of pain evoked by distant sites in the body is referred pain.  It's defined as pain perceived at a location other than the site of the painful stimulus. An example is the case of angina pectoris (chest pain), caused  by myocardial ischemia (decreased oxygen supply to the heart due to a narrowing or complete blockage of the coronary arteries). Angina often results in pain felt in the neck, shoulders, and back rather than in the thorax (chest), which is the actual the site of the injury.
A massage-related field of therapy has evolved around this - trigger point therapy, where trigger points are defined as the cause of pain elsewhere in the body. From personal experience I can add my gratitude to this field of therapy; it's been good to me.

Trigger points. source: Trigger Point Therapy

Another common medical condition that causes pain elsewhere is the spinal disc herniation. The disc pushes against the nerves in the spinal and causes pain, usually in the leg, foot or arm. https://en.m.wikipedia.org/wiki/Spinal_disc_herniation
Sometimes the pain disappears with rest, sometimes surgery is necessary and sometimes the pain partly remains even after surgery.

When I went to a doctor years ago because of pain in my arm that had lasted months, he diagnosed it as tendonitis. It wasn't until a chiropractor recommended I see a sports medicine specialist, who recommended an MRI, that I learned I had herniated a disc in my back that was the cause of the pain in my arm, which didn't go away until over a year later.

@moonpoint It is not uncommon that disc herniation is not immediatly diagnosed. The pain may go away, or it may not, not even after surgery :-(

Just as an FYI, the answer is emphatically yes.  I have two separate areas of my body which exhibit those symptoms.  But my answer does not "track" those of others here.  They talk about (I would guess) some relatively standard off-site pain actions.  In my case, it appears to be more simply the action of (for want of a better term) CrossedNerves.  As one example, there is an area of about two square inches, just right of center, on my chest which, when poked with a sharp object, will cause a stabbing  pain to appear on the back of my right shoulder just below the shoulder blade. This is repeatable and has been that way since as long as I can remember.
Glad to see I'm not the only one with these strange biological oddities.

interesting answer - is there any cited literature on this phenomena that you describe? could you cite that in your answer - it would improve your answer significantly

@VanceLAlbaugh to me this sounds like a specific form of synesthesia.


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Why are there no complex hermaphrodite land animals?
The title says it all.  I know that 'complex' is a pretty ambiguous term to use, but I can't think of a more scientific term/definition for my meaning.  I can't think of any large (larger then a small rodent) hermaphrodite species, or any that we tend to think of as having complex structures; hermaphrodite species all seem pretty boring really.
I get why sex is a huge advantage, but by that regard hermaphrodites seem quite powerful.  The ability to both produce your own young and impregnate others allow for more young.  Plus, it provides the opportunity for a species to choose to self fertilize if no mate is available.  I realize sexual reproduction is preferable, by it's nice to have Autogamy as a backup option just in case.
I understand why there are advantages to two sexes, particularly in terms of sexual dimorphism which allows male to be better at potentially reproducing with many females by specializing in it.  I completely understand how two genders would evolve and be successful.
What I find odd is that nearly all larger or complex species seem to have genders.  I would have thought that, like many other mating strategies, there would be variance across species; with some choosing to be hermaphrodites to increase the maximum children they can produce as a species, by having twice the child bearers, and others choosing to go the sexual dimorphism route by having roles that they are best at.   I mean even Obligate parthenogenesis has evolved separately many larger specie like lizards, despite it arguably being an evolutionary dead end in the long term due to the lose of the advantages of sexual reproduction.  If adaptations that completely toss away the power of sex evolve all over the place why do new hermaphrodite species never seem to evolve, and existing hermaphrodite species never seem to grow bigger or more diverse?
In particular sequential hermaphrodite, like many aquatic fish use, seems a pretty effective strategy.  When your young, and small, play a female role to have guaranteed offspring, only once your big and at your most fit bother competing as a male for access to multiple mates.
A related question, associated with my own attempt to explain why existing hermaphrodite species don't seem to take as many varied forms; but which I'm not really sure I buy.  Is it possible that the lack of sexual conflict (primarily, but not limited to, competition between males for mates, driven from the fact that males would have more drive to compete then hermaphrodites since it's their only reproductive strategy), would mean there was less of a drive towards adaptation in hermphrodite species?  A sort of red-queen scenario, where your own species is the red queen?

I'm no biologist, but what is your definition of "complex"? Land snails and earthworms are hermaphrodites, which makes sense because they move rather slowly and therefore have fewer opportunities to find a mate. Do you mean "vertebrates"? If this is what you mean, the probable answer is that simultaneous hermaphroditism is something that hasn't existed in the verterbrate ancestral lineage for a very long time, if ever, and therefore it needs to "re-evolve." Given that vertebrates are highly mobile and therefore have frequent opportunities to mate, it seems unlikely to happen.

"I can't think of any large (larger then a small rodent) hermaphrodite species, or any that we tend to think of as having complex structures; hermaphrodite species all seem pretty boring really." !!! There are snails much larger than mice. And "boring" is very opinion based.

Please reduce the text by at least two-thirds. Add only info relevant to the Q

@steveverrill Evolution of hermaphroditism is likely not difficult, see http://icb.oxfordjournals.org/content/53/4/736/F1.expansion.html

I was really happy to see this question, cuz it's been bugging me for years too. (Like, I remember trying to get a satisfactory answer from my grade 12 bio teacher.) But it seems like the community in general isn't quite getting the intent, the way you phrased it (it makes perfect sense to me, but then, we're obviously in the same mindspace on this point already). Maybe try making it more concrete?

Like... sketch out an idea for how a species of birds could evolve hemaphroditism, maybe? The selective pressures you think could create and maintain it?

Abstractly, the possible answers to our question that I can think of are: {1 Our ideas of how pressure for hemaphroditism would be generated in species like this are wrong because...?} {2 Our ideas aren't necessarily wrong, but there would be stronger pressure against it because...?} {3 There would be a stable net pressure maintaining hermaphroditism, but there's a barrier against it initially re-evolving from a [antonym of hermaphroditic] population because...?} So write the question to try to focus on concrete examples of those possible explanations, I guess?


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What form of reproduction did the first land animals use?
What form of reproduction did the first animals on land use*? Were they hermaphrodites, or did they have male and female sexes? [Is there a proper term for sexual separation in a species?]
Were any land species believed to have evolved from hermaphrodite ocean species (that crossed to land on roughly the same geological time periods that land creatures first evolved)?
*I know that 'first on land' is a complicated concept itself, since it could mean first creatures be able to survive on land at all, first to freely travel between land and water, or first to only live on land, or anywhere in between.  I assume all three categories were sexual though?

Are you thinking of vertebrates or non-vertebrates?

Your questions are quite wordy. Please be to the point. Condense the question by cutting the fluff, reducing details and exclude irrelevant random thoughts.

I think the term you are looking for is sexual dimorphism. Or just sexual reproduction.


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Parallels between pixelized image and the human retina
On Wikipedia it is explained that the human eye has a certain 'resolution'. Does this mean that the retinal image consists of pixels? If yes, what shape would these pixels have?

Are you asking about the shape of the actual physical representation (rods/cones) or the subjective visual  impression?

I can't imagine this meaning anything other than physical representation, since we do not actually perceive pixels at all.

What shape are stars? Presumably a point light source would illuminate precisely one 'pixel' and you would perceive the shape of that pixel only. In terms of the actual cells, they're roughly round when looked at from 'above'. They're round tubes. Like straws.

Related: What's the smallest size a human eye can see?

You need to realize that the human eye doesn't in any way work as a camera. Only a small area of our eye can see sharp images at high resolution, and resolution and sharpness also differs over the rest of the retina as well. So the resolution varies over the retina. The image we actually see is also a continiously interpreted and updated, and the brain is very creative in this process by basically "filling in the blanks". We therefore don't see in pixels.

I have edited the question in the hopes of saving it from going on-hold. Parallels between cameras and eyes are often made and these parallels are often pretty handy for teachers. However, they lead to confusion in many students when the limitations of the analogy are not properly clarified.

The key to your answer lies in the fact that the brain interprets what we see. What we see is not what we perceive. We see as pixels (logical), which get interpreted as a seemless (unpixellated) image in brain through neural processing.

The pixels of the visual system are represented by the photoreceptors. Their shape is the following (adapted from "The Brain from Top to Bottom, MgGill University"):

There are about a 180 photoreceptors packed on 288 microns on the retina (see "What's the smallest size a human eye can see?") so about 1 pixel per 2 microns. The rods and cones are packed closely together on the retina, referred to as the retinal mosaic. This retinal mosaic is not unlike a photosensitive chip, as can be seen on the folllowing image (Developmetal Neurobiology lab, UCLA, Santa Barbara):

We do not visually perceive this mosaic, as the optics of the eye (e.g., light diffraction by the cornea and the lens, and distortions due to the relatively large pupil size) prevents optimal use of the photoreceptor density (the maximal resolution). Furthermore, especially outside the field of view (the foveal region), the output of many photoreceptors are funneled onto one single optic nerve fiber, thereby fusing the output of many photoreceptors (See the question "Why can we not see around our point of focus of our eyes?"). Lastly, the brain actively 'glues' any gaps in the visual field together. Most strikingly, the blind spot, which is the place where the optic nerve exits the eye is fairly large, is normally not visible to us: see the following picture (PNAS online content):

Hence, any gaps in the retinal image are in fact actively smoothened out by the brain.

Interesting answer. In the field of view do the photoreceptors each connect to a single nerve? Roughly speaking how many photoreceptors may channel into a single nerve fiber, on average (unless there are actual values for different areas of the eye!)? This would ultimately be the smallest "resolution" or "pixel size" then, rather than the size of the photoreceptor itself. Thanks again

Thanks. Good question :) As to neural retinal connectivity see: "Why can we not see around our point of focus of our eyes?" You can click the link in the answer above.

If you by pixels are referring to the photoreceptors (rods & cones), their density differs over the retina, and we can only see sharp images at high resolution in a small region of our eye (fovea). So the resolution varies over the retina. The image we actually see is also a continiously interpreted and updated, and the brain is very creative in this process by basically "filling in the blanks". We therefore don't see in pixels, and our resolution is influenced by (at least) light conditions, contrast, photoreceptor density, signal merging and interpretation of the visual signals by the visual cortex in the brain. However, our eye is also constantly scanning the visual field (see saccade), so even if the "static" visual resolution (when we focus constantly on a single point) is drastically different over the visual field, this does not match our visual perception. As a sidenote, saccades are possibly the fastest human motions, and can reach speeds well above 400°/s (Boghen et al, 1975) - wikipedia reports 900°/s but without a clear reference - and takes place several times per second.
If we focus at the resolution in terms of photoreceptor density (densities of rods/cones), this is drastically different over regions of the retina. For instance, Jonas et al. (1992) reports ~150,000 cones/mm2 close to the center of the fovea to 2500-6000 cones/mm2 towards the periphery. The approximate density of rods goes from 150,000 rods/mm2 to 30,000 in the periphery. Cone & rod diameter also differs over the retina, with larger diameters towards the retinal periphery, which relates to light sensitivity.
A nice summary of the flexibility and limitations of human vision can be seen in this xkcd comic (click for larger version):

(from "xkcd: Our central visual field" at http://xkcd.com/1080/)


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Organisms that contain rare chemical elements
By accident, I found a slide from a Polish chemical presentation, that talks about a small group of biological organisms which contain chemical elements not found in the human body, like:

B (boron),
F (fluorine),
Si (silicon),
V (vanadium),
Cr (chromium),
Se (selenium) and
Sn (tin).

Can someone provide a list of examples of organisms containing these chemical elements?

Our body contains quite some fluorine in bones and teeth...

There is separate wiki page on selenium in biology, and vanadium has this paper dedicated to it. Your assumption that these "chemical elements not found in the human body" is wrong.

Selenium is an essential trace nutrient, what makes you think humans don't have it? For example, we have ~22 (or 25, depending on how you count them) selenoproteins, each of which contains at least one selenocysteine amino acid which is a cysteine analog with Selenium in the place of sulfur. In fact, I would be surprised if any of these elements is not present (at least in trace amounts) in the human body. Do you have any references that support the absence of one of these?

OK. Thank you for your enlightening comments. However, this question is asking about non-human organisms, that contains these elements (for example, tin, which isn't mentioned yet in any comment or answer). You proven, that my assumption was wrong and probably all of these elements are found in human body, but question remains unanswered actually (with little exception for Thaina's answer and silicon).

In that case, please [edit] your question to reflect what you're currently asking. Most of the elements you mention will be present in, basically, most organisms. Which ones are you asking about? Oh, and this article suggests that tin is an essential nutrient in humans as well. Please [edit] and narrow the question down to something specific that we can answer.

This slide only says that these elements aren't used by all organisms there's nothing about small group...

All the elements you mention (B, Fl, Si, V, Cr, Se and Ti) are listed as (probable) essential trace elements in humans by the World Health Organization. The WHO document "Trace elements in human nutrition and health" mentions a host of studies addressing the functions of these elements in species ranging from bacteria and plants to primates. The following list provides some of the functions these trace elements have in humans:

Boron - essential for cell membrane characteristics and transmembrane signaling (Nielsen, 1991);
Fluoride - necessary for the prevention of caries and it is associated with bone health (WHO);
Silicium - probably essential for healthy connective tissue and bone (WHO);
Vanadium - possible role as an enzyme cofactor and in hormone, glucose, lipid, bone and tooth metabolism (WHO).
Chromium - essential trace element that potentiates insulin action and thus
influences carbohydrate, lipid and protein metabolism (WHO);
Selenium - essential component of one of the antioxidant defense systems of the body (WHO);
Tin - expected to have a function in the tertiary structure of proteins (WHO).

References
Nielsen, FASEB 1991; 5: 2661-7
WHO, Trace elements in human nutrition and health 1991

Silicon is not rare at all. Silicon Dioxide is Sand and Sand is content of every soil. Even just rice hull and grass blade contain silicon
If you just read in wiki page of silicon there you would see this

Silicon is an essential element in biology, although only tiny traces
  of it appear to be required by animals.[10] However, various sea
  sponges as well as microorganisms like diatoms and radiolaria secrete
  skeletal structures made of silica. Silica is often deposited in plant
  tissues, such as in the bark and wood of Chrysobalanaceae and the
  silica cells and silicified trichomes of Cannabis sativa, horsetails
  and many grasses

Also in each wiki page you place about each element. Some of them have content about biology/organism chemical component. Such as Boron and Fluoride. You can search their page with {organ} or {bio}


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The mechanism of mechanoreception?
I am interested in knowing the molecular mechanism behind mechanoreception/mechanotransduction (i.e. mechanism behind receptor potential generation on mechanical stimulation). I know that most mechanoreceptors (touch, stretch, pressure etc) respond to mechanical modification of plasma membrane or of some external projection embedded in plasma membrane. I want to know the molecular basis behind this mechanical transduction.
Also, the sensory hairs in lateral line sense organs of fishes, and equilibrium and auditory sensation in animals involve generation of receptor potential when the steriocilia( or any equivalent extracellular projection), externally embedded in gelatin, bends in specific ways, another example of mechanotransduction.
(I don't know if all these receptors function with slight modification of the same basic framework or all of them operate with distinguishable mechanisms. If the latter is true, I just want one example of how molecular mechanism might bring about mechanoreception.)

See this article on mechanotransduction and especially the cartilage section.

I wonder how exactly mechanical stretching can ope ion channels.

i think it distorts the channel ...

A mechanical stimulus can act on a tissue with elastic and viscoelastic properties in two ways [1, 2]:

distort the cellular membrane which leads to opening of ion channels.
create tension on the extracellular matrix or cytoskeleton, to which a ion channel is bound, thus leading to opening of the channel.

Stretch-activated ion channels opening leads to the formation of an action potential, if there is enough ionic flow to trigger depolarization [1, 3].

References:

Wikipedia contributors, "Stretch-activated ion channel," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Stretch-activated_ion_channel&oldid=606349902 (accessed July 12, 2014).
Grigg P. Biophysical studies of mechanoreceptors. J. Appl. Physiol. 1986 Apr;60(4):1107-15. PubMed PMID: 2422151.
Wikipedia contributors, "Mechanotransduction," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Mechanotransduction&oldid=593605473 (accessed July 12, 2014).


text:
Why is the neuronal plasma membrane more permeable to potassium ions than sodium ions?
From what I understand, the greater permeability of the neuronal plasma membrane to K+ ions (which diffuse out) than Na+ ions (which diffuse in) helps to maintain the -60 mV resting membrane potential. However, I am not sure why. After all, K+ ions are larger so should the membrane not be less permeable to them? Could it be to do with the greater charge density of Na+ ions or is there another reason altogether? Does it have something to do with the 'leakiness' of ion channels?
Also, why is it that the resting potential is maintained and does not become increasingly more negative? Should it not be that because 3 Na+ ions are pumped out and 2 K+ are pumped in continuously, and more K+ ions are diffusing out than Na+ is diffusing in, that the potential is becoming increasingly negative? Is movement of other ions also involved in maintaining this potential?

The cell membrane is inherently quite impermeable to any ion, because it is made of hydrophobic fatty acids. Ions are hydrophilic because of their charge and small size. Metal ions are relatively small and, indeed, have therefore a high charge density. They gather a lot of water around them and hence, they are hydrophilic.
Therefore ions, including Na+ and K+ are transported via dedicated ion channels, which form specialized pores in the membrane. They consist of vast families with many members and a host of different characteristics. Hence, the size of the ion does not matter, because they are transported through channels.
There are indeed leaky K+ channels, but not leaky Na+ channels. And exactly this feature is the reason cells are negative on the inside, because positively charged K+ leaks from the cell.
There is just so much the Na+,K+-ATPase can do. In the end  it burns ATP to fuel each cycle to pump out Na+ and pump in K+. At a certain point it cannot transport anymore Na+ out (K+ diffuses relatively freely) because the concentration gradient of Na+ and the electrical gradient (inside negative) gets too steep.

Sal Khan says at the end of this video that leaky Na+ channels do exist. This site also claims that. Are they both wrong?

@OrenMilman afaik, they may exist, but in the standard Hodgkin&Huxley model Na channels are assumed to be non-leaky


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Tubing connector identification request
this may not be on topic but I'm hoping someone here can tell me the name/manufacturer of the connectors used with the thin teflon tubing in this picture:

Try looking for "Luer valves" or "Luer fittings".
For instance, we buy this kind of supplies from WPI.

Thanks, but I don't believe these are Luer fittings - as I understand it they are some type of compression fitting, you can push the teflon tubing through to the desired length, then screw tighten the fitting to seal it in place.

@zephyr: aren't those the ones on the bottom right of the link in the answer (not sure)?

hmm not sure, they do look similar. Looking at the kit contents link though I don't see anything that sounds right.

I think this is what I'm looking for: http://www.westernanalytical.com/pdf/VLp5-8.pdf


text:
What is the mechanism behind tinnitus?
I seem to have come across two contrasting explanations for tinnitus induced by loud noises- i.e. damage to the hair cells in the cochlea.
On the one hand, I have read that damage to the hair cells results in them releasing excess glutamate, the neurotransmitter that carries the impulse from the hair cells to the neurones in the auditory nerve. This would result in the neurones constantly being excited, which I can understand would lead to constantly perceiving sound.
On the other hand I have read that when the hair cells are damaged, the auditory cortex is no longer receiving electrical impulses from the hair cells that detect those frequencies, and so the neurones start to fire (although I am not sure why no input would lead to neurones going off by themselves! Surely there must be some input to cause the initial depolarisation to cause an action potential?) and so you perceive a constant sound.
These seem to me to be two contrasting explanations. My only other guess on how these explanations overlap is that the excess glutamate being released causes death of the neurone, and therefore the neurones after that one do not receive and input and they start firing spontaneously (although again I would appreciate if someone could explain how lack of input results in neurones firing by themselves).
Thank you in advance!

Short answer

The exact mechanism behind tinnitus (ringing in the ear) is unknown.

Background
Of the two theories you pose here, to the best of my knowledge the second one is the most widely accepted. It is a generally accepted phenomenon that whenever neural systems are being deprived of input, they start seeking new input, or even generate it themselves. For example, blind folks rarely have no visual perceptions at all. In contrast, they often perceive spontaneous visual sensations. For example, many blind folks report perceiving a persistent grayish background hue. In other words, it is never black in the eyes of a blind person. They also often see spontaneous spots of light. The most striking example, however, being Charles Bonnet syndrome, where the blind person may perceive complex scenes with faces and objects (Bhatia et al., 2013).
In the case of tinnitus, the perceived sounds are mostly not complex, but repetitive and simple in nature ('ringing', beeps etc.). It is thought that the deafferented auditory cortex actively starts generating sound perceptions. However, many other explanations have been brought forward, such as spontaneous activity in the hair cells in the cochlea and spontaneous activity in the auditory nerve fibers (Luxon, 1993). I will sum up a list of potential causes mentioned in Han et al. (2009):
Peripheral mechanisms
(1) Spontaneous otoacoustic emissions
Spontaneous otoacoustic emissions (SOAEs) are small acoustic signals generated by the electromotile activity of outer hair cells (OHCs) in the cochlea. While normally inaudible, SOAEs may be perceived as tinnitus. Tinnitus due to SOAEs is mild and is more common in subjects with functional hearing.
(2) Discordant theory
Tinnitus may be induced by the dysfunction of damaged OHCs while inner hair cells (IHCs) are still intact. For example, intense noise and ototoxic agents initially damage OHCs in the basal turn of the cochlea, and subsequently, if continued or repeated, affect IHCs, because IHCs are generally more resistant to such damage. IHCs are the receptor cells for sound transduction. In contrast, OHCs work as mechanical amplifiers, enhancing weak sounds by providing up to 50 dB, which can be evaluated by measuring OAEs. When OHCs die, cells in the dorsal cochlear nuclei (DCNs) show increased spontaneous activity due to the fact that IHC input is relatively normal, but OHCs input is decreased due to damage to the OHCs. This spontaneous activity is perceived as tinnitus.
Spontaneous activity in neurons can occur through a host of mechanisms. Basically, a depolarization beyond a certain thresholds sets the neuron off to fire. In case of the disinhbited DCN neurons, the input from the OHCs is taken away. OHC input to the DCN is inhibitory,m as it is believed OHCs activate inhibitory interneurons. The exact mechanism is unknown, but a central inhibitory neurotransmitter is GABA. GABA can activate GABA-A receptors, that open up a Cl- channel, which in turn leads to Cl- influx into DCN neurons and hyperpolarization. When this input is taken away, you can imagine that DCN neurons depolarize and when this depolarization reaches threshold, the DCN neuron may increase firing Kaltenbach et al. J Neurophys 2002;88:699-714. Hence, as you question whether, in the absence of neurotransmitters, cells can fire action potentials, I say: **yes*. In fact, many neurons have spontaneous spiking activity, often with very regular frequency. These oscillating behaviors are often mediated by cation channels that gradually depolarize the cell up until its spiking threshold.
(3) Crosstalk theory
Nerve compression (e.g., due to a tumor) may cause artificial synapses to be formed between nerve fibers of the cochlear and vestibular nerve  (crosstalk). The breakdown of the myelin insulation of the nerve fibers may further enhance coupling. Hence, spontaneous activity in the auditory nerve may be generated through vestibular activity.
Central mechanisms
Some patients may still perceive tinnitus after the auditory nerve is transected. Hence, tinnitus in this subgroup must be caused by mechanisms located more centrally from the auditory nerve.
(4) Auditory plasticity theory
Damage to the cochlea enhances neural activity in the central auditory pathway, specifically in the temporal lobe in the auditory association cortex and inferior colliculus. This theory was touched upon further above in the first paragraph. Basically, when neural tissue is deafferented, it tends to look for new input or even generate activity de novo.
(5) Somatosensory system
The activity of the DCN is also influenced by stimulation of nonauditory structures and the somatosensory system has been implicated in development of tinnitus. Somatic tinnitus can develop as somtaosensory input may disinhibit the DCN.
(6) Limbic and autonomic nervous systems
The aforementioned theories cannot explain why some people suffer from tinnitus while others do not. More than 80% of those perceiving tinnitus for the first time do not associate the sound with any negative meaning and experience spontaneous habituation. However, if the first perception of tinnitus induces high levels of annoyance or anxiety by association with unpleasant stimuli or with periods of stress and anxiety, tinnitus might develop into a problem.

References
- Bhatia et al. Delhi Psych J 2012;15:423-4
- Han et al. J Clin Neurol 2009;5:11-9
- Kaltenbach et al. J Neurophys 2002;88:699-714
- Luxon, BMJ 1993; 306:1490-1
Further reading
- Action potentials in the absence of neurotransmitters: how-does-optogenetics-work

Thank you for your reply! I was just wondering: in the discordant theory section, you said that 'cells in the dorsal cochlear nuclei (DCNs) show increased spontaneous activity due to the fact that IHC input is relatively normal, but OHCs input is decreased due to damage to the OHCs' Do you have a link explaining how this spontaneous activity occurs? I just don't get how there can be an action potential firing in a neurone without some kind of initial stimulus... Thank you!

@21joanna12 - the Han article is open source and that one cites the relevant articles. Basically it is disinhibition playing a role. Also note that many, many neurons in the auditory system display spontaneous spiking activity.

I have read the Han article and looked up spontaneous activity of neurones and disinhibition, but I still cannot find an answer to my question. I simply do not get how an action potential can fire along a neurone without the initial depolarisation to reach the threshold voltage initiated by the neurotrannsmitter...

@21joanna12 - Other processes can depolarize a neuron. If you look at your other question, biology.stackexchange.com/questions/30203/…, you can see in the answer posted there that channelrhodopsins are also able to depolarize a neuron up to the point of spiking without one neurotransmitter being involved. I have explained spontaneous activity in the DCN in my answer.

There are neurons that fire by themselves. For example neurons in the RAS (reticular activating system) fire spontaneously by themselves and are responsible for arousal (alert non sleepy state).

@OneFace - Absolutely - many do. A background firing rate basically doubles dynamic range - it can also go down then. See my first comment here lol

I don't know if a neuron has this mechanism, but the electrical activity of heart which is also spontaneous is due to activity of special channels among which there is one called "hyperpolarization activated potassium channels". This channel activates when the SA nodal cells get hyperpolarized and causes sufficient depolarization to cause an action potential. @21joanna12

Yep Ih channels.


text:
Definition of general anesthesia
To quote Goodman & Gilman :

An alternative way of defining the anesthetic state is to consider it
  as a collection of “component” changes in behavior or perception. The
  components of the anesthetic state include:
  • amnesia
  • immobility in
  response to noxious stimulation
  • attenuation of autonomic responses
  to noxious stimulation
  • analgesia
  • unconsciousness

My question is, does not the state of Unconsciousness already imply other components of analgesia and amnesia? Analgesia is the absence of the perception of pain, which is granted if there is unconsciousness which would be the absence of all perceptions.
I am not certain if unconsciousness also entails amnesia, but it seems that remembering what happened when unconscious seems considerably unlikely.
Apart from a reductionist argument for minimizing the constraints required for classification as a general anesthetic, I am more interested in cases where unconsciousness would be achieved without analgesia or amnesia, which could be a likely rationale behind including the additional caveats in the definition.

Well, I looked up the definition from Merriam Webster. But I guess what you state could be classified under the reflex autonomic loops, which I don't think are included under unconsciousness. And I think, probably, that the sensation of pain would begin only when he becomes conscious.

I guess the issue is what we mean by perception. If it strictly means stimuli perception, I guess it's not lost when unconscious. But I meant it more in the sensation way, the feeling of pain way. Sorry for the vague seemingly unscientific usage.

A state of unconsciousness does not guarantee analgesia nor amnesia. Besides, a muscle relaxant is often paramount to prevent movements. The perfect general anesthetic would do all of this and have hypnotic, analgesic, amnesic and muscle relaxant properties. Such compounds do not exist, because each effect works on a different part of the brain or elsewhere.
In practice, therefore, multiple compounds are administered to obtain the desired effect. A cocktail anesthetic not only ensures all the desired physiological changes, it also reduces the chance of toxic side effects relative to giving one constituent in a large enough dose to encompass all the effects. And there lies an important point, namely anesthetic depth.
If anesthesia is deep enough, all effects may, perhaps, be reached to some degree with a single compound, but the dose likely becomes so high that the side effects become too large. An example in this realm is alcohol, which when consumed in copious amounts, may come close in reaching all desired effects at least to some degree. A related compound is ether. But even with ether, which has been used in early days of surgery, surgical stress caused patients to die intra-operatively due to cardiac hyperactivity. Surgical stress needs to be minimized and that's why an analgesic is needed in the cocktail.
Commonly applied anelgesics in the OR are opiates, such as fentanyl. Anelgesics are critical for invasice surgery, because the body reacts to trauma even when the brain cannot process the information to the degree necessary to turn it into a conscious experience.
For instance, a widely used cocktail is propofol-based anesthesia: A propofol injection might be used to start anesthesia, fentanyl (injectable) is used to blunt the stress response, midazolam (injectable) given to ensure amnesia, and sevoflurane (inhalant) during the procedure to maintain the effects.

Great answer! +1. I was hoping, though, that the answer would give a passing nod to the need for an amnestic. Not a very comforting prospect.

Thanks a lot for a great answer. But my primary concern was the discrepancy in the definition. If there is a loss of consciousness, can there be a memory of what transpires therein? Are there cases wherein a person can be rendered unconscious but still not amnesic about that state? And second, if I understand correctly, analgesia in the definition mean a loss of afferent nociceptor input and not just a loss of the perception of those inputs?

A person may be unconscious but still can retain a feeling of something traumatic having happened during the surgery. This is called recall. You might want to read https://en.m.wikipedia.org/wiki/Anesthesia_awareness


text:
How to bind antibodies to study their properties?
I want to experimentally look at the behavior of antibodies. To do so, I need to be able to bind these antibodies to a substrate.
Eventually, I want to study the specificity of antibodies to know to what substrates they bind. After that, I want to study the biological activity of the antibody over time.
But my question is more basic, namely: to what material do antibodies bind non-specifically? It's not about antigens at this stage, it's just about non-specific binding of antibodies to a carrier material. Also of interest would be howw to get the antibodies of that carrier again.

Like any other protein, antibodies will aspecifically bind nitrocellulose or PVDF membranes, but any other protein present in your antibody preparation will also do.
Depending on the antibody class, more specific binding can be obtained with protein A or protein G, that recognize the Fc domain. It's usual to have protein A/G immobilized on a stationary phase like agarose.
If you know the antigen used to develop the antibody, you can also use the immunizing peptide crosslinked to CnBr activated sepharose as a probe to bind your antibodies.
Knowing something more about your antibody preparation and what exactly is the 'behavior' your want to study could help obtain better answers.

96-well plates made from polystyrene are routinely used to immobilize antibodies with excellent results.  The immobilized antibodies are then used for binding to antigens e.g. ELISA.  The antibody should be free of other proteins for best results as these will compete for binding (many are supplied with carrier proteins such as BSA  that will compete).
A good read here:
https://www.corning.com/catalog/cls/documents/application-notes/CLS-DD-AN-454.pdf


text:
Neomycin resistance gene in E. coli stb3 cells
We use a lentivirus packaging vector called pLenti_puro_DEST. We use puromycin to select for the cloned gene in 293T cells. However, the pLenti_Neo_Dest has been discontinued, so I'm cloning a Neomycin resistance gene into the pLenti_Puro_Dest thus replacing Puromycin with Neomycin. I usually just grow up this gene in Stb3 or Stb4 cells from invitrogen. I'm wondering if I can select for cloned pDEST vectors in these cells using Neomycin or G418. According to the G418 manual, you can theoretically use it for bacterial selection, but I think that may be for libraries and not actually growing up the plasmid.
So is it possible to select for my plasmid in these cells by adding a little G418 to the ampicillin plate? Is this common? I can't find anyone selecting bacteria by Neomycin anywhere.
EDIT - The main reason I ask, is that the resistance gene is under a PGK promoter that I have no idea if it works in bacterial cells.

Mammalian promoters don't work in bacteria basically.

PGK is mammalian (murine) phosphoglycerate kinase promoter. It will therefore not work in bacterial systems. Why don't you select using ampicillin only? You can increase the ampicillin concentration if you want.
Regarding:

I can't find anyone selecting bacteria by Neomycin anywhere.

Kanamycin is generally used for bacterial selection. The Neomycin resistance gene works on Neomycin, Kanamycin and G418 (a gentamycin variant). The gene basically codes for an aminoglycoside phosphotransferase and different variants of the gene have different affinities for different aminoglycoside substrates. For a basic reference see this.

I do select with ampicillin, but any residual parent vector (from the cloning) would also contain ampicillin.

@jwillis0720 For that you have to do screening. You can do colony-PCR screening which is relatively faster than other methods. Also have self ligation controls to have an idea of how many colonies you need to screen. This is sticky end cloning right?

Plasmid  construction is a technique to get plasmids that carry your inserts from empty vectors carrying the same resistant markers. If you want to select with kanamycin/neomycin, you could take a bacterial expression unit of a kanamycin/neomycin gene. In fact, there are plasmids which carry kanamycin with both bacterial and mammalian promoters,

I will just screen by PCR. But it's gibson assembly.

@jwillis0720 not an issue. Just use the end primers and screen for the appropriately sized amplicon.

I understand, but the amplicon is so freaking big, it approaches the template vector size supercoiled.

@jwillis0720 Ohh okay..in that case RD would be better.. Or a colony PCR on a section of insert followed by RD

In this paper (Li and Elledge, Nature Genetics, 2005) it is shown that the PGK promoter works in E.coli but it has very little activity. So, I don't think it is suited to properly express resistance enzyme.
About Neomycin, many aminoglycosides resistance enzymes (not all) that work on Kanamycin works well also with Neomycin. I have personally selected E.coli expressing Kan resistance (from a pET vector) using Neomycin without problems.


text:
Why the length of UTR in the genomic sequence of gene X is too much longer than the same region in the corresponding Refseq mRNA sequences?
I'm browsing in the UCSC genome browser and found that the UTRs length of KIAA0040
gene in the genomic sequences is too much longer than the corresponding the Refseq mRNA sequence. In fact, the total length of Refseq mRNA sequence is 4,721 and the length of its genomic sequence is about 36,107bp, of which the length of CDS is just 300 bp. How to explain this event?
This gene has 4 transcript variant and I know something about that UTR can span multiple exons, but I'm not sure about it and would like to hear more from you.

Doesn't the genomic sequence you refer to contain intron sequence?

What do you mean by "length of the gene" ? The UCSC browser displays the mRNA sequences aligned to the genome, so the sequences can differ only if there were errors in alignment. Are you saying the UTR is longer in the genomic alignment than in the refseq mRNA sequence? Which mRNA are you referring to?

UTRs are involved in post-transcriptional regulation. See the wikipedia articles on the 5' and 3' UTRs. Alternative splicing of UTRs allows for exposing/hiding these regulation sites, which may then be useful for differential regulation in differing tissues.


text:
Where I can download the genome sequence of various species of Fusarium?
I'm looking for genome sequence of various species of Fusarium (a kind of fungus!) on net, but I found no suitable information. Could you please help me out for this purpose?
Thanks in advance

The standard source for open-access nucleotide sequences is GenBank. Searching for Fusarium in GenBank gives 440421 hits, but these are shorter reads, not full genomes. Depending on your purpose, they may be useful to you.
You may also be interested in assemblies, which are collections of aligned reads stitched together, often at the scale of whole chromosomes. Assemblies with 'Fusarium' in their keywords are available here.
Genomes may be found here, but it does not appear that GenBank holds a complete assembled genome for any Fusarium species yet.

There are several strains of three different species of Fusarium available for download at the Broad Institute: http://www.broadinstitute.org/annotation/genome/fusarium_group/MultiHome.html
Follow the links to Download on the sidebar.