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Difference between facilitated diffusion and secondary active transport in cells
Specifically, what is the difference between facilitated diffusion carrier processes (passive transport) and secondary active transport co-transport processes (active transport)?
They seem to be the same thing - doesn't the passive process with the carrier transports substance $x$ against its gradient together with substance $y$ that is moving down its electrochemical gradient?
Similarly, in the active process, substance $x$ is transported against the gradient, and substance $y$ down its electrochemical gradient?
I don't see how energy differentiates the active transport in this case from the passive transport.

it is not very clear what you are asking. Also, have you read through corresponding wiki articles? e.g. http://en.wikipedia.org/wiki/Active_transport

Yes I have, and hopefully after these edits what I am asking is clear. There are many types of transport processes in the membrane but I do not see the difference between two that are listed under completely different processes the active symport, and the passive cotransport. Yes I have read the articles, the problem is I have found listing stating Glut1 is a carrier protein, and also Glut1 is an active symport. I tried to find a difference between the two processes and this furthered my confusion because I cannot find the difference.

Short answer
Facilitated diffusion is a passive process in which membrane channels mediate the transport of polar, or big molecules that are not solvable in the cell membrane. Co-transport, on the other hand, is active transport, as it depends on the electrochemical gradient of ions across the cell's membrane, particularly Na+. Because ATP or other energetic compounds are not directly involved in co-transport, it is referred to as secondary active transport. The electrochemical ion gradient is mainly established by the Na+,K+-ATPase.
Background
As commented upon by others, your question is not entirely clear and the best way to approach this question is by defining the various terminologies and physiological mechanisms used in your question:

Active transport needs an energy source such as ATP. For example, the Na+,K+-ATPase is an enzyme that pumps Na+ and K+ ions against their concentration gradients into the cytosol (K+) or out of the cell (Na+). Note that both Na+ and K+ are transported against their chemical gradients (and Na+ also against its electrical gradient as the cell is negative). Therefore your statement that [...] in the active process, substance x is transported against the gradient, and substance y down its electrochemical gradient is untrue, and likely the cause of your confusion.
Passive transport is mediated by diffusion, which typically occurs through a concentration gradient. Only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates. Examples are gases (such as O2 and CO2) in the lungs, and small polar but uncharged molecules (such as H2O and ethanol) (Cooper, 2000).
Facilitated diffusion is an example of passive diffusion, but aided by membrane-spanning channel proteins that span the lipid bilayer. Therefore the particles (molecules or ions) do not have to dissolve in the cell membrane's hydrophobic lipid bilayer, allowing hydrophylic and larger molecules (carbohydrates, ions) to be transported into the cell. No external source of energy is needed and  travel across the membrane in the direction determined by their concentration gradients and, in the case of charged molecules, by the electric potential across the membrane (Cooper, 2000).
Co-transport is active transport, where the energetically unfavorable transport of a particle against its electrochemical gradient is facilitated by the co-transport of a favorable one down its gradient. In other words, multiple particles are transported so as to neutralize the sum of the transport. For example, sodium-dependent glucose tranporters transport glucose into the cell against the concentration gradient (unfavorable) and Na+ is transported along with it into the cell which is a favorable transport (Haraki & Inagaki, 2012). This is an example of a symporter. An example of an antiporter is the Na+/Ca2+ antiporter found in the heart to transport Ca2+ out of the cell against a steep concentration gradient and electrical gradient, while 3 Na+ is imported into the cell to balance the unfavorable Ca2+ transport. Note that all these mentioned co-transporters and many others are dependent on the Na,K-ATPase that ultimately generates the Na+ and K+ gradients by pumping Na+ out of the cell and K+ into the cell using ATP (Freeman, 2000). This generated membrane potential works like a battery being charged, and co-transporters discharge it by using the energy stored by importing Na+. Hence, it is referred to as secondary active transport, as no direct energy input from ATP is needed, but instead it utilizes the electrochemical gradient created by the Na+,K+-ATPase.

These considerations should clarify your issues and answer your question on what co-transport exactly is. Specifically, the glucose transporter mentioned, GLUT1 as you refer to, is a symporter that mediates secondary active transport.
References
- Cooper, The Cell, 2000
- Haraki & Inagaki, J Diabetes Invest 2012; 3: 352-3
- Molecular Cell Biology, 2000

"Specifically, what is the difference between facilitated diffusion carrier processes (passive) and secondary active transport co-transport processes (active)?"
Facilitated diffusion creates alternative paths for polar/charged substances to move down their electrochemical gradients across the hydrophobic interior of the membrane, thus greatly speeding up their movement into the cell.
Secondary active transport is a form of active transport where the transport of a substance AGAINST its electrochemical gradient (endergonic) is coupled to the movement of another substance DOWN its electrochemical gradient (exergonic), thus providing energy to transport the first substance against its electrochemical gradient.
The key difference is really that passive transport does not require energy whereas active transport does.
According to wikipedia the GLUT1 you mention is a uniporter that facilitates the diffusion of glucose into the cell, so it is a passive transporter. It does not require energy as it simply helps glucose move down its concentration gradient.

It's an old article I know, but after a bit of thinking my answer would be that while facilitated diffusion is a single step process (not counting the confugurational changes within the CARRIER* protein of course), secondary active transport couples a step of facilitated diffusion with the movement of another molecule/ion in the direction against its (electro)chemical gradient. There's both a passive and an active displacement. (*It's a carrier, not a channel.)

Please add some references to your answer.

The difference between the two definitions is not scientifically justified. Here is an example to clarify this point. A facilitated transport through a carrier A will dissipate the gradient of a substance a. This dissipation will consume energy indirectly if the gradient for that substance is maintained by an active (ATP-dependent) pump. Hence a voltage-gated sodium channel dissipates the sodium gradient maintained by the Na/K ATPase. We think of these sodium ion channel as facilitating the movement of Na down its gradient but in fact they also need the energy indirectly provided to maintain the Na gradient. Now let us consider a coupled transport, Na+/glu for instance. The favorable transport of Na down its gradient largely overcomes the energy cost of the transport of glu against its gradient. Our textbooks commonly justify that this type of transport is secondarily active because it needs the energy necessary to maintain the Na gradient. But isn't the same thing for the voltage-gated sodium channel? If there is no Na gradient, then the transport of glucose by the Na/glu cotransporter will not exist, same thing for the Nav sodium channel: there would be limited flux of sodium ions without the Na gradient (there will be a little due to the membrane potential).

I see what you are saying, but isn't the other key difference that a protein involved in facilitated diffusion is only transporting a single substance whereas proteins involved in secondary active transport transporting two substances so that the link between the energy from one gradient being used to move something else is more direct?


text:
What portion of the electromagnetic spectrum do cats see?
I have seen numerous articles and various information about how cats and dogs see into the ultraviolet spectrum with interesting artistic renderings such as this:

http://www.livescience.com/40459-what-do-cats-see.html
But I have been unable to find any specific parameters of what wavelength boundaries actually exist for cats.
We know that humans see from around 750 to 400 nm, but what would a cat's range be?

Short answer
Spectral sensitivity of cats indeed ventures into the UV, but not beyond ~320 nm. Their maximum is likely similar to ours, i.e., ~750 nm.
Background
The spectral sensitivity of blue cones (photoreceptors detecting low wavelengths) of many species, including humans and cats, extends into the UV range (Fig. 1).

Fig. 1. Human cone absorption spectra. Source: University of Kentucky
However, the various structures in the eye, most notably the lens, filter out UV in humans (Fig. 2). Indeed, surgical removal of the lens in humans results in enhanced sensitivity to UV light below 420 nm (Griswold & Stark, 1992).

Fig. 2. Human transmission spectra. Source: Columbia University
In the cat, however, the lens transmits a large portion of the UV light in the range of 320 - 400 nm, while primates transmit virtually no light of these wavelengths. Figure 3 shows the lens transmission spectra of various species. At 50% transmission the second (dotted) line from the left is the cat (50% transmission at ~340 nm), while a primate (squirrel monkey, species representative for humans and other primates) in this graph is line number 7 from the left with (50% transmission at ~410 nm). Hence, cat lenses absorb less light in the UV region, but transmission is virtually nil at 320 nm (Fig. 3). Given that their cones, just like humans, are sensitive to UV, we can reasonably expect that cats can see in the UV region including wavelengths of 320 nm and up. Cats also have the 560 nm (red) cones, like we do, so their maximum wavelength is expectedly similar to ours (~750 nm).

Fig. 3. Lens transmission spectra of various species. Source: Douglas & Jeffery, 2014
References
- Douglas & Jeffery, Proc R Soc B (2014); 281: 20132995
- Griswold & Stark, Vis Res (1992); 32(9): 1739-43

So is it theoretically possible that I could surgically adjust my lens somehow to obtain some sort of extra vision?

@leekaiinthesky - Correct - I have added some text + a reference on aphakia (eyes without a lens) and increased UV sensitivity in humans

Here is a real life account of a very interesting fellow who had this experience after cataract surgery: http://www.komar.org/faq/colorado-cataract-surgery-crystalens/ultra-violet-color-glow/ @leekaiinthesky

Aren't cats missing red cones? That might make them less sensitive to long wavelengths than humans. Too bad there is no spectral plot for cats.

Cats also have the 560 nm (red) cones, like we do, so their maximum wavelength is expectedly similar to ours (~750 nm). Cats indeed cannot see red, i don't know what this conclusion is not corrected.

I'm, likewise, confused by how they have red cones, but can't see red.    I've often heard that cats can't see red color, but I've seen cats play with red balls . . . does the ball look grey to them?

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What produces the strong odor of decaying dead animals?
Are there specific chemicals responsible for producing the strong, putrid odor that is present after an animal deceases? Also, how long does this odor last?

Mostly putrescine and cadaverine. The list of chemicals emitted during decomposition is avalailable here starting from page 59.

Two compounds are specifically associated with the smell of decaying cadavers (Hoffman et al., 2009), namely:

1,5-pentanediamine (cadaverine), and
1,4-butanediamine (putrescine)

Cadaverine is produced by breakdown of lysin and putrescine by the breakdown of ornithine (Science ME). Both are nitrogen-rich compounds and particularly pungent-smelling.

Source: Science ME
Both compounds are also responsible, in part, for the smell of bodily fluids such as urine and semen, smell of rancid butter, bad breath and stinky cheeses (Science ME).
Forensic Science Central UK mentions that after death, the body begins to decay after about 5-11 days (after an initial phase of bloating). The putrid smells subside mostly after 10-24 days, although a rancid cheesy smell might persist due to butyric acid. Note that many factors will affect decomposition rates and will affect this time course. Moreover, trained police dogs may be able to sniff out minute amounts of putrescine and cadaverine long after humans cannot detect it anymore.
Note that, given the complex composition of animals and the complexity of the decomposition process, a host of volatile organic components are released during decomposition besides putrescine and cadaverine.
Reference
- Hoffman et al. Forensic Science International 2009; 186: 6-13

addition: semen contains related molecules spermine and spermidine

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Can an upper forearm amputee correctly control the Median and Ulnar nerves
I'm an engineer who is looking to build a robotic hand for people without their upper forearm(from center of forearm in direction of hand), controlled by the Thalmic Myo(an EMG sensor). I am first checking for the idea's viability.
I was wondering if one who does not have their upper forearm can still send the correct nerve impulses for a desired hand movement through their Median and Ulnar nerves?

Yes, severed nerves still convey neural responses from the brain.
In fact, nerve potential recordings in the ulnar and median nerves of the stumps of arm amputees have already been successfully applied to control arm prosthetics (Jia et al. 2007; Kuiken et al., 2007.

I will work on formatting the refs later. I am mobile. Kuiken et al.: http://www.ncbi.nlm.nih.gov/pubmed/17276777. Jia et.al: http://www.ncbi.nlm.nih.gov/pubmed/17482005

Will such patients have phantom arm syndrome? @ChrisStronks?

@CRags - likely. Many amputees have phantom sensations, but I am not an expert on that. I am only familiar with Ramachandran's work and that suggests it is very common in upper arm amputees. The severity differs.

I am asking particularly about people with prosthesis as they need ulnar, radial and median nerves in functional order. If you find anything incidentally anytime please add it with a comment to me! Thanks!

@CRags - For now I can say that active use of (conventional) prosthetics reduces phantom pain. I will update if I find out more.


text:
How can bats achieve good resolution with wide beams?
I have been reading about the echolocation system in bats. papers state that bats tend to produce a sonar beam that has a beam angle (-3db) of about 30-40 degrees. This would be considered a wide beam given the fact the sonar sensors used by robots have beams 15-20 degrees or down to 10 degrees with multi-sonar.
As the beam width increases, the azimuth resolution decreases. Yet, bats have good navigational capabilities and good object discrimination in azimuth. How is that achieved? what is the technique used?
I searched hard but what I found is that they rely on the timing between two ears. however, given the complexity of the environment and the multiple echos that return, how is it possible to correlate which echo in the left ear belongs to which in the right ear?

I have been contemplating about this question for months and although I cannot provide you with a concise short answer, I do wish to share what I have so far.
First off, the acoustic beam that is sent is not really part of the echolocation resolution (the bat's echo-locating acuity). Consider the human field of view, which is nearly 180o wide in the horizontal plane. Covering your eyes and obscuring, say, half of the field will not substantially improve visual acuity, because it simply blocks half of the retinal surface from receiving light - it does not double the retinal surface devoted to the field of view.
Hence, I think it is not so much the bat's projected beam that matters, it is the incoming echo that matters. Note that objects such as a tree may scatter the sound that is reflected back, so the projected beam of 40o may be a dramatic underestimation of the chaotic signals bouncing back to the bat. What can they do to improve spatial detail in the received acoustic field of view?
Bats may increase the pulse repetition rate when they are approaching a target. Hence, they basically build a map by sampling the environment multiple times. Sampling frequencies may exceed 50 Hz (Grinnell and Griffin, 1985). For example, imagine you are blindfolded and allowed to scan an object with your fingers. Scanning it multiple times will definitely help you to mentally reconstruct the image. Indeed, bats can assemble information about echo delay changes over time, enabling them to temporally integrate information of the auditory scene. Moreover, they can change the spectral content of their calls that may help in echolocation (Moss & Surlykke, 2001).
Furthermore, to conclude with a personal thought - I think that bats must learn to decode complex echo profiles. For example, a chaotic huge blob of echo with low-echo efficiency (lots of sound is absorbed) that only changes when the bat moves is probably a tree. A big blob with a large echo-efficiency (a lot of sound comes back) with well-defined edges that only changes when the bat moves is likely a human structure or a rock. A pinpoint-echo that moves with respect to the bat is likely something tasty.
References
- Grinnell & Griffin, Biol Bull (1958): 10-22
- Moss & Surlykke, JASA; 110(4): 2207-26

I think you are forgetting bats can see as well. Bat's that use echo location are referred to as Microchiroptera. Since we are speaking about echolocation, we can disregard the megachiropteral class since there most prominent sense is their eyes. This doesn't mean though that Micro's don't use their eyes in conjunction with echolocation. In Handbuch Der Zoologie: Eine Naturgeschichte Der Stämme Des Tierreiches, Volume 2; Volume 5, the authors state

In experimental situations, when visual information and echolocation were competing, the bats relied on vision and ignored the acoustical cues [1].

From this we can surmise that even with echolocating bats, they still fall back on vision in ambiguous situations. Moreover, researchers have determined that bats have ultraviolet cone receptors [2].
To answer your question, Micro bats have good object discrimination because they use both their eyes and echolocation to discern objects in their environment instead of solely relying on echolocation.

yes sure  they use vision for mapping in environment but many papers mention they can locate targets using sound only for example:
link.springer.com/article/10.1007/BF00292562    bat located prey  passively using its noise
And here it says they are able to get the target location in 3D using difference in sound intensity but how do they correlate sounds at the two ears if many objects existed in the environment?
sciencedirect.com/science/article/pii/S096098220500686X


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Are there multiple meanings to "clone" as in "clone a gene"?
I originally thought that cloning a gene meant to put it into bacteria and have them express it. But sometimes I see it used and it seems like it's just a synonym for "identify the sequence and/or location of". So what does "clone a gene" really mean"

Possible duplicate of What does it mean to clone a gene?

"Cloning a gene" also just means making tons of copies of it, like in PCR, so you can sequence it

isn't making 'tons of copies' not regarded as 'amplification'?

I think it can be referred to as either amplification or cloning


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Getting read size less then specified in parameter file Flux Simulation
I have tried to use flux simulation tool to generate simulated RNA-seq data.
I gave the following parameter file to flux-simulation shell script
## File locations

REF_FILE_NAME   cElegansAnnotation.gtf
GEN_DIR         chromFa

## Library preparation
# Expression
NB_MOLECULES    5000000
TSS_MEAN    50
POLYA_SCALE     100
POLYA_SHAPE     1.5

# Fragmentation
FRAG_SUBSTRATE  RNA
FRAG_METHOD UR
FRAG_UR_ETA     350

# Reverse Transcription
RTRANSCRIPTION  YES
RT_MOTIF    default

# Amplification
PCR_DISTRIBUTION default
GC_MEAN      NaN
PCR_PROBABILITY  0.05

# Size Filtering
FILTERING   NO

## Sequencing
READ_NUMBER 1000000
READ_LENGTH 100
PAIRED_END  YES

# create a fastq file
FASTA           YES

According to this parameter, flux-simulation should have given reads with length 100. However when I look at the output, I have seen that reads with less then length of 100 are also included in my  fasta file:
>chrI:47472-49416W:Y48G1C.12:3:651:351:594:A/1
CGTCGAAATTAGTGATATTTTTATCGGGAATCGGTCCGTGTGGTTCTCCGGTGAATATTCGATTCGTTGTGGAGACACGAGATCGCTGGGGTCCAAGGAC
>chrI:47472-49416W:Y48G1C.12:4:651:394:467:S/1
TACGCGACAAAAATGGGAAACCGAATCGCGTTTTTTGGCTTCAAGTACAAGTTATTCAGAATCATCAAAATGGG
>chrI:47472-49416W:Y48G1C.12:4:651:394:467:A/2
CCCATTTTGATGATTCTGAATAACTTGTACTTGAAGCCAAAAAACGCGATTCGGTTTCCCATTTTTGTCGCGTA
>chrI:47472-49416W:Y48G1C.12:5:651:126:142:S/2
AGTTGTAAAAGCGGATT

So, is there anyone how could I fix it?

I think it gives a distribution of read lengths. Not all reads would be 100nt. Even in actual experiments you observe that. Can you add a graph of read length distribution. You can use histogram in matlab, python or R.

@WYSIWYG thanks for reply, I'll add it tonight, actually, I could handle with different size of reads but they have to be longer than a specific length. Could it be possible?

You can remove the small reads before mapping. fastx_toolkit has that option or otherwise just do this: awk 'NR%2==1{h=$0} (NR%2==2) && (length($0)>x){print h"\n"$0}' fastafile.fa


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Can connections between neurons be weakened?
Connections between neurons are said (by Wikipedia) to be strengthened as part of learning - can they also be weakened (below the original level)?
I understand the concept of the connections strengthening. After reading the article Ants Swarm Like Brains Think, my understanding is that positive feedback (I forget the words that I should use for positive vs negative action potentials) should strengthen the connection, and negative feedback should weaken it.
I'm interested to know whether neural connections can weaken below their original connection strength.
I'm curious about this so as to grasp the way that the human brain (or even simply the ant brain) learns good and bad. If I'm not completely wrong about what I'm asking, then I think I get it pretty well: The things that are good (like finding food) trigger positive feedback among the associated neuron groups, and the things that are bad (like pain or danger) trigger negative feedback in the associated neurons, and that's basically how brains learn good from bad.

see https://en.wikipedia.org/wiki/Long-term_depression

Have you forgotten anything you learned well at school at some point in the past? If so, you have your answer.

Short answer
Yes, neural connections can be weakened.
Background
Chemical connections between neurons (synapses) can certainly be strengthened or weakened, dependent on their input. Single synapses can undergo long term potentiation (LTP) or long term depression (LTD). As a typical example there are hippocampal neurons. High-frequency (tetanic) electrical stimulation in hippocampal neurons can result in long-term potentiation (strengthening) of synaptic connections in the hippocampus Moreover, when a synapse receives synchronous input from multiple incoming axons they can potentiate each other's responses (Purves et al, 2001). In contrast, low-frequency stimulation and  prolonged inactivity of synapses in the hippocampus can weaken them (Bear & Abraham, 1996).
The connection between learning, let alone good and bad as you ask for in your question, is far from clear. However, LTP and LTD do provide plausible mechanisms that could underpin these processes at the cellular level (Purves et al, 2001).
References
- Bear & Abraham, Ann Rev Neurosci (1996); 19: 437-62
- Purves et al., eds. Neuroscience, 2nd ed., Sunderland (MA): Sinauer Associates; 2001

What you are talking about called synaptic plasticity, and sure it is possible to weaken connection between neurons, that's why for instance you can forget things.

In neuroscience, synaptic plasticity is the ability of synapses to
  strengthen or weaken over time, in response to increases or decreases
  in their activity.1 Plastic change also results from the alteration
  of the number of neurotransmitter receptors located on a synapse.2
  There are several underlying mechanisms that cooperate to achieve
  synaptic plasticity, including changes in the quantity of
  neurotransmitters released into a synapse and changes in how
  effectively cells respond to those neurotransmitters.[3] Synaptic
  plasticity in both excitatory and inhibitory synapses has been found
  to be dependent upon postsynaptic calcium release.2 Since memories
  are postulated to be represented by vastly interconnected networks of
  synapses in the brain, synaptic plasticity is one of the important
  neurochemical foundations of learning and memory.

wikipedia - synaptic plasticity

neural connections can be weaken below their original connection strength. from neuroscience, new memories mean new neural connections, and the new neural connections require repeated activation. neurons that fire together, wire together, so it neurons or groups of neurons donot fire together often enough, new connections do not form.
i am not sure the relationship with ants, i think the neural connections is strength by frequently practice.

So are you saying rather than the strength of individual connections increasing, more connections form which in turn makes the over-all connection between the two neurons stronger?

yes. but i am not sure is there other thing or action can increase the strength of individual connection

It would be great if you provided some references for your response!

I DO not remember where i found that, i only remember it is about Recursive Hierarchical Recognition (RHR)


text:
Are nutrients absorbed in human esophagus?
Following this question regarding absorption in human oral cavity (sadly not yet fully answered), I'm curious if any nutrient absorption occurs during the descent of food through the esophagus.
And if so, what requirements must a nutrient meet for that.

For several reasons, I seriously doubt that this has been studied extensively.
There is a good reason to study absorption through oral mucosa because a drug or glucose can be held there by people who needing rapid absorption of a drug (e.g. sublingual nitroglycerine) or by people who may be unable to swallow (e.g. a hypoglycemic individual who has lost consciousness). Where there is a reason to know, there is a reason to study something.
The esophagus, on the other hand, is normally an area of rapid transport (a pill, or a fluid, for instance, is in the esophagus less than 10 seconds). While it's assumed that some pregastric absorption through the esophagus occurs and might be beneficial to avoid a "first pass" metabolism of the drug by the liver, there is no good method to keep a drug in the esophagus. With that in mind, absorption from the sublingual mucosa (where a pill might be held) is more valuable than what might get absorbed in as little as 6 seconds in transit to the stomach. From that point, it will spend significant amounts of time in the stomach, the various sections of the small intestine, and the large intestine.
Absorption of drugs from the rectum has been studied, because it can be used, once again, as a method of drug delivery when another route for whatever reason cannot,
Esophageal motility disorders occur, so studies of esophageal function are common. But as the esophagus is never normally the place for absorption of nutrients, there is no reason to study it except for the sake of satisfying pure curiosity. Studies take time, involve volunteers (or paid recipients), risk, and money. Pure curiosity is a reason to study something. But to get the all the previously mentioned factors to come together and fund a study, the reason usually outweighs pure curiosity.
Esophageal scintigraphy: reproducibility and normal ranges
Oesophageal transit of a radionuclide solid bolus in normals
DRUG ABSORPTION BY SUBLINGUAL AND RECTAL ROUTES

an exception to the slow transit time is when there is a diverticulum... here is a case study demonstrating altered absorption of drugs caused by zenker's diverticulum: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2429168/ of coarse the solution is not to take into account the altered absorption in the diverticulum and study the rates of absorption of drugs/nutrients... instead the solution is to just close it up...

yea... achalasia, CREST syndrome, esophageal webs, esophageal spasm, cancer etc... just saying that quick transit time is physiologic, but under pathologic circumstances it might not be the case and the esophagus could potential be a site of absorption into venous circulation and lymphatics... not saying it should be studied because it's probably not important, just saying absorption is possible under freak circumstances... also it's clever that he/she noticed that oral absorption, gastric absorption, intestinal absorption, rectal absorption have all been studied and why not esophagus?

@JasandPruski - actually, you just mentioned an important factoid: some people are trying to treat esophageal cancer with mucosal agents to take advantage of that very fact, as well as it's lack of first pass metabolism. Sorry to seem so picky.

what makes it a "mucosal agent"? different pill design or high 1st pass metabolism?

Prolonged contact with the mucosa. It can't be a pill, though.

then it's a solution, I'm assuming


text:
Confusion about resting membrane potential and the Na/K pump
To this day, very few people and sources have been able to clear up my confusion about resting membrane potential and how it is maintained. It seems like this is one of those topics that few people are able to explain very well...
Here is what I do understand:
Chemical Gradients:

at rest, the inside of a neuron is negative and comprised mostly of Potassium (+) and negatively charged proteins (-)
at rest, the outside of a neuron is positive and comprised mostly of Sodium (+) and Chloride (-)

Electrical Gradients:

at rest, the sodium ions are attracted to the negative charge on the inside of the cell and tend to move inwards
at rest, the Potassium ions on the inside of the cell are attracted to the negatively charged chloride ions on the outside of the cell and thus move outwards

So overall, there is a net inflow of Sodium and a net outflow of Potassium. Got it, pretty simple.
However, the sodium/potassium pump is where I get lost. Why does it reverse all that just happened, and why doesn't it cancel out the resting potential if it moves K+ back inside and Na+ back outside? Isn't the voltage fluctuating because of this back and forth movement of K+ out, K+ back in, Na+ in, Na+ back out, etc.? I would imagine this would completely negate the positive/negative charge distribution, but it doesn't. Why?
Clarification: there is a net outflow of Potassium and a net inflow of Sodium. Why does the Sodium/Potassium pump intentionally reverse this by pumping out Sodium and pumping in Potassium? How does that contribute to resting potential?

would you mind clarifying your question a bit?

Sure, just did that

And see http://biology.stackexchange.com/questions/17840/resting-and-action-membrane-potential?rq=1

And this one has a clear illustrated answer to it: http://biology.stackexchange.com/questions/36123/if-the-average-resting-potential-of-a-neuron-is-70-mv-why-is-there-such-a-high

I suggest to skim through these links and search across the site for your answer first. If you are left with a more specific question feel more than free to post.

@Christiaan Thank you. I looked through the first two links before posting and they didn't quite clear up my confusion. Thank you for the 3rd link with the illustration, that picture is a little helpful

The Sodium/Potassium pump maintains the overall concentrations of ions on either side of the membrane. In other words it keeps the neuron's battery charged.

Imagine the neuron like a circuit. We can imagine that the electro-chemical gradient for each ion species (Potassium, Sodium, and so on) as batteries. So When the ions flow according to their electrochemical gradient, the potassium current flows outward and sodium  current flows inward as dictated by these batteries reversal potentials [negative for potassium, positive for sodium].
However, note that this will discharge those batteries, i.e. the concentration of sodium on the outside of the cell will drop (slightly) as sodium flows inward the cell, and potassium flows outward the concentration on the inside will drop slightly. Thus the magnitude of the reversal potential of the Sodium and Potassium drops (they move closer to zero).
To counteract this discharge the Sodium/Potassium pumps expends energy in the form of ATP in order to recharge the batteries. The amount of current that the pumps moves is very small relative to the larger currents of sodium rushing in and the potassium rushing out during an Action Potential. Thus when a neuron fires there is very little overall current contribution from the pumps.
When the neuron is at rest (not firing) then the Sodium/Potassium pump is able to recharge the membrane and the current becomes important. Still this is a very slow process, relative to action potentials.
Another thing to note, even though the cell is at rest the batteries are discharging slightly. Their is a leakiness to the membrane, sodium leaks in and potassium leaks out. Thus the pump's current will counteract these leaky currents at rest, keeping the batteries charged and thus the overall net current  across the membrane at rest will be zero.
Remember though, these currents are very small currents.
EDIT: Based on Discussion with @Christiaan, I decided to post a update to clarify.
At rest potential Sodium Ion influx is much smaller than potassium ion efflux and thus can be ignored. Whether or not Sodium is ignored the above still holds true. The neuron's membrane is at rest which means the net current is equal to zero. This means that the outward potassium current is counterbalanced by the pump's current thus keeping the relative concentrations of Potassium and Sodium constant while at rest and maintaining a steady rest potential.
EDIT 2: Clarifying as per OP comment:
So during an action potential Sodium and Potassium ions move in large currents and this current flow discharges the batteries. At rest there is still current flowing (thus smaller discharging of the battery) but there is no Net current flow thus no change in voltage(thus the neuron is at rest). It is exactly counterbalanced by the sodium/potassium pumps. The reasons the pump doesn't overcharge the batteries is the constant but smaller discharge at rest. When the recharging current is equal and opposite to the discharge via the leak current, a equilibrium is reached.
However when lots of action potentials fire, the resting potential will be altered from the larger discharge rate, thus when the neuron returns to its new resting potential the leak current and pump current will not be balanced, thus the recharging pump current will be larger in magnitude and will bring resting potential back to its normal value.  (Note what constitutes large is relative between species and even neurons.)
Edit 3: Rates of Leakiness and Pump activity.
If only you could say one is stronger than the other. It depends on the conditions of the cell.
Lets focus in on potassium. The leak current for potassium is dependent on two (really three) things. The permeability (or conductance) to the membrane to potassium, and the reversal potential of potassium (which is dependant on the internal and external Concentration of Potassium. Thus varying these things will strengthen/weaken the power of the leak current.
The Sodium Potassium Pump is dependent on three things. The External Concentration of Potassium, The internal concentration of Sodium and the availability of energy (in the form of ATP).
The point where these two strengths are about the same is when there is more Potassium on the inside of the cell. That is to say pump is capable of keeping up with the leakiness of the membrane until the internal concentration of potassium reaches about $140$ $mM$ (again that just a ballpark number). If their is less Potassium in the cell then $140$ $mM$ the pump is stronger, if there is more than $140$ $mM$ the leak of potassium is stronger.

Isn't it so that the K channels leak, but the N channels don't, or at least negibly so?

Yes, at rest there is more K leakage, but there is a Na leakage as well. As for its relative magnitude I cannot say off the top of my head, but over long periods of time this small leak of both Ions must be rectified. At anyrate, the main influx of Sodium is durning the AP by far the major source. I will clarify my post after lunch :)

@Christiaan I ran a quick simulation using the Hodgkin-Huxley model to measure the K and Na currents at rest (~$-65$ $mV$) and it showed that the K current is ~4 times stronger. I would caution that this is just a simple simulation however, but it predicts that the sodium channels don't fully close at rest state, and in fact allow small amounts of Na Ions to leak across the membrane.  Still looking at primary literature however, and not sure this level of detail is necessary to answer the question. Thus a comment.

Question is on resting membrane potential and K+ is the main player in this due to leakiness afaik.

@Christiaan not sure what afaik is? At any rate, I looked more into it and I see your point, Ignoring the small contributions of sodium gives a good description. Furthermore, your answer in from (http://biology.stackexchange.com/questions/21394/what-keeps-the-resting-potential-of-neurons-constant-at-70-mv)  you are completely right the pump counterbalances the leak current. Guess however, my answer didn't make that too clear, updating now to reflect this.

Okay, so I seemed to understand everything until this bit: "This means that the outward potassium current is counterbalanced by the pump's current thus keeping the relative concentrations of Potassium and Sodium constant while at rest and maintaining a steady rest potential". But in your 2nd paragraph, you state that "The amount of current that the pumps moves is very small relative to the larger currents of sodium rushing in and the potassium rushing out during an Action Potential." I'm a little confused there. Could you please explain that part?

So to summarize my confusion: (1) does the NA/K ATPase work at the same rate as the ion leak channels or does it lag behind? (2) Why do so many sources state that the interior concentration of K+ ions is greater than the concentration on the outside if K+ ions are always leaking out into the extracellular fluid?

I apologize that I'm struggling to understand this so much. I appreciate your effort and have accepted your answer. I still don't understand, but that's fine.

@AleksandrH Not a problem, Sorry I can't be clear enough. Always happy to help and I can try to help more if need be. Another way to word an answer to your question is the potassium pump grabs the ions that escape to the extracellular space . However it can only grab so much. thus the two forces eventually come to equilibrium with most of the potassium on the inside.

@AleksandrH May I ask what is your background. I find knowing student's background helps when explaining difficult concepts. I personally come from a math background and sometimes my awnsers can get a little divorced from the biology.

Sure, I'm in my last year of high school and I'm taking AP Biology. We're using Campbell's Biology, but it does a very poor job of explaining this particular concept.

Let us continue this discussion in chat.

I'll try to add some clarity beyond the good efforts xelo747 has made. I will refer to sodium as "Na+" and potassium as "K+", following the standard convention.

Chemical Gradients:
at rest, the inside of a neuron is negative and comprised mostly of Potassium (+) and negatively charged proteins (-)

at rest, the outside of a neuron is positive and comprised mostly of Sodium (+) and Chloride (-)

The main point of the chemical gradient is that the concentration of the various ions is what matters. Concentration gradients drive diffusion, because these ions are at body temperature and therefore slamming into each other constantly, thereby driving each other to areas of lower concentration. For the purposes of talking about the chemical gradient, the charges of the ions can be completely ignored.

[at rest] So overall, there is a net inflow of Sodium and a net outflow of Potassium. Got it, pretty simple.

At rest, there is actually not very much inflow of Na+, because most of the Na+ channels are closed. There is some small outflow of K+, called the leak current. There may also be a very small Cl- (chloride) flow (probably into the cell).

Electrical Gradients:
at rest, the sodium ions are attracted to the negative charge on the inside of the cell and tend to move inwards

at rest, the Potassium ions on the inside of the cell are attracted to the negatively charged chloride ions on the outside of

the cell and thus move outwards

Keep in mind, movements of ions are not only due to the electrical forces of attraction/repulsion. They are also due to the diffusional (chemical gradient) force above. The way you are phrasing things here suggests you are seeing their movements due only to the electrical forces.

So overall, there is a net inflow of Sodium and a net outflow of
  Potassium. Got it, pretty simple.

A very small net inflow of Na+ during rest. During an action potential--which, keep in mind, can happen up to ~200 times a second (!) and is the neuron's main job, there is a big inflow of Na+.

However, the sodium/potassium pump is where I get lost. Why does it
  reverse all that just happened,

Why do you "reverse all that just happened" with the workings of a mousetrap when you want to catch the next mouse? You're resetting it. In the same way, the pumps are there to (continually) reset the imbalance of ions--that is, to make sure there is an imbalance (instead of an equal amount of all types of ions on both sides of the membrane). The neuron needs to have this imbalance of ions so that it is like a set mousetrap, ready to fire an action potential when the Na+ channels are "sprung".

and why doesn't it cancel out the resting potential if it moves K+
  back inside and Na+ back outside?

The potential is due to the difference in number of charges on the inside edge of the neuron's membrane relative to the outside edge of the neuron's membrane, and not due to the small movements of the K+ leak current and the much smaller Na+ leak current. That difference is set up by the pumps, so the order of events is:

The pumps set up (and maintain) the ionic concentration differences.
That causes a voltage difference (think of it as "electrical pressure").
That voltage drives the leak current, mostly through open K+ channels.
The pumps run continually reset the small K+ concentration rundown due to the leak current as well as the small Na+ buildup after action potentials.
This always-on nature of the pumps uses up a good amount of ATP, thus the brain has a blood glucose demand to manufacture more ATP for these pumps (among other needs).

Please see this page, and click on #9, "Na-K Exchange pump".
Note, when I say "small", I mean it. Even in a "dramatic" action potential, the % gain in Na+ concentration inside the cell is only about 0.06%. This is because, when it comes to voltage change, only a small amount of ions can result in a big change in voltage.

Isn't the voltage fluctuating because of this back and forth movement
  of K+ out, K+ back in, Na+ in, Na+ back out, etc.?

At rest, the voltage is not fluctuating: it holds steady. And the movement of ions, in net, is not a back-and-forth movement during rest; it's a steady stream. To illustrate this...
Imagine an office building with many doors. Some are regular doors (K+ leak channels) that say "RED SHIRTED PEOPLE ONLY!", some are gasoline (ATP) powered revolving doors (the pumps). There are also locked doors that say "BLUE SHIRTED PEOPLE ONLY!".
The scene you should picture is the building filled mostly with people wearing red t-shirts (K+), with a small percentage wearing blue t-shirts (Na+). Outside the building, the situation is reversed (many more blue shirts). On both sides, all people are more gathered against the walls of the building (membrane) than elsewhere. Some very small amount of red-shirted people are leaving through dozens of regular red-only doors, in a continual flow. Another very small amount of both red and blue shirted people are going through the revolving doors: two red shirts go in (K+)) while three blue shirts go out (Na+). And there are dozens of these revolving doors in the building. The net effect is that the overall proportion of red to blue shirted people in an outside the building remains the same.
And of course, every now and then, suddenly lots of blue shirt only doors unlock from some magic command from the building computer, and a noticeable amount of blue shirted people enter the building (an action potential)...but not nearly close to enough of them to change the proportions of blue:red in any significant way. They are soon pumped right back out by the revolving doors. (I'm leaving out some other details, but you get the point).
If this scene makes sense, that's a reasonable metaphor for what is happening in the cell with respect to K+ and Na+.

I would imagine this would completely negate the positive/negative charge
  distribution, but it doesn't. Why?

I'm not sure what you mean by "completely negate the positive/negative charge distribution". This is the crux of your whole question and confusion. The pumps are there to set up and maintain the charge distribution, not negate it. In fact, they require ATP as a source of energy to pump ions where they "do not want to go" if it were only up to diffusion and electrostatic forces. They are constantly opposing rundown of the distribution of charges.
Please let me know if this clears it up, and if not, I can try to amend what I've written.

Sorry for the late response. What I don't understand is why the gradients would dissipate in the absence of the Na/K ATPase pump. From what I understand, Potassium leaks out along its concentration gradient from high to low, but this creates an opposing electrical attraction that drives some Potassium back inside. Eventually, the inward movement is equal to the outward movement and there is no "net" movement of Potassium. However, if there is no net movement of Potassium, I don't really understand why the charge isn't neutral but instead is negative. Could you explain that particular bit?

I'll answer you in two comments. 1. The eventual point you refer to for potassium is the equilibrium potential for potassium (about -80 mV in mammals), and yes, at that potential there IS no net movement of potassium. BUT, neurons are NOT sitting at -80 mV when at rest; resting membrane potential is about -65 mV. Therefore, there IS a net movement of potassium outward--the leak current.

"I don't really understand why the charge isn't neutral but instead is negative." Just to clarify terms: we want to talk about the VOLTAGE (aka POTENTIAL), not charge (which is something related but different). Voltage is essentially a difference in the clustering of charges between two locations. It's considered an electrical "potential" because it has potential energy, in that if you dropped an ion from a helicopter in between the two locations, it would feel a push and would be moved by the electrical field of that clustered-charge differential. The point is, the neuron winds up with..

...a difference in charge clustering on either side of the membrane, such that the voltage is negative on the inside with respect to the outside.


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How does natural selection explain how organisms that are poisonous evolved?
Natural selection makes perfect sense when describing the evolution of say camouflage. For example 2 bugs of the same species live on a tree. One is mutated to look slightly more like a tree, so the bird misses it and eats the one that sticks out more.
This logic seems to fail for poisonous animals though. For example, two bugs are equally visible but one has developed a mutation to be poisonous. Since they are both easy to spot they both get eaten. Now the poisonous mutation has died out. How does natural selection explain the poison mutation overcoming the initial hurdle?

@BryanKrause I don't think my question is a dupe of that. I'm asking how poisonousness becomes a species-level change, not why it happens at an individual level.

This should be informative, especially the section on evolution: https://en.wikipedia.org/wiki/Aposematism

@canadianer As a matter of fact what originally brought on this question was the Eastern Red Spotted Newt which has exactly these traits

There is a lot to say on this question. I will try to keep it short, to the risk of oversimplifying the problem. I can think of three main reasons:
1. Predation does not necessarily means death of the prey
Most of predation does not directly kill the prey. Typically herbivory, will often damage the prey but a single individual won't kill the prey entirely. In such systems, being poisonous may eventually either directly stop the predator (because the predator quickly sense it is poisonous or because the predator immediately dies) or will ensure that the predator remembers not to attack this same individual.
2. Kin selection
kin selection (aka. Group selection although there are a few authors who do not equate them), is selection above the level of the population of individuals (see also unit of selection; see this recent answer for some book recommendation on the subject).
In very short, under kin selection, an individual who dies of predation but can either cause suffering to the predator or just kill it, will protect its close relatives that live nearby from the same predator (who is iether dead or who may have learned to avoid these particular plants). As close relatives share of lot of DNA in common, a gene for toxicity - even if it fails to protect the individual being preyed upon - can protect the copies of itself present in the siblings of this individual.
3. Side effect
Let's not make the mistake of assuming that a trait has necessarily come to high frequency because it was selected for the specific purpose we associate this trait with. A plant may happen to become toxic for reasons that are unrelated to predation. While toxicity is often costly to the plant, it may sometimes eventually just be a by-product. Unfortunately, I would not be able to cite an example where toxicity is simply a side effect.


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Electrophoretic mobility of isozymes
If isozymes are seperated using electrophoresis, which of the following will be the principle of separation ?
A.charge density
B.molecular weight
C.polarity of molecule
I think it should be B.

What class is this for?

for general bio class

(B) is incorrect. I think the answer is (C) but to my mind those other two options are badly worded.
Here is an explanation.
The classic example of isozymes is the case of lactate dehydrogenase.
As you will see if you visit the Wikipedia page the enzyme is a tetramer, and there are two subunit types, the muscle or M type and the heart or H type. Consequently there are 5 isozymes, ranging from M4 to H4 with all possible combinations in between. Different tissues express these two subunit types to different degrees and so are characterised by a different pattern of isozymes.
The M type is encoded by the LDHA gene and the H type by the LDHB gene. I obtained the sequences of the two proteins and analysed them:
LDHA: 332 amino acids; 36.7 kD; pI=8.45
LDHB: 334 amino acids; 36.6 kD; pI=5.93
You can see from this that the ability to separate these isozymes depends upon charge and not molecular weight. That big difference in pI (isoelectric point) means that at neutral pH the LDHA protein will carry a net positive charge while the LDHB protein will be negatively charged. Consequently each tetramer will have a unique overall charge. You can find some details and an image of an electrophoresis result here.
In general, protein electrophoresis is much more sensitive to charge differences than it is to molecular mass except in the special case of SDS-PAGE when the large amount of negatively-charged detergent that binds to the proteins masks their intrinsic charge differences.
Another classic example of this is the ability to separate haemoglobin S in sickle cell patients from haemoglobin A in normal blood. In this case the only difference between the two molecules is a single Glu>Val substitution in two of the monomers in each tetramer.


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What is the point of having evolved two nostrils?
How would having two nostrils be advantageous to your sense of smell or your ability to breath? I already hypothesized that either one of the nostrils could act as a back up for when another gets congested, but even then you can still breath through your mouth and at least for me I almost always have either both nostrils congested or neither at all.

I doubt it's so much that two nostrils are that much more beneficial than one as much as that most complex organisms follow bilateral symmetry for their body design. That said, your body will clog one and keep the other clear during fevers, allergies, or when it's cold to prevent it from drying out completely.

There are two aspects to your question.
First, organisms have some kind of symmetry. The field of evolutionary developmental biology has some theories on why our anatomy is the way that it is.  So, we have two eyes, two halves of our nose and two nostrils, one "tube" that becomes the path from our mouth to anus, etc. Our nostrils are just part of that symmetry. It may be evolutionary advantageous to keep two nostrils so that an animal can tell what direction a smell is coming from.
Second, we see that evolution has provided a path to having just one nostril.  Blowholes in toothed whales are just one nostril.  The other nostril does not have an opening to the outside of the whale.  It would be interesting to explore the split between baleen (two nostrils) and toothed whales (one nostril).  This evolutionary divergence may have been caused by differences in communication styles or the different blowholes may have caused a difference in communications http://www.whoi.edu/science/B/people/kamaral/marinemammalacoustics.html .

It's important to recognize that toothed whales with a single blowhole have two nostrils as embryos, as clearly seen in this image (middle of lower panel). http://www.evolutionevidence.org/wp-content/uploads/2013/08/beardolphembnose.jpg

We have two nostrils for the same reason we have 2 ears and 2 eyes. Having 2 nostrils means an odor molecule coming from one direction will have higher concentration in one nostril than the other, so we can determine what direction the smell is coming from, and allows us to find food or avoid predators more effectively. While humans no longer rely on smell very much, our distant ancestors and relatives did. Moles provide an excellent example and recent research displays their "stereo smell" ability, http://news.nationalgeographic.com/news/2013/02/130205-moles-smell-stereo-animals-weird-science/
And nostrils aren't the only example of smelling in directions, insects have 2 antenna, which are their scent organs. Moths can follow a pheromone trail using their antenna with great accuracy.
So why do humans still have two nostrils despite not needing to smell in stereo? There just hasn't been any evolutionary pressure to move towards 1 nostril. In fact, there would probably be pressure against it, because a human with 1 big hole in the middle of his face probably won't get a lot of dates.
Also, not all cetaceans have a single blowhole. Gray whales have 2 nostrils, and sperm whales have a vestigial second nostril that doesn't reach the surface. http://en.wikipedia.org/wiki/Blowhole_%28anatomy%29
The position of the blowhole is interesting because it's on the top of the head, above the eyes. Rarely, other animals will be born with a disorder called cyclopia, where they have 1 eye in the middle of the face. They usually don't live very long at all, but their nose doesn't develop right either, if it develops at all it shows up above the eye, and is often a proboscis instead of a nose.http://en.wikipedia.org/wiki/Cyclopia
Whales must have developed a way to keep the nose above the eyes while not messing anything else up.

I remember something from the anatomy lecture saying that one nostril picks up one, the other other kinds of molecules depending of the molecule's size and other attributes.
Meaning speed is important: if you breathe in through the nose right now, you'll probably feel the air coming in faster from one side than the other.
And still if i remember correctly this blocking of one side is achieved by blood vessels getting bigger.
The choice which one of the airways is blocked more comes from daily rhythms similar to sleep cycles.

Can you add some references to your answer?


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Pectinase Enzyme Assay
I am working on pectinase enzyme assay. I incubated 900 ul of substrate for 10 minutes in the water bath, followed by adding 2ml of DNSA reagent, then 100ul of enzyme extract added finally i read the absorbance @ 540 OD. However the values are high. How can I troubleshoot high enzyme blank values in Pectinase assay ?

So you have the problem that your blank is too high?

Yeah, the enzyme blank is high

Can you exclude having a contamination?

What contaminants ? As much as possible the enzyme production is done in contamination free environment.

You are not doing this assay in your hand, are you? So what about you reaction tubes, the photometer cuvette etc.?

The reaction tubes and cuvette are clean

Dilute the standards so that the values are in the linear range and within high precision range of the spectrophotometer

I diluted the standard substrate to 0.5% w/v, but still the enzyme blanks are high value,

What is the substrate?

Pectin (citrus )

Is the enzyme blank cloudy/turbid?

Yes it's, , there's is a colour change to light brownish

If the blank is at all turbid or coloured you should be using it to calibrate/zero the instrument (rather than using water or buffer). Is that what you are doing?

I am using the Reagent/ substrate blank to calibrate the instrument

So, your blank is everything but the enzyme? That is, substrate and DNSA with 100 uL water? If yes, measure, as negative controls, substrate alone and DNSA alone. If one of them is also highly absorbing light, it may be contaminated, and a new vial should be ordered. If both are highly absorbing, it may be the water you are using, or the spectrophotometer.
Alternatively, you may try to measure a time course. If blank's absorbance is increasing as time goes by, there is contamination, and reordering reagents may help you. If absorbance stays constant, you are not looking at an enzyme contamination, that is, the culprit is spoilt water, or broken spec, or even wrong protocol. (That is, reordering or repeating won't help.)


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Enzyme Assay - pectinase
During assaying an enzyme at high temperature, the substrate (Pectin) is degraded by the high temperature rather than by enzyme, so, how can I minimize degradation of the substrate by the temperature?

Why do you run the assay at high temperatures? The solution sounds easy, run it at lower temperatures, but is there a reason to not do this?

I wanted to check whether the Pectinase (enzyme) is thermo-stable or not

pretreat the enzyme at high temperature before carrying out the assay at the standard temperature

Thats what I would test as well. Incubate the enzyme at different temperatures for the same time. How do you perform your experiment? In small tubes? Is it possible to premix the whole enzymatic reaction without the pectin and the pre-incubate it at higher temperatures?

I perform the the experiment in test tubes, I pre-incubate the enzyme and the substrate for about 5 minutes separately, , then I mix the enzyme and substrate then follow by incubating vfor about 10 minutes,  I tried to draw the graph enzyme activity vs temp. The rexn is good till 65°c , however, in higher temps.the absorbance values are very high

@Oli absorbance values are high even for control?

Pretreat the enzyme at high temperature before carrying out the assay at the standard temperature –  Alan Boyd


text:
Is the thecal sac ectoderm?
The thecal sac, or dural sac, is the membranous sheath of dura mater that surrounds the spinal cord and the cauda equina. The thecal sac contains the cerebrospinal fluid in which the spinal cord 'floats'.
Is the dura matter ectoderm? I know neural crest and such is ectoderm. But the meninges, in particular the dura, where do they come from?

The dura mater is formed by the mesoderm. The mesoderm is the middle layer of the early trilaminar embryo. The three germ layers are the ectoderm, mesoderm and endoderm, formed by gastrulation. The middle germ layer forms connective tissues and muscle throughout the body, with the exception of the head region, where some of these structures have a neural crest (ectoderm) origin. Connective tissues include cartilage, bone, blood, blood vessel endothelium and dermis, but also the dura mater. The muscles include cardiac, skeletal and smooth muscle (fig. 1).

Fig. 1. Germ layers. Source: UNSW
Source
- UNSW


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What are chiasmata?
I have a confusion in understanding what chiasmata are. My ‘NCERT’ book says ‘The beginning of diplotene is recognised by the dissolution of synaptonemal complex and the tendency of the recombined homologous chromosome of the bivalents to separate from each other except at the site of crossovers. These X shaped structures, are called chiasmata.’
I am not able to imagine what chiasmata look like with this definition ‘... X shaped structures... ’ moreover I am not sure whether this definition is correct for whomsoever I have asked gave me somewhat different definition.

A simple google image search would give you a plenty of images of chiasmata. Did you try that?

We need to make a distinction between the genetic map of a chromosome, which is usually built up from meiotic recombination frequencies between linked genetic markers, the physical map of a chromosome, which used to be made up of clones and contigs, but is now usually derived from the reference genome sequence, and the cytological map of a chromosome, which is usually built from micrographs of fixed specimens.
In other words, you can only see chiasmata using a microscope.  They are named after the Greek letter named 'chi' which looks like our letter 'X', and are the cytological manifestation of the physical crossover, or crossing over, that took place after meiotic recombination, but before resolution.
Chiasmata are essential for proper segregation on the meiotic spindle because they provide the physical tension, or glue, that the microtubules pull against.  If the centromere of each replicated pair attaches to a different spindle pole, then as the microtubules pull, the chromosomes will align in the middle of the spindle.


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Do human-ape hybrids exist?
Since humans and apes share up to 99% of their DNA, can they interbreed? For example, a horse and a donkey seem to be just as distantly related and produce offspring. Mules, however, are sterile. Would ape-human interbreds be sterile?

Human-ape hybrids are genetically impossible, because the two species have different numbers of chromosomes - humans have 23 pairs (46 total) while all great apes (orangutans, gorillas, and chimps) all have 24 pairs, or 48 total chromosomes. The egg would likely not get fertilized, due to differences in surface markers, but if by some chance the sperm penetrated the egg, the resulting cell would never* divide.

Welcome to Biology S.E.! If you have any question regarding the site, please visit The Help Center.

Although this question sounds easy to answer in the first place, it is not. The main problem between humans and the apes we are most closely related to is that we have 46 chromosomes, while the apes all have 48. At some point in the evolution of the humans the ancestral chromosomes 2 and 4 fused together to form our chromosome 2, leaving us with only 46 chromosomes (see reference 1).
This makes offsprings much more complicated, but not completely impossible. A good example for this are crosses between donkey and horses (donkeys have 64 chromosomes, horses 62) to get mules (male donkey crossed with a female horse) or hinnys (male horse crossed with a female donkey) which subsequently have 63 chromosomes and are infertile. There are even crosses possible between horses and zebras which even differ wider. Zebras have between 32 and 46 chromosomes (depending on the species) but still zebroids are possible. See reference 2 for some more details.
So far there has been no successfull attempt to produce such hybrids, although there have been some attempts to make them. Some information can be found in reference 3.
Besides this problems (which are also due to ethical restrictions), there is a study available that at least humans and chimpanzees interbred for at least 1.2 million years after diverging and still produced fertile off-springs. See references 4 (for a summary) and 5 (original paper) for details.
Based on this evidence, I would say it is possible for humans and apes to produces off-springs, however, this is relatively unlikely and they will probably be infertile.
References:

Origin of human chromosome 2: an ancestral telomere-telomere fusion.
The chromosomes of two horse x zebra hybrids; E. cahallus x E.
grevyi and E. hurchelli
Blasts from the past: The Soviet ape-man scandal
Human Ancestors May Have Interbred With Chimpanzees
Genetic evidence for complex speciation of humans and chimpanzees


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Do females retain oogonia after puberty?
Oogonia are the precursors of oocytes in females present during embryonic development. I was wondering whether these stem cells are still present in the ovaria at puberty?

I slightly modified your question for the sake of clarity. Please feel free to roll back if the question edits are not to your liking. Welcome to Biology and +1 for your question

From Developmental Biology, 6th edition I learned the following:
In humans, the oogonia divide to form a limited number of egg precursor cells. In the human embryo, the thousand or so oogonia divide rapidly from the second to the seventh month of gestation to form roughly 7 million germ cells. After the seventh month of embryonic development the number of germ cells drops and most oogonia die during this period, while the remaining oogonia enter the first meiotic division. These latter cells, called the primary oocytes, progress through the first meiotic prophase until the diplotene stage, at which point they are maintained until puberty.
Hence, at puberty the cells from the lineage of oogonia are called primary oocytes. So from a terminological perspective, you are correct that no oogonia are thought to be left at puberty.


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Are Humans Considered Keystone species?
Do humans have a huge impact on the ecosystem ? is it possible for other animals to live without us ?

Welcome to Biology! Homework questions are welcomed, but it should be accompanied by some evidence of research effort before it will be considered.

@Remi.b - Someone has undermined my authority with a brilliant answer :)

I am voting to close as homework question.
I felt like I would give you a few hints though.

is it possible for other animals to live without us?

Life on earth have existed for almost 4 billions years. Animals have existed for about 600 millions years. Modern human (AMHS) have existed for 0.2 million years.

Do humans have a huge impact on the ecosystem?

Here are just a few pictures taken by airplane of agricultural lands

and a koala searching its home after a rapid man-made deforestation

I like the aerial pics but they don't show animals :)

ha ha I inverted the OP questions though. I fixed it. The pictures were there to adresse the question of whether human affect their ecosystem (not talking about animals specifically). But I added a picture of Koala just for you @AliceD

oh no, not a remi-alone-in-the-world koala.... That is so sad.... I nearly not +1'd because of this painful addition

I call BS. The photo has clearly been cropped to hide the vast koala paradise of eucalyptus and...and...what else do koalas like? anything? ...just above the frame.

@Corvus yes maybe. This (and other similar) picture went kinda viral in the past weeks. If it was to be true that the koala was living at this exact location before, then it was probably not too far away during the deforestation and therefore, there must be some green stuff not too far outside the frame of the picture anyway.

@Remi.b, I'm just kidding of course. The koala picture is a nice touch in this great answer!


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Are there any de-novo genome assembly programs for HADOOP?
I have access to a small (approx 20 nodes) cluster that has HADOOP running on it, and I need to do some de-novo genome assembly. I'd like to ask is anyone knows of any program that can do this on a HADOOP cluster. Cloud based stuff is not an option right now, unfortunately, so I need something that I can deploy on our cluster locally. Thx in advance.

You can try CONTRAIL and CLOUDBRUSH...


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Involuntary twitches and apnoea during early phases of sleep
I assume most people either experienced or have seen people with the following phenomenon: in the early phases of sleep sometimes involuntary twitches occur that usually accompany the pause of breathing (I'm aware that there's a  chronic sleeping disorder called sleeping apnea but I think it's different because what I'm asking about now is acute). I wonder if the twitching is some sort of emergency signal, so that the person would wake up (to some level not necessarily full awake) and start breathing. Is there any data that these (the pause in breathing and the twitches) are connected or they are independent? Also I'm also interested why this acute pause of breathing occurs?
Edit:
I've researched myself on this topic and it seems that what I've described is more likely a form of Obstructive sleep apnea.

After a discussion I would like to mention that the assumption that "most people have experienced a paucity of breathing" during sleep may be unfounded. The 'sleep starts' are a very familiar phenomenon indeed. However, the paucity of breathing aspect is not & needs clarification, preferably by identifying the cause, or by naming the phenomenon instead of assuming everyone knows what you are talking about. Take this as an objective critique to draw in answers.

Jerk-like muscle contractions occurring while drifting off to sleep are normal and are referred to as "sleep starts" or sleep myoclonus (National Institute of Health - NINDS).
Sleep Education explains the symptoms:

Sleep starts usually consist of one strong jerk that affects much of the body. The arms and legs are most likely to be affected.

So sleep starts may be quite vigorous, but may consist just of small lip movements too.
The American Sleep Association mentions that:

Sleep myoclonus will rarely disturb the subject or any bed partner to the point of waking and disrupting sleep [...].

In fact, sleep starts are associated with tachypnea, i.e., an increased in breath rate (Vetrugno & Montagna, 2011)
Hence, your hypothesis that a myoclonus is a mechanism to wake a person up (for whatever reason) seems unsupported.

Reference
- Vetrugno & Montagna, Sleep Medicine 2011; 12: S11–S16

Thank you, but this is not  I was looking for. What I was talking about is the pause of breath and a twitch affecting entire limb(s) or the body. The text you've linked says that myoclonus only affects lips toes etc - small body parts.

I edited the answer.

Thanks for the edit,but it seems you keep missing the aponea part of my question. Can you link the sleep education part please?

Maybe someone else can elaborate. I have experience related to sleep EEGs and linked to epilepsy (myoclonic seizures). The apnoea part is unknown to me and unrelated to myoclonus afaik.

After researching myself I've found what I've added as edit. Since you put much effort in your answer on a not well formatted question that helped me a lot, in my research, and realize that my question already has an answer on the internet.


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Why do we go blind for a few seconds after switching off the light?
At night, when I switch off the lights, I always seem to go blind for a while. The room becomes pitch black and I am unable to see anything. After a while, however, my vision slowly recovers and I start to see things around me again. I always have to wait a while before my vision returns to that functional state.
I am interested in knowing the mechanism behind this phenomenon. What do we call it?

Short answer
The eyes need to adapt to the low lighting condition after you switch off the lights, a process called dark adaptation.
Background
The process behind the reduced visual function when going from bright ambient light to low-lighting conditions is caused by a process called dark adaptation. The visual system works on a huge intensity scale. The only way to do that is by adapting to ambient lighting intensity.
The sensitivity of our eye can be measured by determining the absolute intensity threshold, i.e., the minimum luminance of a stimulus to produce a visual sensation. This can be measured by placing a subject in a dark room, and increasing the luminance of the test spot until the subject reports its presence.
Dark adaptation refers to how the eye recovers its sensitivity in the dark following exposure to bright light. The sensitivity of the visual system increases approximately 35 times after dark adaptation.
Dark adaptation forms the basis of the Duplicity Theory which states that above a certain luminance level (about 0.03 cd/m2), the cone mechanism is involved in mediating vision, called photopic vision. Below this level, the rod mechanism comes into play providing scotopic (night) vision. The range where two mechanisms are working together is called the mesopic range, as there is not an abrupt transition between the two mechanism.
The dark adaptation curve shown below (Fig. 1) depicts this duplex nature of our visual system. The sensitivity of the rod pathway improves considerably after 5-10 minutes in the dark. Because after you switch off the light the rod system is still inactive, you are unable to perceive much. The reason why rods are inactive is because they are said to be photo bleached. Photo bleaching refers to the visual pigments in the rods and cones to become used up because of the high light intensities when the light was still on. The pigment needs to be regenerated and that takes time.

Fig. 1. Dark adaptation curves of rods and cones. Source: Webvision
Reference
- Kolb et al (eds). Webvision. The organization of the retina and the visual system (2012)

Also this is the reason pirates wore eyepatches (to be able to quick switch between sunlit deck and dark rooms inside ships), and why you should keep your eyes shut or stay in a dark room for several minutes before a telescope session.

@Mindwin There isn't any historical evidence for that theory, beyond the eyepatch wearing pirate being a common trope.

@MJeffryes I stand corrected.http://message.snopes.com/showthread.php?t=86177

Try this, 1- Turn off all the lights in your room for 5 minutes or until you start to make out objects in the room while being in the dark, Now your pupils have adjusted and are in night vision mode. 2- Cover one eye with your palm and turn on the lights. 3- Wait about a minute while keeping the eye closed and covered during the minute. 4- Turn off the lights again and you will be in pitch black darkness, open the covered eye now and "instant night vision"

@TheVoid an easier test, instead of sitting in the dark for 5min, would be to try this in the morning after waking up & before turning on the lights (if the room's dark)

Eyepatch: it works, as illustrated on mythbusters.  Officers whose duities moved between inside and outside woukd have had a competitive advantage if they figured that out.  Btw, I wonder if a red fikter, rather than opaque patch, would work ok.


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Can we change our dopamine baseline levels?
Can we change our dopamine baseline levels? High dopamine levels improve alertness, problem solving, but may also cause anxiety and aggression.
I've read that smiling and laughing, eating certain foods, or having unexpected rewards can elevate dopamine levels in the brain. I also read that expecting a reward in the future (such as an upcoming vacation) elevates dopamine levels. Can these actions, if repeated over a prolonged period, increase baseline dopamine levels? Or will dopamine return to original levels once these actions are stopped?

Welcome to Bio. I slightly changed the wording of the question. Feel free to roll back if it is not to your liking.

Usually the nervous system undergoes an adaptation. So you would need stronger stimuli to elicit the same response.

Feelings of pleasure and reward are transient in nature. Similarly, the dopamine release in the reward centers (the limbic structures) is transient, namely in the order of seconds (Rebec et al., 1997).
One way to chronically elevate dopamine levels is by administering certain drugs. A notable/notorious example is methamphetamine, which elevates mood and generates euphoria for 8-12 hours. However, after chronic use, people may report a lack of motivation and anhedonia when they stop taking the drug. Anhedonia is an absence of pleasure in response to acts that had previously been pleasurable. Anhedonia may be reported as long as 2 years after the last use of methamphetamine in addicts. Chronic use of the drug overstimulates the dopamine neurons in the limbic system (and elsewhere), and destroys the dopamine receptors, explaining the anhedonia.
Hence, even with hard drugs like meth, the effects on dopamine levels are transient, just less transient as with physiological reward responses.
Reference
- Rebec et al., Brain Res (1997); 776(1–2): 61–7

Actually, I was wondering what would happen if a person was born with naturally high baseline dopamine levels. From what I've read, high baseline dopamine levels can also cause anxiety, like low baseline dopamine levels. So I was wondering if this person could permanently lower baseline dopamine levels.

That is an entirely different question altogether, as your original post is quite explicitly asking for dopamine enhancement. When formulating questions be aware that folks like me can't read your thoughts, only your post. I suggest to post your question as a new one. It sounds interesting :)

No worries Yvonne. We're here to help.


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Why do nerve cells convert electric signals to chemical signals?
One would assume that a faster response time in the nervous system would be beneficial. However, nerve cells have to convert electrical impulses to chemical signals and cross a synapse. Why didn't nerve cells evolve in such a way as to transmit signals purely electronically, and what was the evolutionary need for the current, more complicated structure of the nerve cell?
I've seen answers on how synapses ALLOW for more complicated structures, but never how the synapse came to be. Is it even possible to have a brain structure without converting between electrical and chemical signals? If not, why not? If so, why synapses?

You are mingling two questions together. I would suggest editing this one to only ask about the difference between electrical and chemical synapses, and then open a new question asking about the evolutionary story of synapses. Be careful not to ask a question that's too similar to this one.

I concur with @James - there's a concoction of evolution (question body) and neurophysiology (title). The answer below is quite apt but receives the dreaded "yes, but that's not what I'm asking". Please follow James' instructions and make the current questions the physiological counterpart, because that received an answer from Ben2209

There are two types of synapses:

Chemical synapse
Electrical synapse

The first one is the one you are asking about.  The second one corresponds to the faster synapse you are imagining. It consists of two neurones connected by a gap junction. Gap junction form a cytoplasmic bridge between the neurones and thereby allow electrical signal to directly go from one neuron to the next through ion diffusion without converting to chemical signal.
The second one implies release of chemicals (neurotransmitter) in the synaptic cleft, the extracellular space between the two neurons. It is indeed slower than the electrical synapse. However, unlike the electrical synapse, it enables a variety of postsynaptic effects. Some neurotransmitter elicit excitatory effects, some elicit inhibitory effects (electrical synapses where the presynaptic side is an axon only allow excitatory effects). Some postsynaptic receptors to neurotransmitter are ionotropic whereas some are metabotropic. The former are neurotransmitter-gated ion channels, which means that they let specific ion cross the postsynaptic plasma membrane when they bind neurotransmitter. The latter trigger intracellular chemical reactions, such as production of cAMP, which is a companent of a signalling pathway and can for example influence the expression level of specific genes.
This more diverse set of postsynaptic response enabled by chemical synapses explains why they dominate our nervous system.
Reference: Purves et al., Neuroscience, 5th ed., 2012 ISBN 978-0-87893-695-3

Thank you for the answer. I understand now why chemical synapses are more useful, but I still wonder how they came to be evolutionarily. How could there have been a jump from the creation of electrical synapses in organisms to chemical synapses (or vice-versa)?

Please consider adding a couple of references to you answer.

why would an electrical synapse only allow for excitatory events? Gap junctions couple cells in a tissue and mediate, e.g. oscillatory behavior, i.e. wave-like spread of activity. I think you lay out an incorrect view of electrical synapses.

+1 for your answer btw, but some additional referencing and adjustment of the function of gap junctions may improve your answer.

@Christiaan: yes you are right the sign of postsynaptic current equals the sign of presynaptic current in case of electrical synapses. When saying they are excitatory I was referring to synapses involving an axon. An action potential is always hyperpolarizing, thus the postsynaptic effect is excitatory.


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Are epigenetic changes involved in evolution?
Evolution leads to phenotypic changes through changes in DNA such as mutations. Mutations are transmitted to offspring. Cumulative mutational changes across many generations may cause evolution and speciation.
As far as I know, epigenetic changes causes an individual to change in how it appears (phenotypic changes). In turn, epigenetic changes may be transmitted to offspring, just as DNA mutations can be.
Is epigenetics a factor in evolution?

Sorry but this is just not answerable. I'm afraid you have completely misunderstood. Epigenetic features have nothing to do with phenotypic changes (they can, but most certainly not always). Please read at least the relevant wikipedia articles and post again with a more specific question.

@terdon - I'm most definitely no expert in evolutionary Biology nor genetics, but I think this question is actually quite cool. I edited the question in the hopes of clarifying it.

@Christiaan that's much better, thanks. Close vote retracted.

The answer is yes. But the question is very broad. Have you read the wiki article on epigenetics or one of these multiple hits you getwhen you google epigenetics evolution?

Note by the way that you are using the term evolution in a slightly wrong way. Evolution is most often defined as any change of allele frequency through time. Therefore you do not need to wait many generations for evolution to occur. Also the phrasing suggest an eventual misunderstanding between evolution and speciation. You might want to have a look at an introductory course to evolutionary biology such as Understanding Evolution for example

My $0.02. Any change that affects an organisms ability to mate and reproduce, changing the frequency of traits in the gene pool has the potential to drive evolution. Take an imprinting disorder like Prader-Willi. I think that we too often think that evolution leads to the winners, but it is equally relevant to all of those that lost the race, with their lineages going extinct, effectively change the make up of the species and altering its direction.

To start I will repost some of an answer I have previously posted, which will explain what evolution is:
Evolution is simply a process of change.  It is a change in trait values of populations over time. It results from four mechanisms: mutation, migration, drift, and selection.

"Evolution means change, change in the form and behaviour of organisms
  between generations. ... When members of a population breed and
  produce the next generation we can imagine a lineage of populations,
  made up of a series of populations through time. Each population is
  ancestral to the descendant population in the next generation: a
  lineage is an ancestor-descendent series of populations. Evolution is
  then change between generations within a population lineage." - Ridley,
  Evolution

Your Answer:
Evolution depends on the inheritance of information from the ancestral population to the descendant population. Much of the time we talk about information in the form of genetic variation, the information contained within the DNA. However, more and more we are realising that other forms of information transmission can occur, including epigenetic effects, and that these can contribute to evolution.

"Epigenetic modifications are a bit like ornaments on a Christmas
  tree; the tree (the DNA sequence) is still the same, but the
  decorations (epigenetic modifications) change how it's perceived." ...
"Over the past few years, several studies have compared the epigenetic
  modifications of our genome with that of other great apes, leading to
  an emerging picture of the importance of epigenetics in our recent
  evolutionary history." ...
"The role of epigenetics in evolution (particularly primate evolution)
  is an active and exciting area of research..." - Nature Scitable

The edited question is also broad in scope, but one can narrow it down by talking about specific conditions. For example, the role of epigenetics markers helping in survival under stress conditions, especially in A. thaliana, has begun to be much appreciated.
Epigenetics could also potentially be an important mechanism facilitating developmental plasticity-formation of two or more phenotypes from the same genotype, a process which helps organisms to adapt to changing environments (Developmental Plasticity and Evolution-Mary Jane West Eberhard, Oxford Univ. Press 2003).
Under both scenarios described above, epigenetic changes could favour a differential success in survival (e.g. under stress) and/or reproduction (e.g. flowering) of individuals in a population as compared to animals without these markers, thus leading to evolution in the next generation.


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Why is AIDS not a congenital disease?
AIDS can easily pass from mother to the newborn, then why do we not consider it to be a congenital disease (or syndrome)

Technically speaking, a 'congenital disease' is a term used to describe some (or any) disease that you had at birth. From that point of view, AIDS could be considered congenital too. But, usually, or most often, the words 'congenital disease' are used to explain those diseases which the mother does not have but the child has. Typically, those would not be diseases caused by some sort of germ.

@JordiZambrino - I'm not sure that's correct; e.g.congenital syphllis.

Why do you think it is not considered to be acquired congenitally?

@anongoodnurse do you mean congenital syphilis because it is caused by Treponema pallidum? Or because it is transmitted to the foetus pre-birth via the placenta? Are there further exceptions to the "known" congenital diseases?

@JordiZambrino - yes, there are. That was just an example. Maybe the whole thing could be better expressed by the use of "congenitally acquired" instead of simply "congenital," e.g. congenitally acquired HIV?

@anongoodnurse thank you for clearing that up for me

A congenital disorder or disease is a disorder that is present at birth.  This term can be applied to many conditions, including some that are infections.  More typically, the term is used for developmental birth defects such as spina bifida and cleft palate.
Although HIV/AIDS can be congenital (since a mother has about a 25% chance of passing it to her newborn), most cases of HIV/AIDS are not transmitted by pregnancy and birth, but rather by sexual contact between adults.  Hence it is inappropriate to call AIDS congenital since most cases do not occur in newborns.  This can be contrasted with, for instance, spina bifida and cleft palate, which essentially only occur in newborns and so can reasonably be called congenital disorders or diseases.
A specific case of HIV/AIDS, one which has occurred in a newborn, can be called congenital HIV/AIDS, but HIV/AIDS cannot, in general, be called congenital.

Congenital HIV and Childhood AIDS. You should probably add more detail. Of course HIV can be congenital, and should be called so when the criteria are met.

That was my initial thought that we can not generalize that its congenital.Although it could be in case of a pregnant mother suffering from AIDS though a very less chance of occuring is there


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Development and function of spindle neurons
In his book How to Create a Mind author Ray Kurzweil makes some claims about spindle neurons that he provides no source for.
Concretely he states that spindle cells:

Are Involved in handling emotion and moral judgement;
Are believed to first have occurred in the last common ancestor of chimpanzees and humans;
Are non-existing in newborns, but appear around the age of four months, and increase significantly in number from ages one to three.

Is there a scientific consensus backing these claims?

I fell the common origin of these questions justify bundling them. If not, I apologise for the mistake.

The spindle-shaped brain cells you refer to are called von Economo neurons —named after the man who first described them  (source: Smithsonian).

In humans, von Economo neurons reside only in the anterior cingulate cortex (ACC) and the frontal insula (FI) (Allman et al., 2011). These two regions are particularly active when people experience emotion and they are reportedly important for "self-monitoring," such as noticing bodily sensations of pain and hunger, or recognizing that one has made a mistake. The ACC seems broadly involved in nearly every mental or physical effort (Smithsonian). By contrast, the FI may play a more specific role in generating social emotions such as empathy, social awareness, and self-control (Allman et al., 2011), but also trust, guilt, embarrassment, love, and even the sense of humor Smithsonian).
Humans and the great apes (chimps, bonobos, gorillas and orangutans) have von Economo cells. Lesser primates, such as macaques, lemurs and tarsiers, do not. That means the neurons evolved in a common ancestor of all the great apes about 13 million years ago, after they diverged from other primates but well before the human and chimp lineages diverged about six million years ago (Smithsonian). However, elephants and whales have them too, possibly explaining their complex social behavior (Allman et al., 2011).
I couldn't find literature on the development of these cells in children. Note, however, that, as far as I know, the presence of these cells can be only detected using microscopic techniques, i.e., on coupes of post mortem tissue (e.g., Santos et al., 2010)). This will make research in infants and children difficult.

References
- Allman et al., Ann N Y Acad Sci (2011); 1225: 59–71
- Santos et al., Brain Res (2011); 1380: 206 – 17


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What bird is singing at almost 3 AM in Hong Kong? (recording included)
I live in Hong Kong and there’s a bird around my street that sings around 3 AM, when there isn’t the slightest bit of twilight.
I have recorded its song here: https://youtube.com/shorts/0dBNvPAgLmU?feature=share
Can somebody identify it?

+1 for providing an actual recording! Can you describe a bit more about the song? For example, is it several seconds long and repeats, or goes on and on for up to a minute in a somewhat rambling, non-repeating way (which describes what I often hear between 3 and 5 AM in Taiwan)

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Do species which have a closer common ancestor to humans tend to be more intelligent?

Q: Do species which have a closer common ancestor to humans tend to be more intelligent?

Our closest living relative, the chimpanzee, seems to be regarded as intelligent:

Chimpanzees make tools and use them to acquire foods and for social displays; they have sophisticated hunting strategies requiring cooperation, influence and rank; they are status conscious, manipulative and capable of deception; they can learn to use symbols and understand aspects of human language including some relational syntax, concepts of number and numerical sequence; and they are capable of spontaneous planning for a future state or event.

Does this hold in general?  And, if so, how strong is the correlation?

humans being more intelligent than other animals is a hotly debated topic :-D http://www.huffingtonpost.com/2013/12/11/human-intelligence-animals_n_4400395.html

I agree with point 1 in Remi.b's answer; what do you mean by intelligence?
Generally though, no it doesn't. Crows have tools, octopuses and goldfish solve puzzles, dogs respond to human voices, whales have language. There are too many exceptions to say that 'generally' the closer to humans the more "intelligent" the species.
And who said we're top of the "clever test"? Could you do this? http://www.independent.co.uk/news/science/video-chimpanzees-have-faster-working-memory-than-humans-according-to-study-8496034.html

Probably not. Ravens can solve multistep problems, showing some level of premeditation. Border Collies have been shown to associate over 1000 human words with specific objects. Dogs are one of the only animals able to interpret pointing by humans, and their brain responses in fMRIs to photographs of strangers to owners (Loved ones), shows pretty much the same patterns as humans exhibit. Pigs are believed to be one of the only animals other than humans that have self recognition when looking at their reflections in a mirror. Dolphins and whales probable have language. Gorillas do sign language.

Several issues here that make your question unanswerable:

Intelligence is not defined. How would you define it?
What kind of relationship are you exactly looking for? Comparing average intelligence between groups or trying to fit a regression with intelligence on the Y-axis and relatedness to human on the X-axis?
The general issue hidden behind methods of species comparison is "How do you define a species?"

If you want to compare average intelligence between groups, meaning that you want to compare average intelligence of a group of closely related species of human to the average intelligence of all animals? Then the answer to your question will probably be "Yes" as primates seem in average to be more intelligent than the average animal and mammals tend to be in average more intelligent than the average animal. I'd expect too that vertebrates are probably on average more intelligent than the average animal. Let's not forget that some animals have no brain (e.g. Sponge).
But now if you want to fit a regression between intelligence and relatedness to human for all animals, you will probably have some trend (a regression with a significant slope (positive correlation)), but you will have many group of points that will not fit on your line. Many birds for example may be considered as much more intelligent than humans depending on your definition. Many invertebrates such as octopuses are very intelligent, too. If you allow for a broad definition of intelligence, then you may also consider the intelligence of social insects which may be surprising. Some aquatic mammals are very intelligent although other, more seemingly stupid mammals, are closer to humans than aquatic mammals.
In short, keep in mind that intelligence is not easy to define, and depending on the definition, the answer will be different. Typically, if you use a very human-like definition of intelligence, you will probably find that intelligent species are more closely related to human. There is a correlation between intelligence and phylogeny (=tree of life), therefore yes, closely related species to humans may have some tendency to be fairly intelligent, but there are many other clades (groups of species on a phylogeny) that show some impressive intelligence, especially in insects, in mollusca, in  birds, the carnivora and the cetacea.