What are possible reasons for a DNA template not giving amplification? I am trying to amplify ~10kb length fragments using NEB LongAmp Master Mix. I had been using one particular aliquot of DNA (template amount in each PCR reaction of 10ul being around 60ng) and getting amplification results as desired. However, when I switched to a different aliquot of similar concentration, I am not getting amplification all of a sudden. I tried a different DNA sample and different primers and got results. So the problem lies with either the template or the primers. I have tried increasing amount of template, increasing Mg2+ by 1mM in the final reaction etc. but to no avail. The DNA templates/100x primer stocks are stored at -20⁰C and the DNA had been phenol-chloroform extracted. What could possibly be wrong here ?

Lets summarize the comments into a real answer: When the only chemical changed in your reaction is the DNA, which came from a fresh Phenol/Chloroform preparation, I would suspect it. From there, we have a few possibilities, what could have gone wrong.

The most likely cause of an enzymatic reaction not working with
Phenol/Chloroform prepared DNA are left-overs (or carry-over) of the
organic solvents from the reaction. The inhibit (especially Phenol)
enzymatic reactions very efficiently. It would help to do another
round of DNA precipitation.
It is possible that your DNA didn't got dissolved after the drying
step in the precipitation. Depending on the conditions, DNA can form
a pellet which is hardly to see and even harder to dissolve. So your
DNA concentration would be too low to get amplification. To prevent
this measure the concentration of your DNA.
It is possible that the water you used is contanminated with DNAses
(although it shouldn't) and your DNA got degraded by them. Here only
new aliquots will help.
Depending on the size of your amplicon, it is possible that overly
harsh condition during the preparation led to the shearing of the
DNA leaving not enough intact DNA to get a proper amplification. If
this is the case, be more gentle with the extraction.

Additionally your primers can be a problem. It would be good to keep the 100x stock solutions permanently at -20°C and prepare 10x working solutions. These can undergo freezing and thawing (which will degrade them over time) but they can be replaced easily.
I would also try the new DNA prep (if possible side by side with one that is working) with new primers to test if they are the problem.


Find the length of DNA sequence? Given $N=5\times10^3$ and mutation rate is $\mu=10^{-5}$ per site, find the length of a DNA sequence so that the probability of mutation occuring M, is greater or equal than 0.95.

Is there a method or a formula for this type of calculation?

The mutation rate per haplotype per site is $\mu = 10^{-5}$. Assuming diploidy and a population size of $N=5000$, the population wide mutation rate per site is $10^{-5} * 5000 * 2 = 0.1$.

$0.1$ is hence the probability that a mutation occurs a at a given site (in the whole population). For 10 sites the probability that a mutation occurs at at least one site is $1 - (1-0.1)^{10} = 0.65$.

The probability we are aiming for is 0.95. So let's write the equation

$$1 - (1-0.1)^{x} = 0.95$$

, where $x$ is the number of sites we are looking for. You just have to solve for $x$ now and round up to the larger integer.


Can you eat cancer cells without risk? Afaik GMO products are not a real risk to health of course if they do not contain toxins.

But how about cancer cells? Like say rhabdomyosarcoma which is more or less a muscle cancer found also in cows.

Likewise, meat breweries use stem cells, but wouldn't cancer cells just grow faster?

HeLa cells (which are of course derived from a cervical cancer) have actually been injected into humans to see if they would grow; they grew briefly but were promptly rejected. Similarly, surgeons have on occasion accidentally stabbed themselves and inoculated themselves with the human tumors they were operating on.

Injecting human cancer cells is a far greater risk than eating non-human cancers, and even in that case the risks seem to be very low.

There have been rare cases of people with profoundly suppressed immune systems (organ transplant recipients) allowing a transferred tumor to grow, so (though of course the risk there is vastly higher than merely eating a cell) it's not completely impossible.

Pragmatically, it's very likely that everyone who's eaten, say, chicken has unknowingly consumed some chicken tumors.


Can someone provide resources on human electromagnetic frequencies? Pardon all of my questions below.  I'm basically looking to find online resources regarding my inquiry.  If you can answer any of them off the bat, that would be awesome!!

It seems that humans and mammals give off certain frequencies from our nervous systems.  For example, dogs are able to sense when their master is coming home, even when their distance is close to a mile away.  Also, cats are able to sense when a human is about to die.  They can feel the frequency the person is giving off, and react differently.

Where can I learn more about this frequency that humans give off?
Has anyone ever done research on this subject?
Is this electromagnetic frequency or something else?
Are there devices that can measure this frequency that the human nervous system gives off?
Are there devices that can generate this frequency that the human nervous system gives off?

For a start, you could learn about Bioelectromagnetics which is the study of the interaction between electromagnetic fields and biological entities (reference). Electro-magnetic fields are generated by the heart, brain, tissues and cells. These fields are in-turn affected by temperature and the overall mood of a person (reference).

There is a lot of research that is being conducted in the field. You can find a lot of papers relating to the field with a simple search on Google Scholar.

Well technically electromagnetic fields.

There are instruments to measure EMF which are detailed in the Wikipedia page. Here is an article on an instrument made to measure the electromagnetic field of the heart (reference).

Generally, if you have measured the electromagnetic fields in different parts of the body (eg: this article states that the electric field of the heart is up to 50 mV/m, and that of the brain and other vital organs up to 5 mV/m) then it shouldn't be too hard to generate them seeing that EMF generated is a low value (reference).


Microbial Fuel Cell Reaction I found a formula online which explained the reaction which occurred in the anode chamber of a microbial fuel cell but there was a typo

$\small NADH + Ferredoxin_{(ox)} (NADH-Ferredoxin\ Oxidoreductase) \longrightarrow NAD^+ + Ferredoxin_{(red)}\ \
Ferredoxin_{(red)} (Hydrogenase)\#61614;Ferredoxin_{(ox)} + 2H^+ + 2e^-$

I attempted to correct it but I'm not sure if I'm right could you check this and see if it's correct?

$\small NADH-Ferredoxin\ Oxidoreductase \longrightarrow NAD^+ + Ferredoxin_{(red)}$

$\small Ferredoxin_{(red)} \longrightarrow Hydrogenase + Ferredoxin_{(ox)} + 2H^+ + 2e^-$

Anode reaction,

$\small Glucose + 2NAD^+ (Embden-Meyerhof pathway) \leftrightharpoons 2 Pyruvate + 2NADH$

$\small Pyruvate + Ferredoxin_{(ox)} (Pyruvate-ferredoxin Oxidoreductase) \leftrightharpoons Acetyl-CoA + CO_2 + Ferredoxin_{(red)}$

$\small NADH + Ferredoxin _{(ox)} (NADH-Ferredoxin Oxidoreductase) \leftrightharpoons NAD^+ + Ferredoxin_{(red)}$

$Ferredoxin_{(red)} (Hydrogenase)\leftrightharpoons Ferredoxin_{(ox)} + 2H^+ + 2e^-$

[Last one: http://en.wikipedia.org/wiki/Ferredoxin_hydrogenase]

Cathode reaction,

$4 H^+  + 4e^- + O_2 \leftrightharpoons H_2O$

$C_6H_{12}O_6 + 6O_2 \leftrightharpoons 6 CO_2 + 6 H_2O, DG° = - 2870 kj$

Full paper: http://www.altenergymag.com/emagazine.php?issue_number=07.04.01&article=haldia


Are there any intersections between the biochemical pathways of uracil biosynthesis (or metabolism) and methionine degradation in eukaryotes? Is there any way in which uracil biosynthesis or metabolism could help cell in degradation of toxic levels of methionine?

No, I don't think there are any intersections, and I can't see how uracil metabolism would have any influence upon methionine degradation.

Methionine degradation is shown in Figure 1 below. The end product is succinyl CoA which is fed into the TCA cycle. The only obvious by-product is cysteine which doesn't have any connection with uracil biosynthesis.

Uracil biosynthesis (as UMP) is shown in Figure 2: it is built from CO2 and NH3. Uracil degradation produces CO2 NH3 and aspartate.

There are certainly no shared intermediates in these pathways, and I can't come up with any convincing indirect connections either.

Figure 1. Methionine degradation

Figure 2. Uracil biosynthesis


Why do I hear beatings with stereo headphones? When I play a sine wave together with another pitch shifted sine wave I hear the beating very clearly. This is the expected physical phenomenon.

When I use headphones to play the lower frequency sine wave in my left ear and the slightly higher frequency sine wave in my right (or vice versa), there should be no way for them to physically interfere with each other? But I still hear the beatings, just less strongly.

I tested it with a few different people and how strongly one perceives the beatings varies between people, but many do still hear it. Why?

Short answer
Dependent on the auditory stimuli used, it sounds like binaural beats to me.

Background
Binaural beats are the resultant perception evoked by the interaction of two auditory tones with different frequencies when presented to both ears (Lane et al., 1998). The presented tones should be below 1000 to 1500 Hz and differ in frequency between 1 and 30 Hz. For example, if a pure tone of 400 Hz is presented to one ear and a 410 Hz tone in the other, an amplitude modulated standing wave with a frequency equal to the frequency difference (10 Hz in this case) is perceived. Note that these 1-30 Hz beat frequencies are below the dynamic range of acoustic hearing. Hence, the beatings are the result of neurophysiological interactions in the brain, and not the result of physical interactions of the auditory stimuli impinging on the inner ear. From an experimental point of view, limiting the sound levels to 60 to 70 dB should prevent gross cross-over stimulation to the other ear.

Binaural beats are thought to be elicited in the auditory brainstem, and specifically in the the superior olivary nuclei, when the two wave forms mesh in and out of phase within the brainstem.

Reference
- Lane et al., Physiol Behav (1998); 63(2): 249–52

Source
- Web US

Related post
- How can binaural beats change mental state?


Why have people much more different cells than rice plants, while they have roughly the same number of genes? Rice plants have about two times as much of genes in their DNA than humans have. Then how is it possible that people have much more different cells than a rice plant has?

Actually, rice has about twice as many genes than humans (you can check yourself on bionumbers). But who cares? It is not because two species have the same number of genes that they would look alike. Human and rice have quite different genes. Numbers in themselves do not matter.

Consider the situation where Paul has twice the number of clothes in his wardrobe than Jack, it does not necessarily mean that Paul and Jack dress up differently. Conversely, when playing poker, Paul always has the same number of cards in his hands than Jack, yet their hands may well be very different.

Generally speaking 'higher plants' tend to have way more genes than 'higher animals'. There are several hypotheses for that. Plants are more often polyploid and therefore have more neofunctionalization. Also, plants don't move. It is not impossible that they would need more genes to cope with a more varying environmental conditions.


Excess protein consumption effect on kidney How does excess protein consumption through food as well as through supplements affect body especially kidneys?
Why it is advice to consume low protein diet during summer ?

Short answer

The ammonia resultant from the protein metabolism is toxic to the body and specially kidney. (William V. et al.)

Long answer

Protein is a poly-peptide composed by amino acids. Each amino acid has an amine group (-NH2) in its composition. In the metabolism of the amino acids, this amine group is taken, and if it isn't needed is released the to blood vessels to be transported to the liver and be turned to urea.
Needless to say since the kidney filters the blood when there is excess of ammonia in the blood vessels the kidney is the first to suffer.

I've found some papers about the effect of ammonia in the kidney but none of them where about humans. (I may try to fetch some of them later.)

Why summer?
During summer water is lost through perspiration so there's less available for the excretion of urea.
I hope it helps.

References.

1.William V. McDermott, Jr., M.D. ,Metabolism and Toxicity of Ammonia


Carbohydrates- D-Glucose & L-glucose , alpha and beta What's the difference between D-glucose & L-glucose ?

Yes , I know that L-glucose is an isomer of D-glucose . But what differences do they have ? They are the same , they are glucose .

Similarly for alpha and beta glucose ?

Sorry I just started learning on carbohydrates and I'm a little confused about these 2.

They are not the same. Because they are enantiomers, they do not have the same shape. Because they do not have the same shape, enzymes in metabolism that have evolved to use D-glucose cannot work on L-glucose.

L-glucose is not synthesized by organisms because life on earth shares a lineage using the R-enantiomer, so organisms don't encounter it, so there is effectively zero selective pressure to evolve the ability to metabolize L-glucose.

For alpha and beta glucose, see this question on Chemistry.SE; those terms refer to anomer forms of glucose that can interconvert in solution. Given enough time, glucose and similar molecules in solution will form an uneven but consistent ratio of alpha and beta forms.


Is there a preferred sleeping position for humans? I remember hearing various sleep related advice as a child, like "sleep on your right side", or " have your head pointed in X direction".

Is there any biological reason why sleeping on one side versus another, or with a head pointed in some direction is beneficial for humans?

The enWikipedia article summarizes the best/only real research on positions that I am aware of.  I read a book in high school (that is to say it was old and I have no idea what the title was) that claimed that the semi-fetal position was the best, as it supposedly maximized protection without compromising breathing too much.  I can't say I've seen anything that would indicate your head's direction actually matters, except as it depends on the position of the rest of your body.  Do you mean facing North or the door?  That's some Feng Shui stuff or something similar, which is meaningless.

In terms of which side to sleep on, there is actually an answer!  Well, maybe.  Sleeping on your left side aggravates heartburn more than sleeping on the right side1, but sleeping on your left may be somewhat associated with heart problems.2  From what I can read from the studies, the heartburn one sounds more causative, but then again dying is worse than a little heartburn...  In the end, though, about the only thing that matters is that sleeping on yours side can lower the amount of snoring (annoying) and sleep apnea (unhealthy).


What is it called when a dead flower is rotted away and only the veins remain? I've spotted a flower that is dead:

It looks like most of the tissue has rotted away and only the veins remain.

(Sorry, I don't know the proper name for flower veins).

What is the technical term for this phenomenon?

Retting could be a valid term. But I think that the term "skeletonization" is more common. For instance here is a link to the University of Arizona showing how you would take a flower or a leaf and remove all components, leaving the veins:
Skeletonization

I think that "retting" is confined to the industrial harvesting of plants like flax. I would use the term "skeletonization" to include acts of botanical science in which the veins alone were sought. For instance in the above link the botanist Frederick Ruysch published a method of chemical skeletonization in his book Adversariorum Anatomico - Medico - Chirurgicorum Decas Tertia in 1723.

It also became a form of art and craft in the late 1800's in the United States; "Skeleton Leaves & Phantom Flowers" was published by E.Parrish. I would assume that the end result as a craft would be to display the skeletonized flowers or leaves on a display board.

As a natural, observed event the term skeletonization could be used. But if the  underlying causes such as fungus were considered then both rot, or fungal rot, and skeletonization might be used together in the same sentence. The wikipedia entry skeletonization considers animal decomposition. It's a reasonable and analogous step to use the same term for plants that decompose and leave fibres rather than bones.


Help in identifying an unknown Golden Worm/Larvae Can anyone help me to recognize this type of species? Is it a clustered worms or clustered larvae? Location is in Bali, Indonesia. Recently this species is goes viral, but people here always link this species to a myth.
Thanks.

These are larvae of the so called fungus gnat of the order Diptera. Fungus gnats are small flying insects that look sort of like mosquitoes but they don’t bite. In fact, adult fungus gnats live only about 7-10 days and do not feed. It is the immature larval form that can cause damage to your plants.

Source: https://www.projectnoah.org/spottings/30766835/fullscreen
I see, i'm Balinese too, you know everything things were rare are linked to myth.


What is the name of this spider I found in The Netherlands? This spider is smaller than 1 mm and fast.
The spider has tiny hairs on orange coloured legs. The backside of the spider is dark-brownish and has a small red stripe in the middle. I have taken pictures magnifying 25x using a lens of some watchmaker glasses. As a reference the lens of the lamp shining on the spider is 6mm.
Found inside my house on the second floor on the attic.

The location is North-Brabant, The Netherlands, location on maps.

I have searched all over the internet but I keep coming back to mites which this specimen doesn't resemble.

Unfortunately the camera isn't as good as my eyes, although a little zooming is possible.

The spider skittered around again today and I managed to take a picture, unfortunately not a zoomed one but maybe some characteristics will be recognized.

I believe you are looking at a spider mite of the genus Anystis or Tetranychus. Both of these have The Netherlands in their range.
Here is an info page on the two genuses, includes a map of observations and a gallery of photos that you can even filter to only view images from a certain range. You can also filter the gallery to group photos into species categories.
Anystis: https://inaturalist.ca/taxa/249515-Anystis
Tetranychus: https://inaturalist.ca/taxa/203334-Tetranychus


Do humans contract more physical sicknesses and diseases than animals do? I wondered: If I get into the library and look into the medical section it is evident that there are thousands and thousands of different human physical diseases. But if I look into the section of animal diseases it is by no means as large as the human section.
But humans are by no means the only beings with extraordinarily cell complexity. Many other animals have an equal amount of cell complexity. So shouldn't other animals have an comparative equal amount of diseases ?

Naturally as humans we are much more interested in human physiology which would explain the discrepancy. But is there any evidence that animals, especially mammals, have not an equal amount of (still unknown) different diseases ?

Remark:
While a bit similar, this is not this question:

Why do humans seem so much more prone to disease than animals?

I am asking about the quantity of diseases, not if humans are especially prone for diseases.

ADDENDUM:
The difference between the questions is like
"Is building A more prone to fall in natural catastrophes than other buildings because it seems like it ?"

and
"How many faults have building A in comparison to other buildings ?"

A correct answer to the first question is: "We made a statistical comparison and building A is more/less/equal prone to fall in a natural catastrophe. The impression is wrong/right."

A correct answer to the second question is: "Building A has in fact a mean approximately 13 000 faults while other buildings have only 5400 faults. But the reason can be that the other building are inspected with less care." Or "No, they both have very likely something like 9000 faults".

It is a completely different question. The second question does not ask for the severity of faults. It could even be that building A has more faults while being more secure because the faults itself are much less severe.

The issue is more a matter of research focus than anything else. People care more about people than other organisms. Hence, more money is available for research and more money goes around in medical healthcare than in veterinary care. Research and drug development, in turn, focus on where the money is. The diseases of animals other than humans have simply not been investigated in such detail as in humans, because less effort has been done to document them as exhaustively as has been done for humans. Thus, when something is not in the literature, that doesn't mean it doesn't exist.


What species is this orange and black caterpillar from Costa Rica? Does anyone know what type of caterpillar this is? I don't know much about them. Pictured it in January in Costa Rica cloudforest (Monteverde) and am using it in a speech for visiting Costa Rica.

Size about 3,5-4 inches.

Probably it is Cricula silkmoth (Cricula trifenestrata, Saturniidae), in caterpillar stage.


Are common eye defects inherited? If one parent is nearsighted and the other is farsighted.
One parent developed nearsightedness later in life, while the other was born farsighted and they are both the first ones in their family to have any sort of eye problems.
Is there a possibility of their children having a perfect vision since both their conditions are the result of a recessive gene and can the probability of inheriting one over the other be assessed?

Both Nearsightedness and farsightedness are inheritable.

According to Citizen Scientists Look into Nearsightedness, 23andme blog:

  Nearsightedness, a condition in which far-away objects look blurry, is
  a problem of endemic proportions — approximately 30-40 percent of
  adults in the United States are nearsighted.  And, as computers and
  cellphones (which train our eyes to focus on short distances) play an
  ever-increasing role in our lives, we can only expect that this number
  will grow. One study in the United States highlights the rising rates
  of nearsightedness. These researchers found that in the early 1970’s,
  approximately 25 percent of Americans between the ages of 12 and 54
  were nearsighted, but thirty years later that number had skyrocketed
  to 42 percent. While it’s been clear that genetics play an important
  role in nearsightedness, until this month relatively little was known
  about which genes are involved. Two large studies on nearsightedness,
  however, have recently shed light on the subject. One of these studies
  was conducted by the 23andMe research team under the leadership of Amy
  Kiefer and Nick Eriksson.

  Read more at
  http://blog.23andme.com/23andme-research/citizen-scientists-look-into-nearsightedness/#ijOHfuvePBSFOm4A.99

Which types of eye disease are inherited?

Genetic factors play a role in many kinds of eye disease, including those diseases that are the leading cause of blindness among infants, children and adults.

More than 60 percent of cases of blindness among infants are caused by inherited eye diseases such as congenital (present at birth) cataracts, congenital glaucoma, retinal degeneration, optic atrophy and eye malformations. Up to 40% of patients with certain types of strabismus (ocular misalignment) have a family history of the disease and efforts are currently under way to identify the responsible genes.

In adults, glaucoma and age-related macular degeneration are two of the leading causes of blindness, and both appear to be inherited in a large portion of cases. Researchers have mapped several genes for glaucoma and are starting to identify genes involved in macular degeneration. They also are making very significant progress in identifying the genes that cause retinitis pigmentosa, a degenerative disease of the retina that causes night blindness and gradual vision loss.

Can common vision problems be inherited?

Genetics also play a role in vision problems that occur in otherwise healthy eyes. Genetic ophthalmologic researchers now have evidence that the most common vision problems among children and adults are genetically determined. The list includes strabismus (cross-eyes), amblyopia (lazy eye) and refraction errors such as myopia (nearsightedness), hyperopia (farsightedness) and astigmatism.

Can inherited eye diseases be corrected if an early diagnosis is made?

YES

Source: http://my.clevelandclinic.org/disorders/inherited_eye_disease/default.aspx

This Table gives a better insight on Causes of Myopia:


What is the current consensus, if any, about why long term potentiation is not clearly correlated with learning? I was watching a video where a professor said that according to some experiments, Long Term Potentiation (LTP) is correlated with better learning, while in yet other experiments, LTP is correlated with poorer learning.

Are there any models that explain this phenomenon? What's the current theory on this?

I'm going to answer your general inexact question with a general inexact answer. The consensus is that LTP is correlated with learning.
To clarify in more detail, studies have shown that when an animal performs a learning task that involves the hippocampus(which is important for memory), and the animal effectively learns, less LTP is seen in-vitro in brain slices from these same animals. LTP is said to be occluded or blocked since potentiation of those synapses have already maximized through the in-vivo mechanisms. This can be interpreted as learning affecting LTP or at least both acting on the same basic mechanisms of the synapse(strengthening and weakening).

See for ex.
Learning induces long-term potentiation in the hippocampus.", Jonathan R Whitlock, Science (New York, N.Y.), 2006;313(5790):1093-7


Why can't a corn cob have 13 rows of seeds? Every time before eating a corn, I count its lines. I would always find 12 or 14 rows of seeds, but never 13.

Is there any biological/scientific reason behind this?

Most varieties of corn bred for modern use have between 8-20 rows of kernels (Bommert et al. 2013.. Nearly all varieties have an even number of kernel rows.  This is due to the early development of the ear.  Ears of corn are developed from pistillate flowers on the ear (Bortiri and Hake 2007). Pistillate flowers are the female flowers, so they will bear seeds. The seeds are the individual kernals.
Long before the ear of corn has the kernels, it has several rows of flowers. The flowers develop on the ear in long rows. Early in development of the ear, the individual rows of flowers double, forming rows of double flowers, as shown in the simple diagram from Bortiri and Hake (2007). Both male flowers (left) and female flowers (right) have this two-row structure.

You can see the doubled pattern forming in this scanning electron micrograph of the very early development of the ears, also from Bortiri and Hake (2007). Notice the tip of the ear still has the single rows but the rows begin to double a little farther away from the tip. You can usually see this even on mature ears of corn.

You can see remnants of this arrangement if you look carefully at a cross section of an ear of corn. I've drawn arrows to show the connections where the flowers once connected together. If you look carefully at the ear of corn, you can identify the rows. The doubled rows have the kernels exactly opposite of each other. Each doubled row is staggered slightly from the neighboring rows. I've drawn lines to highlight each doubled row.  These two photos are from the agriculture extension office at Purdue University.

The development of corn flowers and all other flowers follows what is called the ABC model of floral development (Krizek and Fletcher 2005). The model has been greatly expanded since molecular genetics has increased our understanding of flower development. Many genes are involved, and the genes are used in different ways by different species of plants. The pattern of gene usage is similar in most grasses, which explains the double-flower arrangement of corn. Most grasses have the double-flower arrangement, and corn is a type of grass.
Some highly inbred variety of corn can produce odd numbers of kernel rows, as shown in figure below, taken from Bommert et al. (2013). KRN is kernel row number.  RIL is recombinant inbred lines, which means different varieties that have been inbred for particular traits. Thirteen is possible, as are other odd row numbers. An odd number of rows is unusual, however.

Citations
Bomblies, K. et al. 2003. Duplicate FLORICAULA/LEAFY homologs zfl1 and zfl2 control inflorescence architecture and flower patterning in maize. Development 130: 2385-2395.
Bommert, P. et al. 2013. Quantitative variation in maize kernel row number is controlled by the FASCIATED EAR2 locus. Nature Genetics 45: 334-337.
Bortiri, E. and S. Hake. 2007. Flowering and determinacy in maize. Journal of Experimental Botany 58: 909-916.
Krizek, B.A. and J.C. Fletcher. 2005. Molecular mechanisms of flower development: An armchair guide. Nature Reviews Genetics 6: 688-698.


Can viruses be deformed? Viruses are created in their fully-formed state and do not grow. But one thing has been bugging me lately:
can a virus be deformed, e.g. in order to fit into an opening slightly smaller than itself? Say you were to apply a force to the virus perpendicular to the smaller hole; would the virus merely break, or is it possible for it to deform and retain its structure on the other side?

Most viruses of human concern are "enveloped", that is, they are surrounded by a lipid membrane. This membrane is usually what determines the shape of the outer layer, and is intrinsically flexible, so most human viruses would be able to deform a bit to fit through a hole. Additionally, the size of individual enveloped virus particles tends to vary quite a bit as seen in this image from a previous answer:
You can also see that biologically active proteins stick out of the membrane. These are likely to break off if the virion experiences any significant forces. My experience with coronaviruses has been that even relatively mild purification procedures remove the spikes from most particles, let alone forcing them to deform through a hole. So, while they might pass through a small hole without rupturing, it's likely their ability to infect cells would be greatly reduced.
In the case of non-enveloped viruses such as adenoviruses or picornaviruses, their outer layer is composed of many copies of a "capsid protein", linked together according to quasi-equivalence. The capsid proteins need to join together over a range of angles, so they should be able to tolerate some flexing. Again, though, any extra proteins that stick out for biological functions (such as the adenovirus' fibers) will likely be damaged or detached, which would remove the virus' ability to infect cells.


What is the direction of current flow in myelinated nerve cells? Is it correct to say electric current flows through the extracellular space, or cytosol of a nerve fiber during impulse conduction?

I know that an impulse is actually a change of membrane potential which is transferred along the length of a neuron through transfer of ions (by a series of ion channels and pumps).

In myelinated axons our professor told us the following:

  When a nerve impulse propagates along a myelinated axon an electric
  current (carried by ions) flows through the extracellular fluid
  surrounding  the myelin sheath and through the cytosol from one node
  to the next.

How exactly does the current flow in myelineated nerve fibers?

During an action potential current flows across the neuronal membrane. Basically, during depolarization, Na+ goes into the cell, during repolarization K+ goes out. This process for a myelinated axon is shown in Fig. 1.

Action potentials in myelinated neurons jump from node to node, a process called saltatory nerve conduction. These nodes, called nodes of Ranvier, lack myelin and contain Na+ and K+ channels. Outside these nodes there is insulating myelin wrapped around the axon and the axonal membrane lacks Na+ and K+ channels there.

What happens during an action potential at a node is the following: Na+ rushes in at the node. Because of the insulating myelin in the next axonal segment leading up to the next node in line, Na+ can run through the axon to the next node without much signal loss. This passive spread of depolarizing current is much faster than repeatedly generate a new action potential along the length of the axon.

To answer your questions now:

  Question: Is it correct to say electric current flows through the extracellular space or cytosol of a nerve during impulse conduction?

Answer: Yes... and no. No, because electric current and notably Na+ and K+ flow perpendicular to the axonal membrane during action potentials. Yes, because the Na+ ions do move through passive current spread through the axon to the next node.

  Question: How exactly does the current flow in myelineated nerve fibers?

Answer: Your professor was spot on. During depolarization, ions (notably Na+ in this case) are carried from the extracellular space through Na+ channels in the node of Ranvier to the intracellular space. From there it spreads through passive diffusion to then next node.

Fig. 1. Action potential generation in myelinated axons. source: Purves et al.(2001)

Reference
- Purves et al. (ed). Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates (2001)


Is there a realistic "family tree" model for the human population? I would like to do some gene inheritance simulations, and I was wondering if there is an accepted model for what mating looks like in the general human population? I am not necessarily looking for the exact graph of any population.

For example, my current model has generations 1, 2, ..., n, n+1, ... where each individual in generation i is the product of a mating between two individuals in generation i-1. This is obviously over simplistic, and I was wondering if there are better models out there?

Well, there are some questions regarding what population. I don't have 50 rep, so I can't really ask for clarifications; populations range a lot, from your typical avoidance of inbreeding (laws against cousin marriage) to Tamils with their high rates of first cousin marriage (so high that they don't have any pedigree inbreeding depression due to selection, so it's not unhealthy).

Mating in humans is often assortative for many traits including education, vocation, etc. When the Americas were settled (after aboriginal Americans were devastated by disease), skin color was a source of assortative mating. Arguably it still is. On the other hand, people tend to mate disassortatively for traits such as Major Histocompatibility Complex.
Furthermore, isolation in human populations tends to be by distance (though this is of course changing, leading to a lot of admixture in recent population history).

As a result, what your population is will have a huge impact on your results; you'll need to calculate f for any particular locus, and take a look at admixture. If f is 0, then you have a random mating scenario (neither preference nor avoidance of inbreeding, and neither assortative nor disassortative mating).

TL;DR if you're doing a very simple analysis on dummy data, you can probably get away with assuming that mating is totally random. But if we're talking about actual populations, you'll need to run the models/calculations of f and other population measures.


What was the reason for some plant and animals to become giant in course of evolution? The dinosaurs, mammoths, giant plants etc are known to be bigger than modern animals. I wonder why they had been lived and why they are not living now? I really don't know much but is it something about oxygen balance or something similar?

Thanks for asking an interesting question which made me think.

The short answer is that something evolves if there is an advantage to the genes involved, and, by 'advantage' I mean it produces more copies of the genes in the next generation so more individuals with that characteristic will be present in the population.

As to what particular advantage increased body mass had to any particular species that would depend on the particular species and its environment at the time.  There is almost certainly not a 'one-fits-all' answer.

Most very big land mammals are herbivores and there is an advantage in having a large digestive tract when you eat a lot of plant material with a fairly low nutrient level.  However, when there are also predators around, getting big and slow might be more of a disadvantage than staying small and fast. With evolution there is often a balance of competing forces which are traded of against one another.

Where large mammals have become isolated on islands with no predators, such as a species of now-extinct elephant on the Flores Island, they tend to become smaller so this suggests avoiding predators by simply being too big for them to kill might be an important factor.

And of course with many species we have the effect of sex-selection. If females select for the biggest males, there will be a selection pressure towards greater size.

With plants it could be something else entirely. Trees, for example, have long trunks basically for one of two reasons.

Firstly to put their leaves and seeds out of the reach of herbivores, so we have a kind of arms race like that between giraffes and acacia trees in Africa.

Secondly, when they grow in close clumps like woods and forests, there will be competition for sunlight and soil resources like water. A species which can reach higher and put it's leaves above those of it's neighbours will win the competition and there will also then be pressure on it's neighbours to evolve longer trunks.  Long trunks mean that water must be pumped a long way to the leaves so the tree with the longest trunks will also need bigger root systems.  Again a trade off between making a long trunk and dominating the water supply underground.

Many trees are also believed to have formed symbiotic associations with fungi in their root systems which help them take in the nutrients and water required to 'service' a long trunk and high-up leaf crown so they may be the only types of plants capable of doing this anyway.

One thing you might like to think about is why some whales are very big and some are relatively small (dolphins, porpoises, killer whales). What is the difference in their life-style, food, habitat, and so on, which could drive these evolutionary differences.


How did giraffes develop their rete mirabile failsafe? Giraffes, being one of the tallest mammals in the world, have a failsafe called rete mirabile to prevent them from dying from excessive blood pressure while lowering their head.[1]

Due to their long necks, a formidable amount of blood pressure is needed (quoted from animals.about.com):

  A giraffe's heart has special adaptations to enable it to pump blood up the animal's long neck to its head.
  A giraffe's heart has the formidable task of pumping blood at high enough pressure so that it can flow up the giraffe's neck to the brain.
  To accomplish this, a giraffe's heart is specially adapted.
  It can weigh up to 10 kg (22 lb) and generates twice the blood pressure of other large mammals.
  Having enough blood pressure to pump blood to the brain when the giraffe's neck is extended upward is one challenge, but when the animal lowers its head it risks injury due to excessive blood pressure.
  To counter this, giraffes have a pressure-regulating system known as the rete mirabile which restricts the amount of blood that rushes towards the brain when the giraffe lowers its head.

How did this evolve? I believe in evolution but I can't wrap my head around this. If an "overload" of blood would reach the giraffe's brain while it is, for instance, drinking water and either instantly killing the animal or severely wounding the animals mental and physical capabilities by rupturing the brain, how could a failsafe like this evolve?

I think what leads to the confusion here is the assumption that the neck was evolved before the rete mirabile.  Giraffes evolved from creatures with shorter necks.  As evolution occurred nature was selecting for longer neck creatures (being able to eat more leaves) but at the same time creatures with longer necks had problems with blood pressure.
At this point this would also not be lethal because we are talking about animals with much shorter necks, just in some way disadvantageous to the animal.
So over time necks got bigger, blood pressure went up, and blood vessels developed that could better and better deal with the change of pressure. Rete mirabile also occur in other animals, so they are not a rare evolutionary phenomenon of giraffes.


Are neural connections one-way? I'm trying to think about how two neurons communicate, typically shown in pictures as an electric pulse traveling along a long, thin connective tissue.

Is this depiction somewhat accurate, and if so, what happens if both neurons fire at the same time on that connection?

Perhaps the connections are one-way, or they can facilitate pulses going in opposite directions at the same time, or perhaps it's something different all-together. It'd be interesting to have this explained, at least vaguely.

Are neural connections one-way?

Yes. Action potentials travel only from dendrites towards axon.

  typically shown in pictures as an electric pulse traveling along a long, thin connective tissue.

What connective tissue? That thin "wire" which carries the action potential is a part of the neural cell body called axon.

Depending on what the axon connects to, there are 6 types of synapses:

"Blausen 0843 SynapseTypes" by BruceBlaus. When using this image in external sources it can be cited as:
Blausen.com staff. "Blausen gallery 2014". Wikiversity Journal of Medicine. DOI:10.15347/wjm/2014.010. ISSN 20018762. - Own work. Licensed under CC BY 3.0 via Wikimedia Commons.

A synapse is the connection between two structures: the axon of a neuron which "outputs" a signal (chemical or electrical) and the other structure ("input") that can be:

a dendrite or any other specific receptor from a cell
a neural body (can receive both electrical and chemical stimuli)

  what happens if both neurons fire at the same time on that connection?

In the situation of an axoaxonic synapse (example 2 and even 5 and 6 from the above illustration), the presynaptic neuron can have inhibitory action (nicely explained on michaeldmann.net at Presynaptic inhibition) from where I quote:

  Activity at the axoaxonic synapse partially hypopolarizes the terminal so that, when an action potential comes down the [...] afferent fiber into that terminal, its amplitude is reduced. Because the amount of transmitter substance released by a bouton is proportional to the amplitude of the action potential in it, less transmitter substance is released, resulting in a smaller EPSP and less excitation of the postsynaptic cell [...]

Links:

http://en.wikipedia.org/wiki/Synapse
http://www.getbodysmart.com/ap/nervoussystem/neurophysiology/synapses/introduction/synaptic_contacts/tutorial.html
http://michaeldmann.net/mann13.html


Understanding presynaptic and postsynaptic inhibition One way to classify neural inhibition is based on the inhibition being "presynaptic" or "postsynaptic".

As far as I understand, the two different types of inhibition refer to the following:

Presynaptic inhibition: A neuron N1 is inhibited "indirectly" insofar as the presynaptic excitatory neuron's action on it are dampened. This is typically achieved by neurotransmitter's impact on the presynaptic excitatory neuron which inhibit Ca2+ channels, and consequently prohibit vesicle release of neurotransmitter's into the synaptic cleft - hence the excitatory impact on neuron N1 is reduced.
Postsynaptic inhibition: A neurotransmitter acts directly on  neuron N1's receptors, leading to hyperpolarization of the membrane potential and hence a reduced probability of firing.

My questions:

(1) When we speak of "inhibitory post-synaptic potentials" (IPSPs), is this hence
always in the context of post-synaptic inhibition?

(2) I often read of "interneurons" (and it seems that this concept is used typically to refer to inhibitory neurons). Is inhibition by interneurons also always post-synaptic?

Post-synaptic vs pre-synaptic inhibition

Yes, inhibitory post-synaptic potentials (IPSPs) are always in the context of post-synaptic inhibition, because they are post-synaptic potentials. They occur because of inhibitory neurotransmitters (for example, GABA) are released and bind to post-synaptic receptors, particularly ligand-gated chloride channels. We often just call this "synaptic inhibition."

Pre-synaptic inhibition, on the other hand, would reduce the frequency/amplitude of excitatory post-synaptic potentials, by reducing neurotransmitter release at excitatory synapses (for example, glutamatergic synapses). You can also have pre-synaptic inhibition at an inhibitory synapse, where the pre-synaptic inhibition is actually disinhibitory from the perspective of the post-synaptic cell (inhibiting inhibition).

In summary: post-synaptic inhibition is reducing the rate or probability of action potentials; pre-synaptic inhibition is affecting the quantity or probability of vesicle release.

Interneurons vs inhibitory cells

Inhibitory interneurons are a major class of interneuron in the neocortex, but not all interneurons are inhibitory (layer 4 spiny stellate cells, for example, are excitatory interneurons). In addition, not all inhibitory cells are interneurons; some brain regions have inhibitory projection neurons, for example the cerebellum (Purkinje cells) or striatum (medium spiny neurons).

Inhibitory cells are those that release inhibitory neurotransmitters, so they are best thought of as involving post-synaptic inhibition. Chandalier cells in cortex are a bit of a special case, because they synapse onto axons and interfere with action potentials that way, but I would not lump them in with presynaptic inhibitory mechanisms.

Sources of pre-synaptic inhibition

In general (because there may be exceptions, and almost certainly are in invertebrates who have very "weird" nervous systems from my mammal-biased worldview), presynaptic inhibition arises from three places: autoreceptors (self receptors), retrograde signalling from post-synaptic cells, and neuromodulation. One could fill textbooks with information on all the mechanisms, but I'll give one example of each of the three types:

Autoreceptors

Glutamatergic synapses, for example, can have pre-synaptic inhibitory metabotropic glutamate receptors. These are G-protein coupled receptors, not ion channels, and they typically respond when a synapse is very active. They are effectively a brake on over-activity: if a cell is firing too much, the effect of its firing will be decreased by pre-synaptic inhibition mediated by these self-receptors. This principle is common for other neurotransmitters, too. (Wu & Saggau, 1997)

Presynaptic inhibition by post-synaptic cells

Although we think of neuronal signalling as one way, that's not entirely true. Post-synaptic cells have mechanisms to communicate with the pre-synaptic cell, and this can include inhibiting that cell.

Endocannabinoids are one mechanism: they are released by the post-synaptic cell and can reduce pre-synaptic release probability (Maejima et al 2001; Melis et al 2004). At an excitatory synapse, that makes them inhibitory; at an inhibitory synapse, they would be disinhibitory.

Pre-synaptic inhibition by neuromodulators

Pre-synaptic cells can also be affected by local concentrations of neuromodulators, like dopamine (Bamford et al 2004). Dopamine isn't necessarily released directly onto a cell but more into the surrounding area. Dopamine D2A receptors, for example, are found presynaptically at cortico-striatal synapses. Release of dopamine in the striatum reduces glutamate release at those synapses coming from cortex.

Bamford, N. S., Robinson, S., Palmiter, R. D., Joyce, J. A., Moore, C., & Meshul, C. K. (2004). Dopamine modulates release from corticostriatal terminals. Journal of Neuroscience, 24(43), 9541-9552.

Maejima, T., Hashimoto, K., Yoshida, T., Aiba, A., & Kano, M. (2001). Presynaptic inhibition caused by retrograde signal from metabotropic glutamate to cannabinoid receptors. Neuron, 31(3), 463-475.

Melis, M., Pistis, M., Perra, S., Muntoni, A. L., Pillolla, G., & Gessa, G. L. (2004). Endocannabinoids mediate presynaptic inhibition of glutamatergic transmission in rat ventral tegmental area dopamine neurons through activation of CB1 receptors. Journal of Neuroscience, 24(1), 53-62.

Nadim, F., & Bucher, D. (2014). Neuromodulation of neurons and synapses. Current opinion in neurobiology, 29, 48-56.

Wu, L. G., & Saggau, P. (1997). Presynaptic inhibition of elicited neurotransmitter release. Trends in neurosciences, 20(5), 204-212.


Why are fifth order Markov Models, the ones most often used for gene prediction? As far as we know that smallest polypeptide chain length is 60 amino acids - so if we found an Open Reading Frame (ORF) of about 60 codons without the interruption of stop codon we can consider it to be a possible coding region or gene.

The fifth order Markov Model uses hexameric frequency to predict coding regions, however this doesn't seem very specific.

Why wouldn't we use higher order Markov Models with higher frequencies and more specificity? Wouldn't increasing the order of Markov models prevent false positive results?

The problem with increasingly complex HMMs is that their parameter space tends to explode with the nth-order of the HMMs. Higher number of parameters is often not great because it reduces the possible number of observations that go into training each parameter and can increase overfitting of the model.

From the information that you are providing it is possible that the 5th order model reaches the sweet spot of having great performance with a reasonably contained parameter space.

It is not clear how your model also works.

Is each state a single nucleotide or a single KMER?

Is it a generalized HMM with separate states for exons and introns with the KMERs being observations?

Work by the Bier lab has shown that 5-mers are very good at telling apart enhancers from background using a SVM model for classification. In your context it seems pretty reasonable to use 6-mers to find genes given this finding.

For more details please check "Biological Sequence Analysis" by Sean Eddy and the work of Dr. Michael Brent @ Washington University in Saint Louis (his lab has done a lot of research on HMMs for gene finding).

It'd be useful to have one or few paper references behind your question.


Do adult mammalian cochlear inner hair cells regenerate? The consensus seems to be no, but I see conflicting evidence.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5361427/

Supernumerary human hair cells—signs of regeneration or impaired development? A field emission scanning electron microscopy study

The combination of scarring and proximity to the supernumerary cells suggests it is regeneration and not just misplacement.
Do adult mammalian cochlear inner hair cells regenerate?

Short answer
The current consensus is that hair cells in the cochlea of humans do not regenerate spontaneously.
Background
I took the liberty to show the linked paper to a colleague of mine. This guy has been doing histology on the inner ear for his entire professional career.
He pointed out that the consensus is that in mammals, cochlear hair cells do not regenerate. This as opposed to birds and fish where they can regenerate. In mammals, vestibular hair cells can also regenerate (Santaolalla et al., 2013).
Where do these 'supernumerary inner hair cells' (sIHCs) the authors of the paper show in their (quite stunning) EM photos come from? I wish to point you to the last lines of the Discussion of your linked paper (Rask-Anderson et al., 2017):

Taken together, it cannot be settled if the sIHC represent renewed or redundant accessory IHCs. Further molecular studies are needed to verify if the regenerative capacity of the human auditory periphery might have been underestimated.

In other words, the extra hair cells may have appeared during development in utero, or perhaps due to regenerative processes later on. Note that the inner ear in mammals is fully developed and doesn't grow anymore in size. The EM photos in the article don't allow for the identification of functionality either. Also note that sIHCs have been identified in the 1800s in other animals and that the beauty of this paper lies more in the fact that it shows that sIHCs exist in humans, rather than showing that IHCs regenerate in man (that would likely not appear in the Upsula journal of medical sciences, but in Nature or the likes). On a side note - the authors of the paper are giants in the field.
Literature
- Rask-Andersen, Ups J Med Sci (2017); 122(1): 1–19
- Santaolalla et al., Neural Regen Res (2013); 8(24): 2284–9


What is this insect or lake dweller? Found on my deck. We live next to a lake. Don’t know if a bird dropped it?  Not sure whether to save it?  Has scalloped front legs and a point from the end of what I think are wings. Antennae, mouthparts. Back legs either deformed or partly missing because can’t propel forward, just rolling side to side   I put it in a pen to keep it safe for now.

That is a mole cricket. Order Orthoptera, family, Gryllotalpidae https://en.wikipedia.org/wiki/Mole_cricket
I'm not surprised you live by a lake. They burrow in sandy soil or sand, often right up to the water's edge. They can fly, but spend most of their time underground. You do not need to save it, as it will find its way back to its home if you just let it go. They are not pests. They don't bite, or spread disease.


Neuron activity on body parts measurable? Is it possible to measure the neuron activity on body parts like the back or the arm? Or is this done already?

Of course neuron activity can be measured on the scalp using an EEG. I wonder if similar technology could be used to do the same on other parts of the body.

I know there is EMG which measures muscle activity and  that's also easier to measure as the voltages are multiple orders of magnitude higher. But I imagine that one could get much richer data by directly sampling neuron activity.

To measure single-unit neuron activity you need to use a microelectrode system, but it is very invasive. How useful the information collected depends on what you searching for. If you interest in studying the neurophysiology of neurons its good way to go. If on the other hand, you are interested actual outcomes stimulation then the average neural response is actually more useful.

Computational work often uses these neural averages as 'the' signal. In the end synchronicity of neurons working together is what really matters in achieving higher order functions.

A good book I have found  " Theoretical Neuroscience: Computational and Mathematical Modeling of Neural Systems " by Dayan P., Abbott, LF., (2005)
really insightful into how brain activity is measured and analyzed. Prior knowledge in Calculus and Statistics will greatly help make sense of the math, but even without it is enlightening.


Manipulating Gut flora in vivo I am tasked with designing an in vivo experiment in humans that requires manipulating the gut flora in one sample group to gauge its effect. Please suggest ways of doing this besides administering antibiotics.

I am of the view that antibiotics may have unintended consequences and may be unethical; explain any opposing view.

I can't think of any way to start with an intestinal "blank slate", so to speak, except with antibiotics.

Perhaps it's possible to at least partially homogenize/standardize a sample group's biota with probiotics?

If it's ethics you're worried about, perhaps draw experimental subjects from a pool already being treated with antibiotics (although this, I suppose, introduces it's own biases?).


Inhibition of beta-oxidation by acetyl- or malonyl-CoA Which molecule, in excess, inhibits beta-oxidation?
a. Acetyl-CoA
b. Malonyl-CoA

The answer to this question seems debatable to me, as I think both are correct.  However, according to my professor, only one is correct — which one I  don’t know because it was a question from the final exam.
Acety-CoA can inhibit thiolase, and malonyl-CoA can inhibit CAT I (Carnitine- acyltransferase), both of which lead to the same outcome — inhibiting beta-oxidation

Mammalian $\beta$-oxidation occurs in the mitochondrion, whereas fatty acid biosynthesis is cytoplasmic.

The rate-limiting in mammalian fatty acid oxidation is considered to be carnitine palmitoyltransferase (CAT), a key enzyme in the transport of acetyl-CoA across the inner mitochondrial membrane.  This enzyme is inhibited by low micromolar concentrations of malonyl-CoA (see Beta oxidation of fatty acids by H. Schulz).

Malonyl-CoA, of course, is a key intermediate in fatty acid biosynthesis.  Salih Wakil showed that CO2  is required for fatty acid biosynthesis, but that carbon atoms from CO2  do not appear in fatty acids, and it is now known that this is due to the formation of .malonyl-CoA by acetyI-CoA carboxylase, the rate-limiting reaction of fatty acid synthesis.

Thus when fatty acid biosynthesis is taking place, the concentration of malonyl-CoA is high and CAT (and therefore $\beta$-oxidation) is inhibited (Schulz, 1991).

However, as the OP points out, micromolar concentrations of acetyl-CoA inhibit 3-ketoacyI-CoA thiolase when the concentration of CoASH is low, and the Acetyl-CoA/CoASH ratio within the mitochondrion may also play a role in the regulation of beta-oxidation (Schulz, 1991).

As the OP says, it is a debatable point, and it seems to me, an example of a badly worded exam question.  I think the 'expected' answer is probably malonyl-CoA, and there is no doubt that this molecule plays a key role in the regulation of both fatty acid oxidation and fatty acid biosynthesis.  Nevertheless, the inhibition of thiolase by Acetyl-CoA may also play a role in the regulation of beta-oxidation.

Perhaps your Professor is an example of the type that Warburg told Hans Krebs to attach himself to? :-)


What hold and inject pressure to be used in microinjection? I am planning to set up micro-injection apparatus in our lab. Normally what hold and inject pressures are used to inject DNA in fly embryo? I couldn't find in any literature as far as I've come across.

It depends on volume that you want to inject and the width of your needle! Try to optimize the pressure by measuring the volume that you inject in mineral oil (I use grid in the objective to measure the drop size). You will decrease the volume by decreasing the injection pressure, of course. I work with zebrafish embryos so I am not sure if it is the same since it's in the water, but for DNA injection (1-2 nL) I normally use Hold Pressure 2 kPa and Injection Pressure 20-30 kPa.


Does Pasteur's experiment contradict an origin of life? To my understanding, Pasteur’s experiment demonstrates that life is only made from life. If this is true, then how could origin of life (aka. abiogenesis) ever have happened?

It seems to me that Pasteur’s experiment and the theory according to which there is abiogenesis contradict each other. Do they?

Consider the context. In Antiquity and the Middle Ages from Aristotle on, people thought that many living things (from microbes to mice) would arise through spontaneous generation. Seemed sensible enough; if you don't pay close attention to animals getting somewhere, and you have no knowledge of anything microscopic, it can easily look like animals just come out of the environment. After the Enlightenment scientists got better understandings of reproduction on the one hand, and made many experiments showing that under certain conditions (like keeping meat sealed so flies couldn't get to it for example), life didn't, in fact, spontaneously generate in the way it was previously thought it did. At this point the idea that all living things come from the reproduction of other living things of the same species became increasingly accepted.

Pasteur's experiment was more or less the death knell of the spontaneous generation hypothesis; some previous experiments had shown microbes growing after a flask was supposedly sterilized, or kept the flask sterile by keeping air out (which opened one to the argument that spontaneous generation required air). His showed microbes not growing in a flask where air could flow but dust did not settle because of its shape, and immediately growing when the flask was tipped and dust fell in.

Pasteur's experiment didn't so much "prove that life only comes from life", as disprove a specific other hypothesis that existed at the time. And in that sense it is still consensus biology: No biologist today thinks that snakes, mice, microbes, or even viruses can arise directly through abiotic processes. If you replace "life" with "modern life", the principle is true as far as we know.

Now biology has advanced a lot, and there is a different context, with people asking different questions and advancing different hypotheses to answer them. The question of the origin of life is one such question, that has nothing to do with what Pasteur was trying to prove. And that's where the "modern life" caveat becomes relevant; while all modern living things are too complex and specific to arise directly via abiotic processes, it doesn't follow that the same is true of the first living things. We know that living things used to be different from how they are now; and in fact when looking into the past via the fossil record and genetic evidence we find clear patterns of gradual development of the modern biosphere's diversity and complexity from simpler and more generic ancestors. While it is harder to find evidence for the evolution of early cells, because the genetic evidence is muddled by the time scales involved and the fossil evidence near-nonexistent for obvious reasons, it is sensible to figure that similar patterns would occur there, and that the earliest cells were as different and simpler than a modern cell as a Precambrian worm is from us.

Here is a video of Nick Lane talking about a promising hypothesis on the origin of life. It sort of illustrates how different, and simpler, those primordial living things could have been compared to current organisms.

https://www.youtube.com/watch?v=gb7pZyks_HE&t=1151s


Can human survive falling from 30,000 ft without a chute? If someone falls 30,000 feet without a parachute; what are the chances of survival if they landed in the water?

Summary: A fall from "any height" may be survivable, depending on what you hit, but with an expectation of severe injuries. A water impact at terminal velocity will in all likelyhood result in immediate death.

The Serbian Flight attendant Vesna Vulović holds the Guiness World Record for surviving a fall without a parchute with an estimated fall height 10,160 metres. However, some doubts have been cast on the accuracy of the record, with claims that the fall was actually only several hundred meters. Vulovic was found partly in the wreckage of the plane, so it can be discussed whether she had a truly "free fall" for the purposes of this question. However, several other persons have been known to survive completely "free" falls from great heights. Although it is hard to verify the exact altitudes, the WW2 aviators Alan Magee, Nicholas Alkemade and Ivan Chisov are reported to have survived falls of about 6700 m, 5500 m and 7000 m, respectively.

The exact altitudes are in any case not necessarily of interest, as it can be assumed that all persons falling from a height of more than about 500 meters will reach terminal velocity, the velocity where air resistance prevents the fall speed from increasing, before hitting the ground. As such, above a certain height, other factors become determining for the survivability of a fall. As has been demonstrated by the listed examples, it is clearly possible to survive a fall at terminal velocity. However, this requires favorable conditions at the site of impact, and will likely result in severe injuries.

Due to the flat surface and the surface tension of water, it is hard to imagine an unprotected impact with water being survivable at terminal velocity. The best chances for survival will likely be in areas with foliage, snow and/or a hilly landscape allowing the kinetic energy to be dissipated through rolling downhill. Of the listed aviators above, Nicholas Alkemade appears to have been the least injured. About him, it is reported that

  His fall was broken by pine trees and a soft snow cover on the ground.
  He was able to move his arms and legs and suffered only a sprained leg


Grouping OMIM disease codes I have ~100 sets of genes, and each set includes between 2 and 70 genes. I'd like to perform an enrichment analysis on each of these sets to test if they're enriched for OMIM disease labels. However, I'm encountering a problem where the OMIM codes are too "sparse", such that each OMIM code only occurs maximum once in all gene sets. As far as I can tell, this makes the codes unsuitable for enrichment analysis in this case.

I believe that grouping the OMIM codes could solve this, as long as each group-label occurs multiple times in my lists. Grouping OMIM codes seems doable: for example, OMIM codes 601495, 613500, 613502, and 613506 all refer to types of agammaglobulinemia. I could imagine grouping codes based on something like gene ontology labels.

My question: is there a standard way to group OMIM codes?

I see some papers doing something like this, e.g. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458913/, but I'm new to the field and don't know how "standard" approaches like these are.

Based on OMIM ID codes
In a broad sense NIH have already divided the IDs. If all you are checking is OMIM code enrichment, this might be an okay resolution since it can tell you the chromosomal locus (autosomal, sex linked, or mitochondrial).

Each OMIM entry is given a unique six-digit number as summarized below:
1----- (100000- ) 2----- (200000- ) Autosomal loci or phenotypes
(entries created before May 15, 1994)
3----- (300000- ) X-linked loci or phenotypes
4----- (400000- ) Y-linked loci or phenotypes
5----- (500000- ) Mitochondrial loci or phenotypes
6----- (600000- ) Autosomal loci or phenotypes (entries created after
May 15, 1994)

Other databases as an alternative method.
If you are interested in specific phenotypes, you may need to get more involved.
OMIM doesn't really attempt to group diseases together beyond their ID nomenclature as far as I'm aware. There have been several projects that set out to do this, like the one the question points out, and the examples below. They mostly use phenotypic data in combination with OMIM information.
Two databases that aim to solve this are:

HPO
LDDB
Enricher web-server see @MaximKuleshovs answer below!

These are tools with controlled vocabulary for phenotypes and associations from OMIM codes. They could help you check for disease/phenotype specific enrichment. This would certainly allow programmatic grouping, although I have not worked with either before and I presume it would be very involved!
It's up to you!
Wikipedia has a list of OMIM codes listed in alphabetical order if you wanted to try to group them manually by whichever criteria you desire.

Without your source code it's hard to tell, but maybe the maximum of one occurrence rate could be a code problem rather than a scientific problem.


Firing rate of retinal ganglion cells I have few questions about the firing rate of retinal ganglion cells.

1) How to explain the baseline firing rate if either the entire receptive field is stimulated or there is no light stimulus at all? That behaviour means that the intensity of light does not have any effect if the entire receptive field receives the same stimulus. I don’t understand how horizontal cells let that possible.

2) When the on-center is stimulated, the firing rate is maximized at the beginning and it diminishes with time to reach the baseline rate. Why does the firing rate decrease? What is responsible for that?

3) Is it possible to have a simple mathematical model of the process with an artificial neural network?

1) This is a bit simplified; in reality, flashes of light or dark that cover the whole receptive field do influence the firing rate somewhat, just not nearly as much as an on-center stimulus for an on-center RGC. Your textbook is using a bit of an idealized interpretation to convey the concept of center-surround organization. I'm not sure what your confusion related to the horizontal cells is, however.

2) This is usually called "adaptation" and is a general principle in nervous systems (particularly on the sensory side). Multiple systems influence adaptation, including depletion of neurotransmitter-containing vesicles, metabotropic receptors activated by high concentrations of neurotransmitter that have opposite-sign effects to ligand-gated receptors, feedback systems that suppress the potency of second-messenger systems, accumulation of extracellular inhibitory neurotransmitters, etc. For the eye, there are additional sources of adaptation that come into play, depending on the experimental paradigm.

Without knowing the exact paradigm your textbook is meaning to indicate, it's probably more important at this point to just recognize adaptation as a normal aspect of sensory processing. The specific mechanisms can be understood later.

3) Yes - but you don't need to go to anything as complex as an artificial neural network. Basic image filters like the Laplacian of Gaussian (LOG) filter are basic approximations of center-surround organization in the retina.


Changing time and rpm of centifuge Inspired by this question, I want to ask a question about centrifugation.

Suppose a protocol says : 10 min at 2500 rpm . Can we instead centifuge for 5 min at 5000 rpm or 20 min at 1250 rpm ?

No, it isn't that simple, because centrifugal force varies with the square of the rotor speed. Have a look at the Wikipedia page for clearing factor.

Those equations are usually used to determine what you need to do if you are going to use a different rotor, but they can also be used to solve your question.

Because you are looking at a situation where the same particles are being centrifuged, the sedimentation coefficient s is the same in both centrifuge runs. Also all of the factors relating to the rotor properties are the same (rmax etc.). So, if you have a set of conditions that work, t1 and RPM1, and you want to choose new conditions t2 and RPM2, you can use the equation:

RPM2 = SQRT(t1/t2) x RPM1

For the example you mention t1 = 10 min and RPM1 = 2500 rpm. If you change the time to 5 min:

RPM2 = SQRT(10/5) x 2500 = 3536 rpm

Because the centrifugal force varies with the square of the rotor speed you don't need to double the speed if you halve the time.


Do alternative start codons code for methionine after transcription? There is some literature which shows that all start codons code for methionine. However, in the standard genetic code, the alternative start codons clearly code for leucine. Does that mean these codons will code for leucine when they are encountered during translation (after start codon has been initialised and translated).

I commented that this was a duplicate, but reading the question more carefully you seem to be asking something slightly different.

In the context of a 'start' these codons will be recognised by fMet-tRNA and a formyl-methionine will be inserted as the first amino acid. Subsequent occurrences of the same codon within the open reading frame will be translated normally (e.g. GUG > valine).

The use of GTG as an initiation codon in the E. coli lacI gene

In this paper

  Frottini et al. (2006) The Proteomics of N-terminal Methionine Cleavage. Molec. & Cell. Proteomics 5: 2336-2349

the authors report assays of E. coli methionine aminopeptidase with model peptides showing that when Lys is the 2nd residue, Met removal is very inefficient. They also show that when Pro is the 3rd residue, Met removal is very inefficient.

This explains the fact that when the lacI repressor protein was sequenced:

  Beyreuther et al. (1973) The amino-acid sequence of lac repressor. PNAS 70: 3576-3580

it was found to have a Met residue at its N terminus (sequence Met-Lys-Pro-).

However, when the lacI gene was sequenced:

  Farabaugh (1978) Sequence of the lacI gene. Nature 274: 765-769

the corresponding DNA sequence was GTG AAA CCA, demonstrating that the N-terminal residue is encoded by a GTG(Val) codon. LacI residue Val23 is encoded by a GTG codon, demonstrating the normal use of that codon in the body of the mRNA.


Isolating the vasculature of an organ? Is there a chemical or process that would dissolve or remove all other tissues in an organ and leave all the vasculature intact? I am planning to make a shelf display of the blood vessels in the heart of a pig for use as a shelf display.

The typical name for this technique is "corrosion casting" - if you search for literature on corrosion casting you will find many many papers detailing the technique. Another answer mentions "plastination" but I don't think this is really what you are looking for; plastination is a technique for preserving the tissues themselves (though the "Body Worlds" exhibit that post references also uses corrosion casts extensively).

Briefly, in corrosion casting, you gravity or pressure-fill the vasculature with a plastic, typically acrylic. It is best if the vessels are flushed free of blood before injecting the plastic, with saline/PBS, for example. (Organs from a butcher will work fine but you will get better results if you can administer heparin premortem to prevent clotting, which of course is not possible for a meat animal.) The acrylic cures, and then the tissues that remain are digested with a basic solution, ranging from 0.5 M NaOH to 6M KOH depending on the protocol (lower concentrations or NaOH will digest more slowly, higher concentrations or KOH will digest more quickly), often at elevated temperature (~37C). Note that this solution technically digests all of the vasculature as well, but you have already filled the vascular lumens with plastic, so that is what you are left with.


Do the claims in this paper have any degree of validity? The paper The waiting time problem in a model hominin population talks about a problem of waiting time, etc. Is the methodology of this numerical simulation, and the conclusion right or is it wrong?

(A quick search reveals that the first author is an intelligent design advocate and apparently believes or believed that the earth is less than 10,000 years old)

I'm afraid I laughed a bit when reading that paper for the first time.

Why? Well, here's what they essentially did: They tried to model evolution by implementing an algorithm. They had a population of 10000 individuals, represented by their genetic sequence, and had an algorithm do mutations of those sequences and modeled selection and reproduction to get the next generation. They did that for a long time. Why did that make me laugh? I did both my BSc and MSc theses in the field of Evolutionary Bioinformatics. Almost every student there implements something like that when they first start, to learn to write that kind of program. It's not exactly novel. They even cite several other studies doing this kind of analysis.

Now, their result is basically that human evolution from human-chimpanzee ancestors couldn't have happened because it would have taken way too long. Not only would the whole difference between these two species have taken too long, every single difference of more than two nucleotides would have taken too long to get fixed.

Since this goes against established science, this algorithm better be good... The paper is lengthy and much of it isn't all that interesting or related, in my opinion. But here's the big problems, in my opinion:

  When natural selection successfully amplified the target string to the point of fixation (i.e., when the allele frequency reached 99–100 %),

Their target is for their target sequence to reach a frequency of at least 99 percent. That's unnecessarily high, and will of course take a long time, especially as they hold their population constant at 10000 individuals. They don't show a figure with how frequency changed over generations - I'd assume that 90 percent is reached a lot earlier than their threshold.

Holding the population size constant is of course also not a realistic model for human evolution. It wasn't at 10000 individuals for millions of years.

  initialization : initialize every individual to the same random or user-specified string (e.g., AAAAA)

Humans didn't start with random sequences and then mutated them to make them do something useful, we started with useful genetic material that then changed. If you start at AAAAA, expect a target of TAGGC, don't confer any benefit to intermediate steps (as they did) at a mutation rate of something like 1 per ten million nucleotides per generation, of course you are going to wait a long time. Mutation rate in genomes also isn't uniform, it varies by region. From what I can see, this was neither taken into account nor discussed.

There is also the problem of them only looking at single nucleotide mutation, not gene duplication, insertions, etc. that also make up a lot of the difference between humans and their ancestors.

Then there's random "mate-choosing", which is a valid simplification to make if you are just looking at some mechanisms of evolution, but not valid if you are going to use your model to estimate time needed for speciation.

They also only allow for one beneficial mutation to arise, then wait for it to be fixed, claiming that anything else would have just resulted in even longer times, without, as far as I can see, just implementing this and then testing that assumption.

At some points, their paper is just going to going for some kind of dramatic effect:

  waiting time was 500 million years – which is still extremely prohibitive. This amount of time approximates the estimated time required for the evolution of worm-like creatures into people

500 million years ago, we had the first animals emerging on land and the first chordates. Chordata and the "worm-like" phyla had already diverged.

Basically, in my opinion, they took a very simple model and drew sweeping conclusions from it. This kind of analysis is suited for looking at how evolution might result in speciation, what parameters might play a part, etc. but it is not suitable for estimating the time this takes.

But these are just my first thoughts, I hope there'll a more thorough review of this on the internet somewhere soon.


How greater magnitude implies greater frequency of action potential? Greater the magnitude of receptor potential, greater is the rate of discharge of action potentials in the nerve fibre.1

Now consider a case where stimulus ( strength ) is large , so there is more accumulation of positive charges near the spike generator region, this would then form action potential , this action potential should then travel in both directions just like at initial segment , where SD spike clears the existing EPSPs, so if I apply same logic here then antidromic Action potential should clear those generator potentials. If I am right then how is more stimulus causing more frequent action potentials?

Case2: If we take the scenario where there is no antidromic conduction of action potential ( for some unknown reasons) then more and more generator potentials are coming at spike generator region(1st node of ranvier) then also how it is causing more frequent action potential generation , if we consider that fact refractory period is constant for all action potentials( in a particular neuron)?

There are several important points to answering your question, each somewhat independent of the others. First, lets think about this problem from the perspective of the axon hillock, where action potentials are thought to be generated.

Conduction of action potentials requires voltage-gated sodium channels

When you talk about antidromic action potentials, you mean when they start at the "end" of an axon and return towards the cell body. You can also get backpropagating action potentials into the cell body and dendrites, but these are impaired by two things: 1) fewer voltage-gated sodium channels, so the action potential is weaker or not really an action potential at all, and 2) impedance mismatch. The axon is very narrow; the soma is very big in comparison (this is less of a factor in the context of peripheral sensory receptors where the soma is located far from the site of action potential initiation, but it is still true for the neurites there). A few sodium ions coming in around the axon hillock is enough to depolarize that membrane enough to start an action potential, but when those ions diffuse passively into the rest of the soma, they have a lot more membrane area to cover, and they don't cause as much depolarization.

What all of this means is that the "strength" of a backpropagating action potential isn't less than that of an action potential in the axon.

Frequency is relative

When people talk about frequency coding of intensity, they are talking about a gradual increase in frequency, not going immediately to refractory period. For example, a cell may fire at 1 Hz, then fire at 4 Hz, then fire at 16 Hz, then fire at 64 Hz. If the cell has a refractory period of 5 ms, even at 64 Hz it is nowhere near it's theoretical maximum firing rate.

Related to that point...moving ions takes time and cells are not isopotential

Threshold isn't reached immediately in the axon hillock when a "refractory period" ends: that's the difference between an absolute and a relative refractory period. Ion concentrations and ion permeabilities set an equilibrium potential, but, it takes time for the potential to actually reach that equilibrium, and both the present voltage and equilibrium potential can be different in different parts of the cell: this leads to current flow, which takes time.

After an action potential, the axon hillock typically hyperpolarizes for a bit, sometimes followed by a brief depolarization. During that time, if there are other parts of the cell (such as dendrites) that are still relatively depolarized from a receptor potential, ions will be flowing from those areas into the axon hillock. This depolarizes the axon hillock, but again, this takes time (I'm purposely repeating that to convey a feeling of this all being a dynamic, moving process, with ions moving through each step). The amount of time it takes will depend on the voltage difference, so a bigger depolarization in the dendrites will bring the axon hillock back to threshold sooner.

Not that many ions flow during an action potential

This has been a recurring theme here, see this answer: Why is it possible to calculate the equilibrium potential of an ion using the Nernst equation from empirical measurements in the cell at rest?

The change in membrane potential isn't just because ions flow: it's because permeabilities change, briefly creating a new equilibrium potential. If you have in your mind massive quantities of sodium and potassium ions flowing, completely upsetting the ionic balance in the cell and drowning out all other electrical activity, you have it wrong.

Stimuli are often long-lasting

Especially if you are talking about a mechanical stimulus, most will last a lot longer than an individual spike, which is only ~1ms long. So although one transient stimulus can cause several action potentials, often what actually happens is that those receptor potentials are quite long lasting. Effectively, they set a new "resting potential" for the cell which is above the cells' firing threshold.

In summary:

Receptor potentials depolarize the cell, bringing them to or beyond firing threshold. An action potential starts in the axon hillock and propagates down the axon, but only has a minor impact on the rest of the cell. Importantly, the action potential is really brief, not many ions move, and there is current flow in both directions, so the depolarized parts of the cell are still depolarized somewhat even after a spike. As the initial axon segment recovers from post-action potential hyperpolarization and sodium channels leave their inactivated state, current from the receptor potential is flowing in, depolarizing the cell to threshold and causing another spike. Repeat.


What are the coverings of femoral hernia? It was my Viva question and I was really puzzled.I know what is femoral hernia and it route like the abdominal content moves down the femoral canal and further through the saphenous opening and all but I have no idea about it's coverings.Can anyone please help me

Femoral hernia coverings (from inside out):

Peritoneum
Femoral septum (extraperitoneal fatty, connective and lymphoid tissue)
Tranversalis fascia
Cribriform fascia
Superficial fascia
Skin

Image source: SurgWiki, Creative Commons Licence

Sources:

SurgWiki: Hernias
SlideShare: Femoral hernia, p. 12
EarthsLab: Femoral canal
Textbook of Anatomy Abdomen and Lower Limb;, Volume 2, By Vishram Singh, p.45


Do reproductive organs function before puberty? Testis means one of the two male reproductive glands that produce spermatozoa and secrete androgens.

Ovary means one of usually two organs that produce oocytes and secrete oestrogen and progesterone.

Do these organs function before puberty?

No, they are not functional before puberty.

For males:

  Most males begin puberty between the ages of 9 and 14, but commonly puberty will begin around 12 years old. When the human body reaches a certain weight (which differs among individuals), the hypothalamus releases gonadotropin-releasing hormone. This hormone signals the pituitary gland to release the two hormones that begin the onset of puberty: leutinizing hormone and follicle-stimulating hormone.7 In males, these hormones stimulate activity in the testes, which start to produce the male sex hormone testosterone and begin spermatogenesis. Spermatogenesis is the process of sperm production.

source (warning: contains NSFW drawings and images)


If you are 30 degrees, and touch something that is 50 degrees, do you only feel 20? First off, I don't know if this is the correct site to post this question as it could possibly fit into others? If so, please flag it to be moved as I would appreciate that very much.

Now, if my body was at a temperature of 30 degrees (celcius), I would feel somewhat warm. However if I then dipped my hand into a bowl of water at 50 degrees, would I begin to feel 20 degrees difference?

This seems likely as when I come out of a freezer (at work, don't stress), and wash my hands to "warm myself up", the water feels boiling hot and painful to touch but indeed is only maybe 30-35 degrees. Until it gradually becomes more bearable.

Or you come out of a spa, into a colder pool and you feel freezing cold?

To add some depth to this question, may I ask why this happens, and how your body actually reacts in this situation?

Your sensation of heat is dependent on the change in temperature of your skin, which is roughly proportional to the difference in temperature between skin and material.

However, temperature difference is much less important than the transfer of heat between your skin and an object, which is heavily dependent on the type of material you are touching.

Why does a cold piece of steel feel so much colder than the surrounding air, despite them being in thermal equilibrium? The answer is that steel is a much better conductor of heat, and can therefore draw heat from your hand at a much faster rate than air, which is a poor conductor of heat.

A very interesting study by Lele, Weddell and Williams (1954) [1] demonstrates that the rise in skin temperature is proportional to the rate of heat transfer. The same paper suggests that the sensation of heat is roughly proportional to the rate of heat transfer.

Now for some physics.

Heat transfer along an object of length L and cross-sectional area A is given by:

Q = kAt$\Delta$T / L

where Q is the heat content, t is time, and k is the thermal conductivity.

As you can see, the transfer of heat is proportional to the difference in temperature between the two ends of the object. So a simple interpretation would suggest that your body senses the rate of heat transfer, which is directly proportional to the difference in temperature between your skin and the object you are touching.

However, this neglects the ability of your body to draw heat away from an area (via blood circulation, passive heat conduction etc). Given that your body maintains a core temperature of around 37 degrees Celsius, this complicates matters somewhat, and probably comes into play when you touch a hot/cold object for an extended period of time (e.g. your example of washing your hands to warm up).

So in summary, you are essentially correct, in that your body feels the difference in temperature between your skin and the surroundings, taking into account the thermal conductivity of the surroundings.

[1] Lele PP, Weddell G, Williams CM. The relationship between heat transfer, skin temperature and cutaneous sensibility. J Physiol. 1954;126: 206–234.


Why is Psoriasis treated with Cortisone, when stress (which releases Cortisol) is known to aggravate the condition? It is well known that stress isn't good for psoriasis , yet why do we treat the illness with Cortisone, a compound very similar to cortisol (and "has a similar name, genesis, and function", according to wikipedia) whilst cortisol is released in the body in stress situations?

For treatment reasons cortisol is named Hydrocortisone (probably to avoid problems with the similar names) and this is often only referenced to as cortisone (although this is not correct). Cortisol (Hydrocortisone) is the active form, while cortison is not. See here for some more details.

Glucocorticoids (like Cortisol or Prednisolone) suppress acute inflammation and also have immuno modulative (downregulate) or suppressive function. Since the immune system causes the problems in Psoriasis it is downregulated to control the outcome of the disease.

First it sounds counterintuitive to use Glucocorticoids for the treatment of psoriasis as this hormone is released during stress (in this case to mobilize energy resources). However, there is a study which looked precisely at the cortisol levels in psoriasis patients and also recorded their stress levels.

What they found was interesting: First they could correlate the peaks in the stress levels with a psoriasis attack about four weeks later. Then they found that the Cortisol levels of the patients where significantly lower in stres situations than for healthy control persons. Additionally they found that patients which had permenant high stress levels also showed significantly lower permanent Cortisol levels. So here the stress seems to negatively influence the cortisol levels which then prepares the way for psoriasis attacks. Using high levels of topically administered Cortisol seems to reverse this effect.
You can find the study here:

How stress gets under the skin: cortisol and stress reactivity in
psoriasis.


List of np-hard problems in biology/bioinformatics I'm not sure if this is the right place for this but...

I am looking for a list of computationally "hard" problems such that if a problem from this list could be solved effectively, it would be (significantly, or otherwise) beneficial in some form or another to the biology community.

Some examples I have found (or atleast were tagged as "np-hard" problems):

Multiple sequence alignment problem
Protein threading / design problem
Map / sequence assembly problem

The list does not have to be extensive, but hopefully more than a few.

Thank you!

(Also, I couldn't think of any more tags to add so feel free to help out there as well.)

Note:
Same question at biostars: https://www.biostars.org/p/98112/

I'm no expert in computational biology but I am very much interested and do some big data analysis using R for my own projects so I will try to provide some information.

This (http://www.ncbi.nlm.nih.gov/books/NBK25461/) is an excellent book talking about all the grand challenges in computational biology and the emerging fields so I definitely recommend looking through at least the list on the page, if you don't want to read the entire book. To me all this points to the fact that we are in the big data era, where we have masses of data but making sense of them all and putting them into prospective and analysing them in a way to show us new insights into problems is difficult.

You might also be interested in BOINC, which runs a few computationally challenging projects through crowd sourcing/grid computing (http://boinc.berkeley.edu/projects.php). In more theoretical aspects, here is a list of unsolved problems (http://en.wikipedia.org/wiki/List_of_unsolved_problems_in_mathematics), solving of which will excel our understanding of many modelling problems, which percolate in biological problems as well although I'm not at all an expert in biological systems modelling.

Hope this helps!


Could you identify which species of ant is this queen? could you identify which species of ant is this queen. I caught it in Bangalore, India. I caught it after a rain at around five to six.

]2

Although absolutely no formal criteria are visible on your photo, the general shape of the ant, especially the wide elongated head and low thorax, is typical of the ant genus Camponotus.

See ref below:

  Bolton, B., Alpert, G., Ward, P. S., & Naskrecki, P. (2006). Bolton’s
  Catalogue of Ants of the World. Massachusetts, Harvard University
  Press (CD-ROM).


What does the hominin phylogenetic tree look like? I'm no biologist, but I'm curious what the rough phylogenetic tree looks like for Hominin.  Could you create a rough sketch that includes:

Homo rudolfensis
Homo ergaster
H. georgicus
H. antecessor
H. cepranensis
H. rhodesiensis
Homo neanderthalensis
Denisova hominin
Homo floresiensis
H. heidelbergensis
H. neanderthalensis
H. sapiens
H. erectus
H. habilus
any others I may have missed

Feel free to correct any incorrect assumptions I may have made here, or clarify anything that could be instructive.

Gonzalez-Jose et al. (2008) published the following cladograms, based on two analyses (parsimony versus maximum likelihood). The table shows the legend. The interesting case of Homo floriensis, among others are not included, likely because of their recent discoveries and limitations of the study cited.

Reference
- Gonzalez-Jose et al. Nature (2008); 453 775-79


Is co-transport within a cell active or passive transport? ATP is used to actively transport H+ out of the cell against the concentration gradient. The H+ & sucrose cotransporter, for example, then uses this proton gradient for transport. H+ goes back into the cell with the gradient (passively) with concomitant sucrose transport across the membrane. Is this active or passive transport?

Co-transport, also called secondary active transport, is a form of active transport because it is using the energy from one concentration gradient to transport another molecule across the membrane against its concentration gradient. The concentration gradient which drives this process requires energy to set up in the first place, which is why co-transport is considered active.


Streamside plant identification - Oregon This is in the western cascades forest in Oregon. Leaves are at the ends of branches only, lives mostly in slightly muddy areas next to streams. Produces small black berries.

It's a plant in the family Ribes, which includes currants.

If it stinks when you crush the leaves, it is probably Stink Currant, or Ribes bracteosum, a plant found in the Pacific Northwest.

  Leaves are large, like maple leaves, sparsely hairy to smooth, with 5 to 7 lobes, stinky when crushed.  Flowers are numerous on mostly erect clusters; with white petals and brownish-purple to greenish-white calyces.  Berries are blue-black with a whitish bloom.

The leaf and berry are a good match. There are ~150 species, so it's a bit difficult.

It could also be Ribes acerifolium, or Maple-Leaved Currant.

  Shrub with spreading branches but no bristles. Leaves maple-like, 1–3 in. across, with 5–7 rounded, finely toothed lobes. Hanging stem of 8–12 greenish flowers, each less than 1/3 in. across with tiny red petals and stamen filaments broad at base. Berry black, coated with bluish powder. Grows from mid elevations to treeline in Cascade and Olympic mountains.

I could not find a photograph that was not copyrighted. The flower color was pinkish to brownish.

It's not a perfect identification, but it's closer than 'in the ballpark'. If you google "Ribes western Cascades", you'll see what I mean. :)