Why doesn't HIV spread through vectors? HIV spreads only through body fluids. If a mosquito bites an HIV infected individual and then an uninfected individual, will the virus spread  to the new individual?

This doesn't take much effort to answer!  Googling "HIV mosquito" brings us straight to this blog post, which gives three main reasons (along with more details, links to other resources, etc.):

Only saliva is injected into humans when a mosquito bites and thus HIV positive blood that a mosquito may have previously ingested is never transmitted to other humans.
Unlike mosquito borne diseases, HIV is unable to replicate within the mosquito's gut and therefore is broken down.
HIV circulates in human blood at a far lower level than would be necessary to create a new infection.


What will happen if we expose the brain to intermittent light? If a brain is exposed to an intermittent light source, are specific areas going to fire? If yes, which of them? Is there a experimental data about this effect?

It is thought that there are no active optical receptors in the brain normally, its possible some effect might show up in the future, it would be minor at best.

Shining light into the brain is standard procedure in optogenetics experiments. A subpopulation of neurons is transformed to express an optical receptor to modulate genetic or signalling properties of the cell.

So the reason I say it would be small effect on a native brain is that these experiments do give good results and are run with controls which do not have the optical receptors added, which typically show no change in brain activity.

  Channelrhodopsin-2 (ChR2) induces temporally precise blue light-driven activity in rat prelimbic prefrontal cortical neurons. a) In vitro schematic (left) showing blue light delivery and whole-cell patch-clamp recording of light-evoked activity from a fluorescent CaMKllα::ChR2-EYFP expressing pyramidal neuron (right) in an acute brain slice. b) In vivo schematic (left) showing blue light (473 nm) delivery and single-unit recording. (bottom left) Coronal brain slice showing expression of CaMKllα::ChR2-EYFP in the prelimbic region. Light blue arrow shows tip of the optical fiber; black arrow shows tip of the recording electrode (left). White bar, 100 µm. (bottom right) In vivo light recording of prefrontal cortical neuron in a transduced CaMKllα::ChR2-EYFP rat showing light-evoked spiking to 20 Hz delivery of blue light pulses (right). Inset, representative light-evoked single-unit response.

Image taken from the linked Wikipedia page and originally from Baratta et al..


Why do you need primers in PCR? I have read that DNA polymerase requires a primer to bind to the DNA, but I am confused as to why this is the case. When DNA undergoes replication in the cell, there are no primers in the nucleus. Why are they needed in PCR?

Many thanks :)

Actually, when DNA replicate in cell, there is primer exists. DNA polymerase only can add deoxyribonucleotide (dNTP) to the 3’end of a growing DNA chain, instead of creating a new strand. Here is the picture for DNA replication in legging strand, but is same principal use in leading strand. Primer is synthesized by primase in replication.

It is also worth to mention that, looking at the last step, there is a primer there and must be removed, and DNA maybe shorter in each DNA replication time, and that is why DNA telomere mechanism is proposed. That may be a key point for aging.

So, in PCR, it also needs primers, for DNA polymerase only can only can add dNTP to the 3’end of a growing DNA chain.


Why is it good to use Glycerol as carbon source to produce intermediates in pharmaceuticals? Why is it good to use Glycerol as carbon source to produce intermediates in pharmaceuticals?

My best guess would be because it produces a lot of ATP per carbon. But I haven't found anything to verify my hunch.

First, glycerol is economically and environmentally interesting as a substrate. It is a side product of first generation biodiesel production, which has been increasing in the past years. So large amounts of glycerol are being accumulated, while we make little use of it. Therefore it has become a necessity to develop glycerol utilizing industries. Another consequence is that glycerol is now a cheap and abundant substrate.

The metabolism of glycerol is quite complex and has many end products that are of industrial relevance. For example, 1,3-propanediol and succinic acid have commercial applications and can be produced directly from glycerol by some microorganisms. So depending on the strain you use, you may not need heavy metabolic engineering.

Here is an article that might help you.


What's the difference between the neuroendocrine system vs endocrine system? This is what I have understood so far:

Neuroendocrine system involved neuroendocrine cells (also known as neurosecretory cells) that receive nerve impulses by a sensory neuron to release neurohormones into the blood stream. The endocrine system releases hormones by endocrine cells into the blood stream when a receptor protein senses a stimulus.

Here are my questions:

When it comes to the brain, are the neurosecretory cells located in
the hypothalamus or the posterior pituitary gland or both?
Is the hypothalamus and the posterior pituitary gland classified as
    neuroendocrine glands and is the anterior pituitary classified as an
    endocrine gland?
If the posterior pituitary gland is indeed a neuroendocrine gland,
    is ADH and Oxytocin, which are both released by the posterior
    pituitary gland, classified as "neurohormones", not just the classic
    hormones?

Neuroendocrine systems can be defined as the sets of neurons, glands and non-endocrine tissues, and the neurochemicals, hormones, and humoral signals they produce and receive, that function in an integrated manner to collectively regulate a physiological or behavioral state.
The neuroendocrine system is the mechanism by which the hypothalamus maintains homeostasis, regulating reproduction, metabolism, eating and drinking behaviour, energy utilization, osmolarity and blood pressure. (Source)

The central neuroendocrine systems serve as an interface between the brain and many of the peripheral endocrine systems. This chapter discusses the hypothalamic control of anterior pituitary systems regulating stress, basal metabolism, growth, reproduction, and lactation. Each of these systems involves one or more hypothalamic releasing or inhibiting hormones, released from hypothalamic neurons that terminate in the portal capillary vasculature that projects from the median eminence at the base of the hypothalamus to the anterior pituitary gland. There, the hypothalamic hormones act upon subsets of anterior pituitary cells to regulate pituitary hormone release and downstream physiological functions. Other hypothalamic neuroendocrine cells control water/salt balance, and lactation/parturition, through the release of vasopressin and oxytocin from nerve terminals that arise in hypothalamus and project to the posterior pituitary gland. Together, these hypothalamic neuroendocrine functions enable the central nervous system to respond rapidly to internal or external environmental change, and to maintain a response through endocrine hormonal transducers. (Gore, 2013).

The endocrine system is a group of glands and other structures that release internal secretions called hormones into the circulatory system.

Endocrine organs are richly vascularized ductless organs that produce hormones. The epithelial cells of the organ secrete their hormone product directly into the bloodstream where, upon binding with specific receptors in target organs, cellular functions are affected. The endocrine systemincludes not only the endocrine glands (pineal, pituitary, thyroid, parathyroid, and adrenal) but also single cells and small clusters of cells in the thorax and abdomen known as paraganglia. This chapter addresses the thyroid, parathyroid, adrenal, pituitary and pineal glands, and paraganglia. In addition to size differences, several features of endocrine tissues differ between rodents and humans, and often between rodents. (La Perle & Dintzis, 2018).

Question 1

When it comes to the brain, are the neurosecretory cells located in the hypothalamus or the posterior pituitary gland or both?

Neurosecretory cells are found in the hypothalamus. (Source)

There are two types of neurosecretory cells: magnocellular cells and parvocellular cells. Magnocellular cellsare large cells, having long axons that terminate in the neurohypophysis (also known as the posterior pituitary). Magnocellular cells release the hormones vasopressin and oxytocin to the general circulation; we will talk about the physiology of these hormones in Conjoint 403.  The parvocellular cells are small cells, with shorter axons that terminate at a capillary-rich bulge at the base of the hypothalamus known as the median eminence.

Question 2

Is the hypothalamus and the posterior pituitary gland classified as neuroendocrine glands...

No

...and is the anterior pituitary classified as an endocrine gland?

Yes.
The following is from: https://courses.lumenlearning.com/boundless-ap/chapter/the-pituitary-gland
(emphasis mine)

The posterior pituitary (or neurohypophysis) comprises the posterior lobe of the pituitary gland and is part of the endocrine system. Despite its name, the posterior pituitary gland is not a true gland; rather, it is largely a collection of axonal projections from the hypothalamus that terminate behind the anterior pituitary gland.

The pituitary gland is an endocrine gland, about the size of a pea, that sits in a small, bony cavity at the base of the brain whose secretions control the other endocrine glands and influence growth, metabolism, and maturation.
While the pituitary gland is known as the master endocrine gland, both of its lobes are under the control of the hypothalamus: the anterior pituitary receives its signals from the parvocellular neurons, and the posterior pituitary receives its signals from the magnocellular neurons.
The anterior pituitary, also called the adenohypophysis, is a major organ of the endocrine system, and is the glandular, anterior lobe of the pituitary gland.
The anterior pituitary gland secretes 7 hormones: follicle stimulating hormone, luteinizing horomone, adrenocorticotropic horomone, thyroid stimulating horomone, prolactin, endorphins, and growth hormone.
The posterior pituitary gland does not synthesize any hormones.  Hormones known as posterior pituitary hormones are synthesized by the hypothalamus, and include oxytocin and antidiuretic hormone (ADH), also called arginine vasopressin or vasopressin (Liu, 2007). The hormones are then stored in neurosecretory vesicles (Herring bodies) before being secreted by the posterior pituitary into the bloodstream.
With regard to neurohormones mentioned in question 3, neurohormones are hormones that are produced by neurosecretory cells and released by nerve impulses (e.g., norepinephrine, oxytocin, vasopressin).
This is the part which can be confusing. Whilst ADH and oxytocin are released from the posterior pituitary gland, which is an endocrine gland, the hormones are produced by neurosecretory cells within the hypothalamus and they are stored in and released from neurosecretory vesicles within the posterior pituitary gland. Therefore they are classed as neurohormones.
References
Gore, A. C. (2013). Neuroendocrine systems. In Fundamental Neuroscience (Fourth Edition) (pp. 799-817). doi: 10.1016/B978-0-12-385870-2.00038-X
La Perle, K. M. D., & Dintzis, S. M. (2018). Endocrine system. In Comparative Anatomy and Histology (pp. 251-273). Academic Press. doi: 10.1016/B978-0-12-415759-0.00058-3
Liu, K. D. (2007). Hyponatremia and Hypernatremia. In Critical Care Secrets (Fourth Edition) (pp. 285-290). doi: 10.1016/B978-1-4160-3206-9.10044-8


What does "count in gene set" mean? I am trying to understand the analysis generated by STRING.
In analysis for biological processes table, there is a column titled "count in gene set." This gives a value for example "68 of 498".

What does this refer to?

It means the software has 4753 genes it has labeled with "biological regulation" and the short list you gave has 45 of those genes.  That is a little higher than you might expect by chance if you'd given a random gene list of the same size.


By what physiological mechanism do we not feel microbes (bacteria, etc.) living on our skin? Background
I know our bodies have a handful of ways to threshold our awareness of sensory stimuli:

Neural density

Sensory acuity
I assume really tiny stimuli could fit between receptors

e.g., Oaklander (2001) found nociceptor densities of 2-4000/mm2

Impacts summative abilities to surpass postsynaptic impulse thresholds

Varying thresholds of individual receptors.

Dubin & Patapoutian (2010), for example, show variations in classes of neurons based on their temperature (°C) and mechanical force (milli-newtons) thresholds (see thresholds listed in Tables 1 and 2).

Reticular formation involvement in regulating what we are consciously aware of

My question:

Which of the above physiological mechanism(s) are primarily responsible for our lack of sensation (or lack of conscious awareness) regarding microbes on our skin?

Update: My question is explicitly about physiology. Regardless of the impacts, benefits, evolution ,etc. of not feeling them, they're there. But even though we're covered in microbes, we don't sense them -- how not? I want to know by what physiological mechanism(s) we don't feel microbes on our skin.

Ask yourself, what benefit would it have?

Keep in mind you will always bee covered in them, this is the state you evolved in. Thus sensing them would serve no purpose, and sensory organs are expensive in terms of resources so why would we evolve a useless sense?


What is the mechanism of cytokine release syndrome in CAR T cells? CAR T cell administration results in cytokine release syndrome (CRS). But what is the mechanism that induces the CRS in CART therapy? Also, what factors correlate with CRS severity? CAR structure? Or tumor burden?

CRS in CAR T therapy is likely the result of hyperactivation of a large number of immune cells, either by antigen-specific/co-stimulatory activation (T cells) or by non-specific activation due to significantly elevated pro-inflammatory cytokines. CRS is the most prevalent adverse effect following CAR T infusion, but does not always happen. These two reviews provide a lot of detail, and reference many primary studies, but I will summarize briefly below:

1) http://www.nature.com/articles/mto201611

2) http://www.bloodjournal.org/content/124/2/188?sso-checked=true

In patients with CRS, it manifests clinically whenever maximal activation of the infused T cells occurs. From ref 1,

"In the setting of early CAR T-cell trials utilizing “first-generation” constructs (without costimulatory signaling elements), insufficient T-cell proliferation/cytokine production and lack of antitumor response were noted.30 The addition of costimulatory signaling in second-generation CAR design (CD28 or 41BB) translated to improved T-cell activation/expansion, cytokine production, and most notably dramatic antitumor responses in patients with hematologic malignancies.3,31,32"

So the 2nd-gen CAR design leads to better antitumor responses, but can also cause an intense burst of cytokine release that sets off a sort of 'chain reaction' wherein many other native immune cells also begin to massively release cytokines. One of the key pathogenic cytokines in this cascade appears to be IL6. From ref 2,

"Emerging evidence implicates IL-6 as a central mediator of toxicity in CRS...[]... IL-6R is cell associated on macrophages, neutrophils, hepatocytes, and some T cells..[]... High levels of IL-6, present in the context of CRS, likely initiates a proinflammatory IL-6-mediated signaling cascade"

and from ref 1,

"As an effective alternative IL-6 receptor (IL-6R) blockade with the Food and Drug Administration-approved mAb, tocilizumab has demonstrated near-immediate reversal of CRS.3,35 Investigators are now determining the effect of IL-6R blockade on CAR T-cell proliferation, persistence, and most importantly, antitumor effect. Despite this unknown, the use of IL-6R blockade has generally been accepted as front-line treatment for sCRS following CAR T-cell infusion.23,31,36"

Finally, it does appear that tumor burden has been correlated with CRS severity, presumably because of the higher antigen load available to activate the CAR T cells. From ref 1 and 2, respectively,

" It has been demonstrated that the degree of CRS severity is dictated by disease burden at the time of infusion as patients with high tumor burden experience a more sCRS.3,31,32"

"In recent reports of CRS following adoptive T-cell therapy for cancer,10,14,8,28 the incidence and severity of the syndrome also appears greater when patients have large tumor burdens, presumably because this leads higher levels of T-cell activation."

Hope this helps. Clearly there is a long way to go in terms of predicting and managing these adverse events.


What is SDS PAGE gel polymerization time? I am working on 20% SDS PAGE. I want to know optimum polymerization time for 20% resolving gel and 6% stacking gel. If I increase the time then would it affect the band pattern?

There is nothing like a general polymerization time, as this is a chemical reaction which depends on many factors. The most important are:

APS: Concentration and and the age of the chemical are important. APS decomposes over time when it is not stored completely dry (which it is not on most benches) and also with freezing thawing cycles in storage. APS provides the free radicals necessary for the reaction; without it no polymerization will happen. In my experience APS is the most critical part of the reaction, with old solutions making the polymerization really slow. I would make a stock solution, freeze it in aliquots. For making gels I thaw on aliquot and keep it in the fridge afterwards for a week and then discard it.

TEMED: Is the catalyst for the reaction, too much of it will start the reaction very fast.

Temperature: The warmer it is, the faster the polymerization will be. In the cold room you will not get complete reaction, if any.

What you can do is to store the remaining acrylamide in the beaker and wait until it is polymerized. Then your gel should also be ok to use. A longer polymerization time (assuming that your gel was completely polymerized before) will not change the resolving capacity of your gel.


How are constitutive enzymes regulated? I found that inducible enzymes can be regulated by many ways, but
I cannot find how constitutive enzymes are regulated...

A constitutive or "housekeeping" enzyme is usually defined as an enzyme whose expression level (amount of protein) is always constant, independent of any environmental factors. Hence, regulation of constitutive enzymes must be post-translational, for example allosteric regulation of the enzymatic activity by substrates or products.

Note that constitutive enzymes is mostly a theoretical concept. There are probably no enzymes whose expression is completely unaffected by any environmental factor.


Why myelin sheat does not cover the whole axon? Is there an optimal lenght for myelin sheats to be effective and lead potential across the nerve cell? This has always bugged me.

The nodes of Ranvier (the gaps between myelin sheath segments) speed up the action potential because the electric current can jump from node to node (or gap to gap). If the myelin covered the entire axon, the signal wouldn't have the gaps to speed up the signal. As for optimal length, the gap is 1μm long, but can be longer, on the order of millimeters depending on the type of cell. The length of the myelin doesn't matter so much as the length of the nodes of Ranvier because they are where the Na+/K+ channels are found so the ion exchange can occur. This is how an action potetial can occur, so the myelin not covering the entire axon is crucial for the ability of neurons to propagate a signal.


What is the name of the condition where no pacemaker cells are active in the heart for a short-time? Assume that the heart is beating, but no pacemaker cells are working for at least 15 seconds.
This would be a very long compensatory pause if extrasystole started it.
There may be some low frequent cells working at lower frequency (less than 10 Hz) but I do not understand what.

What is the name of condition where main pacemaker cells are not beating?
Main pacemakers are SA-node, AV-node and Purkinje-fibers/His-bundle.

Raoul is correct.
This is called asystole.
It is temporal in the above case.

My definition in research but note the difference to current Clinics so you do not get confused: Asystole is a state of no cardiac electrical activity from pacemaker cells when the conduction system and cardiomyocytes can be still functioning (so the case in my thread). The conduction system and cardiomyocytes of the ventricles are responsible for the bradycardia in my case for short-term.

What do you think about this case?
Some bradycardia?
Can you suspect asystole there between?

Please, do not make diagnoses based on just this picture (which is often the current standard).
Assume case where you see Time-Frequency of the heart perfectly and where you can see exactly the functioning of pacemaker cells at different frequency levels.

If there are no pacemaker cells active, no muscle contraction will occur. This condition is named asystole. It can be a temporary or definitive condition. Some would call it "extreme bradycardia" in temporary cases, but this is just an euphemism.

Edit:

Ok, so let's try to clear up the confusion a bit. Technically, there is no asystole involved here (not even temporary). This rhythm is regularly irregular (irregular, but has a pattern), while asystole has no pattern by its very nature.

What you are seeing here is not the consequence of low frequency firing from pacemaker cells. The supraventricular extrasystoles (every 3rd QRS complex) are a consequence of early ventricular depolarization not triggered by SA node activity. The P wave that would normally trigger the 3rd complex does in fact occur, but it is synchronous with the abnormal QRS complex, which is why you cannot see it. The compensatory pause is due to lengthening of the hyperpolarized state in pacemaker cells, and is a consequence of the addition of the hidden P wave and the extrasystole in a short time.

In conclusion, this pattern is not the result of delayed pacemaker firing, but of early depolarization of cardiomyocytes by an accessory pacemaker.

I have marked on this strip the maximal time interval of SA node hyperpolarization. Depending on when the P wave hidden in the extrasystole occurs, the real time may be shorter than the above interval.


Expression of bidirectional promoters How are bidirectional promoters expressed ? (Won't RNA Pol have to go in 3'-5' direction?)
Why are they more commonly found in eukaryotes than prokaryotes?

Genes controlled by bidirectionl promoters are in head-to-head configurations, meaning that their 5' ends are facing one-another.  Remember that DNA is double stranded, so this means one gene is on the 'top' strand and one gene is on the 'bottom' strand.  Check out the diagram below, genes are in capitals, bidirectional promoter in parenthesis.  Both genes are transcribed 5'->3'

                                         --> Gene 1
 5'-atgcagtcatga(ctgactaagt...tcagtcatga)CTGACTGACTAGTCAT-3'
    |||||||||||| ||||||||||||||||||||||| ||||||||||||||||
 3'-TACGTCAGTACT(gactgattca...agtcagtact)gactgactgatcagta-5'
      Gene 2 <--

As for why they are more commonly found in eukaryotes, those questions are definitely hard to answer.  It has been shown that genes on bidirectional promoters are expressed together more often than two genes that are next to each other on different promoters.  That means this might be a eukaryotic strategy similar to prokaryote's usage of polycistronic mRNA, an easy way to have similar expression patterns of genes that should often be expressed in similar amounts.


Lower affinity drugs longer time for pathways to rebound? Do lower affinity drugs take a longer time for pathways to rebound?

Affinity has to with strength of activating a receptor others options.

Do those with stronger affinities result in more likelihood to rebound?

This article is a good starting point for this question.

It states:
"The binding affinity, defined as the strength of these interactions, is translated into physico-chemical terms in the dissociation constant (Kd), the latter being an experimental measure that determines whether an interaction will be formed in solution or not."

The dissociation constant is explained fairly well by Wikipedia.
So, the higher the affinity of a drug with it's target, the stronger it binds.

I'm assuming that by "rebound" you mean that the pathway will regain its ability to function normally.

When someone takes a quantity of a drug, it disperses throughout the body. At any given time, at any given point in the body there is some concentration of the drug. If the affinity of the drug to it's target is very high, lots of molecules will bind to the target, whereas with a low affinity drug, fewer molecules will bind.

As time goes on, the body will filter out some of the molecules, and the remaining drug molecules will diffuse to fill the space where the filtered molecules were located. As this process continues, the concentration of the drug will decrease, lowering the dissociation constant of the drug-target equation, which means that fewer of the molecules will bind, and some of the bound molecules will be released to maintain equilibrium. The longer this process continues, the closer to "normal" the pathway will become, until the concentration of the drug is negligible.

Keep in mind that all of this is dependent on the rate at which the body eliminates the drug (and how quickly the drug degrades on it's own). See here for equations and such. While concentration of the drug is a large factor in it's effects, the half-life of the drug may be a better indicator of how long it takes for a pathway to rebound than affinity of the drug. For that matter, affinity is probably a factor in the length of a drug's half-life.


Why's there no vaccine against Respiratory Syncytial Virus (RSV)? RSV was discovered in 1956. Here’s why we can’t rush a COVID-19 vaccine | AAMC

Respiratory syncytial virus (RSV): This pervasive respiratory virus has proven resistant to vaccination. Children treated with one vaccine in the 1960s developed an  enhanced form of the disease, suffering high fever, bronchopneumonia, and wheezing. Many were hospitalized and two died.
“That set the field back years,” Poland said, as researchers and manufacturers “were afraid” to try again.
Researchers have since tried but still not developed an RSV vaccine for public use, according to the CDC. Babies at particularly high risk for RSV are sometimes injected with an antibody to help fight off infection.

I don't grasp the Canadian government's Overview of the respiratory syncytial virus vaccine candidate pipeline in Canada, CCDR 46(4). E.g. so what if "amino acids do vary in prefusion specific epitopes"?

Challenges to RSV vaccine development
Antigen diversity
A successful vaccine candidate will account for the diversity of antigens presented by RSV in the form of the structural variability of the proteins on the surface of the virus. The protective, neutralizing antibody response to RSV is dominated by antibodies targeting the prefusion F protein on the surface of RSVFootnote 17Footnote 18. Although the genetic sequence of F does not vary substantially between strains of RSV [89% of its sequence is identical in both A and B strainsFootnote 19], amino acids do vary in prefusion specific epitopes [bolding mine]. As new products are authorized and make it into broad usage, it will be critical to understand the sero-epidemiological responses at a population level to understand whether prefusion or postfusion antibodies are dominant responses, and whether these demonstrate equivalent protection against both RSV type A and B.
RSV infection dampens the immune response
[...]
There are no clear correlates of protection
[...]

In answer to the specific question,
This paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741363/ is the one the review was talking about.

The epitope that is targeted (the F protein) varies between strains, so a produced vaccine would only work on that strain. The protein (an obvious vaccine target) was selected because it exists on all strains, and is needed for the virion to fuse with the human cell.

In the vaccine The F protein epitope is fused with an immunostimulatory particle to get a good immune response. That's why they mention "prefusion" and "postfusion". There is confusion in the terminology because the F protein is so-named because of its role in fusing the virion to the cell.


Needle-like crystals observed in wild-grape wine under microscope. Potentially harmful? I recently crushed and strained about thirty pounds of wild grapes to ferment into wine. About a month in, I did a visual inspection of the wine under microscope to try and identify some yeast and bacteria species. However I was more taken by the sight of many sharp, needle-shaped crystals in the wine (along with microbes). Pictures are below:

My best guess is that they are raphides (crystals of calcium oxalate/carbonate), a supposed defense mechanism of some plants. These seem to be complicit in causing acridity in certain plants, and indeed the grapes (and resultant wine) were extremely tart. I've not, however, heard of any wild grape species having known toxicity.

My question is, then: are any wild grape species known to produce such crystals and, if so, are they known to be harmful in any way? Is there another explanation?

you are correct that these grapes have raphides. After doing some research, I found out that the grape raphides are twinned crystals. Raphides can cause much irritation for many herbivores (therefore, it is a protection mechanism) but less so for humans. In grapes, however, the irritation is much less than other raphide-containing species. This probably has to do eith the fact that it has a twinned structure (this is what I think, but I haven't found any research on this).

As a side note, what you have done is known as a whole mount, in which is entire organism specimen is placed on the slide, usually after crushing. It is a geeat way to examine the contents of the cell vacuole, which is where this raphides are commonly found.

References:

http://www.ncbi.nlm.nih.gov/pubmed/10648203
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091341


What happens to the enzymes produced by the digestive system? Our digestive system produces a lot of enzymes and they help to catabolize the food, and after completing their work are they excreted out or as they are also made up of proteins are they catabolized and assimilated back?

The answer is autodigestion fascilitated by denaturation of the digestive enzymes.
EVIDENCES OF AUTODIGESTION OF THE DIGESTIVE ENZYMES
1.The concentration of digestive enzymes is found to decrease from the small intestinal ileum to the large intestine.

There is a general trend to a decrease in the enzyme concentration the furthur down in the intestine the samples have been collected inspite of a concentration of the intestinal content in the same direction (see Figure1).This fact must indicate that the enzymes are partly inactivated or autodigested in the lumen of the small intestine.[pg 1529].

2.Essential amino acids have been found in the small intestinal lumen even if the food ingested didnot contain them which suggests that their source was the hydrolysed digestive enzymes which would eventually be re-absorbed in the small intestine to prevent their loss from the body.

Amino acids from dietary digestion are not alone, because the ingestion of food-even non-nitrogenous food-stimulates the digestive tract to secrete endogenous protein, derived from the sloughing of intestinal cells and used up digestive enzymes. These recycled proteins are a rich source of essential amino acids.Studies by Nasset show that regardless of the amino acid mix of the meal, the intestinal tract maintains a remarkably similar ratio of essential amino acids.[source]


Manufacturing of Bio Molecules Can we Manufacture bio molecules say e.g. the simplest Sugar, C12,H22,O11 the way we do with any other mechanical component. So, we know all about the Structure and arrangement of Atoms in Sugar - so do the design send the commands to the manufacturing machine which will use C,H and O elements and put them in them specified order !

If it's not doable today, what's the reason? -
1. Our lack of understanding of the Structure of Sugar atoms  or
2. The specialized method which will put nascent atoms into the configuration of Sugar. Are people anywhere in the world trying to work this way? Please give references.

There are literally millions of biomolecules.  Some of them we know the structures and chemical properties of others we know nothing about.   I'm going to focus on sugars.  It would be too broad a question probably even to list all biomolecules, much less describe how their chemical synthesis would be performed.

The good news is that industrial manufacturing of biomolecules is done for thousands of compounds and even available.  Certainly chemical synthesis of sugars is possible and even available but is very expensive and often produces side products compared to fermentation processes or extraction from plants say.

Sugars, for instance glucose are very similar, but if you look at this structure you will see that the four OH (alcohol) groups could point up or down.  Any manufacture of glucose would have to get each one of these bonds exactly right.  This is D-glucose, which is commonly available as extracted with water from sugar beets and sugar cane.  I can buy 10 pounds of it at the store for less than $10.

Compare with L-glucose, which is synthesized by a chemist.  Its available (though not really recommended for human consumption because its got impurities and doesn't necessarily pass FDA definitions of purity to be a food) at the cost of $87 per gram.

So the answer is probably best put like this: who would pay \$87,000 for a bag of sugar when they could pay $10?  Cases where one would have to pay a company to produce a biomolecule, its going to cost...


How are melatonin levels measured in humans? I'm wondering how it is possible to measure diurnal variations of melatonin levels in humans. I keep reading that there should be a large difference in amplitude between melatonin levels measured at night and in the middle of the day.

Have there been any studies of melatonin levels in humans where I can take a look at the methods they used for this kind of testing and/or see sample results?

On the analytics of melatonin I have here a german language text by the RKI with references. Translated quote:

  Assay of melatonin is done by serum or sputum using RIA or ELISA.
  Alternatively, to infer the nightly amount of melatonin secretion it
  is possible to look for the melatonin catabolic metabolite 6-hydroxy
  melatonin sulfate (6-OHMS) in urine.[1,2] ... standardized
  conditions of sample taking are a must to get good results.[3,4]

Ref.:

P. Levallois, M. Dumont et al: Effects of electric and magnetic fields from high-power lines on female urinary excretion of 6-sulfatoxymelatonin. In: American journal of epidemiology. 154, 7, October 2001, 601–609. PMID 11581093
D. H. Pfluger, C. E. Minder: Effects of exposure to 16.7 Hz magnetic fields on urinary 6-hydroxymelatonin sulfate excretion of Swiss railway workers. In: Journal of pineal research. 21, 2, September 1996, 91–100. PMID 8912234
E. Gilad, N. Zisapel: High-affinity binding of melatonin to hemoglobin. In: Biochemical and molecular medicine. 56, 2, December 1995, 115–120. PMID 8825074
D. K. Lahiri, D. Davis et al: Factors that influence radioimmunoassay of human plasma melatonin: a modified column procedure to eliminate interference. In: Biochemical medicine and metabolic biology. 49, 1, February 1993, 36–50. PMID 8439449


What is the scientific name of this parrot? I found this parrot at Nehru Zoological Park which is located in Hyderabad city of India.It's head to tail length is between 30cm-35cm.Can anybody tell me the scientific name of this parrot?

Looks like a male plum-headed parakeet (Psittacula cyanocephala)

wiki: the plum-headed parakeet


How can bats hear such high frequencies? I attended a talk that glossed over some biology as it was talking about a certain protein. The speaker mentioned humans can hear up to, often less than 20kHz frequencies, whereas bats can hear up to 100kHz. Presumably this is to do with differences in cochlear anatomy.

What about the inner ear of bats is different form ours, and how does this allow them to hear such high frequencies?

Short answer
Echolocating bats have relatively large sensory epithelia in their inner ear, that may correlate with their high upper frequency limit of up to 200 kHz. The basilar membrane is thinner and stiffer, possibly allowing it to decode higher frequencies.

Background
In terms of the place theory of hearing, the cochlea acts as a frequency transformer, where high frequencies are encoded basally, and low frequencies apically. The cells responsive to sound, the hair cells, are located along the basilar membrane (BM). Going from base (high frequency) to apex (low frequency), the BM becomes wider and less stiff, making it more susceptible to encode low frequencies apically. Note that sound is encoded as a travelling wave, where the point of resonance of a particular frequency corresponds with the characteristic frequency of the hair cells (Fig. 2).

Fig. 1. Rolled out cochlea. Source: New York University.

Fig. 2. Travelling wave and resonance frequencies along the basilar membrane. Source: University of Minnesota.

A study in Microchiroptera species revealed that the basal part of the basilar membrane was relatively narrow and stiff, which increases the resonance frequency of the basal part of the BM and hence may allow it to encode higher frequencies in these bats (Pye, 1966).

Because the high frequencies are encoded basally, it would be tempting to speculate the basal region would be enlarged in echo locating bats. Although this is true in some species, it may have more to do with frequency sensitivity than the upper limit of hearing, simply because a larger surface of the BM allows for more exquisite resolution of the BM. Although there is a tendency for larger BM lengths in echolocating bats, it is not consistent (Davies et al., 2013).

The human BM is 33.5 mm, while the BM of the bat with the highest frequency limit known (200 kHz, Hipposideros bicolor) is only 9.13 mm. However, compared to that of acoustically unspecialized mammals of a similar body size, e.g. Sorex araneus (BM length 4.4 mm) and Mus musculus (BM 7.0 mm) it is relatively long. However, as said, other bats with lower upper-frequency limits have longer BM lengths, e.g., Pteronotus parnellii (13.2 mm) and Rhinolophus ferrumequinum (16.1 mm). Indeed, the BM length has been correlated both with an extension in frequency range as well as enhanced frequency resolution (Dannhof & Bruns, 1991).

References
- Dannhof & Bruns, Hear Res (1991); 53: 253-68
- Davies et al., Front Zool (2013); 10: 2
- Pye, J Morph (1966), 118: 495-510


Can a pyruvate reaction to acetyl coA be called as acetylation in any way? Can the oxidation of pyruvate to acetyl coa be called as acetylation in some ways?
Please include credible sources in the answer.

Acetylation is defined as1:

  Acetylation (or in IUPAC nomenclature ethanoylation) describes a reaction that introduces an acetyl functional group into a chemical compound.

So, any reaction in which an acetyl (CH3CO-) group adds to another compound is an acetylation reaction. A common example is Friedel-Crafts acetylation reaction:

If the reaction is catalyzed by pyruvate dehydrogenase: In this case, first of all the reaction that you refer to is termed as pyruvate decarboxylation (rather than oxidation, although it won't hurt either). As @WYSIWYG has said in comments, it is not a simple reaction, it involves three steps (+ 2 steps for regeneration of complex), each catalyzed by different enzymes. The name given for the whole complex is pyruvate dehydrogenase complex (PDC)2. The steps involved are3:

The keto carbon of pyruvate reacts with the carbanion of TPP on E1 to yield an addition compound. The electron-pulling positively charged nitrogen of the thiazole ring promotes loss of CO2. What remains is hydroxyethyl-TPP.
The hydroxyethyl carbanion on TPP of E1 reacts with the disulfide of lipoamide on E2. What was the keto carbon of pyruvate is oxidized to a carboxylic acid, as the disulfide of lipoamide is reduced to a dithiol. The acetate formed by oxidation of the hydroxyethyl moiety is linked to one of the thiols of the reduced lipoamide as a thioester.
The acetate is transferred from the thiol of lipoamide to the thiol of coenzyme A, yielding acetyl CoA.

Now, pyruvic acid has the formula: $CH_3-CO-COOH$. So, if you look at the step C of reaction, then since CH3CO- has been added to coenzyme A, hence, in a way, it would be considered an acetylation reaction. Pay attention that the complete reaction will not be considered acetylation, only a part of it would be. This is also the reason why calling the complete reaction as oxidation won't hurt, because even decarboxylation is just a part of complete reaction.

If the reaction is not catalyzed by pyruvate dehydrogenase Taking the question out from pyruvate dehydrogenase (as you don't talk specifically about that), there is an enzyme Acetyl-coA synthetase whose job is catalyzing acetylation of coenzyme-A(!)4. The reaction looks like this:

$ATP + acetate + co-A \rightarrow AMP + pyrophosphate + acetyl-coA$

The enzyme is of two types: AMP forming and ADP forming5:

So, as long as the conversion is not one specifically catalyzed by pyruvate dehydrogenase, we can say that Yes, conversion of coenzyme-A to Acetyl-coA is an acetylation reaction.

References:

Acetylation - Wikipedia
Pyruvate Dehydrogenase - Wikipedia
Pyruvate Dehydrogenase and Krebs Cycle - Joyce J. Diwan; Rensselaer Polytechnic Institute
Acetyl-coA synthetase - Wikipedia
Hentchel KL, Escalante-Semerena JC. 15 July 2015. Acylation of biomolecules in prokaryotes: a widespread strategy for the control of biological function and metabolic stress. Microbiol Mol Biol Rev doi:10.1128/MMBR.00020-15


Unable to identify a muscle of the anterior thorax I was watching an YouTube Anatomy Video which goes over the major muscles of the anterior superficial thorax. There is a structure present throughout the video which goes unmentioned, and I can't seem to identify.

It is shown as a pair of structures, each running from the manubrium to the xiphisternal junction along the lateral margin of the anterior sternum, perhaps with a second head attaching to the costal cartilage.

I'm probably missing something obvious, but for the life of me I can't think of what that could be.

This appears to be the sternalis muscle. The reason it is not mentioned may because it is not present in all individuals, and is therefore relatively poorly characterised.

The image is from An Atlas of anatomy by regions by John Charles Boileau Grant.

Another image of the muscle can be found in Pocket Atlas of Human Anatomy by Thieme:


The effects of auto-brewery syndrome Why are some people affected so differently by auto-brewery syndrome differently if the syndrome seems to be caused by the single organism saccharomyces cerevisiae? It is known that the syndrome has been used to waive DUI charges — like most recently for this New Yorker whose blood alcohol level was 0.4 but she had none of the usual symptoms of intoxication, even though she had ingested alcohol earlier that day. She also carried out most of her daily activities normally, even with high levels of alcohol in her system.

On the other hand, there was another case where the carrier experience the effects of auto-brewery syndrome differently:

  Cases involving the yeast Candida albicans and Candida krusei have
  popped up in Japan, and in 2013 Panola College Dean of Nursing Barbara
  Cordell documented the case of a 61-year-old man who had frequent
  bouts of unexplained drunkenness for years before being diagnosed with
  an overabundance of Saccharomyces cerevisiae, or brewer's yeast, the
  same yeast used to make beer.

The quote can also be found at the link of the CNN article.

Could the difference in symptoms and effects due to variations in how the carrier bodies could deal with the overabundance (maybe depending on age, gender, or ethnicity) or are they attributed to variations in the nature of the yeast?

The gut microbiome is extremely complicated, and almost anything related to it is only partially known, therefore prone to oversimplification. Trying to explain the phenomenon of gut fermentation syndrome in such a limited fashion (age, gender, ethnicity, quantity of one particular yeast, etc.) will not help us understand it.

  Common yeasts (C. albicans, C. tropicalis and Torulopsis glabrata) and Saccharomyces cerevisiae are able to ferment sugars through the homolactic, heterolactic or mixed acid fermentation pathways, with ethanol as the major end product.

Candida is a very common yeast found in the environment and in and on our bodies wherever it's warm and moist (therefore the GI tract.) Candida species are the most common cause of invasive fungal infections in humans (followed by Cryptococcus and Aspergillus) and can involve any organ. Yet it's omnipresence does not result in clinically recognized cases of ethanol intoxication in even a minute fraction of people who carry it in their gut.

Case reports started appearing in the literature starting in 1972, yet it is still a rare event to see one. In 2001, the case of a 13 year old girl was published. She had short gut syndrome and became intoxicated after ingesting carbohydrates. She had been placed in a rehabilitation facility with no access to alcohol, but still had positive blood alcohols. Aspirates from her small intestines grew Candida glabrata and Saccharomyces cerevisiae. Short-gut syndrome is complicated.

We have no idea how common fermentation into alcohol is in the gut, or what the results are, but it is probably far more common than recognized, can probably result in effects other than intoxication (for example fatty liver disease in non-drinkers), and probably has a role in other illnesses.
It's complicated:

  Carbohydrate metabolism by gut microorganisms is a central process allowing supply of nutrients and energy to the host. This fermentative process is complex and involves several functional groups of bacteria with complementary metabolic activities that interact to ensure the biotransformation of polymers (resistant starch, nonstarch polysaccharides, proteins, mucins…) into end-products (mainly short chain fatty acids and gases). Hydrolytic communities transform complex substrates into smaller fragments that can also be used by other bacterial groups unable to hydrolyse polymers. Other microbial cross-feeding interactions are related to the utilisation of fermentative products such as succinate, lactate or hydrogen and involve specific groups of microorganisms.

All we know is that it happens in some people, and that it can respond to antifungal treatment and some probiotic supplementation. "Why" is still a mystery, and speculation only.

Gut fermentation syndrome
Invasive Fungal Pathogens: Current Epidemiological Trends
IwataK., “A Review of the Literature on Drunken Syndromes Due to Yeasts in the Gastrointestinal Tract,” University of Tokyo Press, Tokyo, 1972, 260-268. Not available online
Functional dysbiosis within the gut microbiota of patients with constipated-irritable bowel syndrome
Obesity and female gender increase breath ethanol concentration: potential implications for the pathogenesis of nonalcoholic steatohepatitis


What does it mean by “end effects can be ignored” I have been reading a book ( Statistics for Biology and Health) and i encountered many of following bold text.

Consider a long DNA sequence of length N, where N is assumed to be
so large that end effects can be ignored in our calculations.

In Shotgun sequencing also the saw similar thing :

The fragments are assumed to be taken at random from the original
full-length sequence, so that if end effects are ignored, the left-hand ends
of the fragments are independently distributed with a common uniform
distribution over [0,G].

What does " end effects can be ignored " means?

They are considering a model of a DNA sequence of quasi infinite size. They consider a case where the DNA sequence is so long that the fact that it has ends will only negligibly affect the conclusions of their model. This is likely the same as considering the DNA is circular.

To give you a similar logic, imagine a species where individuals live in different populations. All population can be placed on a one dimensional axis. The migration rate from one population to the neighbouring population is 0.1 (this is called a "stepping stone model" btw). Hence, the probability of not migrating is 0.8 (1 - 0.1 - 0.1). I can draw conclusions from such a model but it would be important to specify that I neglected the end effects and hence, I assumed there are a lot of populations (or that the population form a loop). Why did I neglect the end effects. The last population on each side cannot have a migration rate of 0.1 toward a population that does not exist. Hence, their migration rate must differ from the other populations. This is commonly called edge effects (rather than "end effects")


Identification of red, plum-like fruit (probably from Southern Russia) My parents are currently on a holiday in St. Petersburg (Russia). They sent me this photo of plum-like fruits they bought on a market there (toilet paper for scale, I guess).

The fruits are 20-30mm long, have a big stone, taste sourly like red currant (based on my fathers opinion) and are supposed to come from Southern Russia (don't know where this information is coming from).

Can you please help to identify them?

Can't be certain from the picture, but they look a lot like Cornelian Cherry (Cornus mas: https://en.wikipedia.org/wiki/Cornus_mas ).  However, the ones in my garden (western US) don't ripen until late September/October.

Perhaps they could return to the market, and ask for the Russian name?


Does the amplitude of action potentials vary among species? I would like to ask if the amplitude of action potential in animals(for example zebra finch or other bird) differs from the amplitude of action potential in humans which is approximately 70mV.

Does the amplitude of action potential in animals differ from the amplitude of action potential in humans?

Surprisingly, they don't!

The current model that's used to describe biophysical neurons is the Hodgkin-Huxley model, and one of its fundamental assumptions is that, action potentials (APs) are electrical events consisting of a large transient change in membrane polarization (typically around 100 mV). (source)

The reason for this can be seen when quantifying the absolute value of peak conductance during an AP, specifically when considering the average membrane resistance with respect to peak conductance. The following graph is from the original publication by Huxley & Hodgkin, just here, and it illustrates this principle.

This model applies to virtually all excitable cells, and therefore, AP amplitude values aren't specific to the organism. Consider the following table which lists AP measurements amongst various animals, and pay notice to the values in the highlighted column. As can be seen, amplitude values remain fairly consistent across all animal types, hovering right around 100mV. (source)

And then, regarding humans, just as you stated, the resting potential of a neuron is ~ -70mV. When excited, the membrane potential rises to ~ +30mV.

  Most cells in the body make use of charged particles, ions, to build up a charge across the cell membrane. ... The exact value measured for the resting membrane potential varies between cells, but -70 mV is most commonly used as this value. ... The change in the membrane voltage from -70 mV at rest to +30 mV at the end of depolarization is a 100-mV change.

(source)

If you're well versed in math, you can directly compute the ~100mV change in membrane potential using the Goldman/Hodgkin/Katz equation, given that inter & extra cellular ion concentrations are known.


Why 20 amino acids instead of 64? This question got me thinking about amino acids and the ambiguity in the genetic code. With 4 nucleotides in RNA and 3 per codon, there are 64 codons. However, these 64 codons only code for 20 amino acids (or 22 if you include selenocysteine and pyrrolysine), so many of the amino acids are coded by multiple codons.

Is there any hypothesis as to why there are only 22 amino acids and not 64? Is it possible that there were 64 (or at least more than 22) at an earlier time?

Brian Hayes wrote a very interesting article from a mathematical point of view:

http://www.americanscientist.org/issues/pub/the-invention-of-the-genetic-code

especially the "Reality intrudes" section. Basically people had created fancy mathematical reasons why it has to be exactly 20. Nature, being nature, does not follow the reasoning, but has its own ideas. In other words there was nothing especially special about 20. In fact there seems to be a slow grafting of a 21st amino acid, selenocysteine using the codon UGA. Also pyrrolysine is considered the 22nd. The last section suggests that the code was originally doublet, so coded for <16 amino acids. This can partly explain why the third base in each codon is not as discriminating.

So perhaps in the year 2002012 someone will be asking on biology.stackexchange why there are only 40 amino acids.


Where would Saccharomyces cerevisiae be found in highest concentrations in environment? I have bakers asthma specifically to 'Sc' yeast, and know to avoid bakeries, breweries, etc...

I have figured out to not disturb rotting leaf piles, and fermenting bark mulch. Where else?

What percentage higher are concentrations in say Florida, as opposed to New York state?

Here is a link to an interesting article which reports a survey of wild isolates of Saccharomyces cerevisiae in China.

  Wang, Qi-Ming, et al. (2012) Surprisingly diverged populations of Saccharomyces cerevisiae in natural environments remote from human activity. Mol Ecol 21: 5404-5417

A relevant quotation from the article:

  In addition to grapes and oak tree (Quercus spp.) bark, S. cerevisiae was successfully iso-lated from a variety of damaged fruit collected in orchards or markets in different provinces of China; from the bark of different deciduous trees; forest soil and rotten wood collected in primeval, original secondary and planted forests located in different regions covering temperate, subtropical and tropical climate zones from northern to southern China. Unexpectedly, the success rate of S. cerevisiae isolation from fruit samples (6.5%) was lower than that from tree bark (16.5%), soil (10.8%) and rotten wood (9.2%) samples. S. cerevisiae was more frequently isolated from forest soil samples (success rate 13.7%) than from orchard soil samples (success rate 9.1%). Among the fruits giving positive S. cerevisiae isolation, grape samples showed the lowest success rate.

Table S2 in the supplemental information records isolates as follows:

climatic zone    sites   isolates
__________________________________
tropical           5       20
subtropical        2       14
temperate          13      51

Superficially, from this it looks as if there would probably be little difference between New York state (humid, continental) and Florida (humid, subtropical).


How to read this DNA inversion diagram? In the following diagram about chromosome inversion, I don't understand:

Why do we need to take the reverse complement from step 1 to 2? Isn't inversion just reversing the bases in the region?
How is the bottom diagram derived? For example, where does the ACCCCACTC come from? I thought it should be: GACTGCCGT for 5'→3' and CTGACGGCA for 3'→5' (inversion of the sequences in the second step).

http://web2.mendelu.cz/af_291_projekty2/vseo/print.php?page=315&typ=html

Your misunderstanding probably stems from the differences of definition of inverse in bioinformatics (reverse) and cell biology/genetics.

What is shown in the picture is chromosomal inversion, in which the segment of DNA gets cut, flipped and ligated. Note that in the DNA, 5' would be ligated to 3' and vice-versa. So the 5' of the bottom strand i.e. T is ligated to the 3' of the top strand i.e. C. Similarly for the other ends. Therefore, you see a reverse complementation.

The sequence of the top strand however should have been 5'-TTAC-TGCCGTCAG-TAG-3' which has been incorrectly shown as 5'-TTAC-TGGGGTGAG-TAG-3'. That is a mistake in the picture.

Have a look at this picture [1]:

[1] Okamura, Kohji, John Wei, and Stephen W. Scherer. "Evolutionary implications of inversions that have caused intra-strand parity in DNA." BMC Genomics 8.1 (2007): 160.


How Do White Blood Cells Learn? Or Do They? So I get the concept that a vaccine is a weakened form of a virus so that the body can "learn" to fight it and make a person immune to that disease, but how exactly does this learning take place? What learns? The white blood cells? Do they have their own database or something and do they go from cell to cell informing them of what they learned? I read that they only last around 5 to 7 days so that means there's constantly new white blood cells that also need this information for all diseases ever encountered. How does this work? Thanks!

So while some kind of a biological database might have been an evolutionary option, the way we evolved is different from this. Rather than 'planning' what diseases could be recognized in the environment and recording this, our bone marrow constantly pumps out naive B and T cells that have a randomized receptor on them. The effect of this is that every new B and T cell that your bone marrow makes will recognize a unique, random protein sequence, and you will have billions of these cells floating around in your blood circulation at any given time. These cells however will only float around in circulation for a short period of time before dying and being replaced by other cells with new random sequence receptors.

When you get a vaccination, you are injecting in specific protein sequences from a specific pathogen. As these injected protein sequences circulate through your blood they will eventually bump into a B or T cell that has a receptor that recognizes them. When this happens, the B or T cell will now start to divide and give rise to long lasting memory cells that express the exact same receptor and will therefore recognize the exact same protein sequence again in the future. These cells will float around in your blood for most of your life and make you 'immune' to the recognized pathogen. When you get reinfected with the same pathogen or the pathogen to which you were vaccinated these memory cells will rapidly divide upon recognition of the pathogen and give rise to a large number of effector cells that eliminate the pathogen before it can 'make you sick'.

What is really cool about this is that because each T or B cell carries on it a receptor that recognizes a random protein sequence, you currently have in you B and T cells that would recognize a protein that does not even exist on Earth, but might exist on Mars or somewhere else in the Universe. This makes our immune system quite valuable because any protein that nature creates for all of time anywhere in the universe will still be recognizable by our immune systems.


How do trees lift water higher than 10 meters? The atmosphere pressure is 10 meters of water (approx). This means that it is impossible to lift water higher than 10 meters with vacuum or сapillary action (on Earth, under normal conditions).

There are trees higher than 10 meters.

How do they lift water to their tops?

UPDATE

In other words: how cohesion-tension theory can be true if it apparently contradicts the laws of physics?

UPDATE 2

Atmospheric pressure helps to rise the water, not resists rising. What is resisting is water weight. When water column is 10 meters high, then atmospheric pressure can't help anymore.

Any adhesion/cohesion mechanism can't help here too, because it acts only in thin molecular layer. To transfer action force further the pressure is required, which is insufficient at 10 meters.

UPDATE 3

If we had capillary small enough to rise water to 10 meters and then we will build smaller capillary which we expect will rise water higher, we will fail. Water column will break and does not climb higher than 10 meters.

Menisci acts like small piston and can't help rising water higher than 10 meters.

UPDATE 4

Common pressure distribution in capillary is follows:

$P_0$ is atmospheric pressure. As you see, right under menisci, the pressure is lowered by $2 \sigma / R$ where $R$ is the radius of menisci and $\sigma$ is surface tension. The entire term is called "Laplace pressure". As you see, it can't supersede atmospheric pressure, because water continuity will be broken in the case.

I.e. no any menisci can rise water higher than 10 meters.

The existence of higher trees PROVES that there are some other significant mechanisms, not adhesion/cohesion, not capillary.

UPDATE 5

Current version, as I understood it, is based on a declaration, that a water, if put into thin capillary, can behave like a solid body. Particularly, it can resist tension up to minus 15 atmospheres.

This is a tensile strength of concrete, so I don't believe that without additional proofs.

I think it is just not hard to make thin tube, put water into it and check, how high it can climb.

Was it done ever?

Disclaimer: This is not my field of research.

First, this is not a complete answer to our question. A nice explanation of the current hypothesis of water transport in trees (Dixon-Joly cohesion-tension theory, originally proposed 1894) can be found at The Amazing Physics of Water in Trees but also in Tyree (1997). The key points are that the stoma (leaf surface pores) are so small that the menisci can withstand huge water columns, that water has strong cohesive forces, and that water is transported using the negative pressure that is created by transpiration. The webpage linked above contains a beautiful visualization of how multitudes of stomata and menisci create strong negative pressures:

Second, much of the current discussion in the comments (an indication that the question might be a poor fit for Bio-SE?) revolves around the plausibility of the cohesion-tension theory, and specifically on whether water can sustain strong negative pressures. Caupin & Herbert (2006) review metastability and cavitation in water (in a physics journal), and contains experimental results on negative pressures in water. The paper references a large number of experiments under various experimental setups (I cannot fairly judge these). In their conclusion they state that:

  Among the countless cavitation experiments, only the ones with special care about water purity can reach large negative pressures; with a variety of techniques, they all obtain Pcav around −25 MPa at room temperature (see Fig. 3 (b)), which falls far away from the theoretical value (from −120 to −140 MPa). There is a notable exception: experiments with mineral inclusions achieve −140 MPa. The large gap between these data requires special attention.

So basically, the theoretical estimates lie at -130MPa and empirical results at -25MPa (-250 atmospheres), and water can clearly achieve large negative pressures. This would also mean that the current estimates are much larger than what is needed for the cohesion-tension theory to work (atmospheric pressure= 0.1MPa, negative pressure in water column at 50m ~ -0.5MPa).

They also have a section specifically discussing trees:

  7.1. Water in nature
  The law of hydrostatics teaches us that the pressure drop in a water column of 10.2 m is 0.1 MPa. This points out that negative pressures can be reached in the ascending sap of tall trees. In fact additional effects (viscous flow, drought) make the pressure in the sap negative even at smaller heights. The cohesion-tension theory, first proposed by Dixon and Jolly [56], explains that the sap column is held at the top by the meniscus in the pore of the leaves: by Laplace’s law, the meniscus curvature allows a pressure jump between the outside air pressure and the negative pressure in the sap. The trees thus contain large amounts of metastable liquids. Cavitation may sometimes occur, disrupting the liquid column and stopping the flow (xylem emboly). The complex hydraulic architecture of trees limits the damage, and strategies exist to refill the embolied xylem channels. Much work has been devoted to this topic, and is reviewed in Refs. [110,111].

There is also evidence that the risk of xylem embolism increases with tree height, and this creates a trade-off between water transport efficiency and structural adaptations to deal with embolism (Domec et al. 2008). This is for instance facilitated by the pit aperture diameter of tracheids, with apertures decreasing with height along a tree, causing increased resistance to embolism but at the same time lower water conductance. This will clearly limit the height of trees, and the paper indicates that the tallest Douglas firs are at the edge of what they can achieve.

Another recently published paper that should be relevant is 'Methods for measuring plant vulnerability to cavitation: a critical review' by Cochard et al. (2013), but I haven't had time to look closely at this. See abstract below:

  Abstract:
  Xylem cavitation resistance has profound implications for plant physiology and ecology. This process is characterized by a ‘vulnerability curve’ (VC) showing the variation of the percentage of cavitation as a function of xylem pressure potential. The shape of this VC varies from ‘sigmoidal’ to ‘exponential’. This review provides a panorama of the techniques that have been used to generate such a curve. The techniques differ by (i) the way cavitation is induced (e.g. bench dehydration, centrifugation, or air injection), and (ii) the way cavitation is measured (e.g. percentage loss of conductivity (PLC) or acoustic emission), and a nomenclature is proposed based on these two methods. A survey of the literature of more than 1200 VCs was used to draw statistics on the usage of these methods and on their reliability and validity. Four methods accounted for more than 96% of all curves produced so far: bench dehydration–PLC, centrifugation–PLC, pressure sleeve-PLC, and Cavitron. How the shape of VCs varies across techniques and species xylem anatomy was also analysed. Strikingly, it was found that the vast majority of curves obtained with the reference bench dehydration-PLC method are ‘sigmoidal’. ‘Exponential’ curves were more typical of the three other methods and were remarkably frequent for species having large xylem conduits (ring-porous), leading to a substantial overestimation of the vulnerability of cavitation for this functional group. We suspect that ‘exponential’ curves may reflect an open-vessel artefact and call for more precautions with the usage of the pressure sleeve and centrifugation techniques.


Where does the gluteus medius attach to the greater trochanter compared to the gluteus minimus attachment? Where does the gluteus medius attach to the greater trochanter of the femur  compared to the gluteus minimus attachment? Is it above, below, next to it, etc.? Ideally I'd like to know the distance as well and location relative to the greater trochanter.

What I have found so far: some diagrams place the gluteus medius attachment below the gluteus minimus attachment, some place it above and some place it next to it at the same height.

Example of diagram placing the gluteus medius attachment below the gluteus minimus attachment (image source (mirror)):

Example of diagram placing the gluteus medius attachment next to the gluteus minimus attachment (image source (mirror))

Example of diagram placing the gluteus medius attachment above the gluteus minimus attachment (image source (mirror)):

{1} greatly answers the question.

Regarding the insertion location (lateral view):

Note that unlike the gluteus minimus insertion, the gluteus medius insertion can also be viewed anterolaterally:

Table 2 contains more detailed insertion location data:

Regarding the insertion area:

  Gluteus maximus: Average Area, mm^2 (95% CI): 473.4 (381.0, 565.8). Thick, muscular insertion along the posterior femur on the linea aspera
  Gluteus medius: Composed of 2 contiguous rectangular footprints, the lateral facet oriented in the sagittal plane and the superomedial facet primarily in the transverse plane:

  Lateral facet: Average Area, mm^2 (95% CI): 141.1 (117.7, 164.5).
  Superomedial facet: Average Area, mm^2 (95% CI): 501.5 (442.8, 560.2).

  Gluteus minimus: Average Area, mm^2 (95% CI):  280.9 (229.3, 332.5). Two morphologies noted: The majority (11/14) were long, thin, and crescent shaped and ran medial to lateral and concave facing inferiorly, while a few (3/14) were bowtie in shape.

Below are some actual pictures of the gluteus minimus insertion, the gluteus medius insertion to get another sense of their shape and location. Still  from {1}, this picture shows the gluteus medius (but not the gluteus minimus):

From {2}, this picture shows both the gluteus medius muscle and the gluteus minimus muscle:

I also find this picture good to give a better sense as to where the greater trochanter is located with respect to the human body (image source (mirror)):

References:

{1} Philippon, Marc J., Max P. Michalski, Kevin J. Campbell, Mary T. Goldsmith, Brian M. Devitt, Coen A. Wijdicks, and Robert F. LaPrade. "Surgically relevant bony and soft tissue anatomy of the proximal femur." Orthopaedic journal of sports medicine 2, no. 6 (2014): 2325967114535188. https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Surgically+Relevant+Bony+and+Soft+Tissue+Anatomy+of+the+Proximal+Femur&btnG= ; https://www.ncbi.nlm.nih.gov/pubmed/26535335 ; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4555602/ ; https://doi.org/10.1177/2325967114535188
{2} Woodley, Stephanie J., Susan R. Mercer, and Helen D. Nicholson. "Morphology of the bursae associated with the greater trochanter of the femur." JBJS 90, no. 2 (2008): 284-294. https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Morphology+of+the+Bursae+Associated+with+the+Greater+Trochanter+of+the+Femur&btnG= ; https://www.ncbi.nlm.nih.gov/pubmed/18245587 ; https://doi.org/10.2106/JBJS.G.00257


View and plane/section of neural tube I have a question regarding the following image:

In my book, it states that this is a dorsal view which shows the formation of the neural tube. However, isn't this a caudal view of a transverse section? A dorsal and ventral view wouldn't apply to a transverse section right?

It looks like a dorsal view to me, like your book says.
It isn't a section at all, these are embryonic structures visible from the outside.
Maybe you are being misled by the orientation of the neuraxis differing among organisms? The head will develop at the anterior neuropore; the spine will develop down the middle. You are looking at what will be the back.
Here's another view from Gray's (downloaded from Wikipedia at https://en.wikipedia.org/wiki/Somite#/media/File:Gray20.png ):


Rabies in spiders - is it possible? What if we inject rabies virus into an insect body, like spider or a bee, will it contract rabies as humans, cats, dogs, racoons or bats do?

Rabies is a viral disease that causes inflammation of the brain. It is adapted to the nervous systems of vertebrates particularly mammals. Arthropods are too different for lyssaviruses to survive in their body.


How does cytochrome c oxidase inhibition cause cell death? I realise the inhibition of cytochrome c oxidase prevents the release of H+ ions into the intermembrane space, and that the ion gradient is required for ATP synthase action. However, I'm not sure how this causes cell death.

Does this:

a) Prevent oxidation of Cytochrome C, preventing electron movement the cytochrome bc1 complex, which in turn prevents electron movement from earlier parts in the chain, shutting down the electron transport chain altogether? Thus, no ATP is produced and the cell dies due to lack of ATP.

b) Prevent oxidation of Cytochrome C, but not preventing oxidation in the other protein complexes*, merely reduce the number of H+ ions available for ATP synthase action, lowering the amount of ATP produced, and the cell dies due to low ATP levels.

c) other.

I realise in either case, the ATP count is merely lowered, as ATP is produced by other methods, so my statement 'lack of ATP' is not totally explicit.

*This being the case, how are the released electrons dealt with by the cell? Are there electron acceptors to remove this?

Inhibition is rarely binary - it's almost always subjected to stoichiometric effects. So the answer could be either option, depending on the amount of the inhibitor present in the system. If there is a huge amount of the inhibitor in the cell, it may more or less completely ablate ATP production by the ETC.

On the other hand, if there isn't enough of the inhibitor to shut down all cytochrome C oxidase, you'd only see a reduction in the amount of ATP produced by the ETC (which could still be sufficient to kill the cell).

It also depends on the type of inhibition taking place. Is it reversible or does it bind permanently? Does it degrade quickly? These aspects are also important to consider.


What are fish seeds? I stumbled upon this term in a section called Induced breeding of Carps in an Applied Zoogy book.

  Traditional practice is to collect seed from the natural riverine habitatwhich also contain uneconomic,unwanted and predator fish species.

What are seeds? Does it mean zygote ?

Fertilized fish eggs are known as Fish seeds. In simple words, they are the baby fishes used for seeding new Ponds in fisheries.

They can be used in 4 stages:

Hatchling : Larvae stage where it have yolk sac hanging below from where it draws its nutrition for 2–3 days. It can't eat from outside as mouth is not formed yet!

Spawn: Stage where mouth is formed.

Fry: About ~2 cm long, now, it can eat small size zooplanktons!

Fingerling: About ~15 cm long. It is now becomes easier to transport these kinds of fishes to Ponds.

Source (Picture Credits) :

Pic 1. https://www.ucdavis.edu (https://www.ucdavis.edu/sites/default/files/images/article/trout_lg.jpg)
Pic 2. Wikimedia (https://upload.wikimedia.org/wikipedia/commons/f/fe/Anemone_Fish_protecting_it's_spawn.jpg)

Pic 3. Fishbio (http://fishbio.com/wp-content/uploads/2011/03/Oncorhynchus-mykiss-fry.jpg)

Pic 4. Deveron (http://www.deveron.org/wb/media/images/parr.jpg)


Where to put the gene after eukaryotic promoter for best expression levels? As far as I know there is an optimum distance between a promoter and the gene for the best expression levels. What is that distance for common promoters like CMV, SV40? If you have a first hand experience about this (e.g. if you have cloned the gene way downstream of the promoter and didn't/did see expression) and share it I will be grateful.

If you have comprehensive knowledge for other promoters please feel free to add them in the list too; they don't need to be common. I just want to hear people's experience on the subject.

I used pEYFP-N1 (stock vector) where the spacing between the CMV promoter and the EYFP start codon is ~88 nt, and the expression is high.

I also cloned a protein 5' of the EYFP, only 4 nt after the CMV promoter. The expression of this fusion was also high. Because I was only using the chimeric protein in experiments, I did not try to assess differences in EYFP expression.

If you look here: https://synbiota.com/projects/19/sequences you'll see the basic pEYFP-N1 vector and the separation between the CMV promoter and the EYFP coding sequence.

On wiki: "The TATA element and BRE typically are located close to the transcriptional start site (typically within 30 to 40 base pairs)."


Do trees in a forest generally grow in a lattice formation? The closest arrangement of trees in which they are at least a certain distance away from each other is a triangular lattice, much like a honeycomb. I wonder if you tend to see this sort of arrangement of trees in the wild?

I guess this would actually not be beneficial to the trees since it would mean they would all be lined up in certain directions which might not be good for sunlight etc.

I wonder if there is much research on the pattern of distribution of trees in a forest?

For most trees and plants, distribution is spatially highly variable. Thinking about the lifecycle of plants—their seeds are non-randomly dispersed, the seedlings and saplings grow in different biotic (neighboring trees, distance to herbivores) and abiotic (different soils, shading, etc.) environments, all the plants are at different life/size stages, and that they are highly plastic in their ability to have fluid morphologies in different conditions—it's really difficult to detect a clean lattice pattern with little variance.

Nevertheless, for some species of plants, where the conditions are right (e.g., very limited and highly sought-after resources, species poor areas, synchronicity of generations, strong antagonism), we see some evidence of regular patterns. Ecologists often analyze spatial distributions to see if they are random, clumped, or uniform/regularly distributed (link). We see some distributional uniformity that does resemble lattice-/tiling-like patterns, which you may find in the references from the link above. There is reference to only 1 tree species in that link :/ I can't say that I see ecologists looking for lattices explicitly, but I would be surprised if there isn't a subfield interested in it. HTH.


During human ageing, which immune cell sub-types are most affected? It is now well established that human ageing is accompanied by an increase in systemic, low-grade (chronic) inflammation, sometimes termed inflammaging (Franceschi, 2007). This is in part due to more global changes to the body, including an increased number of senescent cells, but of interest to me currently is the change in the composition of the circulating immune cell sub-types that may either cause, or be affected by, the increase in 'global' inflammation.

I imagine the answer to this question is a study that samples individuals of different ages and separates the various leukocyte fractions. Using this it could be determined which immune sub-types are over-/under-represented in the aged, and at what age the changes occur (e.g. monocyte numbers may decrease from age 40, whereas neutrophil numbers may increase...). I have done some fairly extensive research, but have been unable to find a study that has done this - however it seems likely that it has been performed. Thanks.

From my Immunology notes:

*Decrease in hematopoietic stem cells resulting in a reduction of Affector cells. Erythroid and myeloid progeny cells don't seem to be affected.

*Fewer pro-B cells, resulting in fewer affector B-cells.

*Lymphoid progenitors in the bone marrow and thymus mature.

*Lymphocytes in secondary lymphoid organs.

For the Innate system:

*Neutrophils have a reduced capacity for Oxidative bursts, Batericidal activity, and Chemotaxis.

*Macrophages have a reduced capacity for phagocytic activity, oxidative bursts, and MHC II expression (which impairs their ability to present antigen and initiate CD4 Helper T-Cell responses).

*NK Cells have a reduced capacity for Cytotoxicity, proinflammatory cytokines and chemokines,and proliferation in response to IL-2. However, the total number of NK cells increases.

The sources: Both clinical (it was at a teaching hospital) and Aging and Immune System, Chapter 33 of the class text: Cellular and Molecular Immunology


Measuring algae growth or death My daughter (10th grade) is doing a science fair project on the toxicity of triclosan for the algae Selenastrum capricornutum. She is wondering the best way to measure the effect, given the limited resources at the school.

Should she use the school’s UV/Vis spectrophotometer or just do low-tech cell counting?
If she uses the UV/Vis, does she have to do a calibration curve where she manually counts the cells for some number of data points?
Or can she just compare %absorbance to the controls and before/after numbers?
Or is it already know for this particular algae at a particular wavelength that a certain %absorbance equals a certain number of cells?
If she uses the UV/Vis, does that indicate the total number of cells, dead or alive, or does it only measure live cells?

The trial is over 96 hours.    Thanks!

I don't think it's wise to use a spectrophotometer for this experiment, as it is a total count, i.e. it can't distinguish between dead and alive cells very well, and so she might not see a clear difference between her treated and untreated algae. If she has access to a haemocytometer and a good microscope, then she can count the living cells directly, and calculate the cells/ml using a simple formula.

This paper has a nice overview of how to count algae using a haemocytometer, and if her species of algae can swim, then she would need to use the iodine solution mentioned in here:

http://weis.science.oregonstate.edu/files/weis/Protocols/Symbiodinium/Cell%20Counts.pdf

I hope this helps!


Introductory book in genetics? I am working in the field of neuroscience with a background in computer science. I try to find new ways of analyzing brain imaging data (mostly MRI, EEG, MEG, fMRI) with modern machine learning methods.

I would like to take a step up by adding genetics to the data arsenal. My work this far has found connections between some X and Y but not really shed insight to why things should be like that. I hope I could get a partial answer from biology.

To get started, I would need some good material to read. It does not matter if the content would be difficult in mathematical/statistical/technical aspects, but it should be approachable with limited knowledge in biology and/or chemistry and physics.

Suggestions?

GENETICS: Analysis and Principles, 4th edition, Robert J. Booker

This book is used in my school's ( NYU Poly) undergraduate genetics class.


Do snails like water? Simply question, do snail show when it's raining because they like it or/and need hydration and food or are they showing up just to escape somewhere, because they're scared of drowning?

Most types of snails survive droughts (that would kill otherwise through Dehydratation) by producing much mucos around themselves. This mucos will dry out if the sun comes up, so they hide under leaves or in the ground. If it's raining, those rings of mucos hydralise or "melt" and the snail begins to crawl. Like most amphibians snail take their oxygen by their skin furthermore they have lungs. By raninning they start moving for searching food, cause they dry out in sun.


What is this worm-like creature? It is on my bed sheet. The hairy part the the rear end. The length is about the diameter of a US dime (~18mm).

The other answer is most certainly incorrect. Silverfish are silver/grey and (like all members of the Zygentoma order) have three distinct, tail-like caudal appendages from their posterior end -- really, two large cerci with a central long filament.
 [Sources: 1, 2, 3].

The OP's specimen resembles the larva of a dermestid carpet beetle of some type; specifically, the location and appearance make me think it might be a black carpet beetle (Attagenus spp) -- for example A. unicolor.

 Source: Univ of California Master Gardener Program of Contra Costa County Blog

Description:

Tell-tale characteristic: the tuft of numerous "hairs" on the posterior end:

  The larvae of the black carpet beetle, which may reach 12.7 mm in length, are very different from other carpet beetles’ larvae. They are elongate, carrot-shaped, golden to chocolate brown, and have a tuft of very long, curled, golden-brown hair at the tail end of their body.  [Source: Penn state Dept. of Entomology]

A description from IFAS suggests that larvae develop stiff, bristlelike tails when older.

See bugguide.net for more pictures, such as this one

Pest:

According to many of the sources I've linked to already, the larva is the damaging life stage of this beetle.


Crow branch pecking behaviour I was walking through a small park when two crows started cawing at me, and followed me, flying from tree-to-tree as I walked. I speculate that this is a territorial or protective behaviour, but what I found different was the crows were violently pecking the branches nearby them. I have no memories coming to mind of seeing this behaviour beforehand. I speculate that this behaviour could be threat displays, but a quick search on Google did not reveal to me any authoritative studies on this phenomenon. I'd appreciate more information and sources.

This is a good question. This type of behavior -- pecking at a branch, wiping the side of the beak on a branch, pulling off twigs and dropping them, or knocking off pieces of bark -- is quite common among many corvid species, particularly when they are interrupted by something or someone that they might consider a threat. This includes not only potential predators but also potentially hostile conspecifics.

It is typically considered to be a form of displacement behavior. The concept of displacement behavior, from classical ethology, posits that when an animal experiences two conflicting drives to do two different things, it doesn't know which to do and does a third thing instead to dissipate the drive or anxiety. For branch-pecking in crows, see E.g Kilham and Waltermire 1990 Ch. 12.

Referece: Kilham, L., & Waltermire, J. (1990). The American crow and the common raven. Texas A&M University Press.


Do chaperone proteins misfold? If molecular chaperone proteins assist in the folding process of other proteins and misfolded proteins, can chaperone themselves misfold since they are also proteins? What would happen if chaperones misfolded? Can they misfold at all? Why or why not?

Chaperone proteins are still proteins and they can certainly misfold just like any other. If that happens, it will either be assisted by another chaperone and given time to fold successfully or it will be destroyed. If this is happening too often and the amount of chaperones drops too low or the number of unfolded or incorrectly folded proteins becomes excessive*, the unfolded protein response may be triggered and, if it does not resolve the issue and the cell remains stressed, the cell will undergo apoptosis and die.

Some chaperones, especially heat-shock proteins, may be more resistant to misfolding. This is true because they need to be able to withstand noxious conditions that denature other proteins. Not all chaperones are resistant to heat though and many are no more intrinsically resistant to denaturing.

*  It's not uncommon for a "bad" batch of proteins to be created. This can happen with a transcription error during mRNA synthesis since each mRNA molecule is read by many ribosomes. This can naturally happen with chaperones as well.


How is color information transmitted from the eye to the brain? Is color information sent from the eye to the brain frequency-modulated, or are different colors transmitted by different axons?

I know that each ganglion cell is connected to multiple photoreceptors. How do ganglion cells tell the brain which photoreceptors were exactly activated and by what color?

Do ganglion cells correspond to particular colors?

Can one ganglion cell transmit different signals to the brain?

How does the brain know which color the light has, if signals of different receptors are mixed in the ganglion?

Short answer
Color vision is mediated by spike rate modulation (frequency modulation if you like), as well as ganglion-cell specific stimulation.

Background
Ganglion cells exist that transmit opponent colors. The color opponency model predicts that we cannot perceive a greenish-red or yellowish blue, which is quite right. We can, however, see mixtures of the two channels, such as red and yellow (orange), and red and blue (purple).

Then opponent model predicts the existence of ganglion cells that are sensitive to red/green opponency and blue/yellow opponency (in trichromats like humans):

Indeed, it has been shown that these ganglion cells exist, i.e. cells that increase their firing in response to short-wavelength-sensitive (S+) and decrease their firing to middle-wavelength-sensitive (M-) and vice versa (Yin et al., 2009). Hence, it is not so that the frequency of light is represented in firing rate per se, but the frequencies of light are translated in spike rates, because spike rate is the only means in which neurons can transmit graded responses. In other words, every type of graded information is translated into spike rate eventually, including pressure differences, acoustic loudness etc.

Hence, as ganglion cells are sensitive to opponent pairs of colors, they do respond to particular colors. However, a "purple ganglion cell" does not exist, it is the combination of red and blue activations that lets us see colors due to synthetic processes in higher neural centers.

One ganglion cell can send different signals to the brain as it is basically an analogue converter of the red/green and yellow/blue opponent colors.

These inputs are sent to the thalamus (lateral geniculate nucleus) and higher visual cortices, where color-selective cells pick up the signals and integrate them for further processing. Here color mixtures are made to present the full gamut of colors as we know it:

Source: Dot-Color

Reference
- Yin et al. J Neurosci 2009;29:2706-24

Further reading
- Advantage of opponent color?


Boys born in excess - how can the nature draw from non-natural distributions? The probability of a newborn baby to be a boy is not exactly 50% but a bit more. I have been given the explanation that it is because boys act more self-destructive during the early ages and so the distribution evens out during time. But how can the nature know beforehand that boys should be made in excess?

It would make sense that the nature followed natural distributions in its choices like uniform, gaussian, exponential etc. but this seems not to be the case. What are the motivations and mechanisms to deviate from natural distributions? Can you come up with another examples of such "non-natural behaviour" in nature?

Welcome to Biology.SE.

"Natural" vs "non-natural" Distribution

There is no such thing as a "natural probability distribution". Actually, biological system often produce distributions that does not match with commonly used distributions just because the assumptions yielding to these distribution are sometimes poorly met in nature. In other words, many biological variables meet more complicated distribution than the standard uniform, binomial, geometric, beta, exponential, and other distribution you know of.

Of course the gaussian distribution is kind of a special one that is often approximatively reproduced by biological system as a consequence of the central limit theorem.

Some distributions are more used than others but there exist an infinite number of definitions and anyone can construct one. Here is my distribution of the day. $P(x | y,z) =  C \frac{y^x - exp(-yz)}{x+z+y}$, where $C$ is a constant of integration to ensure $\int_{-\infty}^{\infty} C \frac{y^x - exp(-yz)}{x+z+y} = 1$. I will call this distribution the "remi.b distribution". I have no idea what kind or process it can model and nobody will probably ever use it but it is a legit distribution.

Developmental mechanism

You can read this post and that post about the developmental mechanism that yield to such bias sex-ratio at birth.

Evolutionary processes

  how can the nature know beforehand that boys should be made in excess?

Organisms producing a bias sex-ratio are selected for as they increase the average fitness among their offspring. As such the population is selected toward creating such bias sex-ratio. Organism don't know, they just do.

In order to understand the evolution of sex-ratio a bit better, you should have a look at this post.


Is there human Anatomy software that provides great detail? Is there Anatomy software that is exact representation of human body, like let's say virtual reality tour inside human body from head to foot, detailing all organs even small, covering all systems, nervous, blood vessels, muscular, skeleton systems, could be zoomed even to deepest skin layers, neurons,  that can be applied unapplied like layers in Photoshop?
If this does not exist, then which is the most advanced human Anatomy software?

My favorite is this one and it is quite detailed and interactive. It does not use virtual reality technology, but it is a good resource for anatomy students. Then there is this one, but it is more virtually animated and less real. Hope this helps!


Systemic sensory confusion? Sometimes when a person gets touched on one part of the body they feel it else where and may think it came from a different part of the body. What causes this? Other examples are similar to why you can trick your self into thinking your arms are heavier than they really are. another would be that you can close your eyes and move in circles up and down your arm slowly and then when you guess where u are touching your hand is higher or lower than expected. What causes these things?

When our brain works out where a part of our body is in relation to another part of our body, or in relation to anything for that matter, we combine:

visual information
information about how much our muscles are contracted
how much our joints are contracted
different forces being applied on our arms/legs or other body parts
where it remembers we used to be
how much force we applied to move where we wanted to move
where we would therefore expect to be
and many other things

That's quite a few things that our body relies on! The one that's most fine tuned is our vision. Let's face it, whatever we are actively doing with our hands requires the most skill and knowledge of where our hands etc. are. It is also the system that we rely on the most. But other systems are helpful to make sure we don't fall, grabbing on to things and making sure we reflexively contract the opposite muscles to prevent falling, stop us dropping things and lot's more. It doesn't matter if they're not accurate, they just need to be fast and in doing so they can't be extremely exact.

When we don't use vision, we rely on these other things. They're made to quickly adapt (e.g. hold a shopping bag for a while and when you let go your arm feels light or when you get out of a swimming pool your body feels heavy) and it is important that they do this to allow their functions as listed in the last paragraph.


Are two colors (red + blue) necessary for LED grow lights, or would either color be sufficient? Below are some chlorophyll absorption spectra from other answers here. There is strong absorption at both the blue/violet end, and the red end of the spectrum, and presumably both of these contribute to steps in water splitting used in photosynthesis.
Do the two broad but widely-separated peaks correspond to different steps, so that both are required? Or is it sufficient to have light present in one band alone?
If both are required, how are they used differently?
If not, why do LED grow lamps have both? Would twice-as-bright light with either wavelength be just as effective and useful to plants?

That horribly un-natural purple light looks cool in high tech settings, but it's kind-of ugly in ones living room.
note: Originally I had though that Chlorophyl A and B corresponded to the two peaks, but clearly this is not at all the case. From here:

Both Chl-a and Chl-b primarily absorb red and blue light, the most effective colors in photosynthesis. They reflect or transmit green light, which is why leaves appear green. The ratio of Chl-a to Chl-b in the chloroplast is 3:1.

above: From this answer, also seen here.

above: x2 From this answer.

tl;dr: Sort of?

Logically, either red or blue light should be sufficient. Chlorophyll a and chlorophyll b preferentially activate different photosystems, and both photosystems are required in green plants.

Practically, we're in luck and someone has actually done the experiment.

As the original study reports, plants need a little blue light to grow into the right shape. Red-only plants produce oxygen and grow, but they take weird shapes. It seems like plants can grow on red light, but they use blue light to work out where light is. See here for a reasonably lengthy treatment on most of the obvious combinations.