Why don't bacterial cell walls prevent bursting when attacked by the complement? The complement system creates pores in cell membrane which leads to influx of lots of water thereby causing lysis of bacterial cell.

But what I fail to understand is that if bacteria have cell walls around them, why will they burst ? Shouldn't they simply become turgid just like plant cells do ?

Although this seems to be a simple question on the exterior, the answer is going to be confusing and unclear because we still don't know the answer exactly.

Short answer - MACs are bactericidal not because of water gushing in. It is due to other mechanisms effected by damage to membrane integrity.

Long answer

First of all, I am assuming you already know the complement cascade, the pathways and the like, and I won't get into it. But to mention in passing, MAC is not the only way the complement can help the immune system. It can also opsonise antigens and release anaphylotoxins to modify the immune response.

Most studies concerning the assembly of the MAC and the resulting membrane lesions have been conducted in model systems, e.g. erythrocytes and artificial lipid bilayers. The advantage of these systems is the ease of characterizing the membrane lesions compared to bacterial membranes. Also, complement fixation tests (which use erythrocytes and complement) have been widely used even diagnostically until not very long ago. The osmotic damage, ion effluxes that you talk of happen here and leads to the lysis of erythrocytes. Even in their case, there are 2 models of how MACs work - one is by making a pore (in the pic) and the other is by forming leaky patches in the membrane. However, the way bactericidal MACs work is thought to be different and a little more complex than this -

This picture may have been used for just didactic purposes but cannot be applied in a bacterial system simply because bacterial cell envelopes are different. The two major groups - Gram positive and Gram negative cell walls are important to differentiate while discussing the mechanism of MAC bactericidality. It is important to note that MAC mediated bactericidal action has been reported predominantly only in Gram negative organisms. This resistance in Gram positives is thought to be not because of the osmotic turgor or turgidity but because of the thick peptidoglycan in Gram positive bacteria, preventing access to the inner cell membrane where the MAC assembles. There are MAC resistant Gram negative bacteria too, but let's not discuss that here. It is not off-track to mention here that species like Neisseria where the capsule is thin and the peptidoglycan is too, are more susceptible to complement damage.

So, assuring that the MAC mediated bacterial lysis is not just water gushing in, how is it thought to happen??

For this, we need to revisit the structure of the Gram negative cell wall. The cell wall structure is quite intriguing since there happen to be two lipid membranes enclosing a periplasmic space which contains little peptidoglycan that Gram positives have much more.

Since there are two lipid membranes, technically, there's a possibility that the MAC can be formed on both these layers (MAC's assemble on hydrophobic membranes). MACs assembling on the OML (outer membrane layer) are not sufficient to cause lysis. It is confirmed that the damage has to occur to the IML (inner membrane layer). Inner membrane damage is thought to be bactericidal since it is more restrictive in its permeability than the OML. Also, the IML is linked to several important cellular, metabolic functions that require proper ionic gradients. One example is the oxidative phosphorylation that takes place around the IML.

This should answer your question in that the mechanisms of cell lysis seem to be slightly different in bacteria than the model systems (erythrocytes), but let us delve a little deeper into this.

One persistent question is "how can something as huge as the MAC, penetrate the OML and the peptidoglycan layer, to reach the IML to cause damage?" The hypotheses that MAC just forms a hole in the OML and other serum factors seep in and cause damage to the IML has been ruled out since complement alone can be bactericidal in nature. To explain this, two models have been proposed -

One, where the complement attaches at special sites in the membrane where both OML and IML approximate (at special sites where large proteins span both membranes) and another where, the complement creates a pore to allow C9 monomers to leak in, in turn polymerizing to damage the IML.

I assume this explains it all. Still, I implore you to refer to the link below and correct me if I've been wrong anywhere.

  Reference : The bactericidal mechanism of the complement membrane attack complex, Lars Ootes, (PDF)


Why are Lymphatic trunks part of the Cardiovascular system? According to Wikipedia the Terminologia Anatomica (international anatomy standard) the lymphatic trunks are part of the cardiovascular system instead of the lymphoid system.

Why did they make that choice?

The definition of "vascular" is as follows:-

  of, relating to, affecting, or consisting of a vessel or vessels, esp.
  those that carry blood:

By this defninition, the cardio-vascular system doesn't need to include only the blood vessels and the heart. It includes all conducting and distributing vessel elements including those which carry the lymph-Lymphatic vessels. The cardiovascular system stands for the "circulatory system"+ the heart tissues and since lymph is an essential part  of the circulation (of nutrients, hormones, wastes etc), the cardiovascular system must include the lymphatic system.

Lymphoid system is a completely different entity which includes spleen, the lymphoid tissue (MALT), the lymph nodes and the lymph vessels. Hence the lymphatic vessels belong to both, the cardiovascular system and the lymphatic system, but the MALT and Spleen (arguable and disputed) are only a part of the lymphatic system and not of the cardiovascular system.

MALT= Mucosal Associated Lymphoid TIssue


What type of spider is this that just decided to stop my plans of sleeping This tiny little spider decided to stop my plans of sleep at 1am, since I have no plans of getting to sleep any time soon may someone tell me what type of spider could be this monsterous!

It is a male Steatoda, probably S. grossa (picture below).  These spiders are often called False Widows, since the females are generally a large purply black and look similar to their cousins the Black Widows. Steatodas are pretty harmless, though, although a couple of species (in the UK/Europe) are known to sometimes produce bite effects like a mild Widow bite.  Not at all dangerous, but a little disquieting if you're the one that gets bitten.  Presuming that you're in North America, though, you're fine.  Steatodas are Theridiid ("cobweb") spiders common in and around houses, and the harmless males are often encountered when they wander around looking for love as adults.

Bug guide has a good section on S. grossa, including lots of images of male spiders like this one.

https://bugguide.net/node/view/6932

Information on Steatoda envenomation is broadly available, but not in great detail.  The Wiki entry appended below covers the ground as well as any of them.

https://en.wikipedia.org/wiki/Steatoda


Key points of Wagner's theory of innovation What are the key points of Andreas Wagner's "theory of innovation" from his book The Origins of Evolutionary Innovations?

Specifically:

What is new in his theory?
What problems in evolutionary theory does it address*?

Wagner does not propose any new theory. He uses the word innovation to mean evolutionary adaptations that manifest qualitatively different traits. In fact, he has himself not defined it properly in the mentioned book. This is what he has written about the term innovation:

  It may be difficult to define rigorously what an evolutionary
  innovation is [538,616]. However, these and countless other examples
  show that it is usually easy to recognize: a new feature that endows
  its bearer with qualitatively new, often game changing abilities.
  These may not only mean the difference between life and death in a
  given environment (just think of biosynthetic abilities), they may
  also create broad platforms for future innovations, as did innovations
  of photosynthesis and of complex nervous systems.

However the examples he cites in the introduction are not as obvious as he says. Lets say the evolution of nervous system. The innovation that would have led to evolution of nervous system could have been the evolution of electrically excitable cells.

Actually, throughout the introduction he does not actually clarify the meaning of innovation. In page-3 he does list some features of innovation but it is all still vague. Without a rigorous definition nothing is easy to recognize and classify (especially in theoretical terms).

I do not have the book and cannot look through the entirety of it. However, based on what I have read in some of his papers I can comment something about what he possibly means by innovation.

In certain dynamical systems, some parameter changes can lead to qualitative differences in the output (bifurcations). Steven Strogatz's book on Non-linear Dynamics and Chaos is a nice and easy read on this topic.

If you look at some of Wagner's research papers, you would understand this idea better. Some of these papers are about how some parameter changes can affect the overall outcome (which may be drastic). For example, in this paper the authors talk about how differences in cell division rates can affect the outcome of a cell differentiation event.

He also talks about metabolic innovations which refer to changes in metabolic reactions and network leading to new products/optimized growth etc. Details of this can be found in his lab's papers on Metabolic Flux Balance Analysis.

There is nothing new or drastically different about all of this. This is just an addition that was unknown during Darwin's time. All that he says is still quite in agreement with the current evolutionary theory. (But personally, I find the opening of the book too vague).

As far as empirical corroboration is concerned, you may have a look at his lab's research papers.


What would be the effect of excess taq polymerase on the PCR? I just had one question regarding the possible effect of putting to much Taq polymerase in my PCR tube?

Instead of 5µl I put 50µl (10x more).

Do you think it will have a bad effect on the reaction??

Thank for your help.

Costly error.
And yes, it will affect your reaction, since the concentration of Magnesium ions, which are needed as a co-factor by the enzyme, is too low. If you need so much PCR product, you can now adjust the rest of the reagents or you could start over and put this on your personal list of errors. Always check the amount of volume, if it is suspiciously high, check again.

If you decide to proceed and work with a 10x larger volume, make sure that the single PCR reaction is not bigger than 50µl, because the bigger volume also affects how fast the reaction heats up and cools down. If your reaction is too slow to reach 72°C for example, the elongation time might not be long enough to get the full product. If denaturating is too short, your efficiency will drop.


Is there a resource to query gene expression similarity? Stratified by sex? We developed such a resource. The editors of "Bioinformatics" (at OUP) rejected the paper on the grounds that we did not run a comparison with "state-of-the-art" [similar] resources. Can someone help me find similar resources?
Link to our own resource, ExFiles.

There are some similar resources, which at the same time do not mix the ingredients in the same way as your tool. Hope that pointing out the respective differences will help your rebuttal or resubmission! e.g.:

A similar web service is part of flyrnai, where tissue-specific expression can also be compared based on sex, and genes can be queried by the similarity of their gene expression profile to other genes.
A resource which has some conceptual relatedness regarding sex-specific similarity in gene expression, and which is also based on the GTEx dataset, has recently been published in the form of tables by Gershoni et Pietrokovski, BMC Biol, 2017.
A very nice and broad resource of high-quality gene expression profiles on individual tissues, but also on response to stimuli, is EBI GXA. Though the web interface only allows to query sex-specific expression profiles, computationally minded people could readily compute (dis)similarity between samples after downloading the (well-structured) data dump of EBI GXA.
A similar tool in terms of the visualization of sex-specific expression patterns is part of gtexportal, though it seems limited to displaying a single gene.


Dissection techniques for fruits and seeds I'm doing some amateur botany, and I was keying some plants in the Brassicaceae (Cruciferae) family, which requires detailed information about the seeds of the plant. My question is, in a seed, how can one identify features such as:

Cotyledon(s)
Radicle
Endosperm (when present)
Accumbency/incumbency of the cotyledons with respect to the radicle (in dicots)

It also seems like the key parts of the seed will be within the seed coat; it's not always obvious how to remove this seed coat, or what methods exist. Are there resources for this sort of thing?
As a more concrete example, I've identified this Cardamine hirsuta from my backyard, but I'd like to verify some features of the seeds. Unfortunately, the seeds are very tiny, as this microscope photo of the silique shows, and the features are non-distinct.
Flora of North America provides these details for the Cardamine genus:

Seeds uniseriate, flattened, usually not winged, rarely margined or winged, oblong, ovoid, or globose; seed coat (smooth, minutely reticulate, colliculate, or rugose) mucilaginous or not when wetted; cotyledons accumbent, rarely incumbent

How can I figure out from dissection whether the cotyledons are accumbent  or not? At least, that's the sort of question I'd like to be able to answer.

I will answer my own question for anyone that's interested in doing something similar. First, a great reference for seed morphology is A. C. Martin's The Comparative Internal Morphology of Seeds (1954), available on JSTOR and from sci-hub.
To dissect a seed, you’ll probably want to have a good dissection microscope, two pairs of sharp tweezers, a razor blade, and a pin. Begin by opening the fruit to expose the seeds; for a silique, it’s very easy to peel the valves open. Be careful not to crush any seeds. Using the tweezers (and optionally the razor blade) separate a seed from the fruit by breaking or cutting the funiculus. Do this for at least a few seeds, more is better. The seed coats will protect the seeds from drying out, but be aware, once the seed coat is removed, the embryo will only last a minute or two before becoming completely dried out. You'll figure this out pretty quickly, if it's a problem, otherwise don't worry.

Seeds in the silique, all still in their seed coats.
Use the tweezers to position a seed so you can cut it with the razor blade. To get a good idea of how the embryo is arranged requires several dissections, cutting the seed in different ways (vertically, horizontally, parallel to the work surface); seeds are cheap so just experiment. Cut the seed open and you should have something that looks like the image below.

Seed of Cardamine hirsuta cut in half.
What you’re seeing is (a) the seed coat, and (b) the embryo. Use the tweezers and/or the pin to get the seed coat away from the embryo with as little movement as possible to preserve the formation.

Using a pin, separate the embryo from the seed case. Note that the distinct features of the embryo are becoming visible.

With the seed coat (pale green part) removed, the radicle and the cotyledons become visible and distinct. This seed is accumbent.

The two cotyledons are pressed together in this example, but you can still see a separating line between them when you hold the embryo at the proper angle.
When dissecting seeds, do yourself a favor and select the most mature fruit available. Your life will be much easier if you have a larger specimen. These stills were taken from a video I made, available on YouTube here.


Difference between biological control and introducing species for conservation? I have a biology assignment and we have to explain various methods and strategies for conservation, two of which are:

  Biological control
  Introduced Species

What is the difference between these? I was under the impression that they are essentially the same thing – biological control being the introduction of species to predate pests (eg. the abysmal failure of the cane toad).

Any clarification would be great.

After talking to my teacher, he said that biological control is the introduction of species to control another species, however species may be introduced for other reasons (the "Introduced Species" method), such as to "assist an ecosystem cope, flourish or re-establish itself."

The example he gave was the introduction of South African veldt grass to Western Australia in order to stabilise sand dunes, so that they can later be built upon further (eg. plants which may not perform well in sandy, unstable soil can then be planted).

Hopefully this helps anyone else with the same problem.


How is a synapse held in place? Here is a question I've never asked myself until now: All textbooks show synapses with a decently large synaptic cleft between the axon terminal and the dendrite. How is this connection held in place mechanically? How is the axon terminal attached to the dendrite?

The textbooks represent the synapses that way for didactic reasons. But, in fact, there are several protein complexes that keep the membranes (pre and post synaptic) attached. The most famous are the puncta adherentia junctions.

In these structures, several different proteins, like nectins and cadherins, promove cellular adhesion:

(source of the image: http://cshperspectives.cshlp.org/content/1/4/a003079)

These molecules are important not only for cellular adhesion, but for synaptic plasticity as well.

Source: Adherens Junctions: from Molecular Mechanisms to Tissue Development and Disease


Inbreeding of selfing and outcrossing plant I am reading John H. Gillespie's Population Genetics A Concise Guide Section 4.3 Inbreeding. I do not understand these two paragraphs quoted below concerning selfing and outcrossing.

The first paragraph states that an outcrosser individual leaves behind on average two gametes one in an ovule and the other in a pollen.

The second paragraph states that a mutant selfer will leave behind three gametes for every two of the outcrossing plants, with two in its selfed offspring and one in its outcrossed offspring.

What are the effect of the ovules and pollen here? How are these two statistical conclusions drawn? I would like to have a very detailed explanation.

Some interesting evolutionary questions arise with species that are capable
of both selfing and outcrossing. For example, in many plant species there is
an intrinsic advantage to selfing, which leads to the evolutionary conundrum:
Why don't all plant species self? The situation is illustrated in Figure 4.4. The
outcrossing pedigree on the right represents a typical individual in an outcrossing population of constant size. This individual leaves behind, on average, two gametes, one carried in an ovule and the other in a pollen grain. These gametes appear as filled circles in the figure.

Figure 4.4: The gametes produced by a selfer and an outcrosser. The p to the right of
an arrow indicates that the parent’s contribution came from pollen; an o indicates it
came from an ovule. The filled circles represent gametes from the illustrated parents;
the open circles represent gametes chosen at random from the gamete pool.
Suppose a mutant appears that self-fertilizes all of its ovules, M illustrated
on the left side of the figure. Suppose also that there is enough pollen in each
individual of this species that the few grains needed for self-pollination by the
mutant represent a small fraction of the total pollen. As a consequence, the
selfing mutant has essentially the same quantity of pollen available for outcrossing as does a nonselfing individual. All else being equal, the selfing mutant will leave behind three gametes for every two of the outcrossing plants, as indicated by the three filled circles in the figure. Two of the gametes are in its selfed offspring; one is in its outcrossed offspring. Thus, the mutant should increase in frequency, perhaps leading to the establishment of selfing as the usual mode of reproduction.

I don't think it's a terribly rigorous statistical argument, so much as a toy model arguing that there can be a reproductive advantage to selfing in an outcrossing population. Here is the logic as I see it:

Ovule and pollen represent the female and the male reproductive gametes in a monoecious plant (monoecious means that it has both male and female reproductive organs in the same individual).
In sexual organisms that do standard sex (i.e. not a complicated variety of sex), both ovule and pollen (gametes) are necessary to generate a fertilized offspring (zygote).
In outcrossing individuals, pollen is broadcast to fertilize other individuals (1 pollen gamete) and ovules receive pollen from other individuals (1 ovule gamete). Total: 2 gametes
In selfing individuals in an outcrossing population, selfing individuals guarantee that they fertilize their own ovules. Thus, they replace the pollen of other individuals (1 pollen gamete + 1 ovule gamete).
Selfing individuals still broadcast pollen to fertilize other outcrossing individuals (+1 pollen gamete). Total: 3 gametes

The key is in looking at the figure and understanding what it's arguing.
Again, these are not really rigorous ratios, details will be determined by exact biology of any case in real life. As far as I can tell from the text, the argument is not "these are the exact ratios in all organisms", but rather that "selfing gives the advantage that a selfer contributes all of the same gametes as the outcrosser, plus the male gametes to fertilize its own male gametes".
Secondary note: this model is only true when the proportion of selfers in the outcrossing population is very small. Note that as the proportion of selfers increases, everyone is just fertilizing their own ovules, and the net contribution goes back down to 2 gametes per generation. So this does not describe an equilibrium case for population composition. [As noted in comments, it is likely the case that it is equilibrium for population size, e.g. number of individuals.]
For more theory about this, you can read about the evolution of self-(in)compatibility. Here is a somewhat recent review. Evolution of self-compatibility in plants is extremely dynamic, as you might expect from the arms-race aspect.
Update:
Pulling up some notes from the comments on the assumptions of the model:

I think that this example works when population number is at equilibrium, but population composition (e.g. selfers vs. outcrossers) might not be at equilibrium.
I think that for the amount of pollen, we have to assume that all organisms contribute an equal, infinite amount of pollen. So selfers fertilize their own, and then also dump pollen into a pool into which outcrossers also dump infinite pollen.
However, there are only a few ovules; every individual contributes one. That is, outcrossers and selfers contribute one ovule per individual.
On average, everyone's pollen will be sampled roughly once (actually a little less) if every non-selfed ovule takes one pollen from an infinite pollen pool of uniform composition.
As number of selfers in the population increases, less and less of the common pool of pollen will be sampled.
If everyone in the population is a selfer, there will obviously be no outcrossing, because everyone just fertilizes their own ovule. This is the equilibrium state, if selfing is heritable and this stated advantage to selfing holds.


Explain to a layperson how cigarettes smoke might cause cancer I have a very intelligent friend who is a light smoker, and also a Biology layperson.
I wondered whether understanding exactly how cigarettes smoke can cause cancer, might encourage him to smoke less (or quit entirely).

So how would you explain to a Biology layperson how cigarettes smoke might cause cancer?

To clarify, I am looking for a detailed explanation for a layperson, that makes the cause-and-effect much more vivid for them, and thus makes it much more likely that the intelligent layperson would internalize the risks of smoking.

Online resources that I found either gave a too simple answer or concentrated on statistics (which are usually hard for humans to internalize, if I understand correctly).
(Nothing wrong with such explanations, they are just not what I am looking for.)

I encountered the following paragraph in the textbook Life: The Science of Biology:

  Some chemicals add groups to the bases. For instance, benzopyrene, a component of cigarette smoke, adds a
  large chemical group to guanine, making it unavailable for base
  pairing. When DNA polymerase reaches such a modified guanine, it
  inserts any one of the four bases at random. Three-fourths of the time
  the inserted base is not cytosine, and a mutation results.

After finding the following quote in Wikipedia's Benzo(a)pyrene page, I decided to explain specifically how BaP can cause cancer:

  BaP has since been identified as a prime carcinogen in cigarette
  smoke.

My explanation:

A protein molecule is a chain of amino acids. Proteins are hugely important, as they are responsible for most of the cellular functions.
A DNA molecule is a chain of nucleic acids. There are 4 types of nucleic acids in DNA: A,G,C,T.
Having intact DNA molecules is crucial, because they include the encoding of proteins, according to which cells synthesize proteins.
A mutation is an alteration of a DNA molecule.
A mutation might lead to our cells synthesizing a malfunctioning protein. If a protein that should regulate cell division is malfunctioning, then the result might be uncontrolled cell division - cancer.
When you smoke, the chemical BaP (which is found in cigarettes smoke) might alter a G nucleic acid in a DNA molecule in some cell in your body. Later, when this cell tries to divide, it makes a copy of each of its DNA molecules, but it won't be able to identify that G nucleic acid (that BaP altered), so it would put a random nucleic acid in the copied DNA molecule. Thus, there is a 3/4 chance for a mutation.


What is this fluffy bug? I found this bug (actually he found me) while walking through some bushes in the city (Iași, Romania).
It is a small bug, a quarter of a fingernail, white and a fluff tail. He lays a white fluff on bushes (that is how I meet him, I brushed the bush and got the white fluff on me, when I wanted to clean it off I saw 2 moving on my shirt) and it seems they stay around it. I also found it near the plants, on a stone pavement, but I presume he got lost.

Based on the image and on the description, it could be a woolly aphid, a kind of insect that produces filaments of a waxy, cotton-like substance that gives them a fluffy appearance.

The images on Wikipedia aren't convincingly similar, but I found a better reference on abundantnature.com:


Is tyrosine hydrophobic or hydrophilic? I’ve seen tyrosine classified as a hydrophobic amino acid due to its aromatic ring in some textbooks and as hydrophilic due to its hydroxyl group in other textbooks.
How does tyrosine actually function in a peptide under physiological conditions (aqueous polar medium and pH~7)?

The answer to this question emerges from an examination of the structure of tyrosine — or, more strictly, the tyrosyl residue, which is how it exists in proteins, the concern of the question:

  It has both hydrophobic and hydrophilic features and can exhibit both
  behaviours depending on the circumstances.

The ring is aromatic and hydrophobic, but the hydroxyl substituent is hydrophilic.

It is important not to try to fit things into rigid classifications that may not be appropriate for them. Indeed, one should ask how useful a particular classification is in any circumstance, and be aware of its limitations.

The classic illustration of the importance of these dual properties of tyrosine is in Perutz’s description of the differences between the oxy- and deoxy- structures of haemoglobin, where oxygenation of the haem cause the movement of tyrosine from the hydrophobic interior of the protein to the hydrophilic surface. This movement is associated with breaking of ionic bonds between the subunits in the overall change in quaternary structure:

(This is a modified version of Fig. 3 of the original, produced many years ago for teaching purposes. The wiggly line is a cartoon representation of the polypeptide chain of the α-subunit of haemoglobin between His-F8 and the C-terminal Arg residue. For clarity, the preceding region is not shown but its continuation indicated by an arrow head.)


How do plants take in only carbon dioxide? There are only 400 molecules of CO2 in 1 million molecules of air.

How do plants only take in CO2 but not the other gases?

My teacher told me that's because there is less concentration of CO2 in the leaves than the air and the CO2 rushes in the leaves.But, then how does the leaf maintain the concentration of CO2 and other gases?

Plants don't take in only CO2, they take in whatever the atmospheric concentration of gases is: gases travel freely across membranes, so it is difficult to select for certain gases.

What your teacher is explaining is based simply on the laws of diffusion in that diffusion results in a net flow from areas of high concentration to areas of low concentration. If CO2 is being used up in chemical reactions in the leaves of a plant through photosynthesis, that means that concentration of CO2 is low there, so the net diffusion of CO2 will be from outside the plant to inside.

Calling it a rush might be a bit misleading, but in general gases mix fairly rapidly (compared to, say, liquids). The plant doesn't really have to do anything to facilitate this except to have surface area available for gas exchange.


Do all species have asymmetric female meiosis? In all the examples I can think of, (mostly vertebrate), female meiosis, or oogenesis, only haploid gamete is produced while the other cell divisions result in polar bodies. While male meiosis results in 4 haploid gametes. This difference follows the fundamental definition of female and males being defined as resources committed into reproductive cells.

I want to know if this asymmetrical gamete production is truly universal across all organisms. Are all meiosis in plants or unicellular organisms unequal between male and female?

Plant meiosis gives rise to four megaspores but usually upto three of them die by apoptosis leaving only one megaspore. But they are symmetric and three of them need not die all the time as it seems [REF].

Plasmodium being a haploid organism undergoes meiosis after fusion of gametocytes. Sexual differentiation is initiated at some point during the merozoite stage (See here and also the cross references).

Chlamydomonas is also haploid during its vegetative phase, and produces four flagellated haploid gametocytes. Sexual differentiation is apparently stochastic.

Perhaps there are more examples of organisms that do not undergo asymmetric division as seen in metazoa. There may be some stochastic asymmetry which leads to differentiation of sexes in the haploid unicellular eukaryotes and apoptosis in plant megaspores; these stochastic events may happen later as well. For plasmodium this is not really known; others I am not sure of.


Do any birds have established "poke a predator's eyes out" behavior? Is there a pattern/tactics of behavior in any birds species that consists of attacking a predator's eyes with its beak?

I'm looking for established tactics, not 1 or 2 anecdotal examples.

From this paper about black-headed gulls responding to a hedgehog:

  The gull might peck the intruder, or strike it with its feet. Pecks were
  mostly directed at the hedgehog's head and might be delivered after a
  horizontal approach with the wings partly lifted.

Although not directed at the eyes specifically, they observed the birds directing attacks to the predator's head.

There's another paper (Ratner 1975) that also looks promising, but I'm on my home computer and can't access it right now


Identifying a lone bone found newar Rowena Crest, Oregon (USA) I was wondering whether anyone knows how to identify what animal the following bone belongs to.  I assume it a femur, but it seems rather short and squat.  The following photos show two views of this bone and I've placed a 15cm ruler in the frame with the bone.

My guess is that it's a relatively young cow humerus. The strongly grooved trochleas are more characteristic of a humerus than a femur, which usually just has two condyles. The deep pit is where the olecranon process (your bony elbow) goes. The proximal end is missing, which indicates that the growth plate was not fused, suggesting juvenile.

And I guess cow because cows are very common and have robust bones compared to other artiodactyls.

Here's an image pulled from the web:


What does the 4DTv (four-fold synonymous) mean? I saw this sentence "4DTv is the transversion rate at fourfold synonymous codon positions, and ranged from zero (for recently duplicated paralogs) to ~0.5 (for paralogs derived from an ancient evolutionary past)." at this paper and another paper.

I have searched 4DTv or four-fold synonymous on google, but I did not find the answers showed at the following lines.

And my questions:

(1) Does the value of 4DTv range from 0 to 0.5?

(2) Why 4DTv closed to 0.5 indicate that an ancient evolutionary was happended?

After one month of research, I have some insights about it.

First of all, more than "fourfold-synonymous", the correct research is fourfold degeneracy. The genetic code is degenerate, in the sense that there is usually more than 1 codon encoding a certain amino-acid. The degeneracy usually takes place in the third position of the codon, that can be 2-, 3- or 4-fold degenerate. A 4-fold degenerate site would be the third position of a codon, where regardless of which nucleotide you have, the outcome doesn't change. Example: GGT, GGC, GGA, GGG all code for Glycine. As there are four variants at the third site of the codon, the third site is said to be fourfold-degenerate (4D). As the encoded amino-acid does not change, there is virtually no selective pressure on these variants, therefore they can be used as a "clock" to estimate times, given that you know the mutation rates per position.

Now for your other questions:
Yes, the value ranges from 0 to ~0.5, and this can be explained in a simple way. Transversions (Tv) are considered to be more rare than transitions (Ti). Therefore, if you calculate the ratio of Tv among all the variants, you expect this value to be < 0.5 (i.e. to have less Tv than Ti, otherwise it would be >= 0.5). Now, in order to accumulate Tv at 4D sites you need time to pass, so the more of them you have, the more time has passed, and that's why 4DTv ratios define time.


Does drinking coffee have negative effects? From what I collected, coffee is a magical potion that lets you feel energetic, and essentially not-sleepy. But are there any tradeoffs? I mean, if it was so beneficial, wouldn't the human body produce caffeine naturally?

First of all, the fact that a substance is beneficial does not mean that our body will, perforce, produce it naturally. Think of oxygen and water for example1.

As for the negative effects of coffee drinking, yes there are many although coffee has both a positive and a detrimental effect on human health. The main active ingredient in coffee is caffeine which can have the following negative effects:

Caffeine can increase blood pressure in non-habitual consumers.
High blood pressure is associated with an increase in strokes, and cerebral
vascular disease, which in turn increase the risk of multi-infarct dementia.
Caffeine may reduce control of fine motor movements (e.g., producing shaky hands)
Caffeine can stimulate urination.
Caffeine can increase cortisol secretion, some tolerance is developed.
Caffeine can contribute to increased insomnia and sleep latency.
Caffeine withdrawal produces headache, fatigue and decreased alertness.
Caffeine is addictive.
High doses of caffeine (300 mg or higher) can cause anxiety.
High caffeine consumption has been linked to an increase in the likelihood of experiencing auditory hallucinations. A study conducted by the La Trobe University School of Psychological Sciences revealed that as few as five cups of coffee a day could trigger the phenomenon.
High caffeine consumption accelerates bone loss at the spine in elderly postmenopausal women.

The list above comes from the very comprehensive wikipedia page on the health effects of caffeine. In fact, wikipedia is particularly good on this subject, see the following pages:

http://en.wikipedia.org/wiki/Caffeine

http://en.wikipedia.org/wiki/Health_effects_of_caffeine

http://en.wikipedia.org/wiki/Health_effects_of_coffee

1 Our bodies do produce both Oxygen and water as byproducts of various reactions but nowhere near enough to satisfy our need for these substances.


Why is the head/neck of the femur at that 120-150 degree angle? I'm just wondering why the femur is such that there is that head and neck sticking out of the top at an angle, why it isn't just straight up into the hips?

The answer to this great question lies in understanding the "Hip Index". I am afraid I will have to go into some technical details to explain this:

When we stand on one leg, the hip abductor muscles on that side have to work hard to keep the pelvis stable and prevent it sagging. In this case the femur is static and the hip abductors are actually working on the pelvis that tilts up or down around the hip centre of rotation. The abductors are represented as "Fm" in the diagram.

In order to do so, the hip abductors have to exert more force than the actual person's weight. This is because the length of the effective lever arm of these muscles "distance h linking H1 with the hip centre H" is shorter than the opposite lever arm "distance D between H and G representing the vertical line down from the centre of gravity".

The hip index represents the mechanical disadvantage of the abductor muscles and is around "2/1" in normal individuals. Therefor if the person's weight is 70kgs, then when they stand on one leg, the hip abductor muscles on that side are contracting at 140Kgs to stabilise the pelvis, and the person's own weight is pushing down at 70kgs from the other side, resulting in the head of femur coming under 210kgs of weight.

If the neck of femur angle becomes more straight as in your question (approaching 180 instead of the average 135), then the hip index goes up towards infinity due to the reduction in distance "h" which approches zero. This is a deformity called "Coxa Valga". If the opposite happens and the neck of femur angle becomes less straight (less than 120), then although the mechanical advantage of the abductor muscles improves, this is offset by the reduction of the actual length of the abductor muscles "distance from i to T", making the muscles weaker. This condition is called "Coxa Vara". In reality, Coxa Vara in humans is also associated with shortness of the neck of femur, which reduces the length "h" also resulting in an increase in the hip index, and an increase in the forces over the head of femur in spite of the abductor muscles becoming weaker.

Both conditions "Coxa Vara and Valga" result in the hip abductor muscles becoming less effective in stabilising the pelvis. In these conditions, the hip index can go up to 4-6/1. This means that a person weighing 70kgs could eventually end up with over 400kgs on the head of femur, leading to pain and early wear and tear. It also results in the pelvis sagging down when walking, which leads to an abnormal walking pattern called "Trandalenburg Gait".

Therefore, a neck of femur angle of about 135 degrees provides optimum conditions for the minimum possible hip index without compromising muscle length and power. Any variation results in reduced abductor muscle effectiveness, gait problems, increased hip joint wear and tear and eventually pain.


What organs are absolutely needed by the human body? The title is my question: what organs are absolutely needed (fatal if injured/removed) by the human body and perhaps animals in general?

I'm not asking which organs are mechanically replaceable, but more what organs cannot be removed (and not replaced) in order to maintain human life.

--update--

To clarify the question, I'm wondering what organs when removed (and applied no medical intervention) would cause fatal effects in a short amount of time, or cause semi-fatal effects (ex. shortened lifespan). A list perhaps of importance, if possible, would be nice.

note: I have no medical knowledge so I'll leave 'short' open to interpretation.

You can't remove most organs. The heart, lungs and brain are the ones that without you'll die in seconds. The rest you'll live a few hours or more. All depends how long you wish to live. The best way to see which organs are most required is to look at the order organs are shut down when there isn't enough oxygen or blood. That tells you which area most and least important.


Solubility of DNA in water This would seem to be an easy to answer question, but I was unable to find an answer (in g/L) for generic double-stranded DNA or plasmid neither on Google nor on BioNumbers. I would expect the solubility to vary slightly based on the sequence or length, but it probably wouldn't affect it very much due to the relative hydrophobicity of the bases.

I know I have made solutions of plasmid maxipreps of at least 1µg/µl, and the Nanodrop DNA quantifier datasheet has a maximum DNA detectable limit of 15µg/µl, but can anyone find a source for the maximum solubility level of generic DNA? For example, the solubility of a specific plasmid of approx. 5kb in length would be a good ballpark answer for this question.

DNA is a bit more complicated than some molecules due to it's length and composition variability.
In water.
According to Integrated DNA technologies:

DNA oligos can be resuspended to a near maximum concentration of 10mMolar; to achieve such a high concentration will require a lot of vortexing and it may take up to a day for the oligo to go into the solution.

DNA is a polar molecule and as far as I have experienced dissolves in water very readily. However there doesn't seem to be an exact quantifiable number for DNA solubility in water. If I correctly understand it, this paper claims that a 200,000Da-8,000,000Da oligonucleotide is soluble in water, however they never quantify this. An answer on a related question pointed out that high molecular weight DNA oligomers, like genomic DNA, is enhanced in solutions with dilute monovalent cations.
Cleaver & Boyer (1971) have some data on this, however it is somewhat outdated, and they were only using this solubility to demonstrate dialysis in water was capable of desalting the oligonucleotides.

Oligonucleotides larger than 5 bases in length remained within the dialysis
bag (Fig. 2) and losses of 10% and 40% occurred for tetra- and trinucleotides,
respectively.

There is a lot of work done on optimal temperature and pH for solubility of DNA so perhaps a more specific query might throw up some results.
In ethanol.
Ethanol precipitates at least 10–20 % of all classes of oligonucleotides. Oligonucleotides longer than 15–16 nucleotides are precipitated to about 65%.


How do we share pain? When somebody else tells me about his or her itching or pain in some specific body part, I sometimes begin to feel similar feelings.

I can think of about three explanations:

I feel pain all over my body all the time for many different reasons but my entrance neural pathways stop it as unimportant of these signals but when I focus on a single signal, it begins to be important for me.
Mirror neurons are doing their job.
For an unknown reason, I psychosomatically induce my friend's feelings.

Which of these theories is at least partially engaged in said phenomenon?

There has been a study by Jackson, Meltzoff & Decety (2005) who investigated the neurocorrelates involved in the perception of pain.
In order to assess this, they carried out an fMRI study in which their subjects were shown photographs of of feet and hands in situations that are likely to evoke pain and also a control set of photos that were free of any pain evoking stimuli.

Their results display that with the experimental photographs, there is a strong increase in bilateral changes in several regions that we know are involved in the perception of pain, namely:

  the anterior cingulate, the anterior insula, the cerebellum, and to a lesser extent the thalamus

Notably, the activity of the anterior cingulate was most strongly correlated with the participants rating of the other persons pain, which suggests that the anterior cingulate is especially modulated according to the subjects reactivity to pain of others.

Source:

Jackson, P. L., Meltzoff, A. N., & Decety, J. (2005). How do we
perceive the pain of others? A window into the neural processes
involved in empathy. NeuroImage, 24, 771-779.
doi:10.1016/j.neuroimage.2004.09.006


Why can't humans use dietary citric or acetic acid as a primary source of energy? As the Krebs cycle is involved with the conversion of food in to citric acid, why can't eating citric acid be used as a temporary primary source of energy - in place of fat/carbohydrate/protein?? It seems like a waste of energy to convert food into citric acid if there is freely available citric acid in your diet why wouldn't that preferentially be used for energy - as it would skip a lot of steps and therefore be more efficient. And what about drinking acetic acid for similar benefits, as "it is changed to citric acid by combining with oxaloacetic acid with the help of CoEnzyme A and ATP".

Why can't eating citric acid be used as a temporary primary source of energy - in place of fat/carbohydrate/protein?

No reason it can't. Citric Acid technically contains 2.5kcal/g -- which is almost half of protein/carbohydrates, almost a third of alcohol, and a fourth of fat.

So if someone needed 2500kcal/day, they'd need 1kg of straight Citric Acid. There's about 47g/L of Citric Acid in citrus fruit juice. So if you wanted it all from "natural" sources you'd need to drink 21.3L of your favorite citrus juice, though that's a bit comical.

In terms of being more efficient since Citric Acid bypasses the first two enzymatic reactions,the part where Citric Acid is processed into alpha-ketoglutarate via Isocitrate Dehydrogenase is the rate limiting step of the entire cycle. You wouldn't be saving any time by flooding your system just before the bottleneck.

Interesting question, though!


Is there a comprehensive life science techniques/methods database? There are so many techniques/methodologies in the life sciences that we can use to interrogate interesting questions. The thing is, most of us are completely unaware of the available methods we can employ. Rather, we go with the techniques we are familiar with or that are popular in our subdomains at the time. But that's pretty limiting.

So I'm wondering... we have databases for everything else... is there one for life sciences techniques/methods? Something like this could be immensely helpful in experimental planning. In particular, I think a comprehensive database would help scientists break outside of their spheres of familiarity and to employ less known (but potentially illuminating) methods to their questions.

I know there are journals that publish protocols and methods, but they are fragmented and don't encompass everything.

Does what I'm looking for exist? If not, how might one go about creating such a tool?

There's Benchfly, which is a video-based protocol library:

http://www.benchfly.com/video-protocols.php

There's also JOVE, which is a peer-reviewed video journal that sometimes covers protocols:

http://www.jove.com/


Insect identification by example Upstate NY USA here.

I am trying to identify the type of insect that this is:

Top-side:

Bottom-side:

Is this a cockroach? If so what type/sub-species might it be? If not, what other type of bug have I stumbled across here?

This is some species of Ground Beetle (family Carabidae); the trochanter of the hind leg (just before and somewhat overlapping the femur) and the threadlike antennae helps point to that group.  The book The beetles of northeastern North America by N. M. Downie and Ross H. Arnett (Sandhill Crane Press 1996; now out of print but in at least some libraries) may help with a species identification (fair warning: the keys are not profusely illustrated).


Do bile salts enter into enterocytes? Wikipedia says :

  The contents of these micelles (but not the bile salts) enter the enterocytes (epithelial cells lining the small intestine) .....

So, where do the bile salts go? Additionally, what prevents them from being absorbed by the plasma membrane?

The fatty acids within micelles are taken up by enterocytes in the upper/middle part of the small intestine (duodenum/jejunum) through selective transporters in their plasma membrane, which do not accept bile acids. The SLC27A4 protein is thought to be the principal transporter for fatty acids in enterocytes, although there has been some controversy about this.

As a result of this selective uptake of fatty acids in this part of the intestine, the bile acids are left behind in the micelles, as they are emptied of fatty acids. They travel down the small intestine until they reach the ileum, where enterocytes express a bile acid transporter, SLC10A2, which performs active uptake of the bile acids. The bile acids are then secreted on the opposite (basolateral) side of these enterocytes; enter the portal vein; and travel back to the liver, where they are reused. This is known as the enterohepatic circulation. A review of these mechanisms is found here.

So the uptake of fatty acids and bile acids differs by location in the intestine. First the emulsified fatty acids are extracted, then the bile acids are recovered in the ileum. There is also some passive transport (diffusion) of bile acids into enterocytes throughout the intestine, but this is considered a minor mechanism.


Do all bacterial cells have a double membrane? I’m reading that gram positive and negative bacteria have an inner plasma membrane surrounding the cytoplasm, then a periplasmic space, then an outer membrane.
How does this compare to my general knowledge of bacterial cells having one plasma membrane surrounded by a cell wall?!

Do all bacterial cells have a double membrane?

No. There are a number of bacterial membrane and cell wall structures. Some of them have a double membrane, some of them don't.

In microbiology, we often make the initial distinction between two groups of bacteria based on whether or not they take up an iodine based stain called a Gram stain. Gram negative bacteria have an inner membrane, a rigid cell wall, and an outer membrane around the cell wall, so they don't take up that stain. Gram positive bacteria have an inner membrane and a rigid cell wall, without the outer lipid membrane, so they do take up that stain.  There are other bacteria that don't stain well with either the Gram stain or its red counter stain (typically safranin), but most medically important species of bacteria fall into one of these two categories (gram positive: blue, no outer lipid envelope, or gram negative: red, has an outer lipid envelope).

You can read about gram-negative and gram-positive bacteria on Wikipedia, but it's surprisingly technical. This biologywise post might be a more approachable introduction.

  How does this compare to my general knowledge of bacterial cells having one plasma membrane surrounded by a cell wall?

When the concept of prokaryotes and eukaryotes is introduced, you're taught about key distinguishing features between the two. One of the key distinguishing features of (most) prokaryotes is a rigid cell wall. This is present in both gram negative and gram positive bacteria. They just didn't tell you about the outer lipid envelope in gram negative bacteria. At that point in your education, the idea is to introduce you to the concept of prokaryotes vs. eukaryotes, not to catalogue or understand all the different kinds of prokaryotes.

The more you learn, the more you'll see that life is quite varied. Many eukaryotic cells are coated in a layer of complex sugars and proteins that is in some ways similar to the cell wall of prokaryotes. It just doesn't provide rigidity against an osmotic challenge like prokaryotic cell walls. On the prokaryotic side, mycoplasma don't have rigid cell walls.


What are some examples of scaling laws in biology? I've seen that metabolic rate scales logarithmically as function of mass for many animals over an extremely large span of parameters. What other scaling laws exist at the individual level?

Here are some off the top of my head.

The height an animal can jump depends on the muscle cross-sectional area ($l^2$) and its mass ($l^3$). Mass grows faster with body size ($l$) so small animals can therefore jump higher relative to their body size ($l$) than large  animals. Very similar scaling exists for strength of limbs vs. mass, ability to fly vs. mass, etc.
In pinhole eyes (as found in clams and nautilus) sensitivity to light depends on the size of the pupil ($l^2$), the bigger the hole the more light gets in. However the ability to focus depends on the reciprocal of the size of the hole (but I don't know the scaling, so $l^{-n}$). Therefore there is a trade off between sensitivity and  ability to focus.
There are some recent models about foraging behaviour in a 2D terrestrial environment (with the front of the animal being a length  $l$) vs. foraging in a 3D marine environment (with the front of the animal being a surface $l^2$). The model predicts different behaviours for the size of prey animals should aim for.
The rate at which sound attenuates scales with the frequency of the sound as $1/f^2$. The frequency of a resonator scales with the reciprocal of volume $1/l^3$. So small animals make high pitched sounds which attenuate quickly and don't travel very far.
Finally, the properties of fluids change with size. The Reynolds number describes viscosity and is dependent on linear scale $l$. Therefore small animals experience fluids as viscous and can "crawl" through water whereas large animals have to "swim" through water.

However, any directly physical or chemical-physical property of biology will experience scaling laws.


Defining Resistance and Sensitivity Thresholds for IC50 I have a dataset containing IC50 data for each of my cell lines and up to 80 drugs. Basically for each drug I want to be able to define an IC50 threshold where if a cell line has an IC50 above that threshold it is resistant, and if it is below that threshold it is sensitive.

I'm trying to think of the best way of doing this: I was thinking of taking the median for each drug as the threshold but I realize that's quite crude. Are there any more robust statistical techniques I could use to define such a threshold for each drug?

Thanks!

IC50 has an exact definition, that is half-maximal inhibitory concentration. To get this you need to make a series of dilutions of each of your drugs and test your cell lines in each concentration and assess how they grow (eg measure Optical density, colony size, cell count or whatever applies to your cells and setup). Then you can set up a inhibition curve that is a function of the concentration. This most likely looks like a sigmoid curve and the inflection point gives you the IC50 value.

An example image form the wikipedia page of IC50 (recommended to read):

So in your case, you already have IC50 values (for wild types I assume), and you need to assess your (probably mutant ?) cell lines to see if they are sensitive or resistant. Standard lab practice recommends using wild-type controls and at least 3 parallel controls. You can compare the average growth of WTs to your cell line at the IC50 concentration you already got in your dataset, and calculate standard deviation, and 95% confidence interval. With some simplification if the 95%CI of your cell line is greater than the wt 95%CI it is most likely that your cell line is resistant to that drug, on the other hand if its lower then that cell line is sensitive to the drug in question.


Help with molar ratio What is meant when asked write molar ratios in 3 parts? For example I am currently assembling a vector that requires annealing several oligos to two pcr fragments prior to ligating them into my vector; which will be used for future transformations. I was told to "assemble the annealed oligos with the 2 pcr fragments. Use a 100:1:1 molar ratio of annealed oligos:each pcr fragment." I'm thinking this means- concentrated oligos:diluted pcr frag #1:diluted pcr fragment #2. I am confused about how to determine the final concentrations of my pcr fragments in relation to the concentrated/undiluted annealed oligos. Why? Because I only know their concentrations as ng/uL not as 5x, 2x or 1x. Should I calculate it as 1(part) divided by 102 (whole) for each fragment? Then multiply that number by the actual concentration of my pcr fragments.

I am sure the answer to this is probably simple but I'm sorry I don't understand it and am hoping someone helps me with understanding calculations of this sort. Thanks.

The whole point of this problem is that for each 100 molecules of annealed oligos, you need to have one molecule of each fragment.

You need to take into account the following:

The MW of each fragment is approximately proportional to the length of the fragment. Thus if you divide the concentration by the length of each fragment, you can get a value that simulates the molarity, meaning that you can use these values to fix to the ratio that you are asked between the different fragments.

For example, if the fragment1 is 100 bp and you have 10ng/µl, fragment2 is 200 bp with the same concentration, then you need to add 1 volume of fragment1 and 2 volumes of fragment2 to get the 1:1 molar ration.

In a similar way, you can calculate the amount of oligos added to have 100x more (of the ratio of concentration to bp length) than the respective fragments.


Is it possible to be allergic to the yolk of an egg but not the egg white? At lunch one day, my friend had a hard boiled Easter egg. When he pealed it he squeezed the yolk, or yellow part, of the egg out. I asked him what on earth he was doing and he said, "I'm allergic to the yellow part of the egg not the white." I was very confused by this, he also sad he was allergic to tomatoes but could still eat pizza with sauce on it, apples but only the skins, and some other strange things. I didn't think this was possible at all. Can anyone explain this and tell me if it's even possible to be allergic to one part of an egg and not the other, or is it all in his head. If this is possible, is there an actual name for this condition?

The protein composition of the egg white and egg yolk differ appreciably. Hence, it is plausible for one to countenance symptoms of indigestion when consuming the egg yolk as opposed to the albumen, egg whites. It is important to stress that your friend may only an indigestion towards egg yolks as opposed to an immune response to an antigen.

If we consider the protein family, the egg yolk comprises a family of phosvitins, a group of highly phosphorylated proteins capable of mustering iron and calcium metal cations - serving a role in embryo development.

These are primarily absent from the albumen which comprises (with an unexpected name!) a highest percentage of suspended ovalbumin, ovotransferrin and ovomucoid. As demonstrated by the American College of Allergy, Asthma & Immunology, it is feasible to suffer an intolerance towards the egg yolk and yet suffer no gastro-enteric indigestion to the egg whites.
More information regarding the American College is available from: https://acaai.org/allergies/types/food-allergies/types-food-allergy/egg-allergy

Your friend evidently does not suffer a severe anaphylactic shock after consumption of the egg yolks otherwise he/she may be adverse to both the egg whites and egg yolk. In conclusion, it is possible that he/she may simply have a mild intolerance towards certain proteins in the egg yolks.


ChIP-seq data Analysis Database Where can i find already analyzed ChIP-Seq Data? Is there any database or any web tool that takes ChIP-seq raw data and automatically analyzes them? Or is there any database that provides some API to analyze the raw data it provides. I am new to ChIP-seq data analysis and i really need these to create a web-based platform for mapping ChIP-seq data. Thanks in advance.
I found some interesting data in genome.edu. Is there another database?

The largest database of curated ChIP-seq data is currently Encode and it supports an API.  You can use JSON to get at all tracks.

That page will have a link to Getting Started that should get you going. You can visualize raw data, normalized data, and processed data tracks in genome browsers that load in ENCODE data.  My favorite genome browser is:

WashU Epigenome browser


What is the full name of E. G. Gray? E. G. Gray is Neuro scientist who found and described first the two major morphologically defined synapse types (Gray Type I (asymmetric) and II (symmetric)) in his work
E G Gray (Oct. 1959). “Axo-somatic and axo-dendritic synapses of the cerebral cortex: an electron microscope study”. In: Journal of Anatomy 93.4, pp. 420–433

However I am unable to find his full name nor further information about his life.

Edward George Gray went by the first name of George, which isn't evident from his initials (he was born Edward George), but I happened to stumble upon the Wikipedia article below.  From there, I found his obituary.

From his obituary:

  GEORGE GRAY was a pioneer in the study of brain ultrastructure. He was Professor of Cytology in the anatomy department at University College London from 1967 to 1977 and then headed the Laboratory of Biological Ultrastructure at the National Institute for Medical Research.

From the Wikipedia article for synaptosome:

  In a collaborative study with the electron microscopist George Gray from University College London, Victor P. Whittaker eventually showed that the acetylcholine-rich particles derived from guinea-pig cerebral cortex were synaptic vesicle-rich pinched-off nerve terminals.  Whittaker coined the term synaptosome to describe these fractionation-derived particles and shortly thereafter synaptic vesicles could be isolated from lysed synaptosomes


What causes the opaque green colour in Lepidoptera? Link here to what I mean by 'opaque' colouration on the insect, the colour intensity remains constant despite changes in light intensity and angle (not shown by the picture but the moth exhibits this in the field). This is different to 'metallic' colouration on other moths like the Forester moth (image here), where the colour intensity changes with light angle and intensity.

Through reading R.F. Chapman's book ('The Insects:
Structure and Function'), I know that metallic colours are caused by interference patterns produced by the micro structure of the scales, the book says this is how most higher frequency colours are produced, including green in this category. Obviously I've looked for pigments that could give this colour but I haven't found anything that is produced in insects.

So my question is: Is there a pigment that gives this colour in the insect and if so, what is it?

According to this paper, green pigments are found in lepidoptera. The study focused on Geometridae, and found that the primary pigment in emerald moths, such as Hemistola chrysoprasaria is also found as secondary pigment in Pseudoips prasinana. The authors dubbed the substance 'Geoverdin' and suggest it may be a derivative of chlorophyll consumed during the larval stage. I cannot find any further studies mentioning 'geoverdin' or its chemical identity.


Why is allolactose the LacI inducer? For what reason(s) is allolactose, instead of lactose, the "natural" inducer of lac operon repressor?

When lactose is present in a cell, some of it is enzymatically converted by $\beta$-galactosidase from the $\beta(1,4)$ linkage (typical of lactose) to the $\beta(1,6)$ glycosidic linkage (becoming allolactose). Allolactose and other analogues can then bind LacI to induce the appropriate conformational change and unbind the lac operator (one such review here).

Why does allolactose act as a signal of lactose presence instead of just lactose? From the perspective of the lac operon, there is no operational difference between lactose and allolactose -- either way one molecule binds LacI and cannot be metabolized while bound. The full paradox is explained by Edgel and summarized by well-known biochemistry textbook author and scientist, Larry Moran, on his personal blog. The short version is that neither allolactose nor lactose are the intended substrates for $\beta$-gal and instead a different sugar entirely is the "natural" inducer and substrate.

Juers DH, Matthews BW, Huber RE. LacZ β-galactosidase: structure and function of an enzyme of historical and molecular biological importance. Protein Sci. 2012 1792-807.
Egel R. The 'lac' operon: an irrelevant paradox? Trends Genet. 1988 Feb;4(2):31.


Is there any research paper state the pros and cons for human to be taller? Is there any research paper state the physical health pros and physical health cons for humans to be taller?

For example, shorter people seems to more likely to get involved in heart diseases and taller people to be more likely to be involved in cancer

People with Shorter height may outlive Taller ones.

It is a statistically established fact that they are more successful in terms of money,
as the study published Journal of Applied Psychology, (Vol 89(3), Jun 2004, 428-441).
But, still in the health, the counterpart succeed over the former.

  The Effect of Physical Height on Workplace Success and Income: Preliminary Test of a Theoretical Model.

  Author: Judge, Timothy A.; Cable, Daniel M.

  In this article, the authors propose a theoretical model of the
  relationship between physical height and career success. We then test
  several linkages in the model based on a meta-analysis of the
  literature, with results indicating that physical height is
  significantly related to measures of social esteem (p = .41), leader
  emergence (p = .24), and performance (p = .18). Height was somewhat
  more strongly related to success for men (p = .29) than for women (p =
  .21), although this difference was not significant. Finally, given
  that almost no research has examined the relationship between
  individuals' physical height and their incomes, we present four
  large-sample studies (total N = 8,590) showing that height is
  positively related to income (β = .26) after controlling for sex, age,
  and weight. Overall, this article presents the most comprehensive
  analysis of the relationship of height to workplace success to date,
  and the results suggest that tall individuals have advantages in
  several important aspects of their careers and organizational lives.
  (PsycINFO Database Record (c) 2012 APA, all rights reserved)
  Source: http://psycnet.apa.org/journals/apl/89/3/428/

Long back in 1975, the relationship between breast cancer and height had been nearly established.

  Breast Cancer Incidence and Nutritional Status with Particular Reference to Body Weight and Height

  Author: F. de Waard

  Cancer Res 1975;35:3351-3356.

  Summary The epidemiological literature on breast cancer is reviewed with particular emphasis on the possible etiological role of
  nutritional status as reflected by weight and height. The results of a
  prospective study and preliminary results of a population-based
  case-control study seem to indicate that body size or body mass rather
  than overweight (obesity) is a risk factor. A considerable proportion
  of the differences in incidence between the Netherlands and Japan can
  be explained by differences in body mass. The biological mechanisms
  mediating nutritional status and breast cancer are believed to be of
  an endocrinological- metabolic nature.

Primarily the investigators started with overweight problem but they have found a better correlation with height. They have concluded:

  A further lead to biological mechanisms might be derived
  from the fact that several endocrine and metabolic functions
  (e.g., basal metabolic rate and cortisol production rate)
  seem to correlate better with body surface area than with
  body weight. The rationale for using surface area is often
  lacking except for the fact that it is estimated from both
  weight and height.

Height and cancer risk are fairly clearly linked, with a 16 per cent higher relative risk for every extra 4 inches of height.

The answer may lies in the metabolic rate:

  For one, taller people tend to weigh more than shorter people, even if
  their BMI isn’t any higher. For another, poor nutrition and stress can
  stunt height growth, and higher calorie diets have been associated
  with increased height. And that doesn’t even begin to take into
  account the psychosocial variables like increased income, education,
  and socioeconomic status.

Other Diseases

On the contrary, in a study examining cardiovascular disease risk and height in men found that men who were taller than 6′ 1″ (185 cm) had a 35% lower risk of having a heart attack than men who were shorter than 5′ 7″ (170 cm). Every inch a man gained in height resulted in a 2-3% decrease in heart attack risk.
In a study in among, Israeli civil servants, shows height was also associated with lower stroke risk. Taller people are more likely,around 76%,  to suffer from recurrent blood clots.

LINKS:

http://blogs.discovermagazine.com/crux/2013/11/08/is-being-tall-hazardous-to-your-health/#.U79p3vmSzQJ
http://scienceblog.cancerresearchuk.org/2011/07/21/height-and-cancer-risk-%E2%80%93-the-long-and-short-of-it/


Explanation of the terms "downstream signaling" and "upstream signaling" In molecular biology, what's the meaning of the terms "downstream signaling" and "upstream signaling"? What's the difference between them?

It simply means after and before with respect to the flow of information in a given pathway. For example, consider this schematic representation of a pathway:

TF1 ==activates==> gene1 ==produces==> Kinase1 ==phosphorylates==> ProtA

In this schema, Kinase1 is downstream of TF1 and upstream of ProtA. Or, to take a classic example (source):

MEK1/2 is downstream of Raf and upstream of ERK1/2.


What kind of skull is this? We found this skull on a beach in southwestern Sweden, and are curious as to what kind of animal it was.

It's definitely a bird pelvis (synsacrum). Based on the size (~30 cm), it came from a very large bird. Unfortunately, comparative images of bird pelves are rare on the internet. Some possibilities (large birds of Sweden possibly found on the coast):

Great northern loon
Golden eagle
Common crane

A loon skeleton (from http://paolov.wordpress.com/2011/08/05/friday-mystery-object-107/) shown below.


How to confirm secondary structure formation of Precursor miRNA on gel? I want to fold precursor-miRNA into its secondary structure and then confirm it on gel. At first, I heat it in annealing buffer at 95°C for 5 minutes and cool down slowly. Then I run it on gel but the samples are at same position as the original dilution.

Disclaimer: Although I have attempted northern blots for miRNA, I haven't actually done the kind of experiment you are talking about.

First of all you need controls.

A negative control: a same length RNA that will not fold (you can introduce some mutations in your pre-miRNA sequence to disrupt the base pairing). You can use the miRNA secondary structure prediction tools for rationally designing such controls.
A positive control: perhaps a folded pre-miRNA that is crosslinked. Frankly, I haven't come across anyone using such crosslinking agents to study RNA secondary structure. I had however, seen some old papers on this topic (Wagner and Garrett, 1978, Rabin and Crothers, 1979). You may also try some conditions (salt concentrations etc) under which the RNA will fold (studied using biophysical assays).

Now, you cannot run agarose gels. You would need long polyacrylamide gels ~15%. You also need to use the right buffers. 0.5-1x TBE supposedly works. You may want to run your sample in two conditions: denaturing (with 8M urea) or non-denaturing. You can refer to this protocol (Petrov et al. 2013).

Your positive control should migrate faster than the negative control. If your RNA is folded (fully or partially) it should migrate between the positive and negative controls in the non-denaturing gel. In the denaturing gel, your RNA should migrate at the same level as the negative control. Positive control (if it works) should not be affected by urea.

Also, the gel heats up during electrophoresis which in turn can dentature RNA. You may want to run the non-denaturing gel in the cold room.

Having said all this, I would advise that instead of putting in so much effort in gel based assay you can use more sensitive equipment to study RNA folding. There are many biophysical studies on in vitro RNA folding. You can check them out.


Would it be more genetically efficient to have shorter lifespans? If, for example, humans had an average lifespan of, say, 30 years, and we reached sexual maturity at age 10, then we could "evolve" more quickly and theoretically "weed-out" more genetic diseases because we would live for shorter times, hence more natural selection.

  Why don't we continually evolve for shorter lifespans (or do we)?

Extremely briefly, we do not evolve shorter lifespans because natural selection does not act for the good of the species.

As an interesting historical aside, August Weismann proposed essentially the idea you are suggesting in 1889, in his Essays upon heredity and kindred biological problems. Within a few years, however, he backed away from this hypothesis.


Why does alcohol cause the hemolysis of RBC in a large proportion? I had today an experiment that we put 95% alcohol to the blood which made it completely transparent so hemolysis must have occurred.
I started to think about the reasons.

I think that this is because alcohol dissolved the lipid membrane of cells outside of the cell.
Alcohol molecule is also very small.
I think that I can go through the bilayer too.
So I started to think that the other possible reason was that alcohol went inside the cell so caused

dissolution of the membrane from the inner side
increase in the volume of the cell so bursting

What are the main reasons why Alcohol cause hemolysis to the red blood cell?

Well, it turns out the situation is more complex. I had assumed the answer was what rwst suggests or something to do with osmotic pressure. It seems that we don't really know that well.

In a paper from 1991, Chi and Wu suggest the following possible mechanisms :

Membrane fusion during the shedding of exovesicles might produce a transient decrease of the permeability barrier.
Increase of lipid dynamics by the alcohol could decrease the packing of the
bilayer. The membrane barrier behaves like a soft polymer, which can sieve solutes. The meshes in the polymer might become larger if its packing density is
reduced.
Lateral phase separation of lipids could induce packing defects in the lipid domain. This has been observed for long chain alcohols and postulated to be responsible for the increase of membrane permeability by amphiphiles.
Increase of the dielectric constant of the membrane by the alcohol would also increase the partition of hydrophilic solutes into the membranes. Such an increase has been postulated to be responsible for the increase of the permeability by aliphatic alcohols.
Modification of the intrinsic membrane domain might follow modification of the membrane skeleton by the alcohol. Accordingly, aggregation of intrinsic proteins might cause membrane modification mentioned under point 2 to 4.

The authors state that it is not possible to decide between the
various possibilities, but they seem to prefer point 5:

  Although it is not possible to decide between the various
  possibilities from the present data, we showed that the
  release of membrane fragments from ethanol-treated RBC was not a
  requirement for the creation of membrane pores since it occurred at a
  time much later than the detection of K ÷ leakage. In addition, we
  found that changes of membane rheological properties preceded the
  permeability increase. These properties have been related to
  the membrane skeletal protein spectrin. Moreover, ethanol has
  been shown to affect the skeleton. The processes leading to
  the formation of pores in ethanol-treated RBC may thus relate to a
  deranged cytoskeletal network, followed by the aforementioned
  alteration of membrane properties.

The plot thickens, apparently, low concentrations of alcohol protect erythrocytes from hemolysis while higher concentrations can cause it. The following are extracts from Tyulina et al:

  The seeming paradox between the direct haemolytic effect of ethanol on
  erythrocytes (Fig. 1) and the stabilizing effect of ethanol on
  erythrocytes undergoing NaOCl-induced haemolysis (Fig. 2) could be
  explained by the relatively small destabilizing effect of ethanol
  which is observed (<1% haemolysis) over 16 h. This effect would be
  negligible in the short time period (generally <10 min) assay for
  NaOCl-induced haemolysis where 100% of the cells are haemolysed. An
  alternative explanation for this paradox is that the mechanisms of
  haemolysis induced by ethanol and NaOCl are different.

  It therefore appears that ethanol does not induce significant
  oxidative stress in the human erythrocyte, and these data are in
  agreement with previous studies (Seeman et al., 1971), in which it was
  found that low ethanol concentrations could protect erythrocytes
  against haemolysis. Although the mechanism for this protective effect
  is unknown, it has previously been suggested (Halliwell and
  Gutteridge, 1999) that ethanol can serve as a hydrogen donor in the
  elimination of the hydroxyl radical with formation of water and the
  2-hydroxyethyl radical.

The authors then state (emphasis mine):

  In summary, we conclude that the damage to erythrocytes which occurs
  on in vitro exposure to ethanol may be caused, at least in part, by
  unmetabolized ethanol directly, rather than by the oxidation of
  ethanol to acetaldehyde or its conversion to FAEE.

I would guess this "direct effect" is something very much like what rwst suggested but the fact that the authors, who clearly work in this field, do not say so makes me think that the situation is more complex.

So, in conclusion, the exact details of alcohol's hemolytic properties don't seem to be understood in great detail. Admittedly, neither of these articles is very recent, if anyone can find a more up to date account I would love to read it.

REFERENCES:

Chi LM, Wu WG. Mechanism of hemolysis of red blood cell mediated by ethanol.
Biochim Biophys Acta. 1991 Feb 11;1062(1):46-50.

Tyulina OV, Prokopieva VD, Dodd RD, Hawkins JR, Clay SW, Wilson DO, Boldyrev
AA, Johnson P. In vitro effects of ethanol, acetaldehyde and fatty acid ethyl
esters on human erythrocytes. Alcohol Alcohol. 2002 Mar-Apr;37(2):179-86.

Trandum C, Westh P, Jørgensen K, Mouritsen OG. Association of ethanol with
lipid membranes containing cholesterol, sphingomyelin and ganglioside: a
titration calorimetry study. Biochim Biophys Acta. 1999 Aug 20;1420(1-2):179-88.


What plant is this? (Found in South Thailand) Have tried to recognize with PlantSnap App, no results.

It looks like Desert Rose, commonly used for Bonsai plantings.


Pedigree Probability of Autosomal Recessive Trait Here is a pedigree:

The trait is autosomal recessive.

The question is:  What is the probability that the bottom 2 people (4 and 5) have a child with the trait?

I tried doing 2/3 * 2/3 * 2/3 *1/4 and got 2/27 but this is wrong. I thought that the probability of III 1 being a carrier is 2/3.  The probability that IV 4 is a carrier is also 2/3.  The probability that III 6 is a carrier is 2/3 and IV 5 must be a carrier.  So IV 4 and IV 5 must be carriers.  The probability that they have a child with the trait is 1/4. But I am not getting the right answer.

The right answer is 1/6.

Starting with the left hand side of the diagram:

III:2 is definitely a carrier (Tt) as one parent (II:2) is affected (tt).
III:1 is also definitely a carrier (Tt) as when mating with III:2 they produce an affected (tt) offspring (IV:1)
This means that we can work out the possibilities for IV:4 as we know the parent genotypes.  It follows the standard arrangement for two carrier parents giving the options of:

TT (1/4)
Tt (2/4 = 1/2)
tt (Normally 1/4 but in this case 0 as individual not marked as affected).

Therefore for this scenario, the probabilities for IV:4 are :

TT (1/3)
Tt (2/3)

Now if we look at the right hand side of the diagram.

IV:5 is definitely a carrier (Tt) as one of their parents (III:5) is affected.

This gives two possible Punnett squares to be examined:

|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

This gives nil affected offspring so we can disregard this option for your question (as we are ONLY looking for scenarios which produce affected individuals).

Therefore the alternative is:

|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         t |              TT                |                tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

Giving 1/4 affected offspring.

As mentioned above, in order to have affected offspring then IV:4 must be Tt.  There is a 2/3 chance of this being the case.  If this is the case, then there is a 1/4 chance of the child being tt.

Both conditions need to be true for this to happen so we multiply the fractions:

2/3 * 1/4 = 1/6


Can it be said that proteins determine phenotypic traits? I am not ignoring the function of genes, or the gene-environment interactions. What I want to know is if behind every "observable characteristic" we can find a protein -or a group of proteins- which is responsible for that trait. The idea comes from a school curriculum, and it is expressed as follows:

  In this unit the core topic is the central role of proteins as executors of fundamental biological functions and thus as responsible of an organism phenotype...

Thank you in advance.

Yep, that is correct in general. However, sometimes proteins indirectly determine phenotype. For example, the skin colour is dependent on melanin (not a protein) but the melanin producing cells work because of proteins. Further, melanin production is also controlled by proteins. Thus, skin colour is not DIRECTLY determined by proteins but because proteins produce the pigment melanin, proteins are ultimately the reason behind our skin colour phenotype.


Are stroma lamellum and grannum lamellum the same? I have a picture in my textbook that is confusing me as to how they are different.I tried looking for some info on the internet, but could'nt get it clear.Please help me.

I will try to help. But, in the future, please post a picture of the confusing diagram to help us help you.

edit: now that I see your diagram, I'm not sure if this answer is helpful. Will re-consider and possibly edit this response. Thanks for including it!

Grana lamellae refer to the lamellae (membranes) in direct contact with photosynthetic stacks (grana), where the stroma lamellae are the ones that are connecting between individual stacks (see here). My understanding is that they are functionally and compositionally very similar, the only difference being the region of the lamellae in question (link to paper, sorry for JSTOR paywall). Check out the Wikipedia page for Chloroplasts for some more diagrams. Maybe one here will help this make more sense to you!


Sequencing rtPCR product So I have a validated set of primers for rtPCR from Biorad that contains SYBR green.  If I do rtPCR, can I use the rtPCR product after purifying it with a Qiagen PCR purification kit?  Also, I'm under the impression that the sequencing company needs primers to do sequencing, do I just use the PCR primer or one of the "universal" primers the company has?

You can use the PCR purification kit for cleaning up the DNA.

You can use the primers that you used for RTPCR for sequencing. The universal primers would work only if the sequence complementary to it is there in the 3' end of your amplicon.


What is this butterfly? The following guys (about an inch long) were seen in the Willamette Valley of Oregon in summer.  When one would fly by a resting one, they'd get into a high-speed little "dogfight".  What genus might they be (or species, if you know).  Are they in the "skipper" group of butterflies?

Yes, it is a skipper (family Hesperiidae) and very similar to European species in Ochlodes, and my guess is that it belongs to one of the North American species in this genus. For instance, it is very similar to Ochlodes sylvanoides (also called Woodland Skipper), which is common in the western parts of the US. However, I'm not familiar with North American butterflies, and there might be closely related similar species that I'm ignoring.

Images of Ochlodes sylvanoides from http://butterfliesofamerica.com/t/Ochlodes_sylvanoides_a.htm:

More pictures can also be seen at Bugguide.net


Range of dry matter yield per kg CO2 of different plant species The photosynthetic equation tells us that for every sugar molecule produced 6 molecules of carbon dioxide are used.

I'm interested in how much organic matter is produced by a certain quantity of CO2. Obviously there are differences between plant species so I'm basically looking for a list of plant (categories), which tells how much CO2 does produce how much dry matter.

A plant contains about 50% of it's mass absorbed from the air, from CO2 which it converts with 45% efficiency. 40-45% CO2 fixation/respiration seems to be optimal for all plants, it's the balance of how much their cells need aerobic respiration day and night, compared to photosynthesis. That 50% absorbed from the air is fixed with H2O which provides most of the other 50%, and the rest is ashes.

According to this research:
The CO2 captured by plants is the result of the differences between
atmospheric CO2 absorbed during the process of photosynthesis and the CO2
released by the atmosphere during respiration. This difference is converted into
biomass and tends to fluctuate between 45 and 50% of the plant’s dry weight.
(the research states dry weight C measurements, they don't seem to measure CO2 absorption directly)

So it's better to search for "photosynthesis respiration ratio" to find research that measures the efficiency of the CO2 absorption:

the ratio of respiration and photosynthesis (R : P) was relatively constant, 0·40–0·45, and independent of temperature. This was consistent with earlier work by Ryle et al. (1976) [...] Some mechanistic understanding of the constancy of R : P was provided by Atkin et al. (2005), who found that respiration and photosynthesis in most examined plant species acclimated similarly after temperature change. More recently, Atkin et al. (2007) confirmed homeostasis of R : P, in Plantago spp., but this was not maintained when plants were subjected to higher temperatures than usually experienced in their habitats. Differences between photosynthetic and respiratory acclimation to temperature have been reported by Campbell et al. (2007) and Hartley et al. (2006). Cheng et al. (2000) found that the R : P of sunflower was also insensitive to changes in atmospheric CO2 concentration. Overall, the research confirms Monteith's (1981) assessment that the ratio may vary over short time periods but is constant over periods of weeks and longer.

That document has lots of research references and technical words and concepts to follow up.

It's good also to see google images for R P ratio graphs and tests.
https://www.researchgate.net/publication/263676467/figure/fig1/AS:278855131648023@1443495652845/Figure-3-Bottom-curve-simulated-10-d-running-average-leaf-respirationphotosynthesis.png

The conversion ratio is visible here, day is white, respiration is black.
https://www.researchgate.net/profile/James_Bunce/publication/43291524/figure/fig1/AS:273738792960009@1442275822297/Figure-4-The-ratio-of-average-night-time-respiration-rate-R-to-average-day-time.png


Human Body "Fat" Equilibrium Here's my theory:

If you consume x calories each day with y amount of caloric expenditure each day you gain zero weight, regardless of x and y being out of balance.
If you then mechanically remove a large percentage of body fat (surgically), the fat should not come back.

Is this a true theory or not? It seems to me that if the body is stable at the current consumption of x and expenditure of y then the removal of excess weight/fat should not affect anything.
Anyone have thoughts on this? Is my thinking flawed? Why? Even if x and y were equal why might the fat come back if there is no net gain when the fat exists?

I'm not quite sure what you mean by

  regardless of x and y being out of balance.

Surely it would make more sense to assume you gain 0 weight if x and y are balanced? The prime reason why people get obese is probably because x and y are not balanced for them (there are other reasons though, as well as reasons why people can have it imbalanced and still not gain weight).

Even if you consume exactly as many calories as you expend in a day, you may gain weight depending on how (ratio of protein/fats/carbohydrates) and especially when you consume the calories. The body may for example store consumed amounts as fat after eating and then use carbohydrate storage from liver and muscle when starving, so long term you would still gain weight.
Adipose (fatty) tissue requires energy too. If you consume in the same manner after as before cutting a large amount of it away, you may just regain it until x=y again.
Also consider: if people ate just half an apple a day more than the exact amount of energy they need, they should gain more than a kilo on average every year. But they don't, and you can hardly assume that people manage on average to consume the exact amount their body needs.

The reason for that is probably leptin. It is a hormone produced by adipocytes (fat cells) and essentially indirectly reduces food uptake and increases expenditure, among others by decreasing your appetite. This has been regarded as a sort of "adipostat"; your leptin system creates a genetically determined level of body fat that you will tend to obtain. Dieting or cutting away fat will cause a drift to return to the previous weight because of a lower level of leptin (due to reduced fat cells). Of course it's not as simple as that though, so it's also possible that you will actually long-term reduce weight through those methods. E.g. exercise seems likely to be an exception somehow.


Does the modern synthesis theory of evolution deny that acquired characteristics can be inherited? The following is an wikipedia article on Lamarckism.
https://en.wikipedia.org/wiki/Lamarckism

According to Ernst Mayr, any Lamarckian theory involving the inheritance of acquired characters has been refuted as "DNA does not directly participate in the making of the phenotype and that the phenotype, in turn, does not control the composition of the DNA."[75] Peter J. Bowler has written that although many early scientists took Lamarckism seriously, it was discredited by genetics in the early twentieth century.
The evolutionary biologist T. Ryan Gregory contends that epigenetic inheritance should not be considered Lamarckian.

It seems to me that the assertion that acquired characteristics can be inherited was denied by the modern synthesis theory of evolution.
Is this true?
If yes, what is the reason of the denial?

Generally, yes, this is not part of theory of evolution as it is generally accepted by most of the scientific community.

For a trait to be subject to natural selection over several generations, it needs to have heritability, meaning it needs to show up in offspring (or their offspring). Generally, what is called an "acquired trait" does not fit that criterion. What's passed on is the genetic material of the parents and that doesn't change when the parent acquires these traits.

For example, bonsai trees are kept small by environmental conditions, as such, their height could be called an acquired trait. Their offspring does not naturally grow as a bonsai tree. Giraffes did not grow longer necks because they stretched them, but because those giraffe ancestors with longer necks (which just happens randomly through mutation - you have varying neck lengths in a population) could reach food more easily and could survive when those with shorter necks didn't. The giraffe example is a classic one that was proposed by Jean-Baptiste Lamarck, whose theory of evolution (called Lamarckism) was superceded by Darwin's.

There are traits where acquired versus genetic traits are hard to differentiate - while a good athlete does not have children who are athletic because their parent did sports, they are often also good athletes. For one thing, the parent might be genetically "suited" for sports and has passed these genes on. Another reason is that they will probably train their children and want them to become more athletic.

I know of one example where something that could be called an acquired trait is passed on to offspring - methylation patterns. Those are modifications of the genetic material that happen during an organism's lifespan and aren't modifications of the actual genetic code - they can be passed on to offspring. Since these patterns influence gene expression, they have an effect on the offspring. However, that's usually not what people mean when they talk about acquired traits.

Lamarckian inheritance


What happens if we continuously stimulate a mimosa plant? I know there is some mechanism in humans by which we start to ignore a certain stimuli if it persists for a long time (e.g., we don't feel our shoes all the time !).

Can the same thing happen in Mimosa pudica? Can it again get it's original arrangement of leaves if it is stimulated without interruption?

I think it should do this, otherwise it will not be able to grow if it is surrounded by bushes from all the sides as it will be stimulated constantly and so will be unable to photosynthesize properly.

Mimosa leaves have mechanoreceptor cells which sense the mechanical stress through proteins called mechanoreceptors (they are similar to the ones responsible for sense of touch in animals). When stimulated the mechanoreceptors cause ion channels to open leading to depolarization. This generates an action potential (AP; like neurons) which in turn activates the motor cell (Visnovitz et al., 2007). Motor cells cause leaf movements by change in their interior turgor pressure (similar to opening and closing of stomata).

Repolarization (like in neuronal AP) takes time and Mimosa would not respond to stimuli that are too frequent. The time required for the turgor pressure to relax would be an additional factor.

I am no plant biologist but if I compare this situation with that in neurons, I can speculate that long term non-responsiveness similar to LTD may happen because of down-regulation of mechanoreceptors. It has actually been shown that Mimosa does actually become insensitive to a persistent stimulus such as a continual water drop and moreover exhibits a long-term "memory" of this non-responsiveness (Gagliano et al., 2014). However, the exact molecular mechanism has not been elucidated. Again, there would be thresholds (on amplitude and frequency) for the signal to elicit these kind of changes.

References

Visnovitz T, Világi I, Varró P, Kristóf Z. Mechanoreceptor Cells on the Tertiary Pulvini of Mimosa pudica L. Plant Signaling & Behavior. 2007;2(6):462-466.
Gagliano, Monica, et al. "Experience teaches plants to learn faster and forget slower in environments where it matters." Oecologia 175.1 (2014): 63-72.


Does Alzheimer affect more than day-to-day memory? I know that Alzheimer's damages a part of the brain called the hippocampus, which has a central role in day-to-day memory.

But, could it affect also on things in other memory centers, things such as taste and moves?

Oh, yes, though short-term memory loss is often an early sign.

"For many, decline in non-memory aspects of cognition, such as word-finding, vision/spatial issues, and impaired reasoning or judgment, may signal the very early stages of Alzheimer’s disease."  from https://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet.  Warning: grim.

Whatever your brain does, Altzheimer's eventually undoes.  For more details:  http://www.alzheimers.net/stages-of-alzheimers-disease/