Why is fructolysis independent of glycolysis? In glycolysis, glucose is converted to fructose-6-phosphate before further breakdown. However fructose, instead of being phosphoryated to fructose-6-phosphate by glucokinase (and thereafter to pyruvate via glycolysis), yields fructose-1-phosphate in the reaction catalysed by fructokinase.
Why is this so?
It should be just as easy to phosphorylate fructose to both compounds. Wouldn’t it be more economical to use a single reaction, so everything would be easier to regulate? As there are several disorders that arise from the deficiency of enzymes used in fructolysis, wouldn’t there be a selection pressure against two separate metabolic pathways?
Edit:
Thanks for David's criticism; I see the confusion, I actually meant that it is mainly metabolized in the liver. I don't really have any real sources as I do not have access to much and quite a large portion of online resources is behind paywall. After a bit of digging I was able to find an overview that reiterates most of my claims. Sorry for not being able to provide more.

In the liver, fructose is rapidly converted to
fructose 1-phosphate via fructokinase. Fructose 1-phosphate is then converted into the trioses dihydroxyacetone
phosphate and glyceraldehyde via aldolase B.

The liver can extract 40–70% of dietary fructose in
both rats and humans. The high efficiency of
fructose extraction by the liver is due to the fact that the
liver is the main source of GLUT-5. Anatomically,
the liver is the first organ to receive absorbed nutrients
via the portal vein; in that way, it contributes to fructose
extraction. In contrast, the liver accounts for a smaller
percentage of glucose extraction for glycogen restoration

Above are two excerpts from Chapter 19 - Fructose-Induced Hypertriglyceridemia: A Review. This source also (albeit vaguely) states that the resulting triose phosphates (glyceraldehyde and dihydroxyacetone phosphate) can and will enter pathways like glyconeogenesis, gluconeogenesis etc.

Up until this point in fructose metabolism, there have been no rate-limiting steps and, as a result, there is an increased amount of substrate leading to metabolic pathways from triose phosphate (i.e. glycolysis, glycogenesis, glyconeogenesis, lipogenesis, and fatty acid esterification).

Another source for my assertion that fructose is mainly metabolized to fructose-1-phosphate (Elsevier's Integrated Biochemistry):

Unique Characteristics—Aldolase B Specificity
Fructokinase, like glucokinase, is found primarily in the liver. Unlike hexokinase and glucokinase, it phosphorylates the sugar at the C-1 position. Aldolase B, which is specific to the liver, works on both F1,6-BP and F1P. In extrahepatic tissues such as muscle or adipose tissue, fructose is phosphorylated to F6P by hexokinase.

Also, a possible lead, from Fructose: Absorption and Metabolism. Encyclopedia of Human Nutrition:

The allosteric inhibition of PFK effectively reduces the rate of glycolysis and decreases hepatic glucose uptake overall. In contrast, the entry of fructose carbons through the pathway proceeds without this limitation.

Using different enzymes (and therefore a different pathway) allows regulation of glycolysis in the liver without unnecessarily affecting fructolysis.

Summary

The mechanistic reason why fructose is converted to fructose
1-phosphate by fructokinase rather than fructose 6-phosphate by
hexokinase is explained in terms of the Km values of fructose and
glucose for the latter enzyme.
A possible general rationale for the two distinct pathways of
metabolism is to allow them to operate and be regulated independently
of one another. Although plausible, I am unaware of further data
support this idea.
The manner in which the fructokinase pathway evolved is a matter for
conjecture. I discuss what types of approaches to this question may
be valid, and the types of arguments that I consider invalid.

“Why?” Questions — A Note of Caution
Before addressing this question I think it important to consider what is meant by a “Why?” question in biology. This can be a trap for the unwary if one is not clear whether a question is answerable objectively or only speculatively. There are two main types of “Why?”questions:

Mechanistic “Why?” questions. For this SE Question this would seem to be: “What is the mechanistic explanation of the fact that
fructose is converted to fructose 1-phosphate, rather than to
fructose 6-phosphate, in liver?”
Rationalization “Why?” questions. In this case it would seem to be
“How can one rationalize the fact that a separate pathway for
fructose metabolism exists?”

Mechanistic questions can be answered objectively if there are sufficient experimental observations. Rationalization questions cannot.
Rationalization is helpful to try to make sense of observations — to provide a framework for further experimental work. It is useful in teaching and learning, which is why one encounters it frequently in text books. But just because it is in text books it should not be regard as on a par with the facts described therein. It is just an opinion, an interpretation, which should be regarded critically. There is a danger in accepting an inadequate explanation, just because it is the only one that has been proposed for something that is difficult to understand but we think that must have an explanation.
Rationalization “Why?” questions are often confused with questions about how something Evolved. These should be clearly distinguished. Rationalization explanations refer to the functional utility of a system, not its evolutionary history. If the only explanation is in terms of evolution, then there may be a plausable evolutionary explanation but no rationale.
An Answer to the Mechanistic Question
Fructose is not converted to fructose 6-phosphate in the liver because it has a much higher Km for hexokinase than glucose does. Furthermore, glucose is present normally at a higher concentration and will therefore act as a competitive inhibitor. Instead, as the poster writes, there is a specific fructokinase, which converts it to fructose 1-phosphate and a further enzyme converting to the fructose 1-phosphate to glyceraldehyde and dihydroxyacetone phosphate. The glyceraldehyde is phosphorylated to glyceraldehyde 3-phosphate.

Trying to Answer the Rationalization Question
“How can one rationalize the fact that a separate pathway for fructose metabolism exists?” The explanation given in the Encyclopedia of Human Nutrition — that it allows separate regulation of glucose and fructose utilization — seems possible, but fails to explain the circumstances in which it would be advantageous for fructose to be converted to pyruvate, but glucose to, say, glycogen. In the absence of this I would say that there is no convincing explanation, and that one should carefully consider a number of different possibilities:

It is chemically difficult to create a enzyme specific for fructose
to catalyse the formation of fructose 6-phosphate.  This seems
unlikely — we are not dealing with two molecules as similar as serine
and threonine.
Fructose 1-phosphate has functions (metabolic fates or regulatory
roles) other than energy generation in the latter stages of
glycolysis. The Kegg pathway map doesn’t suggest anything in the
former respect, but the entry in the Encyclopedia of Human Nutrition
states: “As fructose-1-phosphate is formed, it feeds forward and enhances the activation of pyruvate kinase thereby facilitating the passage of fructose carbon to pyruvate and lactate.” I do not have access to the book, so cannot say whether this argument is developed further. However as pyruvate kinase is also activated by fructose-1,6-bisphosphate (generated from fructose 6-phosphate) there would seem to be no regulatory difference between fructose and glucose metabolism in this respect.
Fructose 1-phosphate lacks some regulatory role of fructose
6-phosphate (or fructose-1,6-bisphosphate) and hence results in
different flux of fructose and glucose through glycolysis. This is
the converse of the previous possibility. It is true that
phosphofructokinase is activated by fructose 2,6-bisphosphate, which
is formed from fructose 6-phosphate, and so there is a feed-forward
effect when the concentration of fructose 6-phosphate is high.
However the fact that fructose 1-phosphate does not have this effect
would not seem to have any significance as it does not use
phosphofructokinase. Another possibility is proposed in the
Encyclopedia of Human Nutrition: “Since fructose enters the glycolytic pathway [later than the phosphofructokinase reaction] it does not exert an inhibitory effect on the gluconeogenic rate-limiting enzyme, fructose-1,6-bisphosphatase” As the only
relevant molecule that regulates fructose-1,6-bisphosphatase is
fructose 2,6-bisphosphate — inhibiting it — the argument would seem
to be that the entry of fructose into glycolysis through fructose
1-phosphate allows more glucose production for other tissues. Why
this would be a “good thing”, however, is not clear to me.
Unphosphorylated glyceraldehyde has other roles in metabolism, so its
production independently of glyceraldehyde 3-phosphate is more
energy-efficient. Unfortunately the other metabolic fates of
glyceraldehyde are specialized and minor, and do not seem to support
this possibility.

In conclusion, I personally cannot see a rationale for the separate pathway of fructose metabolism to pyruvate, although I believe that there must be one.
The Evolutionary Question
Let us use the question to consider arguments in this area. The approaches that I suggest may — in principle — be valid are those relating to actual mechanism. One can consider the number of evolutionary events that need to occur for a new pathway to evolve — the more steps, the more difficult. (I have used a similar argument in another SE answer). In this question the implicit argument is:

“The evolution of the pathway from fructose to glyceraldehyde
phosphate via fructose 1-phosphate requires three steps, whereas that
for a highly specific enzyme that converted fructose to fructose
6-phosphate would require only one.”

If one accepts this argument, it would suggest that there is some rationale for the fructose 1-phosphate pathway that has escaped us. Although this also seems likely for other reasons, one needs to ask whether the argument is correct. Did three separate enzymes really evolve to accomplish this, or were perhaps some of the enzymes already present and serving other purposes?
Two examples of common type of argument that I think are invalid are in the original question.

“As there are several disorders that arise from the deficiency of
enzymes used in fructolysis, wouldn’t there be a selection pressure
against two separate metabolic pathways?”

Selection pressure against causes of a human disease require them to have a severe effect on the survival of the species, to cause death before the individual is of a reproductive age, and to be relevant to early humans. Minor enzyme deficiency disorders of fructose metabolism, or even disorders arising from modern over-consumption of sucrose would exert absolutely no selective pressure. As it turns out fructokinase (EC 2.7.1.3) is widely distributed in nature — If one looks up fructose metabolism in fruit flies on KEGG one can follow a trail to a long list of species in which the enzyme is present. The point that I think this demonstrates is that for biochemical evolution, one needs to think when and where the pathway might have evolved.
The second example of argument that I think are invalid is

“Wouldn’t it be more economical to use a single reaction, so
everything would be easier to regulate?”

I refer to this type of argument as “playing God” or “second guessing Nature” as to me it presumes that one is in a position of such knowledge and wisdom that one is able to propose the optimal design for life.
Economical in what sense? Is our concept of economy the over-riding feature driving mammalian evolution? Multiple reactions and isoenzymes abound in the metabolism of animals. Apparently ‘wasteful’ energy- or material-consuming reactions like splicing are everywhere. And the regulation of intermediate metabolism is mind-boggling in its complexity. Regulation clearly evolved after the pathways, and “ease” of doing this does not seem to have been a driving force in evolution.
The lesson I draw from this is that even the most knowledgeable molecular scientist is in a poor position to say what is economical or efficient, and to predict the outcome from the cost/benefit tradeoff Nature will make or has made to do things “better”. And it is difficult to say what is “better”.


Solubility of Forskolin in ethanol I am interested in using forskolin in cell culture medium. Does anyone know how to make solution of 10 microM forskolin in 5% ethanol or less. I would like to avoid using DMSO as a solvent.
Thank you. L.

Sigma gives a solubility of 200 microMole in water containing 2% ethanol.
They state:

  Forskolin is soluble in water (with 2% ethanol) up to 0.2 mM by first
  dissolving in ethanol at 5 mg/mL and doing subsequent dilutions with
  water.

The datasheet can be found here.


Is Sda a protein, or is it a protein domain of DnaA? I initially thought that a domain was a specific part of a protein, with it given tertiary structure, to which a given molecule is able to bind. (I think I recall phrases such as "the haem binding domain of protein X..." being used in lectures?)

Having consulted Wikipedia on protein domains, I see the definition is a bit more subtle:

  A protein domain is a conserved part of a given protein sequence and (tertiary) structure that can evolve, function, and exist independently of the rest of the protein chain. Each domain forms a compact three-dimensional structure and often can be independently stable and folded.

I can understand this, however the reason why I started questioning what a 'domain' actually refers to was because if it's use in reference to Sda in control of endosporulation of bacteria. In my lecture notes, it is stated that "KinA is bound and destabilised by Sda, a DnaA target,"

From this I was under the impression that Sda is a protein (although to the best of my knowledge DnaA only binds DNA, so I do not know why Sda would be target of DnaA. Anyhow,) on the other hand Wikipedia states "the protein domain Sda is short for suppressor of dnaA or otherwise known as sporulation inhibitor A.", which seems to me to suggest that Sda is a part of DnaA whose modifications allow DnaA suppression?

Also, on Wikipedia, it is later written "Sda protein domain is a checkpoint which prevents the formation of spores." How can a protein, if Sda is one, be a checkpoint?

On the other hand my lecture notes later talk about the regulation of Sda levels, so it again is referred to as a separate protein!

I would very much appreciate if someone could explain what 'domain' means in this context.

Short answer

Wikipedia has unnecessarily made an already confusing situation much worse. Sda is its own protein, it is regulated by DnaA, and it prevents sporulation.

Full answer

I don't think your misunderstanding is based on the meaning of 'domain' - the definition you give sounds quite reasonable - but rather the use of the term domain with respect to Sda and the naming of Sda itself, which I agree is quite confusing and made much worse by Wikipedia in this case.

Sda is a protein that inhibits KinA activity (Burkholder et al., 2001) and is a completely separate protein from DnaA. I don't see where you jumped from your notes to the idea that Sda is a domain of DnaA except for from Wikipedia: I don't know why Wikipedia thinks Sda is a protein domain, it is a protein. It is a very small protein, so perhaps it would be appropriate to think of it all as one domain, but there is not a single result for "Sda protein domain" on Google Scholar - no one else is using this terminology. A full Google search only returns a few (~150) results, most of which are direct copies/translations from Wikipedia, or Wikipedia is a direct copy of them. Wikipedia can be useful, but if it starts to cause you confusion, don't assume it is correct.

The phrasing "KinA is bound and destabilised by Sda, a DnaA target" means that Sda binds KinA and destabilizes it, and notes that Sda is a target of DnaA; since DnaA is a transcription factor, you can infer that this means that DnaA controls expression of Sda in some way.

In biology a checkpoint just refers to a place that a process can be halted/arrested, often in reference to the cell cycle. Sda is considered a checkpoint because when Sda is expressed, it prevents cells from sporulating by indirectly preventing activation of Spo0A (Burkholder et al., 2001).

Another source of confusion is that the name "suppressor of dnaA" on Wikipedia is WRONG, but further, molecular biologists sometimes have an impenetrable way of naming things, owing to the complexity of control of gene expression and the circuitous way that new proteins are identified and understood.

The correct name for sda is "suppressor of dnaA1". dnaA1 is NOT DnaA - dnaA1 is a MUTANT ALLELE of DnaA that results in cells that are completely unable to sporulate. But! sda is also NOT Sda: sda is a MUTANT ALLELE that produces non-functional Sda (the protein).

I'll quote from the title of the table in Burkholder et al:

  sda Mutations Suppress the Sporulation Defect of dnaA1 Mutants

Or, stated again, in dnaA1 mutants, there is a defect in DnaA which prevents sporulation. The researchers searched for mutations that would reverse this effect. They found one, and named it sda, because it reverses (suppresses) the effect of the mutation they were studying. The dnaA1 mutant's effects on sporulation seem to be caused by an increased expression of Sda, which is why the sda mutant reverses the effect.

References

Burkholder, W. F., Kurtser, I., & Grossman, A. D. (2001). Replication initiation proteins regulate a developmental checkpoint in Bacillus subtilis. Cell, 104(2), 269-279.


Do multiple axons innervate a single skeletal muscle fiber? The typical text-book illustration of innervation of muscle fibers shows branches at a single position along the fiber. Does any given muscle fiber have more axons that innervate it though, given that muscle cells can be quite long, up to half a meter in Sartorius?

Until a better educated person contributes a more detailed answer, Hunt's article here from 1954 will likely be the best source,

  studies have shown that muscle fibres in the frog's sartorius are innervated in two major zones and most of the fibres receive motor
  endings at at least two regions along their length (Katz & Kuffler,
  1941). In this case a multiply-innervated muscle fibre may derive its
  several end-plates from the same motor nerve fibre. The possibility
  also exists that a muscle fibre may receive end-plates from more than
  one nerve fibre, i.e. polyneuronal innervation.

HUNT CC, KUFFLER SW. Motor innervation of skeletal muscle: multiple innervation of individual muscle fibres and motor unit function. J Physiol. 1954;126(2):293–303. doi:10.1113/jphysiol.1954.sp005210

He in turn references an article by Kats and Kuffler from 1941,

KATZ, B. & KUFFLER, S. W. (1941). Multiple motor innervation of the frog's sartorius muscle. J. Neurophysiol. 4, 209-223.

As those are both 70 years old, it is likely that more documentation has been produced, and that it could contribute to a competent answer to the question.


How many ommatidia does a honeybee have? European honeybees (Apis mellifera) have compound eyes made of tiny facets called ommatidia. The number of ommatidia is usually known in most model insects, but I cannot find reference for the European honeybees, despite bees being highly studied. How many ommatidia does a European honeybee have on average?

4700 - 5400, according to Somanathan et al. (2009). They base their reported values on two other papers.

Reference
- Somanathan et al., J Exp Biol (2009); 212: 2448-53


Why doesn't ovulation occur in both ovaries simultaneously? I know that in human body ovulation takes place at only 1 ovary every month. But development of a follicle depends on FSH levels in the blood, and since both the ovaries are exposed to the same blood supply, how does it make sense for development of follicle to be seen only in one ovary? Aren't both ovaries exposed to same FSH levels every month?

I am not able to figure out the solution to this anomaly and would appreciate some answers.

Each ovary has hundreds of thousands of follicles. And, of course, each one of those follicles is exposed to the same blood supply.
Therefore, your question...

Why isn't ovulation seen in both ovaries together?

... is the same of:

Why isn't ovulation seen in two follicles (regardless the ovary)?

All follicles are stimulated by FSH and they indeed start to mature at the same time. However, in a given cycle, normally only one follicle fully grows1. What we have here is a competition among follicles.
Guyton is not my favourite book on physiology, but it suggests an explanation for this:

Only One Follicle Fully Matures Each Month, and the Remainder Undergo Atresia:
After a week or more of growth — but before ovulation occurs — one of the follicles begins to outgrow all the others; the remaining [...] developing follicles involute (a process called atresia), and these follicles are said to become atretic. The cause of the atresia is unknown, but it has been postulated to be the following: The large amounts of estrogen from the most rapidly growing follicle act on the hypothalamus to depress further enhancement of FSH secretion by the anterior pituitary gland, in this way blocking further growth of the less well developed follicles. Therefore, the largest follicle continues to grow because of its intrinsic positive feedback effects, while all the other follicles stop growing and actually involute.
This process of atresia is important, because it normally allows only one of the follicles to grow large enough each month to ovulate; this usually prevents more than one child from developing with each pregnancy. The single follicle reaches a diameter of 1 to 1.5 centimeters at the time of ovulation and is called the mature follicle.

Therefore, the reason why we don't see both ovaries ovulating at the same time is the same reason why we don't see one ovary ovulating twice at the same time: the fastest growing follicle inhibits the growth of the other follicles (in the same ovary or in the contralateral ovary, it doesn't matter).
Besides that, it also explains the pattern of ovulation: in a given cycle, the left and the right ovary have equal chances to ovulate. Thus, the ovaries don't take turns like this (L is left and R is right):
L → R → L → R → L → R → L → R → L → R → L → R → L → R → L → R → L → R etc...
The real pattern is probably random:
L → L → R → R → L → R → R → R → L → R → L → R → L → L → R → L → L → L ETC...
According to Ecochard (2000):

It is concluded that in normally fertile women, the cycle length and the hormonal profile are independent of the, most probably random, site of ovulation. (emphasis mine)

Sources:

Hall, J. and Guyton, A. (2011). Textbook of medical physiology. Philadelphia, Pa.: Saunders.
Ecochard, R. (2000). Side of ovulation and cycle characteristics in normally fertile women. Human Reproduction, 15(4), pp.752-755.

1Note that, for answering this question, we will (wrongly) assume that there is no polyovulation in humans. However, as polyovulation does occur in humans, ovulation can sometimes be seen in both ovaries.


What determines whether an action potential is inhibitory or excitatory? What determines whether an action potential is inhibitory or excitatory? Is it determined by the receptors, the neurotransmitters, or some other mechanism?

Short answer
The physiological state of the postsynaptic cell ultimately determines the effect of an incoming action potential.

Background
An action potential occurring in a chemical synapse is neither inhibitory or excitatory. An action potential is a binary '1', an-all-or-nothing signal without any information, i.e., there is not a -1 or +1 action potential. Similarly, there are no excitatory or inhibitory neurotransmitters.

Notably, the principal excitatory neurotransmitter in the nervous system, glutamate, can have inhibitory effects dependent on the receptor activated. While most metabotropic glutamate receptors (mGluRs) and ionotropic AMPA and NMDA receptors are indeed all excitatory, the inhibitory glutamate receptors (iGluRs) are not (Cleland, 1996).

Conversely, GABA, the principal inhibitory neurotransmitter in the nervous system, can have excitatory postsynaptic effects. For example, hyperpolarized neurons may actually depolarize upon GABAA receptor activation, simply because the resting membrane potential is more negative than the reversal potential of Cl- (i.e., Cl- flows out of the cell due to the negative membrane potential) (Marty & Liano, 2005).

The existence of both excitatory and inhibitory glutamate receptors shows that it is the postsynaptic receptor that determines whether an action potential will inhibit or excite the postsynaptic neuron. The excitatory effect of GABAA activation shows that on top of that, even principal inhibitory neurotransmitters (GABA) with principal inhibitory receptors (GABAA) can excite a neuron dependent on its physiological state.

Besides chemical synapses there are electrical synapses. In these synapses action potentials are transmitted directly electrically through gap junctions. In this case, any action potential is excitatory as the signal will be carried forward if it is strong enough (Purves et al., 2001).

References
- Cleland, Mol Neurobiol (1996); 13(2): 97-136
- Marty & Liano, Trends Neurosci (2005); 28(6): 284-9
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates; 2001.


How does the body count time in the short term? So I've done some research and found out about the different circadian cycles that use chemical clocks to help us keep time in the long term (hours, days, etc.). This doesn't seem to explain how we can so accurately count seconds. Musicians can count time extremely precisely in even shorter intervals than seconds. Is it a chemical clock responsible? If you could explain the whole process to me it would be great. Thanks.

Detection of rhythm is a separate function from general musicality, but both can be affected by the same brain damage, or they can be independently affected:

  A range of rhythmic deficits has been described, including the inability to reproduce rhythmic patterns or to discriminate between them, and the inability to perform music rhythmically, or to keep time to music, including dancing in time. These deficits may occur in combination with other musical deficits, such as impaired vocal and instrumental skills ... rhythmic and metric organisation can be differentially impaired in brain damaged patients, supporting the relative independence of functions of the rhythmic system. In terms of cerebral lateralisation, Peretz and Morais [43] suggested that metric organisation may be ascribed to the right hemisphere, whilst smaller rhythmic groupings are encoded by the left hemisphere. ... Neuropsychological studies of groups of patients, however, have generally shown more variable lateralisation effects, particularly in recent research [25,36,46]

--Modelling rhythmic function in a musician post-stroke

So it seems that the detailed neuroanatomy and function of rhythm isn't completely understood, but it is a fairly specific function.  One suggestion is that it's  linked to language ("We conclude, then, that this effect is linked to language dominance and not handedness." -- Rhythm and dominance), but I don't know how widely this is accepted.  Possibly Common neural mechanisms for explicit timing in the sub-second range. offers more insight, but I don't have access to the full article and the abstract isn't very helpful.


are the spontaneous generation and evolution the same idea but in a different time scale? I was in my biology class, learning the history of spontaneous generation and how this idea was discarded. I told my teacher that is the same as evolution but in a different timeline. I Argue that evolution does not explain how life formed, but complemented by abiogenesis. Ultimately it is almost the same thing. Therefore it could not rule out spontaneous generation.

I got an F.

My appreciation is so wrong?

You are right in the sense the evolutionary biology doesn't try to explain the origin of life as it is not within its scope. Other fields of biology investigate the question of origin of life (abiogenesis).

Now, there is a very important difference between spontaneous generation and evolution. Life originated at some point and the through repetitive speciation events, created the whole diversity of species existing on earth. You could say that what really happens is that there was one spontaneous creation of life (although there is more a continuum from non-living to living things than a sudden switch from non-living to living) out of non-living things.

The main fallacy of spontaneous generation is that under the spontaneous-generation-conceptualization of life, every species are made de novo and independently which is definitely not the case as in reality species speciate (split in two) causing the existence of to two new species. There are tons of fallacies hidden behind the spontaneous generation conception of life, one of which relates to the concept of species and another one is the origin of within population variation.

So, in short spontaneous generation is definitely something different from a single abiogenesis and evolution and the hypothesis of spontaneous generation has been ruled out a long time ago already.

So I am not so much aware of the grading philosophy in your school but your argumentation was wrong and probably the F was worth. Next time, you will probably want to discuss your opinions with your teacher before the test to make sure you agree.


Why don't our cells merge when their phospholipid membranes touch each other? Membranes of our cells consist of lipid bilayer (with some other components mixed in).  Why wouldn't those lipid bilayers glue to each other and make the cells merge? If you suppose that it's due to additional components in the membrane that prevent them from gluing together, consider the case of liposomes, which don't contain additional components, but seemingly don't glue as well.

I'm primarily interested in quantitative physical chemistry aspect of the matter.

Phospholipid bilayers found in cells are usually negatively charged. The phosphate groups repel each other by like charges and prevent two membranes from coming too close to each other. Membranes are also full of proteins and often coated with carbohydrates, which serve to keep membranes from interacting too strongly. See this diagram of a membrane bilayer:

Even this diagram is probably cleaned up.

From a more physical chemistry perspective, the energy barrier for flipping a lipid in a bilayer is pretty high, since the polar head group doesn't like passing through the hydrophobic layer. Bringing two membranes together would require overcoming the charge-charge repulsion and flipping around the inner two layers of lipids, so you go from 4 layers to 2.

Interestingly, there are mechanisms for fusing membranes, such as using cationic lipids. These would turn charge repulsion into charge attraction. The lipid ion pairs tend to have shapes that don't support bilayer formation, and tend to prefer micelle or inverted micelle shapes. These have been utilized to break down vesicle membranes and allow large molecules to pass through, like DNA or proteins, and are used in genetic modification of cells.


Mutation That Loses Stop Codon Someone asked this in my class and my instructor wasn't sure in her answer, doesn't anyone know what happens in protein synthesis if a mutation causes mRNA to not possess a stop codon? Would the protein eventually stop? Would it keep coding into the poly-A chain and insert a bunch of phenylalanine?

No, this will not happen. mRNAs are inspected in the nucleus before they are exported into the cytoplasm (at least in eukaryotes), where transcription and translation don't happen at the same place. This ensures that no mRNAs without stop codons or premature stop codons are exported. This phenomenon is called
"mRNA surveillance". mRNAs that do not pass this quality check, are degraded. See the Wiki reference for some basic information and the references below for more.

References:

Process or perish: quality control in mRNA biogenesis.
The exosome and RNA quality control in the nucleus
A faux 3′-UTR promotes aberrant termination and triggers
nonsense-mediated mRNA decay


How to create a 3D density map of a system of varying number of particles? I have a time-dependent system of varying number of particles (~100k particles). In fact, each particle represents an interaction in a 3D space with a particular strength. Thus, each particle has (X,Y,Z;w) which is the coordinate plus a weight factor between 0 and 1, showing the strength of interaction in that coordinate. Here http://pho.to/9Ztti I have uploaded 10 real-time snapshots of the system, with particles are represented as reddish small dots; the redder the dot, the stronger the interaction is.

The question is: how one can produce a 3D (spatial) density map of these particles, preferably in Matlab or Origin Pro 9 or ImageJ? Is there a way to, say, take the average of these images based on the red-color intensity in ImageJ?

Since I have the numerical data for particles (X,Y,Z;w) I can analyze those data in other software as well. So, you are welcome to suggest any other analytical approach/software

Any ideas/comments are welcome!

R packages misc3d and rgl. The function image3d in misc3d does what you need and is very parametrizable via rgl (change the transparency, the view angle, axes, etc...). I used it with fairly big arrays (~10000000 data points/plots) and it produced great 3D density plots.

Both R (e.g. package biOps) and Matlab (image processing toolbox) have very powerful tools for image analysis if you need to get for example RBG levels in your plots but as far as I understood, you have the 3D arrays containing the interaction values, right?

Matlab proposes similar tools if you prefer Matlab (don't remember the exact functions) over R and both will require a fair amount of RAM as the data must be loaded in the environment.

As your system is time dependent you can also create movies fairly easily if you wish so (e.g. rgl's movie3d function).

Here a quick example of a 3D density plot:


Strongest muscle of Human Body Which is the strongest muscle of human body ?

Confusion b/w Masseter muscle (Muscle of Jaw) and Tongue and Muscle of Heart and Muscle of Uterus.

You'll be interested in THIS Wikipedia article. It really depends on how you define "strongest" (Newtons, Wattage, Newtons per Kilogram, etc.). Here are a few relevant excerpts from the article:

In ordinary parlance, muscular "strength" usually refers to the ability to exert a force on an external object—for example, lifting a weight. By this definition, the masseter or jaw muscle is the strongest. The 1992 Guinness Book of Records records the achievement of a bite strength of 4,337 N (975 lbf) for 2 seconds. What distinguishes the masseter is not anything special about the muscle itself, but its advantage in working against a much shorter lever arm than other muscles.
If "strength" refers to the force exerted by the muscle itself, e.g., on the place where it inserts into a bone, then the strongest muscles are those with the largest cross-sectional area. This is because the tension exerted by an individual skeletal muscle fiber does not vary much. Each fiber can exert a force on the order of 0.3 micronewton. By this definition, the strongest muscle of the body is usually said to be the quadriceps femoris or the gluteus maximus.
The heart has a claim to being the muscle that performs the largest quantity of physical work in the course of a lifetime. Estimates of the power output of the human heart range from 1 to 5 watts.[14] This is much less than the maximum power output of other muscles; for example, the quadriceps can produce over 100 watts, but only for a few minutes. The heart does its work continuously over an entire lifetime without pause, and thus does "outwork" other muscles. An output of one watt continuously for eighty years yields a total work output of two and a half gigajoules.


What does it take to start producing(cultivating) probiotics? Is there a DIY way?
Is it possible to make a bacteria strain from scratch based on an existing one ? (for example lactobacillus reuteri).

I did a master's thesis involving enzymes from a probiotic bacteria. Many of the known probiotics were cultivated from faeces but others have also been isolated from breastmilk. Many of the probiotic bacteria are strict anaerobes and can only be succesfully cultivated in modified atmosphere. You may need to use selective plating with various prebiotic compounds such as Galactooligosaccharides or similar compounds in order to control bacterial growth. I recommend incubating at 37°C or slightly below depending on how well controlled your incubator is.


Identify this large exotic bird spotted in Taipei, Taiwan A few months ago while backpacking in Taipei I found this very intriguing large bird facing off a curious puppy in a fairly busy pedestrian area.

The bird did not attempt to fly. None of the Taiwanese locals could tell me what it was and attempts to Google it via description all failed.

I'd appreciate learning the species name, common name in English, and/or common name in Chinese:

For me it looks like a Malayan Night Heron, Gorsachius melanolophus.

They seems to be common in this part of Asia, see the distribution.

It looks strange because he probably get scared.


How do you write genotypic and phenotypic ratios? If two homozygous recessive parents are crossed, I know that all of the offspring will be homozygous recessive as well. Would you write the genotypic ratio as 0:0:4 then and the phenotypic as 0:4? (Does order matter? i.e. compared to 4:0)
Also, if the results are 2 homozygous dominant and 2 heterozygous, is it necessary to put the zero for recessive (2:2:0) or would 2:2 be fine?

I don't think there is formal notation for those ratios.

One would note that perfect dominance and recessivity, perfectly discrete phenotypes without pleiotropy and without environmental variance is extremely rare and these examples are pretty much only encountered in intro classes but never in the real life. There is hence, for the phenotypes at least, really no need for any formal notation here.

That being said, out of clarity, I would definitely prefer 0:0:4 (genotypes) and 0:4 (phenotypes) over 4 (for either genotype or phenotype) and I would definitely prefer 2:2:0 over 2:2


How do rare mosquito borne diseases get transmitted if they are so rare? I recently read a somewhat alarmist notice by the state board of health in NH who claimed that some man had tested positive for Jamestown Canyon virus, a rare disease even in its natural environment of Colorado. Supposedly the man has not travelled out of state.

So, I am wondering how it is possible for such a virus to be transmitted. My understanding is that a mosquito only bites twice then it breeds, so basically what has to happen is the first bite has to be on an infected human (or animal) and then the second bite on the victim. So, if this guy got Jamestown Canyon virus, then he must have been in mosquito range of some other infected creature of which we have no knowledge.

Now, unless there is some type of animal that is endemically infected with Jamestown Canyon virus which is transferable to humans, it would seem unlikely to me that there would be any source from which the man could have gotten the virus.

So, I am wondering what kind of plausible scenario would have made this disease transmission possible, assuming it really occurred?

Via Wikipedia:

The virus is transmitted in saliva to a vertebrate host when an infected mosquito takes a blood meal. It thus cycles between mosquito and vertebrate amplifier hosts, mainly white-tailed deer. In a study from Newfoundland, JCV was significantly associated with large mammals such as sheep, cattle and horses. In Michigan and Ontario moose and bison are believed to be the primary reservoir.[3]
The virus winters in mosquito eggs, which it reaches by transovarial transmission. The female mosquito lays eggs that carry the virus, and the offspring can transmit the virus to deer or ruminants and humans. Infected mosquitoes were found equally distributed throughout the state of Connecticut, irrespective of land use.[4]

So, the virus has a reservoir in (primarily) deer, an infected deer gets bitten by a female mosquito, the mosquito lays eggs with the virus, the resulting mosquitoes can spread the disease by biting another large animal or human.
The reservoir needs to be large enough to ensure the virus survives year over year, but there doesn't need to be any special mechanism for it to travel outside the predominant range; there have been cases in several states in the northeast, though rare.

References [3] and [4] are:
[3] Goff G, Whitney H, Drebot MA (2012). "Roles of host species, geographic separation, and isolation in the seroprevalence of Jamestown Canyon and snowshoe hare viruses in Newfoundland". Appl. Environ. Microbiol. 78 (18): 6734–40. doi:10.1128/AEM.01351-12. PMC 3426688. PMID 22798366.
[4] Andreadis TG, Anderson JF, Armstrong PM, Main AJ (2008). "Isolations of Jamestown Canyon virus (Bunyaviridae: Orthobunyavirus) from field-collected mosquitoes (Diptera: Culicidae) in Connecticut, USA: a ten-year analysis, 1997–2006". Vector Borne Zoonotic Dis. 8 (2): 175–88. doi:10.1089/vbz.2007.0169. PMID 18386967.


Can anyone identify these mushrooms? Found in the Dolomites, Italy

in a wooden fence:

The first one is dyer's polypore or rusty gilled polypore.
https://en.wikipedia.org/wiki/Gloeophyllum_sepiarium
The second one looks a bit like orange peel fungus, although it could be something different.
https://www.wildfooduk.com/mushroom-guide/orange-peel-fungus/


Does adding antibiotic after 5-10 mins of innoculation affect the protein yield or growth? I've asked a lab colleague the same question. She said, it would loosen the bacterial cells in the LB medium and plasmids would come out. Is that true? and why?

That is not true. If you had forgotten to add the antibiotic before inoculation then you can add it before the bacteria starts growing. Make sure you add it when the bacteria is still in lag phase. If you add it later then it won't be effective as some non-resistant (non-transformed) bacteria would have already expanded their population. Ampicillin and kanamycin are best effective when the bacteria are growing. Even though these antibiotics are considered bacteriocidal, you would end up having unnecessary biomass in your culture.

So 5min delay for E.coli is not an issue. (I think this happens to all of us: forgetting to add antibiotic).


Phenotypic Variation of cattle - looking for academic sources Can someone please point me in the direction of a good academic article on the following:

What are possible sources of phenotypic variation of different 400 day weights of cattle?

Furthermore how much variation is likely to be due to each contributing source?

I have tried the following searches in google scholar:

Phenotypic, genetic, environmental cattle weight
Phenotypic variation cattle weight
Phenotypic variation
Phenotypic variation, genetic
genetic variation, dam, sire

Online Mendelian Inheritance in Animals (OMIA) is a database of genes, inherited disorders and traits in more than 135 animal species (other than human and mouse). At the moment, it has about 400 entries for Bos taurus, mostly disease phenotypes. This is probably the only attempt to exhaustively list such phenotypes.


Can someone identify this Brazilian bird? Photographing and documenting the local fauna (Brasília, DF, Brazil - Near Coordinates [-15.696506 -47.860013]), I found this rather unusual-looking bird whose name I couldn't find:

(Image was now uploaded to Wikimedia under my account "AlephGuira")

Possibly useful information:

One was seen preying on
what looked like Taturanas (https://en.wikipedia.org/wiki/Lonomia), but due to their venomous nature, I'm not sure.
The observed flock was composed of 7 birds.
There seems to be sexual dimorphism (The other one, not pictured, seems to be smaller, has shorter head feathers, whiter wings and lacks the orange-pointed beak).
They were first seen on a Pequi Tree (https://en.wikipedia.org/wiki/Caryocar_brasiliense).

These look very similar to the Guira cuckoo (Guira guira) which are found in this part of Brazil.

Source: https://en.wikipedia.org/wiki/Guira_cuckoo


Do muscles still hold glycogen reserves if there is no carbohydrate input Afaik skeletal muscles take glucose from the blood to store it localy as glycogen, to be used in the case of intensive exercise.

Does this still happen

if the calorie input is exclusively made up of fats and proteins?
while fasting / starving?

I know that muscles can run on fatty acids and ketone bodies.
And that the liver can create glucose by gluconeogenesis.

But is this "backup"-glucose still used to refill the glycogen stores in the skeletal muscles in those two respective cases? (while resting)

If not, how would the performance of exercises like sprinting, that normally make use of those stores, be affected?

Most of it isn't but a little bit is.

When your body has very little glucose and a lot of fat(Which can be the case if an overweight or obese person goes on a low carb diet) the ketones and fatty acids and glucose produced by the liver are used almost exclusively to keep the body alive although a little is synthesized into glycogen.

Specifically when you don't eat anything gluconeogenesis alone supplies enough for 1 day. Then the fat metabolism accelerates because gluconeogenesis is not enough. This is when you get into a state of ketosis(this can also happen in bodybuilders since increased muscle = increased fat metabolism). This ketosis causes fast weight loss from not just water like a lot of other diets but also from fat. This fat then eventually depletes and it metabolizes protein exclusively(during all this time it does metabolise some protein). However that can't continue forever even if the amino acids get reused over and over again because some are used to produce ATP. Thus you eventually would die from starvation with obese people surviving longer than underweight people.

Anyway as far as exercise assuming that you start off obese, getting your body into a state of ketosis makes your performance even better than on just glucose alone after a while of adjusting to fat metabolism since 1 molecule of palmatic acid(16 carbon fatty acid) produces 106 ATP compared to 32 ATP for 1 glucose molecule so your muscles can go longer without being exhausted. Theoretically someone who is 50 pounds overweight could exercise 24/7 for several days if he/she is in a state of ketosis.

Here is a reference to the low glycogen and increased muscle performance:
http://www.bodybuilding.com/fun/glen12.htm

As to why it is 106 ATP it is because each NADH produces 2.5 ATP and each FADH2 produces 1.5 ATP and because of the activation step using 2 ATP just like how NADH transport from cytoplasm to mitochondria takes 2 ATP, 1 per NADH in glycolysis.


Do distinctions between dry, tickly and chesty coughs have any medical basis? Background

At least in Britain you normally come across distinct kinds of cough medicine "chesty", "dry" and "tickly".

Questions

Are "chesty", "dry" and "tickly" coughs always due to microoganisms?
For the types of cough that are infectious, are differences due to different species of micro-organism or the same micro-organism at different stages of its development?
Do the alternative treatments (e.g. levomenthol, squill, liquorice for chesty vs. glycerol for dry/tickly) merely deal with symptoms or do they actually help fight the infection?

Related

A related question is: What is the cause of dry cough?

If I may add to what Resonating has said, when it comes to infections, dry cough is usually associated with a viral infection, whereas wet cough is usually caused by bacteria. The two are treated very differently - dry cough is remedied with cough-supressing drugs (antivirals are rarely needed), whereas bacterial infections are medicated with antibiotics (antivirals are NOT antibiotics) and drugs that help clear the mucus from the respiratory pathway. Treating wet cough with dry cough medications is not only ineffective, it can also be dangerous. One more thing - not all bacterial infections necessitate antibiotics which should be used sparingly because the world is running out of antibiotics.


What comes out of this bump in this vegetable? I live in Denmark, Europe and I have in my garden this gigantic vegetable.

It has a big bump on the top and i was wondering about what comes out of it?

I think your vegetable is a leek, or a closely related allium. If this is the case, you are seeing its flowerbud. Congratulations, it will become quite pretty in some days, I know people who use leeks as decoration plants instead of vegetables.


How to find a gene sequence? So I need to learn how to find the sequence of a gene, polyphenoloxidase. Please do not do this for me. Tell me how to approach the problem.

I have found : https://www.ncbi.nlm.nih.gov/gene and searched for polyphenoloxidase and get a list of results.

Here is one PPO page:
https://www.ncbi.nlm.nih.gov/gene/107923401
There is a FASTA sequence there under " NC_030099.1 Reference ASM98774v1 Primary Assembly" but I am not sure if PPO gene is there.

You can find the sequence in the gene database, but it is perhaps easier to search the nucleotide database if you are only looking for the sequence of nucleotides.


What arthropod is this? Location: Johannesburg, South Africa

Colour: Brown/Grey

Legs: 6 or 7 pairs

Size: ~10mm

I've been finding these guys in my bath tub the past two mornings. I've caught and released them. I'd like to know what they are so that I can decide whether pest-control measures are needed.

That is an Isopod crustacean, in the suborder Oniscidea https://en.wikipedia.org/wiki/Woodlouse. These are harmless, so I would not worry about contacting pest control. They are also known as "pillbugs".


How Does The Presence of Livestock on Land Increase Net Methane Production? It's a hot topic, and I've just read this article that debunks the claim I'm about to make - But even though I read it, I still don't really understand it. I'm happy to change my opinion if I understand the facts.
Suppose we have a closed system, imagine a pasture in an aquarium. Light goes in, grass grows, dies, decays, is recycled, all that good stuff. I imagine the air going into the aquarium is pretty atmospheric, and the air exiting has been changed depending on the amount of CO2 that is absorbed through photosynthesis, the amount of O2 is absorbed through plant respiration, and the amount of greenhouse gasses produced from decaying plant material in the thatch/soil.
(I think I have that right - my biology education doesn't go past high school level)
Now suppose we add a cow into the mix. If anything, to me, the cow reduces net emissions while it grows because less grass decays, and is instead turned into cow. Once the cow is mature, in this closed system, it's only eating and "processing" the grass that was already part of this natural cycle of growth/decay.
Here's where I think I am possibly going wrong:

Does the cow increase the amount of "decay"? Does eating the grass make it re-grow faster, thus speeding up that natural cycle?
Or, does the cow output different (more harmful) greenhouse gasses than the grass would normally produce through decay?

In short, how does the cow increase emissions? It can only have eaten what has already been grown -  And what has grown is doomed to someday decay and be re-released into the atmosphere anyway. I don't particularly like having contrary opinions, so help me out!

Ruminant digestion produces a lot of methane.
Cows are ruminants, and ruminants produce a LOT of methane. Sheep and goats are also ruminants but their are far fewer of them. Ruminants use methanogenic bacteria to breakdown their food, these bacteria, as there name implies release methane as a byproduct.  Ruminants produce a lot more methane than other herbivores becasue of this.
Decaying grass normally produces CO2 as do many native herbivores. Cows like most herbivores only convert a very small amount of the grass they eat into cow. Herbivore digestion is not terribly efficient, not surprising the grass does not what to be easy to digest.
Farming also puts a lot more herbivore mass on a piece of land than it would normally have, further increasing the effect, that is the purpose of farming to get more out of the land than simple hunter/gathering could. This is an issue becasue methane is a FAR more effective greenhouse gas than CO2.
Feeding cattle often involves replacing existing ecosystems which high yield feed crops and this can release a lot of CO2 and/or Methane depending on the original ecosystem just from the change, but it also means that feed is now producing methane instead of CO2 it would be if eat by non-ruminants.
Source
Source 2


How would one track a mineral nutrient in a plant in order to prove that nutrient has been re mobilized? Before abscission - senescence of a plant structural components that contain mineral nutrients (E.g. Magnesium, Potassium...) are re-mobilized from the senescent tissue and used in other plant tissue for anabolic activities.
Could we design an experiment to prove this?
I was told that radioisotope method would work. We can detect the presence of the radioactive particle in one part at a time-point, but how would we know whether it is the very same particle that shows up elsewhere after abscission?

It is not possible to track individual molecules within a plant. However, one can track the level of radioactivity from place to place. So, in the case you are talking about, one would find that some level of radioactivity persisted for a time at one location, then it is observed to decline while it increases in another. There also might be a delectably increased level of radioactivity along the pathway between those two areas - regardless, one would logically connect decreased activity in one area with increased activity in another.


Forensic genetics- why is mtDNA comparison sometimes better than nDNA comparison? Why is (in forensic genetics) in some cases more appropriate comparison of nuclear DNA but in some other cases comparison of mitochondrial DNA?

Is it because geneticists are sometimes unable to find nDNA or if nDNA is too damaged? Also could it be because of the structure of mtDNA (it's more protected against degradation, which is good for identifying old biological material)? I can't see any other advantages, since mitochondrial DNA mutations occur frequently, due to the lack of the error checking, but are there any that I am missing?

Thank you in advance.

mtDNA is present in a much higher copy number per cell than nuclear DNA.

According to this paper, there are approximately 4000 or so mitochondrial DNA copies per human muscle cell.

  copy number of mtDNA per diploid nuclear genome in myocardium was 6970 ± 920, significantly higher than that in skeletal muscle, 3650 ± 620 (P = 0.006).

This makes it far more likely that a non-degraded copy of mtDNA exists, considering that there are normally only 2 or 4 copies of nuclear DNA per cell per locus for almost all kinds of cells.


Inbreeding depression and dominance From this article,  second paragraph of the second page

  A classic theoretical result is that the mean of a character controlled by a single locus i with two alleles Ai1 and Ai2 is only affected by the value of f if there is some degree of dominance.

where f is the Wright's inbreeding coefficient.

The authors then add:

  Assume that the trait is scaled such that the values for the genotypes Ai1Ai1, Ai1Ai2, and Ai2Ai2 are -ai, di, and ai respectively. The quantities ai and di measure the effect of the locus on the character and the degree of dominance of the locus, respectively. With two alleles, there is a linear decline in the mean of a trait
  with increasing f either with overdominance (di > ai) or if the allele associated with an increased value of the trait is dominant or partially dominant (ai ≥ di > 0). With additive joint effects of different loci on the trait, this conclusion can be extended to a polygenic character; inbreeding decline occurs if the average value of di over all i is positive.

I don't understand why "[..] there is a linear decline in the mean of a trait
with increasing f either with overdominance (di > ai) or if the allele associated with an increased value of the trait is dominant or partially dominant (ai ≥ di > 0)"

Can you please explain why the mean of a character controlled by a single locus is only affected by the value of "f" if there is some degree of dominance.

Recap of the question:

Looking at a single locus trait ($A$) controlled by two alleles, $A_1$ and $A_2$, the phenotypic mean is only affected by inbreeding depression, $f$ (Wright's inbreeding coefficient), if there is some degree of dominance, $d$. Why?

Answer:

If we take inbreeding as a higher than expected frequency of homozygotes, such that if the frequencies of alleles $A_1$ and $A_2$ are $p = q = 0.5$ the expected frequencies of the genotypes in an outbred population, $P_{outbred}$, would be $p^2 = 0.25$, $2pq = 0.50$, and $q^2 = 0.25$.

Each genotype has the following phenotypic result on a trait $A_1A_1 = 5$, $A_1A_2 = 7.5$, $A_2A_2 = 10$... this is an additive trait with allele $A_1$ having an additive effect of 2.5, and $A_2$ an additive effect of 5.

We can then compare an inbred population of 100 individuals, $P_{inbred}$ where the frequency of $A_1A_1 = 0.5$, $A_1A_2 = 0$, $A2_A2 = 0.5$, to $P_{outbred}$ , where I use $\bar{X}$ to symbolise trait means.

$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 7.5) + (50 \cdot 10)}{100} = 7.5$

$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 7.5) + (25 \cdot 10)}{100} = 7.5$

So when the trait is additive the population means are equal. It is onlt when we add dominance to the situation that the population means will differ as a result of inbreeding. Continuing from the above example, the populations are the same size and structure, but $A_2$ is now completely dominant to $A_1$ such that $A_1A_2$ individuals now have a trait value of 10. Now

$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 10) + (50 \cdot 10)}{100} = 7.5$

$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 10) + (25 \cdot 10)}{100} = 8.75$

Thus inbreeding has affected the population mean in a trait which has dominance, it is basically because the heterozygotes are less common in an inbreeding population and this is where dominance effects are seen.

  "there is a linear decline in the mean of a trait with increasing f... with overdominance (di > ai)"

This is because in the case of overdominance, the outbred population mean becomes even more elevated - if we say now the $A_1A2$ trait is a phenotype of 15 the means become

$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 15) + (50 \cdot 10)}{100} = 7.5$

$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 15) + (25 \cdot 10)}{100} = 11.25$

  " there is a linear decline in the mean of a trait with increasing f... if the allele associated with an increased value of the trait is dominant or partially dominant (ai ≥ di > 0)"

The mean will increase if the dominant allele produces a smaller phenotype. Here we say $A_1$ is now completely dominant,

$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 5) + (50 \cdot 10)}{100} = 7.5$

$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 5) + (25 \cdot 10)}{100} = 6.25$

I hope that answers the question, I tried to answer last night but was too tired to think - this is just what I came up with on the walk to work today so I haven't had the time to check it/overthink it


How to define "Quasifixation" in continuous approximation of finite population? Background

Many models including the famous very first models derived by Sir Ronald Fisher in his early career, assume infinite population size. In an infinite population, an allele can rise in frequency (if its fitness is greater than the fitness of its counterpart(s)). This increase follows a logistic curve that never exactly reach a frequency of 1. Therefore, the term fixation does not apply to these model and in consequence the concept of quasifixation has been created.

Question

An allele is considered to be quasifixed if it reaches a frequency that is very close to 1. But how close? The decision is obviously arbitrary but when using a continuous approximation model in a finite population the question is necessarily raised and a decision needs to be made. How close should the frequency of an allele be to 1 so that it is considered to be quasifxed? The answer is probably a function of the population size $N$. What threshold do authors usually use in the theoretical population genetics literature? It would also be nice to have the definition of the author who first coined this term.

As I haven't found any guideline, I just went with chosing a threshold at $p = 1-\frac{1}{4N}$ for a diploid population. Allele $A$ is therefore considered quasifixed if its frequency $p$ is greater than $1-\frac{1}{4N}$ i.e. the number of occurrences (count) or the other allele is lower than $\frac{1}{2}$.


What are the blue and white things on this Sunburst lichen? I am a amateur photographer I found some interesting things when I got home and looked at my photos. There are some blue/white cocoon. I  like structures on top of the sunburst lichen. I live in Colorado and took these photos on January 23.

The small blue creatures coould possibly be (oribatid) mites.
I have them under my the binocular when I study lichen pretty often.
Their asociation with lichen is well documented


Serious question about a piece of meat Does anyone know some scientific rigorous way to look at a slice of meat. I am not asking what kind of meat it is or which part of the animal it came from. I wonder what is the different lining on the meat, what is that huge white spot in the middle and what do the cells of that red part look like and what they are called.

If someone can provide a reference on that it would be great.

The white circle in the center is a bone, probably the femur. The muscles are covered with an external later of fascia, the epimysium (here's a question with some information). These layers separate muscles from each other, and often fat will also deposit in the spaces between muscles, which is what the white lines between muscle bellies are. There is also some cutaneous fat.

This is probably a section through the thigh, possibly a pig (though it looks a little too red). Regardless, the muscle will have the same basic layout as the image below of a pig thigh from pork.org, even if your image is from some other mammal.

You have to rotate your image clockwise about 45 degrees to get them to match up. The back of the thigh is at the top of the image.


A trivial question on the meaning of "relatives" in an article on horizontal gene transfer Am I right in suggesting that by close relatives the author meant closely related species, or did he have individual organisms in mind?

  DETECTION OF HORIZONTAL GENE TRANSFER

  There are several approaches to identify genetic changes due to HGT,
  including:

  (1) experimental evidence, whereby a genetic marker is monitored for
  gene transfer to a recipient organism;

  (2) phylogenetic analysisof gene sequences to identify topological
  inconsistencies between different gene families;

  (3) nucleotide compositional analysis to identify any gene that has a
  nucleotide pattern that differs significantly from the overall genome;
  and

  (4) evolutionary scenarios to explain the patchy appearance of a
  genetic signature, sequence or function that is not shared by close
  relatives.

(From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese)

You are correct.

From the author's point of view there is not much difference, however. Phylogenetically speaking 'species' are kind of artificial distinctions that exist only as sets of individuals and don't usually convey information, so it makes sense to forget that species exist when talking about HGT. Hopefully that helps provide context for why such imprecise wording is so common.


Reliability of Sanger sequencing Hailed as the "gold standard" of sequencing, I was wondering to what Sanger sequencing owes its incredible accuracy to. If possible, I would like a quantification of the accuracy (because I doubt it is 100%, though possibly very close).

I understand ddNTP chain termination and the strategies involved in Sanger sequencing but I lack the connection to accuracy.

Thanks!

Reliability comes from the fact that in Sanger sequencing (AFAIK) the synthesis of the new strand to the template and the actual reading of the sequence is separated. As you may know Sanger seq uses capillary gel elfo. thus separating the newly produced DNA fragments on a single nucleotide difference, and the reading is done by fluorescence detectors (then base calling etc.) Now compared to this the other sequencing methods like Illumina and 454 detect each nucleotide incorporation that may produce less reliable signals. For eg. in Illumina colonies may overlap on the plate, or in 454 incorporation of multiple nucleotides at homopolymer regions cause a hard time deciding how many nucleotides have actually incorporated. Also it must be noted that quality of the singals / reads is not constant through out Sanger sequencing. The beginning and the end of the reads tend to have noisy and low quality signals, thus actually only the 100-500(-600)bp segment of the whole fragment can be read reliably. Also ABI's SOLID uses a 2 color color-space and each base is read twice and is extremely reliable (99.96% is said by the inventors). Also clever base calling and error correction algorithms may improve accuracy.

It is noteworthy to say that next gen sequencers also achieve high accuracy by taking advantage of their immerse throughput / output - due to clonal amplification of template sequences each original fragment is sequenced multiple times and errors in a single read can be corrected by the use of others.


How does food intake affect medicine? Why pill instructions recommends taking them before (after) meal? Even simple vitamins seem to have this in the instruction. Why is is so? Is there some simple model of how do pills interact with food? Does it depend on the food type? (What about drinks?)

Should not eating at all on some day be considered "before food" or "after food"?

From the Merck website :

Drug absorption is the movement of a drug into the bloodstream after administration.
Absorption affects bioavailability—how quickly and how much of a drug reaches its >intended target (site) of action. Factors that affect absorption (and therefore >bioavailability) include
1.The way a drug product is designed and manufactured
2.Its physical and chemical properties
3.Other ingredients it contains
4.The physiologic characteristics of the person taking the drug
5.How the drug is stored
If a tablet releases the drug too quickly, the blood level of the drug may become too high, causing an excessive response. If the tablet does not release the drug quickly enough, much of the drug may be eliminated in the feces without being absorbed, and blood levels may be too low. Drug manufacturers formulate the tablet to release the drug at the desired speed.

Essentially, most drug's absorption rates are slowed down by food in the digestive tract, which is beneficial for various reasons depending on the drug.
Some pills are irritants to the stomach, in which case they usually have a coating that may need an acidic environment to break down. Food would assist in this, as well as serving as a sort of diluting agent and even a physical barrier for the stomach.
Conversely, some nutrients (and certain pharmaceuticals) are absorbed by the stomach lining and small intestine much more efficiently when the body is actively digesting food, which is why vitamins and other supplements have the food recommendation.
I think that 'before or after' food should be read as 'shortly before or after', i.e., so food and pill are digested simultaneously. Otherwise, I believe they just don't mention it. Of course, this is a simplistic rendering of pharmacological absorption vis a vis food (there are some very specific interactions; grapefruit and various blood pressure medications come to mind), but this is the general answer to your general question, I believe.


Do young children grow in spurts It is a commonplace of my friends and relatives to remark that a young child (younger than 3 years) has had a recent "growth spurt". The underlying assumption is that young children do not grow taller continuously and steadily,  but have periods of rapid growth between periods of slow growth. But is that assumption true? I'm sceptical; I'm inclined to believe that growth is steady, and the idea of growth spurts is a flaw of perception.

So, what research have I done so far on this question? I've seen the height-age charts for children, and they are smooth, so there are no growth spurts synchronised across all children. But that smooth averaged growth could result from the average of many non smooth growth rates. So the question is about when considering a single child. A web search about children's growth spurts shows numerous parenting web-sites that assume that growth-spurts happen, without asking whether growth spurts actually happen. I found an old press release from Emory University about some research supporting the idea, but no better information.

Growth is neither even nor constant, It can vary quite a bit from month to month as hormone levels change, the growth curves you are seeing are a rough average.

You are having a hard time finding anything because it one of those pieces of knowledge that is so old people only rarely research it directly focusing more on deviations from it and you will likely only find good reference to it in textbooks. For a layman this means searches based on the terms you think you should use never find what you want, something as simple as adding the word "textbook" can make a huge difference. Google scholar will also help.

http://adc.bmj.com/content/51/3/170.short

https://books.google.com/books?id=YA-LdtyHJ9QC&pg=PA226&dq=evolution+of+the+growth+spurt&hl=en&sa=X&ved=0ahUKEwjkl4zCztjRAhVB74MKHRiuB7kQ6AEIHzAA#v=onepage&q&f=false


What is the importance of urea in mass spectrometry? What is the importance of urea in mass spectrometry? We use 8M urea to FASP our proteins prior to mass spectrometry.  What is the significance of using 8M urea? and how does it affect the proteins?

I think that the OP was asking about relevance of using urea with respect to the FASP method. In the FASP method, the primary denaturant is SDS . Protein are denatured with a ~4% SDS solution (buffered to pH 7.5 - 8.0). Then 8 M urea solution is used to replace the SDS. Urea serves two purposes here, first it keeps the protein denatured and in solutions as SDS is replaced/washed off. Second, because urea is a chaotropic agent, it reduces the size of SDS micelles which otherwise would block the pores of the membrane filter.

Read the original article here: http://www.nature.com/nmeth/journal/v6/n5/abs/nmeth.1322.html


Do viruses compete with each other or even infect each other? (Virus vs Virus) I have read on a few websites that there can be competition between
the viruses in a host for replication, nutrition etc. Do viruses fight against each other, i.e. are there viruses that infect or attack other viruses directly or indirectly?
If yes, can this property help in curing or limiting hazardous viruses such as HIV
using less hazardous viruses which can be cured and can compete with
these hazardous viruses?

From what I understand virus on virus action is not particularly common but it isn't unheard of.

Consider the Sputnik virophage which

  reproduces in amoeba cells that are already infected by a certain helper virus; Sputnik uses the helper virus's machinery for reproduction and inhibits replication of the helper virus.

Also consider the Mavirus virophage, which

  is a double stranded DNA virus that infects the marine phagotrophic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus. Mavirus can integrate into the genome of cells of C. roenbergensis, and thereby confer immunity to the population.

As a last example, consider the Organic Lake virophage, which

  is a double stranded DNA virus that infects the marine phagotrophic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus. [...] [It] preys on Organic Lake phycodnaviruses, which in fact may rather belong to Mimiviridae than to Phycodnaviridae.

So yes, viruses do at least occasionally attack viruses and inhibit their infectious potential and grant a sort of immunity. I'm not aware of any applications of this in medicine for now but maybe somebody else can add something to this if they know.


Check on 23andme what type of CYP2D6 substrate metabolizer I am CYP2D6 is responsible for the metabolism and elimination of approximately 25% of clinically used drugs. Which SNPs do I need to check on 23andme in order to determine if I'm a poor or ultrarapid metabolizer of CYP2D6 substrates, and how reliable would the results be?

I've found one article on this topic, but I'm not sure how accurate it is, and it doesn't cite sources.

PS: why isn't this information more readily accessible to 23andme users, given the relatively large risks incurred by not knowing one's reaction to a large number of drugs?

Unless your polymorphisms have been tested against a particular drug, you can't extrapolate a starting dosage for it based only on your genotype.  It's better to actually take the drug, and change dosage based on observations.

See this paper

https://www.ncbi.nlm.nih.gov/pubmed/24935087

  CONCLUSIONS AND RELEVANCE: In this meta-analysis of randomized
  clinical trials, a genotype-guided dosing strategy did not result in a
  greater percentage of time that the INR was within the therapeutic
  range, fewer patients with an INR greater than 4, or a reduction in
  major bleeding or thromboembolic events compared with clinical dosing
  algorithms.

.

  why isn't this information more readily accessible to 23andme users,
  given the relatively large risks incurred by not knowing one's
  reaction to a large number of drugs?

Because no-way no-how does 23andMe want to be in the business of giving medical advice.  Nor should they be, because for most things, we have no idea how to convert genotype knowledge anything medically actionable.


Can insects feel pain? Insects do have a nervous system, even if it isn't nearly as complex as that of other animals. Can insects or other arthropods sense pain? Does their aversion to harmful stimuli suggest that they can 'feel' pain in the sense that other animals seem to?

This question has been asked in different forums and many of the answers say that there is no nociception in insects. This book, however claims that Drosophila do have heat induced nociception and is mediated by TRPA ion channels. Also, there is a gene called painless whose mutation causes loss of nociception.


Are there organisms that "branch more" near the leaf? (I'm a computer scientist)

Tree branching is a fractal patterns in nature. I know stems typically branch in two at each level (self-similarity). I guess there are plants or other organisms that branch in 3 at each level (still self-similar).

But are there organisms where the stem first branches in 2, then at the next level branches in 3 or more? And maybe at the next (maybe the last) level branches even more, say in 7? It doesn't need to be the stem of a plant, it could be any part of any organism (fungi,...), e.g. the "flower part" of a plant, or a micro-organism.

I'm looking for places where just the branching factor changes, but otherwise little else. What I'm not looking for "branch by 2, branch by 2, branch by 2, and then the very final step is one level of fascicle where branching is 5". I would be fine it's "branch by 2, branch by 3, then fascicle where branching is >3".

I'm trying to find if there is something in nature (e.g. organism, geological, or physical structure) that follows this pattern found in a computer science algorithm, RecSplit, which I co-authored.

Like the following: it first branches in 3, and then branches in 8. The actual numbers don't matter to me, it might as well be branch in 2, then in 3, then in 5, or so.

I can't say that your question is very clear to me, but perhaps something of interest to you would be a common type of inflorescence called an umbel. specifically, a compound umbel with associated umbellets.

Compound Umbel:

 Source: Educational Technology Clearinghouse

Some examples can be found here

Again, since your post is not clear to me, I'll also include images of other complex inflorescences:

 Source: texaswildbuds.com   [the compound cyme might be of interest to you]


What is this spider I found in Idaho? I live in Moscow, Idaho and saw this guy early in the morning last week. It was about quarter sized if I recall. I've never seen one before and was in a hurry so I couldn't get a better picture, sorry.

This looks like a black trapdoor spider (I'm guessing male by the size of the abdomen), check out the photos on the page I've linked below and see what you think - and this is a pretty good picture, usually the photos friends send me are far more blurry!

http://www.spiderzrule.com/trapdoor1.htm


From which ancestor species did humans inherit orgasm? From what ancestors did humans inherit orgasm?

Do fish experience orgasm?

Are the male and female orgasm the homologues that can be traced to the time when there was no difference in sex between individuals (as in fish) or developed independently?

Let's assume that pleasure from sexual intercourse might be indicative of some sort of orgasm. Then this would suggest that any evidence of autoerotic behaviour would point to the existence of orgasm, or certanly physical pleasure.

I found this quotation on the Wikipedia page for Animal sexual behavior, amongst a lot of information about mammals :

  Many birds masturbate by mounting and copulating with tufts of grass, leaves or mounds of earth...

apparently from Bruce Bagemihl: Biological Exuberance: Animal Homosexuality and Natural Diversity. St. Martin's Press, 1999. ISBN 0-312-19239-8

If this is taken to imply that the last common ancestor of birds and mammals experienced this pleasure then we have got fairly deep into evolutionary history, although not as far as fish.


How can one calculate "probability of possessing a ‘perfect’ profile" from "typical optimal genotype frequencies"? Can anyone please explain how the "Probability of possessing a ‘perfect’ profile" was calculated from "typical frequency of optimal genotype" in Table 1 in this paper?

Paper link here

They appear to have simply considered each allele independently. This means that if there are say 2 alleles for a trait, and they are both present at a frequency of 0.1 in the population, then you have a 0.01 chance of having both of them. This is probably an okay assumption for their purposes (in reality some might be linked and would associate non independently). Their point is simply that as the number of alleles go up, having all the best ones becomes increasingly unlikely.


Genetic mutations in plants I am trying to plant some trees which are usually native to colder climates into Subtropical climate, is there any possibility that if i plant these 20 trees saplings in winters they will grow to be a tree, due to some random genetic mutation, given all nutrients all provided to it?

Tree in Question is Deodar

I think that the potential survival of your seedlings could more likely be credited to your care and management than random genetic mutations. While, of course, DNA mutations happen during cell replication, evolution at the whole-plant scale primarily occurs over the course of generations, not the lifespan of a single plant. You may well be able to get these trees to thrive in your environment with some care and love, although they may not grow as vigorously. Here is a link to a gardening website with tips on growing ceaders in a home garden, although I agree with the commenter that you'll get much better help at the Gardening and Landscaping Exchange!

Best of luck with your horticultural endeavors!


How long could Earth's oxygen supply last if no new oxygen were produced? I read in an article or heard in some documentary that there's so much oxygen in the atmosphere that even if all photosynthesis stopped, there's already enough to last us a long time.

Is this correct? Why or why not? If so, how long is this 'long time', roughly? I've seen estimates between 15,000 to 150,000 years.

Disclaimer:

This is going to be a very mathematical answer. Before answering it, I assume that you are only asking about humans, assuming that all other organisms don't require $O_2$ to survive (as it will complicate the answer many many times).

List of variables:

V     = total volume of air on earth (in l)
V'    = total volume of oxygen on earth (in l)
V(1)  = volume of oxygen used by 1 person in whole lifetime (in l)
V(a)  = volume of oxygen used by whole mankind (one generation) in whole lifetime (in l)
V(p)  = percentage of total oxygen used by whole mankind (one generation) in whole lifetime

Method used:

$ \%\hspace{1mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}per\hspace{1mm}generation = \underline{\hspace{3mm}Volume\hspace{5mm}of\hspace{5mm}O_2\hspace{5mm}in\hspace{5mm}air\hspace{3mm}}\times\hspace{1mm}100$
$\hspace{83mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}by\hspace{1mm}humans$

$Number\hspace{1mm}of\hspace{1mm}years = \underline{\hspace{2mm}Number\hspace{1mm}of\hspace{1mm}years\hspace{1mm}in\hspace{1mm}1\hspace{1mm}generation\hspace{2mm}}$
$\hspace{42mm}\%\hspace{1mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}per\hspace{1mm}generation$

Procedure:

Lets first find out the total amount of air on earth.

From this:

  The air sphere measures 1999 kilometres across and weighs 5140 trillion tonnes.

From here:

  At sea level and at 15 °C air has a density of approximately 1.225 kg/m3

Total volume of air:

$volume = mass \hspace{1mm} / \hspace{1mm} density$

$V = 5140 \times 10^{12} \hspace{1mm} tonnes \hspace{1mm} / \hspace{1mm} 1.225 \hspace{1mm} kg.m^{-3}$

$V = 4195.9 \times 10^3 \times 10^{12} \hspace{1mm} m^3$

$V = 4195.9 \times 10^3 \times 10^{12} \times 10^3 \hspace{1mm} l$

$V = 4195.9 \times 10^{18} \hspace{1mm} l$

Now, from this, 20.95% of this is $O_2$ i.e.

$V' = 4195.9 \times 10^{18} \times 20.95 / 100$

$V' = 87904.489 \times 10^{16}$

$V' = 879.04 \times 10^{18} \hspace{1mm} l$

Moving on to next part, from this:

  a human being uses about 550 liters of pure oxygen per day.

From this:

  71 years was the average life expectancy at birth of the global population in 2013.

$V_1 = 550 \hspace{1mm} l.day^{-1}.person^{-1} \times 25915 \hspace{1mm} days$

$V_1= 142.53 \times 10^5 \hspace{1mm} l.person^{-1}$

From this:

  The world population (the total number of living humans on Earth) was 7.349 billion as of July 1, 2015.

So

$V_{a} = 142.53 \times 10^5 \hspace{1mm} l.person^{-1} \times 7.349 \times 10^9 people$

$V_{a} = 1047.452 \times 10^{14} \hspace{1mm} l$

Finally

$V_p = V_a / V' \times 100$

$V_p = (1047.452 \times 10^{14}) / (879.04 \times 10^{18}) \times 100$

$V_p = 1.191 \times 10^{-2}$

$V_p = 0.0191 \hspace{1mm} \% $

This gives the percentage of total $O_2$ in air used by one human generation. From this, we can find the number of years for which $O_2$ will last, as I have done below:

$25,915 \hspace{1mm} days = 71 \hspace{1mm} years$

$71 \hspace{1mm} years = 0.0191 \hspace{1mm} \%$

$1 \hspace{1mm} \% = 71 / 0.0191 \hspace{1mm} years$

$100 \hspace{1mm} \% = 3717.277 \times 100 \hspace{1mm} years$

$\hspace{13mm} = 371,727.748 \hspace{1mm} years$

Conclusion:

So, yes at least humans can live for a very long time without plants doing any photosynthesis (ideally). 371,727 years seems too large a period of time, but it is just based on ideal assumptions, this number would come down (maybe into your specified range) when more variables are added.

For example:

To show extent of deviation by addition of factors, I add a very general, but complex factor in the expression: air pollution.

How much $CO_2$ is released per year can be estimated from this:

  In 2011, utility coal plants in the United States emitted a total of 1.7 billion tons of CO2

And with the contribution of countries like China, India, Europe, etc. that number should rise up to at least 2.5 million tonnes (its just that I couldn't find the worldwide data on it).

Now:

$1 \hspace{1mm} C + 1 \hspace{1mm} O_2 \rightarrow 1 \hspace{1mm} CO_2$

$2.5 \times 10^9 \hspace{1mm} kg \hspace{1mm} CO_2 \Rightarrow 2.5 \times 10^9 \hspace{1mm} kg \hspace{1mm} O_2$

So, 2.5 million tonnes more $O_2$ is being used each year from the environment. But, there is another twist in this. From this:

  WHO reports that in 2012 around 7 million people died - one in eight of total global deaths – as a result of air pollution exposure.

It means that 7 million people less will consume $O_2$ each year i.e.

$Net \hspace{1mm} population = 7349 \times 10^6 - 7 \times 10^6$

$\hspace{32mm} = 7.342 \times 10^9$

$V_{a} = 142.53 \times 10^5 \times 7.342 \times 10^9$

$V_{a} = 1046.455 \times 10^{14} \hspace{1mm} l$

$V_p = V_a / V' \times 100$

$V_p = (1046.455 \times 10^{14}) / (879.04 \times 10^{18}) \times 100$

$V_p = 1.1904 \times 10^{-2}$

$V_p = 0.01904 \hspace{1mm} \% $

$25,915 \hspace{1mm} days = 71 \hspace{1mm} years$

$71 \hspace{1mm} years = 0.01904 \hspace{1mm} \%$

$1 \hspace{1mm} \% = 71 / 0.01904 \hspace{1mm} years$

$100 \hspace{1mm} \% = 3728.991 \times 100 \hspace{1mm} years$

$\hspace{13mm} = 372,899.159 \hspace{1mm} years$

So, overall number increases instead of decreasing. This example was just to show how adding more factors to the equation would deviate the overall answer, and how large that deviation can be.


Powdered meal replacement vs regular meal Can a person live with this alternative nutrition? Of course, assuming that eating pleasure is assumed the same.

The nutrients that contain are far better than average meal a person eats the majority of times, al least me. However, since is not solid food, do our digestive system need to work harder?

Scientific reports would be appreciated, comparing these two modes of feeding.

Yes you could live off a protein shake type supplement if it had the vitamins, minerals, protein, carbohydrates, and fats you would need. Would you want to? Probably not.

First thing we must determine is the protein whey or soy? If a male is consuming this meal replacement and the only protein is from soy, their estrogen levels will be elevated. In Soy Protein Isolate Increases Urinary Estrogens and the Ratio of 2:16α-Hydroxyestrone in Men at High Risk of Prostate Cancer, Dr.s Jill M. Hamilton-Reeves, Salome A. Rebello, William Thomas, Joel W. Slaton, and Mindy S. Kurzer concluded that soy does elevated estrogen in men which helped with the reduction of prostate cancer [1], but as a male, you wouldn't want to have a lifetime of increased estrogen [2].

Infertility. Estrogen is partly responsible for creating healthy
sperm. When estrogen levels are high, sperm levels in semen may fall.
This can lead to fertility issues.
Gynecomastia. Estrogen may stimulate breast tissue growth. Men with
too much estrogen may start developing larger breasts.
Erectile dysfunction. A balance of both testosterone and estrogen is
important for healthy sexual growth and development. Sexual function
may be impacted when these hormones become imbalanced. Men with high
levels of estrogen may have difficulty getting or maintaining an
erection.

So to be on the safe side, let's assume that the protein is from whey and we have one less thing to worry about. Now as for the vitamins and minerals, the Mayo Clinic states that [3]:

  Supplements aren't intended to be a food substitute because they can't replicate all of the nutrients and benefits of whole foods, such as fruits and vegetables.

and there are three main differences:

Greater nutrition. Whole foods are complex, containing a variety of
the micronutrients your body needs — not just one. An orange, for
example, provides vitamin C plus some beta carotene, calcium and
other nutrients. It's likely these compounds work together to produce
their beneficial effect.
Essential fiber. Whole foods, such as whole grains, fruits,
vegetables and legumes, provide dietary fiber. Most high-fiber foods
are also packed with other essential nutrients. Fiber, as part of a
healthy diet, can help prevent certain diseases, such as type 2
diabetes and heart disease, and it can also help manage constipation.
Protective substances. Whole foods contain other substances important
for good health. Fruits and vegetables, for example, contain
naturally occurring substances called phytochemicals, which may help
protect you against cancer, heart disease, diabetes and high blood
pressure. Many are also good sources of antioxidants — substances
that slow down oxidation, a natural process that leads to cell and
tissue damage.

So you could live off of some meal replacement shake for the rest of your life but should you? Probably not.


In what animal species is the sex ratio skewed in favour of the fertile female? Ants have something like a single fertile female to several males. The same applies to bees, and larger animals - elephants too. Is the sex ratio universally skewed in favour of the female? What animal species exhibit this ?

It is advantageous to have a skew towards more males. Males can be expendable as they are only required briefly for impregnation and can then focus on providing resources for the mother and young and protection. This breaks down when this is no longer the case, for example in humans we are closer to a 50/50 divide.

This article notes that in aphids, there are twice as many females as males, the same is true for daphnia. I don't think the reason behind this is known. In reptiles, the female to male ratio can depend on temperature of incubation thus this can lead to strong fluctuations.

An interesting principle is Fisher's principle:

  Fisher’s principle explains why for most species, the sex ratio is
  approximately 1:1. Bill Hamilton expounded Fisher’s argument in his
  1967 paper on “Extraordinary sex ratios” as follows, given the
  assumption of equal parental expenditure on offspring of both sexes.
  Suppose male births are less common than female. A newborn male then
  has better mating prospects than a newborn female, and therefore can
  expect to have more offspring. Therefore parents genetically disposed
  to produce males tend to have more than average numbers of
  grandchildren born to them. Therefore the genes for male-producing
  tendencies spread, and male births become more common. As the 1:1 sex
  ratio is approached, the advantage associated with producing males
  dies away. The same reasoning holds if females are substituted for
  males throughout. Therefore 1:1 is the equilibrium ratio.
  Source


What is the nature of plasmids? What are the plasmids composed of? Are they composed of genomic or non-genomic DNA?

I guess the answer is "genomic DNA" but I'm not sure.

You probably mean genomic and non-genomic DNA - Plasmids are small rings of non-genomic double-stranded DNA in Bacteria. They replicate mostly indepently of the genomic DNA can can occur from a few to several hundred copies per cell. See the illustration from the Wikipedia:


Proteomics data Vs Transcriptomics data? I want to use either of Proteomics or Transcriptomics data for integrating it into my kinetic model. Before proceeding, I want to know what are the advantages of using either of them so that I could make an informed decision on it!

Many studies have shown that the best we can do is integrating both transcriptomics and proteomics data with our kinetic model, but I've some time constraints and have to proceed with only one of those.

My effort and findings: I've found from discussions with researchers that gathering transcriptomics data has an amplification step which increases the chance of finding a particular one whereas gathering proteomics data has no such step but has fragmentation and then rejoining which creates many problems(such as splice variants etc) and thus leads to a loss of data. But a PostDoc told me that even after the loss of that data, I'll get more information from Proteomics data.

I want to know such type of points and want to know if these are valid or not!

This is what I found from doing some research. Comments are welcome at any point!

Capture percentage for data gathering:

Transcriptomics Data: There's an amplification step in Transcriptomics data gathering methods. Hence, it's possible to capture almost the totality of the Transcriptome using those methods(scRNA seq methods, Nanopore tech, Spatial transcriptomics, etc)
Proteomics Data: There's no amplification step in Proteomics data gathering methods. Those methods have fragmentation and a rejoining step which leads to a loss of the data.

Scalability of methods:

Transcriptomics Data: Scalable methods available
Proteomics Data: Less scalable methods for protein studies

Reference availability:

Transcriptomics Data: Fully annotated references available on consortiums such as ensembl biomart, etc
Proteomics Data: Universal and Comprehensive Human Proteome reference is still in question and because of the incomplete and inaccurate references, much of the newly generated data is being rendered useless

Uniformity

Transcriptomics Data: Lots of publications on pipelines, and their benchmarking available
Proteomics Data: Lack of uniformity across labs/research groups and lack of related literature lead to differences in protein fragmentation and solubilization and differences in algorithms to run analyses

Technical Bias

Transcriptomics Data: Many methods available to tackle cell-bias, noise in data, and batch effects, so as to capture maximum biological variability
Proteomics Data: Cell-wide Mass spectrometry has a bias towards the identification of peptides with higher concentration or contamination from other experiments


What do red ants secrete while marching in a line, one after the other? Red ants often move in a group, and seem to follow a trail one after the other.

Once, I rubbed a part of the path along which they were moving and surprisingly found that the successive ants roaming around the rubbed region became confused as to where to go. It seems that the preceding ants secrete some kind of chemical (hormones, excretory wastes or body secretions) which guide the other ants to follow it. What is this secretion?

The simple answer is that ants secrete a substance called trail pheromone as they forage for food and each ant follows the trail of trail pheromone that is laid down by the preceding ant.

The term 'trail pheromone' can be a bit indistinct, however. Rather than consisting of a single chemical, trail pheromone is composed of many different chemicals, the exact compositions of which appear to be used deliberately to deliver complex information about the details of a given foraging site.

In the linked paper, the authors suggest that the

  use of several trail pheromones that differ in their persistence
  provides memory over differing time scales. In particular, a
  non-volatile pheromone can provide a longer-term memory, while a
  volatile pheromone can allow rapid choice among potential feeding
  locations by quickly ‘forgetting’ depleted locations.

This means that ants may be able to use pheromones to assemble a sort of "collective memory" for the colony, concerning the locations of food and the quantity of food found at each location.


Can microdialysis be made in Drosophila melanogaster? I've asked this before in stack overflow's cognitive science community, and someone recommended me to ask here:

I've found a couple of studies using microdialysis on insects, but didn't found any in Drosophila. I've found that the membrane diameter are from 240um, and it seems that Drosophila melanogaster brain must be between 200-300um , but I was wondering if the lack of studies of perfused drugs in Drosophila is due to this technical constraint, or is just I'm searching wrongly.

--
Edit: I specified the original target, Drosophila melanogaster, since there are bigger parients like Hawaian D. heteroneura and D. cyrtoloma. that could be subject to MD with current probes.

It seems highly unlikely to me. The smallest microdialysis probes I've ever seen are about 250 µm in diameter, so about the size of a Drosophila hemisphere. You can deliver drugs by microinjection (well, I assume you can, seeing as a) you can do it in honey bees and b) you can perform whole-cell patch clamp recordings in Drosophila).


Inexpensive way to determine mass of tiny seeds? My niece is doing a science project and she wants to weigh various seeds, determine their volume and density. She tried using my kitchen scale, but it is not sensitive enough.

I've suggested weighing 100 seeds then dividing to get an average weight, but she (she's 11) wants to weigh each one. I don't want to get in the way too much. I don't mind buying a scale, or other simple equipment as long as it isn't expensive.  Is there any way to do this inexpensively?

A pharmacy is a public business, and they should have a scale sensitive enough to weigh seeds.  They will have to let you in back to use it of course.  If you show up with her and she has the seeds and she asks the manager nicely, they might let you back and help you use it.  I would show up rather than call; if you show up you will see the manager / pharmacist but if you call you will not talk to the manager.

If this works she needs to be sure to credit the pharmacy in her project!

I recommend she weigh several seeds of each type - they might vary.

Your 100 seed idea is a better one, I think.  I understand your sentiment.

You did not ask about volume but this could be done with a graduated cylinder.  Put some water in it up to, say, 5 ml.  Then drop in a seed.  How much farther does the water level rise?  That is the volume of the seed.