How do you write genotypic and phenotypic ratios?

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


What causes DNA gel electrophoresis bands to swirl?

It can possibly be one of two problems:

Either the gel poorly prepared, in that it was cooled for too long, resulting in parts that solidified before pouring it into the mold.
This I have seen before, the pH of the electrophoresis buffer and the buffer used to make the gel was not the same. It has to be the same throughout the gel to ensure that the DNA moves evenly to the positive electrode.

Do you perhaps have a gel image of the bio-transilluminator? It could provide more insight.

Hope this helps


The distance the electromagnetic field of the heart can be detected

The electomagnetic field of the heart actually changes with emotions so there is no fixed range as such (reference). It could also change with temperature and other external magnetic disturbances (reference). The heart generates the largest electromagnetic field in the body which is up to 50 mV/m, and that of the brain and other vital organs up to 5 mV/m. Here is a paper on the exposure of human beings to electromagnetic waves (reference). This paper details some of the current medical treatments focusing on the electromagnetic fields (reference).


What roles do circular connection structures play in the brain?

'Circular connections', as you refer to them, are super common in the nervous system. This motif usually referred to as feedback connections, and serves a variety of roles.

Connectivity studies can be broadly grouped in to those that look at brain areas, and those that look at individual neurons (usually within a single brain area).

My background is more the latter, so that's what I'll focus on.

Firstly, your question misses an important distinction: inhibitory neurons. So if neuron C was inhibitory, we would have a negative feedback loop, a classical circuit that can be used to produce a homeostatic like signal, keeping a system within certain bounds; a delayed feedback loop can also act as a 'signal terminator', allowing an action to be stopped once it reaches a certain threshold. Lastly, under some circumstance, feedback loops can produce oscillations, which are applicable to a number of tasks.

But more generally, recurrent connectivity is hugely important in the cortex. The majority of inputs to neurons come from neighbouring excitatory neurons (see https://www.ncbi.nlm.nih.gov/pubmed/7638624), and if A connects to B then B is more likely to connect to A than by chance (see http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1054880&tool=pmcentrez&rendertype=abstract for a really nice study on this).

So why? For a variety of reasons. Networks with feedback mechanisms can do more, is the basic answer; from negative feedback for homeostasis, to persistent network states. My personal feeling is that too much of computational neuroscience models a network as an operator - it takes an image, say, and outputs what it thinks the image is. And whilst that is important, it's not what the brain is. We need to maintain a constant internal model of the world around us, rather than going 'that thing is a cat. That thing is a burger'. Perhaps recurrent activity maintains the cortex in a certain state - knowing that the cat is there - and inputs serve to move the state so that we can update our internal models when the sensory environment changes.


Why can cones detect color but rods can't?

The spectral sensitivity of photoreceptors expressed is the key to color vision. See figure below for the sensitivity of three-types of cone cells (S, M, L) and rod cell (R, dashed line).

From this figure, one can say rod cells provide information about the "blue-greenness" of vision, however, despite their spectral sensitivity, it seems that in human vision rod cells do not contribute to color vision, because they are highly sensitive to intensity, and thus they are mostly saturated in their response (does not induce firing of downstream bipolar cells) during normal daylight conditions. Rod cells specialize for night vision (scotopic conditions) which is crucial for survival, and under this condition the cone cells are pretty much useless.


What kind melanin do fair or light skinned black or mixed people have, eumelanin of pheomelanin?

Pheomelanin is associated with paler skin, while eumelanin predomominates in people with darker skin — this is influenced by alleles of the MC1R gene Swope and Abdel-Malek, 2018, NIH article on MC1R.


What are the various types of protein-protein interactions

There are so many types of protein-protein interactions via various domains, such as SH2 binding (in RTK signaling), Pleckstrin Homology domain (involved in signaling) among others. This site gives a nice list: http://pawsonlab.mshri.on.ca/index.php?option=com_content&task=view&id=30&Itemid=63

Of course, protein-protein interactions rely on the premises of basic biochemistry:

van-der waals interactions (at the most basic level)
Electrostatic interactions
"Lock and Key" model: Some proteins have specific binding pockets for domains of other proteins
Induced fit

There are many ways to study protein-protein interactions, including, but not limited to

Pull-down assays
2D SDS-PAGE / MS
Yeast two-hybrid
Immunoprecipitation


Will Fst (inbreeding coefficient) always be a value close or at 0 in asexual populations?

It depends on whether mutation exists. Generally mutation is happening in biology, but in its absence, yes it will be at or near zero:

Note that in the absence of any mutation, $F_{ST}$ would be defined but equal to 0, as all the genetic variance is within individuals and none between individuals and subpopulations.

From that paper, see this figure:

So, basically, the exact level of $F_{ST}$ in such cases will be controlled by the mutation rate. That figure shows a value above zero at 100% clonal reproduction because it does have a nonzero mutation rate. There is also nonzero migration between populations, so that will have the effect of reducing $F_{ST}$ somewhat. So here the value is controlled by those 2 factors. Another thing worth noting is that, if there is no initial variation between populations before the split, that will tend to increase $F_{ST}$. So it does matter how much variation exists overall.


Why is Botulinum toxin the most potent poison known?

The biochemical mechanism of BT is pretty well laid out at Wikipedia already. The toxin is likely very potent because (1) it is targeted to neurons; (2) neurons endocytose BT; and (3) the BT light chain's protease activity is able to cleave a wide range of SNARE-complex proteins which effectively disrupt the neurons ability to secrete monoamine neurotransmitters, and peptide hormones. Basically, the neurons are completely inhibited from transmitting nerve impulses.


Mechanism by which $lacI^{d}$ is a dominant mutation, impairing the function of normal copies of the Lac Repressor

The lac repressor act as a tetramere molecule and requires all 4 of the subunit to be able to bind DNA to act on the operon and repress β-galactosidase expression.

The "all 4" is the key here, if any of the 4 subunits is unable to bind DNA then the whole complex cannot attach to the operon. The lacId mutation produces a repressor subunit that cannot attach DNA, yet can tetramerize with other lac repressor subunits, therefore impeding WT subunits to bind the operon.

For your question on the protein structure. Mutations can occur at different locations in a gene and therefore impact different proteins domains. Proteins contain different type of domains, such as an active site for an enzyme or a binding sites for attaching to the DNA. A mutation might act on one of the domain while leaving others fully functional.

In your case this is exactly what happens, the mutation is in the protein region involved in binding DNA but does not affect the region involved in the protein-protein binding with other subunits.


What is the role of glucose in plasmid isolation?

This is a common misconception: in fact, in the alkaline lysis method for plasmid isolation, the glucose does not act as an osmotic stabiliser.

Glucose is present in the resuspension buffer at 50 mM. This concentration is not high enough for osmotic protection of spheroplasts formed by lysozyme treatment: from memory, 0.5 M glucose is typically used for stabilisation. So why is the glucose included?

The original method for plasmid preparation by alkaline lysis was published by Birnboim and Doly in 1979. They explain that the method relies upon achieving a pH of between 12.0 and 12.5 after addition of NaOH so that linear dsDNA (sheared chromosomal DNA) is denatured but closed-circular DNA (plasmid) is not. They state in the paper that:

  further pH control is obtained by including glucose as a pH buffer.

According to this site glucose has a pKₐ of 12.3, which aligns nicely with the claim that it helps to keep the pH within the desired range.


Chromatography is one of the best ways to isolate a protein, full stop. It is extremely widely used in both academia and industry.
Before we get into the details, though, a definition is in order. Chromatography is a means of separating components of a mixture using a mobile phase (liquid or gas) traveling though a stationary phase (a solid, gel, or very small beads, frequently with something attached to them). Chemical and/or physical interactions between the components of the dissolved mixture and the stationary phase cause those components to migrate at differential rates, separating them out from each other.
There is a huge variety of protein-stationary phase interactions that can be utilized in chromatography. Microscopic beads made of different substances can be used to create a matrix of pores where larger proteins will migrate more quickly than smaller ones. Epitope tags such as Myc or FLAG can be recombinantly added to a protein's sequence and purified using beads that have epitope-specific monoclonal antibodies covalently bound to them. The tagged protein is "grabbed" by the antibodies while the rest of the mixture washes through, then the binding is reversed by various chemical means that interrupt the protein-antibody interaction, such as high salt concentrations, varied pH levels, or chaotropic agents and the concentrated protein collected all at once.
Sometimes it is known that a certain class of proteins (such as antibodies, for example) will bind very specifically with another protein or protein fragment (in this case, the bacteria-derived Protein A). That protein is covalently bound to beads and used to purify and/or concentrate all antibodies in a solution, regardless of the antibody's specific target. Protein A binds to a section of an antibody known as the Fc region, so that sequence is sometimes fused to a non-antibody recombinantly-expressed protein so that it can be easily purified by this method. Antibodies that are specific for the protein of interest itself can be used for purification.
Many other chemical reactions can be harnessed to cause a protein of interest to bind to a stationary phase substrate and later eluted by reversing or inhibiting the chemical reaction. One example is purification based on electrical charge, called ion-exchange chromatography. If it is known that a protein has an overall positive charge, negatively-charged beads can be used to bind it (and all other positively-charged proteins in the mixture). Once washed, the protein(s) can then be eluted by changing the pH, hence neutralizing their overall charge and breaking the ionic bonds which bound it to the stationary phase. Positively-charged beads can also be used to purify negatively-charged proteins.
There are many other strategies besides the ones I've highlighted here – the term chromatography encompasses a huge range of possibilities for protein purification. I would say that in the majority of large-scale industrial purifications, combinations of different types of chromatography are the only methods used. There are of course other methods involved in the manufacturing of a protein therapeutic, such as cell lysis, filtration, concentration, dialysis, formulation, etc., where chromatography is not used, but for purification it's typically the only one. One reason for this is automation. Chromatography columns can be loaded, washed, eluted, cleaned, and regenerated without the need for any human interaction other than to provide the necessary buffers and materials. It can often also be scaled up quite a bit from benchtop to manufacturing suite, allowing for more material to be processed per batch. And, once everything is tweaked and optimized, you can get extremely pure material out of it.
There are some other protein purification methods, such as organic extraction, density centrifugation, and differential precipitation/solublization, but these are typically (but not always) used more in research and development than manufacturing, for various reasons. You don't want toxic organic chemicals like phenol, chloroform, ether, etc. involved in your manufacturing process if at all possible, because it takes a lot of work to prove to the FDA that all traces have been removed at the end. Centrifugation is not very scaleable, and is rather difficult to automate. One of the issues with precipitation is ensuring that re-solublization is both complete and consistent between batches. The amount of work that goes into validating manufacturing processes for injectable drugs and getting FDA approval is absolutely mind-boggling. Trust me :)
Hopefully I've answered your question! Please let me know if I missed anything or you want to know more about something.


Why would Aspergillus Oryzae produce lactase when no lactose is present?

"Although beta-galactosidase is mainly produced for utilization in the hydrolysis of lactose in milk or whey, in natural systems this enzyme is also involved in the breakdown of galactan-based hemicelluloses. Wheat bran contains almost 30% hemicellulose, including considerable amounts of galactose residues (Salo and Kotilainen, 1970). Similar residues are presumably also present in spent grain (wheat). "

From the paper linked in the question.


How do you keep track of past/new lab protocols?

The best match to what you're looking for is probably https://www.protocols.io/, which hosts protocols for free and generates a digital object identifier (DOI). It is not indexed by PubMed or other similar engines, however.

Some journals permit methods papers, but not a high proportion (and it sounds like you're looking for a place to find them, not to send them).


The question is interesting at many levels. Of course, in biology and in any other science there is no absolute or 'objective' truth about some given phenomenon if we really care to look at the nuances. Lamarck seems to be vindicated mainly by a wave of empirical work on patterns of transgenerational inheritance, particularly in the field that is known as epigenetics. You can read a good intro-level review here for some recent developments, some particular examples here, or a more conceptual reading here.

As an evolutionary biologist myself, I will say that most other biologists acknowledge that epigenetics and transgenerational inheritance are important and have solid empirical support, but (for various reasons) some of them are hesitant of calling that 'Lamarckian'.

By the way, Dawkins was a very effective science popularizer, but he does not practice science nowadays, and many of his ideas lie in what is known as 'scientism', which is a blind confidence in science as an absolute truth that is inflexible. The same applies to many positions of Steven Pinker, deGrasse Tyson, etc.


How can an infection of lower respiratory tract lead to a skin infection?

One might argue that since replication takes place in erythroblasts (Brown, Anderson, & Young, 1993), that it's not actually a respiratory infection either.  Fluids are simply more hospitable to the virus and more transmissible.

As for the rash, perhaps it is because the P antigen receptor that erythrovirus uses to infect erythroblasts is also expressed on endothelial cells, like those in skin (and alveolar) capillaries .


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


1x is the final working concentration of the solution (it could be anything depending on the type of the solution). Stock solutions are made at a higher concentration; if it is 10 times more concentrated than the working solution then it is 10x.

  Why 50x TAE but 10x TBE?

The salts in TBE precipitate at higher concentrations. In other words, the salts in TBE have lower solubility compared to those of TAE. Therefore stock solutions of TBE are usually 10x or even 5x.


This national geographic post discusses many mammals that sneeze. It doesn't come right out and say all, but suggests most mammals have a cough and sneeze reflex:

Mammal coughs and sneezes come from throat and nasal passages, respectively, says Bill Milsom, a comparative physiologist at the University of British Columbia.
Mammals, he says, are the only animals that process food in the mouth by chewing. In other types of animals, like reptiles, "food is swallowed whole or by chewing, and breathing is suspended during the event."

The same expert discusses non-mammals that sneeze, marine iguanas and fish.
You don't even need nerves or muscles to sneeze, per this Cell Press article

Sponges 'sneeze' without the benefit of nerves or muscles


Is there a correlation between muscle fibers and body types?

A recent paper called 'Genetic Influences in Sport and Physical Performance'[1] states:

  "Muscle fibre type determination is complex. Whilst initial composition is likely to be strongly influenced by genetic factors, training has significant effects on fibre shifts."

They also go onto say that:

  "However, the role of genetic variation in determining psychological state and responses remains poorly understood; only recently have specific genes been implicated in motivational behaviour and maintenance of exercise."

Finally:

  "With the current state of knowledge, the field of genetic influences on sports performance remains in its infancy, despite over a decade of research."

An older paper which also examined fiber types stated that:

  "These results reveal the existence of large interindividual variability and gender differences in the most common characteristics of the human skeletal muscle."[4].

Another study hypothesises that there may be racial differences in muscle fibre types.[2]. It's also said that a large variation in fiber composition of skeletal muscle within subgroups of athletic ability. This suggests that factors other than fiber-type composition contribute to performance.[3].

A small study carried out in the Croatian Navy found that ectomorphs had a better ability to sprint than endomorphs.[5]. They also found a positive correlation between calf girth and sprinting ability.

The information is a bit disjointed and sparse. However, to finally come around to the question at hand, it seems that although there may be differences according to body type initially (which obviously also has a genetic basis), training and physical activity contributes significantly to what number and types of fibres individuals possess.

There are lots of sport-specific research papers examining individuals' performance and suitability on body types.

A note on somatotyping: I guess it might also be handy note that somatotyping (endomorph, ectomorph and mesomorph) is just one theory on measuring an individual and it does have critics. The theory was initially developed in an attempt to link body type to behaviour.

It's been suggested that measurements like BMI are much more objective and useful.[6]. Another point made was that bodies change according to a number of environmental variables, nutrition etc.[7]. For example, one study suggested that intense labour during adolescence may affect somatotype (there are a few similar studies).[8]. So perhaps while using somatotypes to identify a person at one point in time is useful, it has limits in use as a long term classification.

This point probably has more relevance to the question at hand since with training and physical activity, a person can potentially change their somatotype at least to some extent; and also the number and types of muscle fibers (which evidence supports).

Puthucheary Z, et al. Genetic influences in sport and physical performance. Sports Med. 2011. 41:845-59.
Nielsen J. Glucose intolerance in the West African Diaspora: a skeletal muscle fibre type distribution hypothesis. Acta Physiol. 2011. 202(4):605-16.
DeLee: DeLee and Drez's Orthopaedic Sports Medicine. 3rd ed. Saunders.
Simoneau, et al. Human variation in skeletal muscle fiber-type proportion and enzyme activities. AJP - Endo. 1989. 257(4):567-572.
Sporis G. Impact of body composition on performance in fitness tests among personnel of the Croatian navy. Coll Antropol. 2011. 35(2):335-9.
Maddan, et al. The BMI as a somatotypic measure of physique: A rejoinder to Jeremy E.C. Genovese. The Social Science Journal. 2009. 46:394–401.
Parnell. Simplified somatotypes Original Research Article. Journal of Psychosomatic Research. 1964. 8(3):311-315.
Ozener, et al. The effect of labour on somatotype of males during the adolescent growth period. Homo. 2008. 59(2):161-72.


Why does exhaled air still contain oxygen?

You seem to be confused about diffusion versus bulk flow of fluid (air/gas).
In the lungs, there is diffusion between blood and the gas in the lungs. There is sufficient surface area that these equilibrate fairly quickly, and the partial pressure of oxygen in blood leaving the lungs is very similar to the gas in the lungs. Partial pressures are the best way to understand and explain diffusion of gases.
When you breathe out, a fraction of the bulk air moves out and mixes with outside gas. The partial pressures don't matter for this part, however, all that matters is that you have a big opening (as far as a gas is concerned) through the mouth/nose. Then again, when you breathe in, a fraction of bulk external air moves in and mixes with gas that remained in the lungs (you never completely breathe it out). This mixture will initially have more oxygen in it than the mixture that was exhaled, but it again quickly equilibrates with the blood via diffusion.
If you were to breathe in and wait long enough, eventually the partial pressure of oxygen in the blood would drop (used up in metabolism), and the concentration in the lung gas would also drop to match. However, you would lose consciousness far far before this would ever approach "zero".
The lungs are not a machine to pull all the oxygen molecules out of the air and provide it to the body. They are a gas-exchange surface to provide a massive surface area to help make the internal oxygen concentration as close as is possible to the external oxygen concentration. It never quite gets there, of course, but it gets relatively close.


Understanding what passes through and doesn't pass through the plasma membrane

Great questions! Your 3 questions can be answered in 2 parts:

1. How do small, uncharged gasses (ie: O₂, N₂, CO₂) diffuse through lipid bilayers?

First it's important to clear up some terminology: Absorbing a compound isn't the same as being permeable to that compound. If you say that a compound is absorbed (or partitions) into a bilayer, you're assuming that the absorption of the given compound by the bilayer increases the entropy of the system (and is thus energetically favorable). For example, lipophilic compounds partition into lipid bilayers because of the hydrophobic effect; by partitioning into the bilayer they break a number of hydrogen bonds and thus increase the disorder of the system.

Small, dissolved gasses like O₂, N₂, and CO₂ are not absorbed into lipid bilayers, they simply diffuse through passively because of their small size and because they are non-polar.

Water is also able to passively diffuse through a lipid bilayer even though it is polar. We might think it should be fairly rare for a polar water molecule to pass through the hydrophobic center of a lipid bilayer, but typically living cells are found in aqueous environments, where concentrations of water outside the cell are extremely high, so this does occur at biologically relevant rates. In fact, the passive diffusion of water in and out of cells is so important that many cells have developed special transmembrane proteins to facilitate the passage of water in and out of cells (most notably aquaporins and pressure-gated channels).

2. How do non-polar molecules pass through lipid bilayers?

This is answered in the related question posted in the comments section of your question. Briefly, it has to do with the same electrostatic problem I mentioned above: Though there is an energetic cost for non-polar compounds to pass through the hydropilic layer of a lipid membrane, in most cases the partitioning of the compound into the membrane still raises the overall entropy of the system (due to disruption of the hydrophobic effect), making it an energetically favorable process.

It should be noted that for the most part, polar compounds do not spontaneously cross cell membranes because of the hydrophobic region of the lipid bilayer. When passage of these compounds into or out of the cell is required for life, cells typically produce transmembrane proteins which can act as either active or passive transporters to allow these compounds through.


How well does the radius of a tree correlate with its age?

The radius of tree is not a good measure of the tree age, the most efficient technique to know the age of a tree is with dendrochronological methods, this is the less invasive technique. However, knowing very well the dynamics of growth of each species you can infer the age, check out this study:

Jan Lukaszkiewicz and Marek Kosmala. 2008. Determining the Age of Streetside Trees with Diameter at Breast Height-based Multifactorial Model (note this is a direct link to a pdf)


Fish you are referring to by description "fish with a hanging lantern over its head", are not lanternfish. Fish with "lantern" bait above head are members of group of fish named anglerfish (Lophiiformes).

You can find more information about them here: https://en.wikipedia.org/wiki/Anglerfish

Lanternfishes or myctophids are smaller fish that use bioluminecence for communication during mating season.

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


Why can't two different genetically species reproduce to give a viable offspring?

The short answer is that "different species" are defined as "not being able to produce viable offspring".  So the answer to your question is that it's a tautology; it's that way because that's how it's defined.  You're asking a question about words, not about biology.  If you were able to persuade people that a "species" was "anything living in the same area", then "different species" would be perfectly able to reproduce.

More specifically, there are many different definitions of "species", and you're asking a question about one particular definition, the "biological species" concept that was first presented by Ernst Mayr in 1942 in his book Systematics and the Origin of Species.  Mayr's definition is a useful one, but it's far from the only one; there are literally dozens of other definitions of "species".  See Wikipedia's The Species Problem for more information.

Still, it's worth asking why there biology does (to some extent) have "species" that don't interbreed; Mayr's definition has stuck because it is useful.  The first thing to consider is how remarkable it is that any two individuals (of the same species) can interbreed at all.  It's not the default option! There are thousands of highly specialized quirks that allow fertilization to happen at all. Males and females have to be incredibly fine-tuned to recognize each other, to have sperm and egg meet each other, to have the sperm identify the egg, to enter and mix genetic material ... the cascade is tremendously unlikely and has to be rigorously maintained.

So when it's not maintained -- when there's no selection pressure on two populations -- inevitably there will be genetic drift that will randomly disrupt this fine-tuned system. If a population of, say, voles is isolated on an island, they will continue to have pressure to be able to interbreed with other voles on the island, but if they can't interbreed with those on the mainland there won't be any consequences, and so over long enough time they'll drift and lose that ability -- just as many apes, not suffering any consequences from not synthesizing vitamin C, gradually lost that ability from random drift.

There's another side to it. Two populations in the same location may be positively selected to not be able to interbreed. Think about two groups of finches, one with small fine beaks that eat tiny seeds deep inside pine cones, and one with heavy beaks that crush and eat thick-shelled nuts. They each do fine, but they can interbreed and produce offspring that have intermediate beaks -- too thick to reach the fine seeds that one parent eats, but too delicate to crush the nuts that the other parent eats. Those intermediate offspring will die off, and both parents will have wasted their resources raising them.  Both parents would be better off not breeding with each other,  but only breeding with their own kind to produce specialized and efficient offspring. There is now selection pressure on the birds to recognize their own kind (perhaps through songs or mating displays) and ultimately to be inter-sterile, so they never waste resources on the un-fit offspring. There's a gradation of separation over time, in which the different populations become more and more distinct. Eventually, at some arbitrary point, humans start calling them "species", but that's just us, not biology.

"Species" is an important concept, but it's not special in evolution; speciation is just one aspect of natural selection, there's nothing magical about it.


Does every nerve ending send information to the brain separately?

There are two main structures in the human nervous system:

The central nervous system, which includes the brain and spinal cord
The peripheral nervous system, which is all of the nerves in the rest of the body (fingers, arms, feet, etc.)

The signals taken by the peripheral nerves mainly travel to the brain through the spinal cord, and the brain sends signals back to the peripheral nerves through the central nervous system.

There are a lot more complex mechanisms and various exceptions, but essentially: the nervous system is a vast network of signals, and the majority of these signals travel through the spinal cord to the brain and from the brain to the target nerves.

The signals travel via different nerve "branches" — think of it like a tree of nerves, with the common root being the brain.

For more information please see:

Overview of the nervous system for dummies

Wikipedia (with strong references and lots of detailed information)


Appears to me to be a Yucca tree, from the family Asparagaceae, whereas palms are typically a member of Arecaceae.


Drs. Swan and Ganz developed a direct method of measuring cardiac output by thermodilution. They invented a multilumen catheter with a thermal resistor on the end (a Swan Ganz catheter) which could be advanced into the pulmonary artery. Through another lumen, a cold saline solution of known temperature and volume is injected into the right atrium. Using a computer model, the temperature of the blood at the catheter tip is used to determine stroke volume. Stroke volume x heart rate = cardiac output.

  The injectate mixes with the blood as it passes through the ventricle and into the pulmonary artery, thus cooling the blood. The blood temperature is measured by a thermistor at the catheter tip, which lies within the pulmonary artery, and a computer is used to acquire the thermodilution profile; that is, the computer quantifies the change in blood temperature as it flows over the thermistor surface. The cardiac output computer then calculates flow (cardiac output from the right ventricle) using the blood temperature information, and the temperature and volume of the injectate. The injection is normally repeated a few times and the cardiac output averaged.

The same principle is used with a dye study but measuring the concentration of dye downstream.

Although this is considered to be the "gold standard", because it is so invasive and carries a serious risk of complications, it has largely been replaced by echocardiography and Doppler techniques.

Measurement of blood flow by thermodilution
Measurement of Cardiac Output
Invasive and non-invasive methods for cardiac output measurement


Are there any thermogenic plants which are suitable as houseplants?

The heat the plant produces ultimately comes from the light it uses. Unless the plant produces heat just in the wanted time (winter?) from light absorbed another time; then you would be just as warm by letting the light directly warm your environment regardless of plants.


One word. DOPAMINE

See this article on Reward System and this one on Dopamine Those basically answer your question as to addiction, urge, and feelings of relaxation.

There is absolutely nothing wrong with masturbation, so long as you realize that it is a healthy expression of one's sexuality, that is observed, quite frequently, in our nearest relative, the Bonobo. There is no shortage of the study of primate masturbatory practices in the literature, and one could make a career out of its scientific study and analysis, so if you are interested in learning more, conducting a Google Scholar search on Primate Masturbation should give you literally years worth of reading material.

As for an actual addiction, it would only develop into a pathology if it became disruptive to one's life and was pursued at the exclusion of other basic activities.


This is only true because the chloride concentration happens to be slightly less negative than potassium, therefore the weighted (by permeability) average of all the other ions is near the reversal potential for chloride.

Even if you assume the permeability of every ion except sodium and potassium is zero (i.e., if chloride doesn't contribute at all), you will end up with a resting potential near chloride's reversal potential.


How do poikilotherms thrive in a wide range of core temperatures?

I'm not an expert in this topic but I have read a reasonable amount on animal thermal regulation, especially in insects, so maybe I can give some insight into your question.
First of all, an important thing I learned is that one must differentiate poikilotherms from homeotherms and endotherms from ectotherms.
According to Randall et al (1997):

Endotherms are animals which generate their own body heat through metabolism, while ectotherms have a hard time generating enough body heat to maintain their physiological functions, as they have low metabolic rates.
Homeotherms are animals which are able to maintan their body temperature at a more or less constant rate, while in poikilotherms body temperature fluctuates more or less with the environmental temperature.

This a somewhat troubling classification. Insects, for example, are considered ectotherms/poikilotherms, but they may show a condition called heterothermy: they are (most of the time) ectotherms, but they may be able to generate heat through some metabolic activity, and in this situation, they are showing endothermy. This happens quite often in winged insects, which may raise their body temperatures by flapping their thoracic muscles which move their wings. They may also ventilate themselves using their wings, lowering their body temperature, which (I'm not sure about this) may be considered an endothermic behaviour, as they are lowering their temperature in spite of the ambient temperature. Bees and wasps are even able to control their nest temperatures when the whole colony uses their wings to heat or cool their nest. So classifying animals in one of these categories is not so straightforward, but I'm just pointing this out because this is important. I don't think this invalidates your question, so I will talk about poikilotherms/ectotherms for now on.

One important thing to know about these animals is (Randall et al 1997):

  Often, ectotherms have low rates of metabolic heat production and high
  thermal conductances-that is, they are poorly insulated. As a result,
  heat derived from metabolic processes is quickly lost to cooler
  surroundings. Accordingly, heat exchange with the environment is much
  more important than metabolic heat production in determining an
  ectotherm's body temperature. On the other hand, the high thermal
  conductance allows ectotherms to absorb heat readily from their
  surroundings.

As for how they control their temperatures...well, there are lots of mechanisms. I'll state some of them.

As Remi.b stated, behaviour is an important mechanism of temperature regulation in poikilotherms/ectotherms. This happens with basking/avoiding sunlight (as previously said), but also happens in the example of wing flapping I mentioned. Another interesting behaviour mechanism for temperature control is microhabitat selection: desert ants, for example, may face soil temperatures as high as 70° C when searching for food. They lower the harmful effects of such a high temperature by standing high on their legs and/or climbing onto small grasses or rocks which they find through their way. This may seem useless to us, but it plays a big difference between life or death for them (Marsh 1985).
Some animals have antifreeze substances in their blood which prevents them from freezing to death (see Randall et al 1997). This is common in arthropods.
Colour may play an important part in temperature regulation, as lighter body colours make the animal absorb heat less quickly than darker colours.
Some bumblebees may heat up by producing heat at the cost of ATP (a clearly endothermic characteristic) (May 1979).
Body size plays a huge part in body temperature regulation, not only in endotherms, but in ectotherms too. Lighton et al (1994) demonstrate that bigger workers from a species of ant called Veromessor pergandei can withstand dessication from higher temperatures for longer than smaller workers (and they show only a few milimeters difference in their sizes).

Well, as you may see, I don't think there is a straightforward answer. The way I look at it is that, as almost anything in biology, different organisms may show different strategies of coping with thermoregulation. I suggest you take a look at the following book if you want to know more or if I haven't quite answered your question (and the articles I have cited are the ones below):

Book: Randall et al. 1994. Eckert Animal Physiology: Mechanisms and Adaptations. W. H. Freeman  and Company.

Journal articles:
May, M. 1979. Insect thermoregulation. Annual Review of Entomology.

Lighton et al. 1994. Is bigger better? Water balance in the polymorphic desert harvester ant Messor pergandei.
(The name of the ant above changed, that's why I called it Veromessor pergandei)

Marsh, A. C. Microclimatic factors influencing foraging patterns and sucess of the thermophilic desert ant, Ocymyrmex barbiger. Insectex sociaux.


I found a book chapter for you here

Quick summary:
3 hypotheses to Origin of viruses

From pre-cellular world (virus first hypothesis)
From reductive evolution of parasites (reduction hypothesis)
From fragments of cellular genetic material (escape hypothesis)

Drawbacks:

virus require cells (to infect) so how can they come first
virus do not look like known reduced parasites from Bacteria/Eukarya/Archaea
unlikely that genetic fragments form complex viral structures for viral function

  Because of these drawbacks, the problem of virus origin was for a
  long time considered untractable and not worth serious consideration

The rest of the chapter looks more in-depth into the 3 hypotheses


[Old question, but...]

There is an old adage in MRI:  High signal to noise, high resolution, short scan time... choose 2.

The question of "How much SNR is enough?" can't be answered without talking about specifics, primarily, what is the scan going to be used for?

For example, a typical MS diagnostic scan doesn't really need to be too high a resolution or signal to noise as typically the lesions are large and hyperintense.  BUT with higher field scanners one is able to see smaller and smaller lesions.

If one is doing quantitative work off of an MRI scan, then it will depend on the type of quantification, algorithm etc.

So, in some ways the question is very broad and it depends, significantly, on a lot of other factors.

Doing some Google Scholar / Pubmed searches for SNR and MRI might help with specific areas you are interested in (e.g., https://scholar.google.com/scholar?hl=en&as_sdt=0%2C9&q=minimum+signal+to+noise+ratio+in+magnetic+resonance+imaging&btnG=)


What causes Pseudomonas fragi to smell sweet?

The strawberry-like odour that you perceived is mainly attributed to three ethyl esters, namely the ethyl esters of butyric, hexanoic and 3-methylbutanoic acid.

There are other odour-active volatiles produced by Pseudomonas fragi, about 26, which are said to add to the richness and complexity of the odour of the three aforementioned main compounds.

Source:

Analysis of odor-active volatiles from Pseudomonas fragi grown in milk - Cormier et al. 1991

The study by Cormier et al. should be a good starting point for further reading as it references a variety of scientists who have worked on this.


What would be the conduction speed of A-alpha fibers, were they unmyelinated?

The provided relation for unmyelinated axons only holds up to certain diameter value of the axon and is valid only as long as the sodium conductance iNa is uniformly distributed along the cross-section of the axon. This explains why non-myelinated fibers are so thin, being only 0.2-1.5 μm in diameter.

In axons having a larger diameter the axon potential can only move between Ranvier nodes. If this fiber gets unmyelinated the axon potential just stops propagating, due to several reasons:

Sodium concentration through the complete axon surface is too high so that it diffuses internally along the axon and reduces the concentration gradient in the direction of AP propagation.
AP is propagated not only along the length of axon but also laterally, that leads to its flatenning over the axon surface, decreasing its amplitude etc.

Unfortunately I couldn't find the reprint of the original publication in Biofizika referenced by the webpage you provide the link to, so I cannot investigate the constraints of their model for AP propagation.

In order to estimate the propagation velocity in unmyelinated axons of large diameter I would take some theoretical papers investigating the properties of nerve fibers undergoing demyelination. Z. J. Koles and M. Rasminsky "A computer simulation of conduction in demyelinated nerve fibres", J Physiol. 1972 December; 227(2): 351–364. seems to be one of the earliest publications on this topic and it is freely available online.

In this paper the authors tried to simulate the conductance of demyelinated motor axon with diameter of 10μm and 5μm myelin sheath. They gradually decreases the amount of myelin width until 2.7% of the initial value where they saw the abolishment of AP propagation. The propagation time was 12.5 times higher than in normally myelinated fibers (for the distance where AP could travel). If we consider the initial propagation velocity being 80-120 m/s then after demyelination it is reduced down to 6-10 m/s and fade after a short travel.


How does the adaptive immune system store information?

There is probably no precise answer to this question since, as others pointed out, the adaptive immune system is not really comparable to a computer. That said, here are a some items you might want to look into.

Question 1: the main site of information storage for the adaptive immune system is a special region of DNA in T and B lymphocytes that encodes immunoglobulins, the proteins that these cells use to recognize foreign organisms. The sequence stored in this special DNA region can be rearranged by hypermutation and recombination mechanisms. This occurs early in the life of T and B lymphocytes, so that each cell gets a unique DNA sequence. Those cells that later on happen to recognize invaders will multiply as part of the immune response, and they will later survive as memory cells, so that their specific DNA sequences are retained. If the same infection happen again later in life, these memory cells will help the immune system respond more quickly.

Question 2: the region of DNA used is on the order of 1 million bases long, and it has been estimated that the human immune system can generate around $10^{11}$ different immunoglobulins. How to interpret these numbers in terms of "memory size" is not clear to me though. On one hand, 1 million bases is equivalent to 250 kbytes (each nucleotide base storing 2 bits); but on the other hand, $10^{11}$ as an integer can be stored in 37 bits. I guess it depends on what level of information you consider.

Question 3: there is no mechanism for directly transfering information between lymphocytes. Lymphocytes cannot read and write their DNA at will, and they are not able to simply copy sequences from each other. Rather, their diversity comes from first randomly re-shuffling their immunoglobulin-coding DNA, followed by selection of the successful cells --- this is a brute-force, random-search method, like evolution itself. Also, lymphocytes from unrelated individuals will generally interpret each other as invaders, causing an immune response. However, it is possible to experimentally "edit" the "memory" of lymphocytes extracted from blood using genetic techniques. This has for example recently been explored to "train" cancer patients own lymphocytes to attack cancer cells, in some cases with remarkably good results.


Is the start codon regarded as part of the UTR (untranslated region)?

Because the start codon is translated into methionine, it clearly can not be part of the 5'-untranslated region, as @Johnny writes in his answer.

The more contentious question would be for the stop codons and the 3'-untranslated region. Then it really is a question of semantics. One might argue that as no amino acid is inserted in response to these codons, they are not translated. However if one considers the meaning of the word ‘translate’ and its application to the genetic code, a stop codon clearly is translated — it is read and translated into information which initiates the release of the nascent peptide from the ribosome.

And so in the Wikipedia entry on Untranslated Regions it (together with the start codon) is shown in the coding sequence, and not in the untranslated region. The annotations used by GenBank also include start and stop codons in the coding sequence (CDS in their annotations) — see, for example the annotation for this insulin precursor sequence.


An efficient and free method of assembling a large number of Sanger sequencing reads?

Have you considered SPAdes? It's a popular, state of the art assembler that should work with Sanger sequencing reads.

http://cab.spbu.ru/software/spades/


How was the guided daily amount (GDA) calculated?

The total calories are not in fact a recommended value - they are an example amount that is derived from some calorie intake that seemed reasonable to someone (I don't know the details). It does not mean that the government is recommending that you eat exactly 2000 calories per day.

The relative content is, however, a recommended value, based on presumably research. So, if you do take 2000 calories a day, then you know how much of it should be fat/carbs/proteins.

I think that there is some controversy about whether the recommended values were influenced by industry lobbying. Moreover, science is definitely not clear on what the optimal food content for a human is, which is why we keep having the different diet fads, oscillating from no-fat to no-carbs.


It's complicated.

The simplest explanation is that sound amplitude/level/loudness is encoded by the number of participating units, including off-best frequency cells that get recruited when amplitudes are high (the concept of 'tuning width' is helpful to understand). Loud sounds will recruit cells of a wider best-frequency range with high coincidence, for example (see Carney, 1994).

In some experimental paradigms, this hypothesis holds; in others, it does not. It is most likely that the perception of loudness is quite context-dependent and also depends on background, the presence of energy in other frequencies, and adaptation.

Similar to how absolute brightness is not all that perceptually useful (and therefore humans display incredible invariance over very wide brightness ranges), loudness is probably perceptually most useful in terms of relative loudness: sounds that are getting louder may be approaching, for example.

References

Carney, L. H. (1994). Spatiotemporal encoding of sound level: Models for normal encoding and recruitment of loudness. Hearing research, 76(1-2), 31-44.

Heinz, M. G., Issa, J. B., & Young, E. D. (2005). Auditory-nerve rate responses are inconsistent with common hypotheses for the neural correlates of loudness recruitment. Journal of the Association for Research in Otolaryngology, 6(2), 91-105.

Neuhoff, J. G., McBeath, M. K., & Wanzie, W. C. (1999). Dynamic frequency change influences loudness perception: A central, analytic process. Journal of Experimental Psychology: Human Perception and Performance, 25(4), 1050.

Relkin, E. M., & Doucet, J. R. (1997). Is loudness simply proportional to the auditory nerve spike count?. The Journal of the Acoustical Society of America, 101(5), 2735-2740.


Confused about definition of bulk flow of water by osmosis

Bulk flow and osmosis are different; I'm guessing your text might be talking about using osmosis to drive bulk flow, but they are occurring at different stages.

For example, if you get your water from a water tower, your house's water pressure is driven by gravity. However, the water tower could be filled by an electric pump. You could say your water pressure is driven by an electric pump, but the pump isn't really pushing water into your house, it's just pushing water up a tall tower so that gravity can act, and if you didn't realize this fact you might be confused about how you can still have water pressure even when the power goes out.

Similarly, you can drive bulk flow by osmosis. If you have a closed space (e.g., a "tube") and pump salt (or anything else water soluble) into it, it can pull water from the surrounding tissues via osmosis. As the pressure of water increases in that closed space, it can now flow in bulk through that tube. Plants can use this mechanism to deliver nutrients up a stem: they pump in ions/molecules inside the stem, which pulls in water from the soil around. Because the space is rigid, instead of expanding the water goes up the stem in "bulk": anything else carried in the water will be pushed up with it. Then, when target tissues pull in solutes, osmosis again causes water to follow, and by only pumping solutes in one place and out another you produce a bulk flow of water.


CO2 forms carbonic acid in water, which helps to dissolve rocks and mountains in envitonmental science. It would slightly acidify your body with what is called a weak acid.

5% can cause acidosis and loss of conciousness, without lack of oxygen.

3% would devastate most chalk based sealife, corals and shells.

Perhaps lifelong breathing of 3% co2 would have serious effect on alkaline processes in the body, osteoporosis, and would have to be counterbalanced by the body to maintain its blood ph above 7.35, with alkaline chemicals like sodium.

Also check out this fact sheet.


Do we come to know which allele is dominant by seeing family genration tree only?

Addressing Your First Question
We can tell whether an allele is dominant or recessive based on patterns in family trees, that is true, and it is very helpful! However, that is not the only way, since by looking at the molecular function of the alleles, the dominant and recessive relationship between alleles can be assessed without needing to look at family trees!
I think a deeper understanding of what it means to be dominant versus recessive would be helpful, because usually biology isn't just that simple! In most scenarios where there is a distinct recessive and dominant trait, it is because the dominant trait causes some specific activity/functioning protein while the recessive trait does not. Let's look at an example of this:
Let's choose eye color:1
There are multiple genes that affect eye color but let's just look at one: the one that codes for the brown pigment (melanin) to be produced in the iris [specifically the HERC2 gene]. As you probably already know, brown eyes are dominant and blue eyes are recessive.
Let's call the dominant allele B and the recessive allele b. The only way for blue eyes to be the phenotype is for the allele combination to be bb. Now think about why this would occur on a molecular level. Alleles are just forms of genes, which then in turn code for some protein. Think back to what we said earlier about how most of the time dominant alleles cause some certain activity within the cell and recessive alleles do not. We can now use that knowledge to uncover the molecular basis of this eye color scenario: The B allele codes for the brown pigment to be produced in the iris, while the b allele codes for a dysfunctional protein that does not lead to melanin being produced, leading to a blue-ish color seen. So, if the B allele causes the production of melanin and the b allele does not, it makes sense by the B allele would be dominant in this case. In the case of Bb, melanin is still being produced (even if it is because of just one allele), so there still would be brown eyes! Therefore this makes sense by bb is the only allele combination that results in the blue-eye phenotype, because it is the only combination with no allele still producing melanin. This is why brown eyes are dominant to blue eyes, because blue eyes can only exist without the presence of any B allele.
So, by knowing how an allele actually functions on a molecular level, that can help us to understand if it is in fact dominant or recessive to another allele. We should also acknowledge that genes do not necessarily need to be in this black-and-white relationship of recessive or dominant. There is also incomplete dominance and co-dominance!
Now to Your Second Question
When talking about three alleles, it is important to understand that allele dominance only is used when comparing one allele to another allele. So with three alleles, the dominance, recessiveness, co-dominance, or incomplete dominance is between two of the alleles.2 So if we are talking about alleles A, B, and C. We could say things such as:

A is recessive to B, B is dominant to C, C has in-complete dominance with A, etc...

However, it is really up to the molecular function of each of the alleles and to determine how those interactions would take place. But to answer your question directly of "can we have 2 dominant alleles," the answer is sort of. Allele B and C can both be dominant to allele A, but that says nothing about the interaction between Allele B and Allele C.

1 This is a simplification of the actual molecular mechanism of eye color, but at a simplified level this works to illustrate our point. You can read more into the genetic/molecular basis of eye color here.
2 This article is very good at discussing alleles and clarifying the point that dominance is only between two alleles.


What tools can help me determine if a plant homologous protein interacts with an ncRNA in the same way?

The ncRNA sequence from human may bind to the plant protein in the plant cells, but so what? You may be able to say the plant protein works as RNA binding protein, but no more than that.
Another concern is that the plant protein may not recognize the same RNA sequence to the human protein.

There are several ways to find RNA partners of RNA binding proteins.

SELEX

This method is used to find consensus sequences that your protein recognizes in vitro. Once you find consensus sequences, you can search ncRNAs from the plant.

CLIP

This is similar to Chip assay. You could find real targets of your RNA binding proteins


I came across a this Wikipedia page which said blue green algae from ponds can be used as dietary supplement (in tablet form).

Many other articles on the internet like  here suggest it is included in many diets in many places across the globe.

However, without proper regulation one can include a heavy metal contaminated vegetable to their diet which is detrimental to health. Furthermore cyanobacteria are known to produce toxic substances known as microcystins which can cause damage to human organs as well.

So unless you are certain of the biochemical balance of your pond I would  recommend not integrating it in your diet. Rather you can find commercially available ones which your local regulatory authority(s) recommend for dietary purposes.


Electrocardiogram: Missed beats in presence of Ectopic beats or Premature Atrial/Ventricular Contraction beats

After developing and checking the algorithm with simulated ECG data, i found out that premature beats (as the name suggests) itself arrive prematurely i.e. their R-R peak interval is less then the R-R peak interval between normal beats.

In that case, i am considering the averaged interval between normal beats and compare it to the interval between next arriving beats. If that interval is more than twice the averaged normal interval, then i classify it as a missed beat.


Basis of enzyme nomenclature — pyruvate dehydrogenase

The pyruvate dehydrogenase complex catalyses the oxidative decarboxylation of pyruvate. A description of this is easy to find on the web (e.g. Wikipedia), but I would recommend the section in Berg et al. Biochemistry (online), as it is an authoritative book with a high reputation.

Pyruvate + CoA + NAD+ → acetylCoA + CO2 + NADH

In the overall reaction, shown above, pyruvate is being oxidized (hydrogen removed) by NAD+, which is reduced to NADH. Hence there is nothing surprising in the enzyme having acquired the description, dehydrogenase.
Before asking questions about enzyme nomenclature, one should consider the historical and scientific context in which names arose. This was general scientific ignorance of the overall metabolic pathways in which they occurred or even the direction in which the reaction normally proceeded. There is also the question of focus — here on oxidation of carbohydrates. The working names that arise — trivial names, as they are called — tend to stick: they are in the literature and everyone in the field knows what you are talking about. Eventually, when the dust has settled, scientific commissions assign systematic nomenclature. In this case there are three enzymes involved, so that each has its own systematic name:

Pyruvate dehydrogenase (acetyl-transferring) — EC 1.2.4.1
Dihydrolipoyl transacetylase — EC 2.3.1.12
Dihydrolipoamide dehydrogenase — EC 1.8.1.4

It can be seen that even the systematic name for enzyme E1 (which catalyses the decarboxylation) does not refer to the decarboxylation, but to the transfer of the acetyl group (to thiamine pyrophosphate and then to lipoamide), which is of more interest mechanistically.
Details of the reactions and alternative names corresponding to the EC numbers  (Enzyme Commission numbers) can be found either on the Queen Mary University site or Expasy.


Here is a link to the Public Health Statement for Aluminum produced by the Centers for Disease Control and Prevention (CDC) in the United States.  There is much more information on the web page but the following are some of the more pertinent points to your question.

Potential Health Effects

Workers

  Workers who breathe large amounts of aluminum dusts can
  have lung problems, such as coughing or changes that show up in chest
  X-rays. The use of breathing masks and controls on the levels of dust
  in factories have largely eliminated this problem.

  Some workers who breathe aluminum-containing dusts or aluminum fumes
  have decreased performance in some tests that measure functions of the
  nervous system.

Humans

  Oral exposure to aluminum is usually not harmful. Some studies
  show that people exposed to high levels of aluminum may develop
  Alzheimer’s disease, but other studies have not found this to be true.
  We do not know for certain that aluminum causes Alzheimer’s disease.

  Some people who have kidney disease store a lot of aluminum in their
  bodies. The kidney disease causes less aluminum to be removed from the
  body in the urine. Sometimes, these people developed bone or brain
  diseases that doctors think were caused by the excess aluminum.

  Although aluminum-containing over the counter oral products are
  considered safe in healthy individuals at recommended doses, some
  adverse effects have been observed following long-term use in some
  individuals.

Some regulation and recommendations:

Drinking water

  The EPA has recommended a Secondary Maximum Contaminant Level (SMCL)
  of 0.05–0.2 mg/L for aluminum in drinking water. The SMCL is not based
  on levels that will affect humans or animals. It is based on taste,
  smell, or color.

Consumer products

  The FDA has determined that aluminum used as food additives and
  medicinals such as antacids are generally safe.

  FDA set a limit for bottled water of 0.2 mg/L.

Workplace air

  OSHA set a legal limit of 15 mg/m3 (total dust) and 5 mg/m3
  (respirable fraction) aluminum in dusts averaged over an 8 hour work
  day.


What are the key differences in giant and large unilamellar vesicle preparation processes?

Giant unilamellar vesicles (GUVs) are made by methods like hydration of phospholipid membrane generally by use of some solvent , use of electric current, combining small vesicles etc.
large unilamellar vesicles (LUVs) are made by methods like evaporation with low concentration of phospholipid, dialysis etc.
Small unilamellar vesicles (SUVs) are made by methods Injecting solution spontaneously, microfludic methods etc. There are many methods reviewed extensively (just search in pubmed you will get lot of them)

Now coming to your question, factor which affect sizes are depends on method you are using. I will list out few, rest you can check in references of each method I gave above. Most of times these methods will have all kinds of vesicles. Success of these methods relies on which method gives you highest proportion of vesicle size you desired.

Microfludic method - total flow rate, ratio of solvent to aqueous phase (Kastner et al 2014)
Electric method - rate of application of electric field (Angelova and Dimitrove 1986)
Hydration method - amount of phospholipid, evaporation rate (Lasic 1988)

Besides all of this, basic physics behind this explained here like energy difference shown below
(Image taken from (Lasic 1988))


Why is atropine a CNS stimulant, although it blocks the muscarinic receptors in the brain?

Short answer
Atropine inhibits an inhibitor and hence its effects are excitatory.

Background
According to the wiki page on muscarine M2 receptor:

  M2 muscarinic receptors act via a Gi type receptor, which causes a
  decrease in cAMP in the cell, generally leading to inhibitory-type
  effects.

Atropine is an antimuscarinic (anticholinergic) drug.According to the wiki page on atropine:

  [R]eactions to atropine include ventricular fibrillation, supraventricular or ventricular tachycardia, dizziness, nausea, blurred vision, loss of balance, dilated pupils, photophobia, dry mouth and potentially extreme confusion, deliriant hallucinations, and excitation especially among the elderly.

So atropine blocks inhibitory muscarinic receptors, and hence causes excitation.


Why is an increase in the amount of oxygen in the atmosphere favorable for life?

Because it's favorable for the process of aerobic respiration which requires O2 to produce ATP, which is the little power storage unit.

With a bigger concentration of O2, it was possible to produce more ATP, should you evolve in that direction and you needed that constraint to be removed.


Can qPCR primer with several mismatch works?

QPCR is extremely sensitive, so I would not do this. Instead I would get those primers you mention in your question and instead sequence using them instead of doing qpcr with them. Then I would make new primers specific for the region you want to do qpcr on based on the sequence.The advantage of this is that you would now know the sequence and so you would have better primers for qpcr.


What would be the Hardy-Weinberg equilibrium condition for a population of haploid organism?

What is HW rule?

HW rule is a rule allowing one to compute genotype frequencies from allele frequencies and vice-versa. See Solving Hardy Weinberg problems and eventually Assumptions of Hardy-Weinberg rule for more information.

HWr in haploid organisms

In haploid individuals, the genotype frequencies and the allele (or haplotype) frequencies is the exact same thing! This is because the genotype is a simple haplotype. In other words, once you have the allele frequency, you necessarily have the genotype frequencies without need for any calculation. We can consider the haploid organism would display a special case of HW rule, where there is no assumption and where

$$p = f_{A}$$

$$q = f_{B} = 1 - f_{A}$$

, where $f_{A}$ is the frequency of the genotype carrying the allele A and $p$ is the frequency of the allele A. $f_{B}$ is the frequency of the genotype carrying the allele B and $q$ is the frequency of the allele B.


The rate of photosynthesis varies from plant to plant. Some plants require more light and some require less. If you move light closer to the plant, in most scenarios the rate of photosynthesis is likely to be increased. For some plants a minimal light is enough for their photosynthesis, so for those plants, moving light source closer or further will have less effect.


Are There Rules for How Proteins Are Formed?

It sounds like your question is "what are the rules to protein folding?"

That's not the only way to read your question.

Protein Folding is a unique problem - a 1D sequence maps to a 3D object.  Since proteins mediate nearly all biochemical transformations and therefore mediate life's processes, protein folding one of the great unsolved problems in science today.

You can see in the example folded structure above there are helices and flat sheets of connected strands.  You can see below in the schematic alpha beta barrel motif of triose phosphate isomerase (TIM) how elegant these structures can be.

Although the combinations and overall organization of the beta sheets and the alpha helices are boundless, there are some unifying motifs in these structures.

Long ago, a couple of researchers tabulated the amino acids probability of being in alpha helices or beta strands.  The Chou-Fasman model is important in that it has approximately ~70% chance of detecting alpha helices and beta strands.  Its not a great accuracy but what's really amazing about these algorithms is that they show that local forces - the interaction of amino acids near each other in the sequence have something to do with the formation of at least alpha-helices and beta strands.

There have been pounds worth of papers written since then.  In general, statistical surveys of protein sequences have been able to identify folds or motifs by a long list of string and machine learning algorithms.  Hidden Markov Models and Bayesian profiles are popular. Of course all these are similar to Chou-Fasman in that they work on the sequence in short segments more or less.

For a while it was thought that molecular dynamics and other discrete simulations might help to solve protein folding by allowing long distance interactions to be involved.  Just simulating the entire protein molecule in a computer program as it moves into a folded conformation, but this has not proven to be possible for a couple of reasons: (1) it takes a long time for a protein to fold relative to the length of a tractable simulation (2) the forces involved in protein folding and molecular size scales are not really easy to simulate - they do not precisely simulate the forces and behavior experienced by molecules and they involve many more solvent molecules than most computations can involve - even today's server farms would get clogged up with respectable protein folding simulation.

Since 1994 the Critical Assessment of Structure Prediction (CASP) have provided an open competition every 2 years where 3D structures that have been determined experimentally is held from publication.  While its well attended a new class of algorithms showed up around 2000.  These algorithms work on the assumption that local forces are important to protein folding, but often incorporating molecular dynamics.  Using MD or statistics based on protein structures (see the RCSB for the repository), segments of the protein sequence are tested for structural tendencies.  chaining these predictions together, initial protein folds are put together.  Once put together long term interactions can assemble a protein structure.

BTW that is not to say that Protein folding is solved - the solutions that come out often produce a structure that is really similar to the final structure, but often there are substantial differences.

Just looking at the individual sequence there are no simple rules to decide how the protein fold - ultimately molecular physics of the individual sequence determines where the fold will go.

This is incredibly terse, but it could get you started.  Study of protein without any helices or beta strands is a topic in itself - they can be treated the same way as above.  Then there are also proteins who do not have a single fold, but are dynamic and flop around all the time, or only have a shape when in contact with a surface of some kind.  So there's even more.


What is the difference between the basal membrane and the basal lamina?

The basal lamina is a specialised type of extracellular matrix. It is found on the basal side of all epithelial tissue but can also surround other cell types like myocytes and adipocytes. It is also called the basement membrane, although it is not the traditional plasma membrane that we have come to know and love. Rather, it is composed of proteins (often glycosylated) and polysaccharides.

The basal membrane is the actual plasma membrane on the basal side of an epithelial cell (adjacent to the basal lamina/basement membrane).


What influences the timing of human bowel movements in the morning?

The bowel movements are influenced by a lot of factors. For example, when you eat a meal it induces a movement in your large intestines, to defecate and clear up space for new food.

Also, there is MMC, migrating motor complex, which is responsible for the bowel movements when you are fasting. It causes a flushing effect, which prevents bacteria to overproduce in intestines.

So, the daily bowel movements are mainly influenced by the timing and content of the food that you eat. But as I said there are many other factors. The gastrointestinal system has a very complex nervous system. Even psychological factors can effect the bowel movements greatly, for example extreme physical pain may induce the symphatetic system and cause constipation.

Also caffeine may affect it, like many drugs do.


How cotranscription events affect splicing?

Co-transcriptional splicing (CTS) is very widespread. Different studies (which are done on different cell types) report different frequencies of CTS. Most of them report a frequency of ~0.8 in different cells except for mouse liver which was reported to have a frequency of 0.45
This is the article that summarizes these different studies.

Can transcription regulators influence splicing during cotranscription?

Yes.. including factors such as nucleosome positions.. this post may be helpful.


How are hereditary neural circuits created in the brain during early development?

This is one of the most important question in neurosciences and we are far from understanding it. This is also the topic of the entire subfield of neurodevelopment (to answer your last question).

First, you are right that the exquisite degree and physiological correspondence between individuals of a species, and even between species, indicate a strong genetic component. But you are also right that we have good evidence for a developmental component to brains physiology. Here are a few random examples (at the top of my head, so maybe not the most important/influential papers):

Cells selectivity in the primary visual cortex depends on visual experience. Animals housed in an environment with only horizontal or vertical stripes will have cells selective only to horizontal or vertical orientations (Blakemore & Cooper, 1970).
At birth the primary visual cortex doesn't have cortical maps. They develop over time (e.g. Chapman, Stryker & Bonhoeffer, 1993).
Due to synaptic pruning, newborn have actually more connections than later in life. These connections will be progressively eliminated during youth.
Inserting a third eye in the forehead region of frogs makes connections to their optic tectum and creates columns of ocular dominance just as their normal 2 eyes (Constantine-Paton & Law, 1978). Even though having a 3rd eye is clearly not genetically encoded.
Similarly, rewiring the retinal projections of ferrets to their auditory cortex will form orientation columns just as in the primary visual cortex (Sharma, Angelucci & Sur, 2000), even though this area usually processes a completely different modality.
Putting amblyopic (a developmental visual disorder) rodents in complete darkness for some time seems to "reboot" their visual system and cure them from amblyopia (He, Ray, Dennis & Quinlan, 2007).
Efficient encoding of natural statistics mimics the response properties of cells in the nervous system (e.g. Olshausen & Field, 1996).

What these different experiments suggest is that the overall structure of the brain is genetically determined, but development is truly what shapes the function and selectivity of cells.

Blakemore, C., & Cooper, G. F. (1970). Development of the brain depends on the visual environment. Nature, 228(5270), 477-478.

Chapman, B., Stryker, M. P., & Bonhoeffer, T. (1996). Development of orientation preference maps in ferret primary visual cortex. Journal of Neuroscience, 16(20), 6443-6453.

He, H. Y., Ray, B., Dennis, K., & Quinlan, E. M. (2007). Experience-dependent recovery of vision following chronic deprivation amblyopia. Nature neuroscience, 10(9), 1134-1137.

Constantine-Paton, M., & Law, M. I. (1978). Eye-specific termination bands in tecta of three-eyed frogs. Science, 202(4368), 639-641.

Sharma, J., Angelucci, A., & Sur, M. (2000). Induction of visual orientation modules in auditory cortex. Nature, 404(6780), 841-847.

He, H. Y., Ray, B., Dennis, K., & Quinlan, E. M. (2007). Experience-dependent recovery of vision following chronic deprivation amblyopia. Nature neuroscience, 10(9), 1134-1137.

Olshausen, B. A. (1996). Emergence of simple-cell receptive field properties by learning a sparse code for natural images. Nature, 381(6583), 607-609.


Can mutation take place in G1 and G2 phases during the cell cycle?

Yes, it can. A mutation can potentially occur at any given moment in the cell cycle, not only in S phase, which is why revision mechanisms remain alert during the whole cycle. Such mechanisms not only make sure every important event in the cycle takes place adequately (e.g. DNA replication, chromosome segregation) but also repair any damage associated with DNA (e.g. AP sites, single strand breaks, double strand breaks, to name a few). Once DNA damage takes place, specialized sensors detect such events and activate several mechanisms. One of these will pause the progression of the cell in the cell cycle, and another will repair the DNA-associated damage, in case that it can actually be repaired [1].

[1] Karp, G. (2009). Molecular and Cellular Biology: Methods and Concepts. Wiley. New York.


According to the key given, the one shaded black on the right is autosomal and one on the left is sex linked.

Yes, the answer to b is half because Maria is XhX ans Peter is XY and so the probability of the child having this disease is 1/2.


How does Organ Transplant work well despite having Foreign DNA

4. Forever contain both DNAs
Yes, the donor kidney still has (and will remain to have) the donor's DNA. That is irrelevant to the acceptance and continued functioning of the organ, though.
The thing that could make an organ transplant fail is the recipient's immune system. If it detects the organ as "alien", it will attack it like any other foreign particle, and the body will reject the transplant.
To avoid this, two things are being done:

A donor is sought whose organs have similar protein markers to those of the recipient. (Those markers, and not the DNA, are what the immune system looks for when trying to tell friend and foe apart. DNA is inside the cell, the protein markers are on the outside.)
Similar protein markers are usually found in people with similar DNA, which is why close relatives are tested for this kind of compatibility first.

The recipient recieves special drugs that partially suppress the immune system.

If the recipient's body does not reject the organ, it can continue to function normally despite its different DNA. If, for example, there is a genetic defect in there that will lead to some kidney-related issues at a later time, it will be the donor's defect. If there has been a defect in the recipients kidneys that would have led to issues later in his life, that defect would be gone with his kidney. Other cells in his body would still carry the same defect, but those cells are not kidney cells, and thus that particular issue will not manifest itself.
Replication of cells will follow the same pattern: Cells from the recipient will replicate the recipient's DNA, cells from the donor's organ will replicate the donor's DNA.


As @AlexDeLarge mentioned, all non-photosynthesizing plans are holoparasites because they lack the mechanisms for autotrophy. Although it is worth mentioning that it is not always chlorophyll that is doing the photosynthesis in all plants, and that even "non-green" plants can still photosynthesize (see note below).

There are generally two classifications of holoparasitic plants: those that require fungal mycorrhizal hosts called myco-heterotrophs and those that require other plants as hosts. Some examples of non-photosynthesizing myco-heterotrophic plants include those in the genus Monotropa. Examples of plant-specific holoparasitic plants include those in the genus Boschniakia.

In both cases, the parasite is partitioning nutrients directly from its host plant through a specialized root called the haustorium that penetrates the host's roots or hyphae, essentially bypassing the need for its own photosynthetic production. Technically, those parasites that attack other plants are still relying on photosynthesis (of the host), although indirectly.

This is a good review paper on some of these species:
Leake JR. 1994. The biology of myco-heterotrophic ('saprophytic') plants. New Phytologist 127(2): 171-216.

Note: For instance, when deciduous trees turn yellow and red in the fall, they are relying on the carotenoids, xanthophyll and carotene. So, while the plant is not utilizing chlorophyll to absorb light, the carotenoid compounds are incapable of transferring light energy directly to the photosynthesis pathway themselves, and thus still require chlorophyll as a pass-thorough.


The thing about DNA is that it's very durable, compared to the rest of the cell. It's not too difficult to extract DNA from cooked and processed food, even though the definition of "cooked" is "denatured and broken many of the proteins in the cell". The long DNA strands may be broken into long pieces, but overall the DNA holds up very well to heat. There's no risk of DNA damage to neighboring regions with RF radiation because the primary way RF energy destroys DNA is through heating, and at the temperatures where DNA starts to accumulate damage the cell around it is cooked/destroyed.

The quantum explanation for why ionizing radiation can destroy DNA is that high-frequency radiation is powerful enough to zip through the surrounding tissue and break/damage individual DNA molecules. Individual radio photons can't "gang up" on a DNA strand to do the same thing because of how quantum mechanics works, so you won't be able to break the strand or damage the bases without high-energy ionizing radiation.

Metaphorically speaking it's like trying to get at a peach pit. Ionizing radiation is like a knife, it zips through the flesh and can get at a peach pit without damaging the peach much. RF radiation is like a belt sander. You can definitely get at the peach pit, but you'll cause a lot of collateral damage doing it.

Mutations or DNA damage that might cause cancer can only happen to cells that are alive that receive DNA damage. If the DNA is damaged by heat, the cell around it is dead, and that DNA damage doesn't really matter.

I encourage you to read about ionizing radiation and the photoelectric effect.


"Wouldn't obese people die faster and clean the gene pool for people who are slim?"

If your hypothesis is right, the selection for such traits would only have begun in the last 20-30 years ("Worldwide obesity has more than doubled since 1980" http://www.who.int/mediacentre/factsheets/fs311/en/)

Natural selection wouldn't have had time to select against people showing tendency for obesity.

Also, obesity is a lifestyle choice, and not merely predictable by genetic disposition. I could be a "fit" person, but genetically predisposed to obesity.

Look up also genotype vs phenotype for further reading (http://evolution.berkeley.edu/evolibrary/article/genovspheno_01)


Free-flowing cells and those that are stuck together?

Cell-cell adhesion is a well-regulated mechanism, cells don't just stick together randomly, this interaction is mediated by specific molecules on the cell surfaces. The responsible proteins for that are the Cell Adhesion Molecules (CAMs) like integrins, cadherins and selectins. Which of these CAMs are present on the surface of a cell determines if those cells will bind to each other or not.

Cells can change their ability to adhere to each other or the extracellular matrix by expressing or not expressing different kinds of these molecules.

You can find a lot more information about this topic in the cell-cell adhesion chapter of "Molecular Biology of the Cell", available on the NCBI homepage.


Can the RNA in the HIV virus make viral enzymes without entering the nucleus?

I am afraid your question is really not clear. You are asking one thing in the title of your question, another in the question body and a third in your comments. If you are asking (as you did in your comment above) what would happen if a virus with no enzymes were to infect a cell, see below.

In the case of HIV (and other retroviruses) some of the most important enzymes contained in a normal viral particle are:

A reverse transcriptase (RT): this enzyme reverse-transcribes the viral RNA genome to cDNA,
An integrase: incorporates the cDNA produced by the RT into the host cell's DNA.
A ribonuclease : an enzyme that can degrade (cut up) RNA. In the case of HIV this is the same protein as the RT.
A protease: an enzyme that can degrade other proteins.

Viruses work by copying their genetic material (their DNA or RNA) into the host cell's genome and then hijacking the cell's replication machinery to make more copies of the virus. So, what would happen if these enzymes were absent?

Without an integrase, the virus would not be able to insert its reverse transcribed DNA into the cell's genome.
Without an RT, the virus would not be able to copy its RNA into DNA.
The ribonuclease activity is also needed for successful reverse transcription to double stranded DNA (see [1] for a review and explanation of why.)
The protease is necessary for the formation of new viral particles. Mutations in this enzyme result in aberrantly assembled virus particles with low infectivity [2].

What you really must remember is that viruses are extremely streamlined. Everything they contain is essential. In some ways, you could say that viruses are the most highly evolved species (assuming they are living species), they are the most highly specialized "life forms" we know of and they have managed to get rid of all non-essential functions. The flip side of this is that everything that is left is essential, the virus cannot function without it.

So, to answer your question, a virus without any enzymes is, essentially, not a virus. It would not work, would not successfully infect cells.

References:

Greg L. Beilhartz and Matthias Götte, HIV-1 Ribonuclease H: Structure, Catalytic Mechanism and Inhibitors, Viruses 2010, 2:900-926
Bukrinskaya A. HIV-1 matrix protein: a mysterious regulator of the viral life cycle. Virus Res. 2007 124(1-2):1-11.


COPI/COPII proteins and kinesins/dyneins

Interesting question. The term anterograde refers to movement in the forward direction. In the context of vesicular trafficking, anterograde refers to (1) movement from the site of protein synthesis in the rough endoplasmic reticulum (RER) towards the Golgi and then (2) movement from the Golgi towards the final destination in the cell.

Both processes rely on microtubules for transport. Microtubules are polar and radiate from the microtubule organizing center (MTOC) with their (+) ends directed towards the periphery of the cell:

There are two broad classes of molecular motors that facilitate directed movement along microtubules. Kinesins are generally (+)-end directed motors whereas dyneins are (-)-end directed:

These images should already give you a hint. Your question may have arisen due to the assumption that the ER is centrally located near the MTOC with the Golgi somewhat peripheral. This is incorrect. In reality, the Golgi complex is actively clustered near the MTOC by movement on microtubules. Furthermore, the ER extends along the microtubule network towards the (+)-end periphery. Taken together, it is evident that microtubule (-)-ends are located near the Golgi and transport to it from any part of the cell, including the RER, requires the (-)-end directed motor dynein. Subsequent anterograde transport from the Golgi to a specific destination in the cell, or through the secretory pathway, requires the (+)-end directed motor kinesin. Retrograde transport from the Golgi back to the ER would also use kinesin:

The article cited in the question (which I also reference in this answer), mentions that COPII vesicles are coupled to microtubules via dynactin. Dynactin is a protein complex that is used to both activate and adapt cargo to dynein (ie COPII vesicles are coupled to microtubules via a dynein/dynactin complex):


Speed of passive transport of ions in the dendrite

Your edits do improve the question, but you are still asking two very different questions.
We don't really need to answer these questions:

How fast are ions transported passively inside the dendritic tree (and soma), probably depending on their atomic mass, charge, and of the local geometry?
What is the order of magnitude of the speed of passively transported ions in the dendritic tree?

to answer this part:

Especially I want to know when a post-synaptic potential generated x μm away from the axon hillock "arrives" there, i.e. can be detected/summed up with other PSPs

The speed of propagation of electrical signals in neurons don't depend on particular masses of particular ions or diffusion per se. Instead, passive electrical conduction is best understood using the cable equations which treats conductance within neurons as electrical RC circuit. The electric field propagates at the speed of light.
Therefore, EPSPs actually propagate almost instantaneously (given how short the distances involved are relative to speed of light) in that they produce an electric field. However, the peak decays with distance, and the rise time of an EPSP depends on the compartment because of capacitive filtering along the length of the dendrite. The decay peak is described by the length constant:
$$\lambda = \sqrt{\frac{r_m}{r_i+r_o}}$$
In this equation, rm is the resistance of the membrane, ri is the resistance of the intracellular space, and ro is the resistance of the extracellular space and is effectively negligible.
The length constant is the distance at which the peak amplitude will have decayed 63% from the peak at the signal origin.
The temporal filtering comes from the capacitive properties of the membrane along the length of the dendrite. The authoritative works describing these properties are several papers in the 1960s from Rall, Rall, W. (1962). Theory of physiological properties of dendrites. Annals of the New York Academy of Sciences, 96(1), 1071-1092. and Rall, W. (1969). Time constants and electrotonic length of membrane cylinders and neurons. Biophysical Journal, 9(12), 1483-1508. are good references.
The effective time constant for signals originating closer to the soma is much faster because there is less membrane to charge along the way. Exactly "how far" you have to travel to make a certain amount of difference depends on the properties of the membrane, which vary across neurons, vary in different parts of the dendritic tree, and vary dynamically within a neuron due to synaptic transmission.
Magee, J. C. (2000). Dendritic integration of excitatory synaptic input. Nature reviews. Neuroscience, 1(3), 181. is a fairly accessible review that covers a lot of these issues and more. It's important to recognize that although passive propagation of signals is important in dendrites, it's never purely passive and active conductances have important roles as well; in many cells, these active conductances plus differences in the initial shape of EPSPs throughout the dendritic tree act to mitigate the effects of distance.
See also Koch, C., Rapp, M., & Segev, I. (1996). A brief history of time (constants). Cerebral cortex, 6(2), 93-101. for more on the time constant and some evolution of the ideas about neuronal time constants since Rall.


Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?

Yes, it is perfectly possible for both pairs of non-sister chromatids to cross over in a single tetrad. The "standard textbook" depiction is a simplification, true tetrads can sometimes be very complicated and the nested crossing-over would be difficult for entry-level textbooks to cover.

This microscope image clearly shows two chiasmata occurring on two sets of chromatids, with both of the "blue" chromosome's chromatids undergoing crossing over.

In fact, even more complicated chiasmata complexes can form during meiosis. For example, this slide depicts many chiasmata occurring in a single tetrad. More examples can easily be found by searches.


Weighing 2 vertical halves of the human body

The two halves likely do weigh approximately the same. Since the density of most tissues that are not filled with air is basically equal, it doesn't matter that, e.g., heart, spleen, and stomach are on the left and liver is (mostly) on the right. In the left/right axis, it evens out.

As for the location of the center of mass of a human: it's located about 10 cm below the navel, at the level of the S2 vertebra approximately midway between dorsal and ventral surfaces of the body (assuming that the person in question is neither pregnant nor obese).


Polar means there's a higher density of electron on the oxygen and a lower density of electrons on the hydrogens. This has to do with the electronegativity of the elements in question. Hydrogen is in group 1 which likes to lose it's electron and oxygen in group 16 which likes to get two electrons (in this case one from each hydrogen) in order to complete the octet in it's valence shell.

Also it has to do with the shape, water molecules are not linear, but rather bent in a 'v' shape. the two sides are positively charged and the middle is negatively charged. if it were linear then the middle wouldn't matter, but because it is bent, on side has a negative charge and the other side has positive charge. It's not an negative/positive change the way it is in an ion, just a slight negative/positive charge.


Mass Spectrometry (proteomics): How isotopes can be used to to determine charge of the peaks?

If you have an ion of mass 100 and charge 2, the m/z ratio (let's exclude the root) will be 100/2=50. If you have isotopes, then you expect to find several peaks for a given fragment. For example, the masses of different isotopes of the same molecule could be like: 100, 102, 105 and 107. In this case the spectrometer will detect four peaks, instead of one, for the same molecule (will look something like this): 100/2, 102/2, 105/2 and 107/2. The charge of all that peaks is the same.. it's only the mass that differs.

The page you linked simply makes an example, "singly charged ion will show isotopic peaks that differ by 1" example m=10 z=1 m/z =10, for the isotope m=11 z=1 m/z=11 (difference of 1). If you have a doubly charged ion m=10 z=2 m/z=5 and for the isotope will be 11/2=5.5 (difference of 0.5).

So, if you take the spectra of a compound and you see the isotopic peaks having a distance of 0.5 among each other, you are looking at a doubly charged ion, if the distance is 1, it's a singly charged ion.

What do the isotopes have to do with the charge?
Given that the isotopes peaks are around 1 units far from each other, you can conclude that the ion you are looking at has 1 charge.

The last question is not clear to me.


Am I entitled to the latlong coordinates of all specimens used in a species revision paper?

No - you're not entitled to anything. Authors may refuse to share because they want to control future publications arising from their data, either simply to inflate their own publication record or to prevent certain types of anlaysis of their data (see the 'data parasites' fiasco last year for an example of attitudes towards data sharing in some parts of the medical community - this, this, and others).

Alternatively they may simply no longer have the data. Nowadays this is less common, but if you contact an author about a publication from the 1960s it's pretty unlikely that any unpublished data is still in usable form.

Finally, certain aspects of data may not even have been recorded. Before GPS was widely used, accurate lat-longs of collection sites are unlikely to have been measured. As @Kara notes in the comments, it is not uncommon for the collection sites of older samples to be recorded at the country level.

This is why journals are increasingly adopting data-sharing policies (see BES, for example)

However, many authors are happy to share their data, and you lose nothing by asking. Good luck!


Relationship between DNA strands and mRNA

I would add this as a comment to your question but do not have enough reputation. A simple look at Wikipedia (which is a very good source for general questions like these) would have provided you with an answer. I just did this to see how long it would take if I did not know the answer. It was about 20-30 seconds.

Protein synthesis: Transcription

  In transcription an mRNA chain is generated, with one strand of the DNA double helix in the genome as a template. This strand is called the template strand.

Template strand

  Only one of the two DNA strands serve as a template for transcription. The antisense strand of DNA is read by RNA polymerase from the 3' end to the 5' end during transcription (3' → 5').

If I understand your confusion correctly, you also do not understand how the seemingly "non-coding" strand can be the "coding" one which seems to be a paradox. If this describes your confusion adequately you have to think of the semi-conservative replication of DNA. The "non-coding"/antisense strand is transcribed by the RNA polymerase into its complementary RNA sequence. As this sequence is complementary to the "non-coding" DNA strand, the mRNA sequence is identical (with U replacing T) to the "coding"/sense DNA strand.


insect paralysis in response to predator echolocation frequency

Many different species react to bat echolocation sounds by altering their flight path or diving. This includes moths and mantids, but also other insects such as crickets, flying beetles, and likely many others as the following list (taken from this review by Miller and Surlykke (2001): How Some Insects Detect and Avoid Being Eaten by Bats: Tactics and Countertactics of Prey and Predator) is in no way exhaustive:

Crickets

"Many bush crickets can hear bats, but few seem to react to bat echolocation. However, the bush cricket, Neoconocephalus ensiger, shows an acoustic startle response during tethered flight in the laboratory (Faure and Hoy 2000). When the insects hear intense batlike sounds with frequencies from 15 kHz to at least 60 kHz, they dive."

Mantids

"Flying mantids (Parasphendale agrionina) react at distances as great as 10 m from a loudspeaker emitting batlike signals at natural intensities. They react by turning or with dives and spiral flight. The responses are all nondirectional, as would be expected from a functionally monaural system."

Flying scarab beetles

"In response to pulsed ultrasound, flying scarab beetles, Eutheola humilis, dropped or flew toward the ground, and walking beetles stopped."

Moths

"Freely flying, unidentified moths exhibit a variety of behavioral responses to bats and to synthetic batlike signals (Roeder 1967a; for recent results, refer to Acharya and Fenton 1992). Moths far from the source often turn and fly away, whereas those close to the source show zigzag and looping flight, power dives, or passive falls."

For a more recent review of the literature for the specific example of moths, I suggest reading Evolutionary escalation: the bat–moth arms race by Hofstede and Ratcliffe (2016).