Can ant colonies have two "branches"? Could an ant colony have 2 or more "branches" located far from each other (i.e. physically separated but interconnected nests) ? If so, how far is the limit?

Yes, sub- or satellite colonies are common in many species (see e.g. Hölldobler & Wilson, 1990; Debout et al. 2007), and these are then labelled as polydomous species. Subcolonies can either contain extra queens, but sometimes only contain foraging workers. The purpose can be both to expand foraging grounds or as a pre-stage for colony budding. The distance between colonies can differ dramatically between species, but there are cases of supercolonies (especially in the Argentine ant) streching over hundreds of square kilometers (Moffett 2012).

Satellite colonies are also common in e.g. Carpenter ants (Camponotus) and wood ants (e.g. Formica rufa), and when colonies are found inside a house there is often a primary colony somewhere outside the building (see e.g. Ants in the home).


Does the given pedigree show a Y-linked dominant trait? I think that since every generation has males affected only, the trait must be Y-linked. Also, since every generation expresses the trait, I think it should be dominant. However, the answer key says that the answer is autosomal dominant. Could someone please clarify this and give a tip on how to recognise the difference?

You're right that this could just as well be Y-linked dominant (althought that is pretty rare due to the small size of the chromosome).

The only reason pointing more towards autosomal dominant is the mention of "extra fingers and toes". Most cases of polydactyly are inherited in an autosomal dominant way.

Does seem like an unfair question, though, since (at least in theory) there's more than one possible answer.


Dimensional analysis Question So I'm new to the dimensional analysis world and I'm little confused and the answers I'm getting are not convincing :(

if the concentration of hemoglobin in a 5ml sample of blood is 34 g/dL. and red blood cells are 31.45 hemoglobin, what is the mass of red blood cells in the sample?

So.. any thoughts on how to do it?

Thank you so much

It doesn't seem like you need the 31.45 hemoglobin number (which is good because no units are given:

5ml * 34g rbc /dL * 1 dL/ 100 ml = 1.7 g rbc

would fall out from unit analysis


Why do microarrays require a priori knowledge of the genome? Reading this paper they said this:

Contemporary microarrays emerged in the wake of genome sequencing
projects for one obvious reason: arrays require a priori knowledge of
the query genome

Why do you need a priori knowledge? Thanks.

If the query genome is unknown, a microarray cannot be made for a target species. Microarrays have DNA fragments of what you want to amplify on them. Those fragments must be known.
From nature:

DNA microarrays are microscope slides that are printed with thousands
of tiny spots in defined positions, with each spot containing a known
DNA sequence or gene.

From wikipedia:

Scientists use DNA microarrays to measure the expression levels of
large numbers of genes simultaneously or to genotype multiple regions
of a genome. Each DNA spot contains picomoles (${10^{−12}}$ moles) of a
specific DNA sequence, known as probes (or reporters or oligos). These
can be a short section of a gene or other DNA element that are used to
hybridize a cDNA or cRNA (also called anti-sense RNA) sample (called
target) under high-stringency conditions.


Which monkey species features two distinct male phenotypes? I remember coming across a popular science article years ago about a monkey species which featured two male genotypes: the first were good looking males who acquired social status (as alphas or betas) within the group and could thus achieve reproductive succes. The alternative (less frequent) phenotype achieved similar fitness by adopting an outgroup (omega) lurking rapist kind of reproductive strategy.

Does anybody know which species and whose observervations I could be referring to? I'm curious to find out if this was a valid observation and if any further research has been done on this phenomenon.

Patas monkeys exhibit "sneak mating" where a male other than the resident male sires offspring. Resident males do sire more offspring than sneaker males, but both strategies do co-occur. I'm pretty sure there are other species that have a similar mating strategy as well.


How are fingerprints formed? I know what influences the fingerprints to be unique always. But what actually process is taken to make these as we grow?

Fingerprints are called epidermal ridges in Biology. These are formed between the 3rd and 4th month of the fetus. The epidermal layer looses its strength, becomes like a cloth from a piece-board and falls on the underlying layer of skin cells, the dermal papillae. Now, you must realize that not all tissues are as smooth as the skin for evolutionary reasons. This tissue, although a part of the skin, is irregular and some its cells get little more swelled up. After falling, the epidermis begins to harden up and thus takes its shape.
This phenomenon has probably evolved from providing friction for traction and increase in surface area for sweat to come out.
Read more at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1013024/


Does depolymerisation take place at the minus end of microtubule? Wikipedia says that

  Dynamic instability refers to the coexistence of assembly and disassembly at the 'ends' of a microtubule.

but Karp's Cell Biology, 7th edition says

  Dynamic instability is an inherent property of microtubule itself, more specifically, of the plus end of the microtubule.

I was of the opinion that the GTP bound to the minus end does not hydrolyse and so no depolymerisation take place at the minus end.

But again from The Cell: A Molecular Approach. 2nd edition I found that

  treadmilling is a dynamic behavior in which tubulin molecules bound to GDP are continually lost from the minus end and replaced by the addition of tubulin molecules bound to GTP to the plus end of the same microtubule.

The concept I have developed so far is completely shattered by this treadmilling thing. Can somebody explain,

i) Whether GTP remains attached to the minus end?

ii) Whether depolymerisation occurs at the minus end?

iii) If depolymerisation does not occur, then is treadmilling a special condition?

Often microtubule (MT) dynamics and actin dynamics are taught side by side, which can be quite confusing as MTs display unique characteristics relative to actin filaments. Indeed, treadmilling is an in vivo behavior primarily associated with actin, while dynamic instability characterizes MT growth. But why?

Both actin filaments and MTs are "sided" (polar), with actin having barbed- and pointed-ends and MTs having plus- and minus-ends. This polarity emerges from two properties: 1) the energetic state of the individual monomers that make up the filament and 2) the rate of growth.

For actin, the barbed-end is compromised mostly of ATP-actin (high energy), while the pointed-end is made up of ADP-actin (low energy). This composition preferentially adds new ATP-monomers to the ATP-rich barbed-end, yielding a faster rate of growth than at the pointed-end. Disassembly at the pointed-end occurs more readily as ATP-actin is converted to lower energy ADP-actin. Treadmilling occurs when the rate of assembly at the barbed-end is equal to the rate of disassembly at the pointed-end (Pollard and Borisy, 2003).

Similarly to actin filaments, MTs are polar, with their plus-ends made up of GTP-tubulin monomers and GDP-tubulin concentrated at their minus-ends (Desai and Mitchison, 1997). Unlike actin filaments, which can form sporadically almost anywhere in the cell (Pollard and Borisy, 2003), MTs are initiated at what we call a microtubule organizing center, or MTOC (Kollman, 2011).

The bulk of MTs within the cell are attached to the MTOC through their minus-ends, though there are unattached sub-populations. Both in vivo and in vitro data indicate that growth and shrinkage at the minus-ends does occur, but that the rates are slow relative to those occurring at the plus-ends (Hendershott, 2014). In these instances, MTs can undergo treadmilling in a manner similar to that as actin and this behavior is readily observed in vitro (Waterman-Storer, 1997). Recent studies have suggested that MT minus-ends are under tight regulation in vivo, likely limiting their dynamics (Akhmanova, 2015). Therefore, MT growth and shrinkage primarily occurs at thee plus-ends. Enter dynamic instability.

MT plus-ends undergo a cyclical process of growth and shrinkage known as dynamic instability (Mitchison and Kirschner, 1984). The key to this process is the difference in shape between GDP-tubulin and GTP-tubulin (Buey, 2006). One can imagine GTP-tubulin as a rectangle, with perfectly straight lines connecting its angles. On the other hand, GDP-tubulin has a small bend in the center of one of its long ends.

As a MT grows, GTP-tubulin is added to the plus-end forming a "GTP cap." The role of this cap is to counteract the inherent desire of GDP-tubulin to bend outward, thereby forming a straight filament and ensuring continued growth of the MT (Desai and Mitchison, 1997). However, the MT will lose its cap when the rate of GTP-tubulin addition drops below the rate of GTP to GDP conversion, thereby exposing GDP-tubulin. This event characterizes the "catastrophe" stage of dynamic instability (Mitchison and Kirschner, 1984). The shape of GDP-tubulin is no longer constrained in this stage, and instead, bends outward causing rapid disassembly of the MT. Because the cell is chock full of GTP-tubulin, recovery of the GTP cap rapidly occurs and the MT re-enters productive growth. This cycle of growth-catastrophe-recovery is the hallmark of MT dynamic instability.


Estimation of the amount of bacteria For my first research project in microbiology I've chosen to determine the effectiveness of sanitizers and soaps in killing bacteria from our hands, however, after putting the bacteria on agar plates using cotton swabs, why do we incubate them? Won't their numbers increase and give us the wrong results?

This is a very standard method. The idea is that you have a culture of bacteria on an agar plate. During the incubation each bacteria forms a colony. After a few hours of growing the colonies grow and become visible for human eyes. So you can easily count them.

Then you can compare the number of colonies before and after washing your hands with the sanitizers and soaps and find which method has the lower amount of colonies on average and therefore whihc one is the most efficient one.


Why would yeast grow but not produce alcohol? I'm studying for my intro to microbiology test and I have a question asking why a culture of yeast responsible for producing alcohol would be growing, but not producing alcohol?

The multiple choice answers are:
a) the maltose is toxic
b) O2 is in the medium
c) Not enough protein is available in the agar
d) The temperature is too low
e) The temperature is too high

EDIT: There is not much more context that what I gave here. The question simply asks me to assume the position of a scientist at a wine production company, and then asks the question I posed above - nothing too specific.

I think it is (b) because the presence of O2 would cause the yeast to respire aerobically, but I can't eliminate (d) and (e)

I figure it probably isn't (a) because a toxic chemical would inhibit the growth of the yeast. I don't believe protein is relevant so I don't think it is (c).

I think only b.) is true.

a. I cannot find evidence that maltose is toxic to yeasts (and I would hardly believe it, because it is a glucose dimer), however I found evidence, that yeasts might need the presence of oxygen to process maltose.

1977 - The Requirement of Oxygen for the Utilization of Maltose, Cellobiose and D-Galactose by Certain Anaerobically Fermenting Yeasts (Kluyver Effect)
1994 - Effects of oxygen limitation on sugar metabolism in yeasts: a continuous-culture study of the Kluyver effect.

b. Alcoholic fermentation is an anaerob process, so it won't work in the presence of oxygen.
c. Alcoholic fermentation is for creating energy. Proteins are normally not involved as substrate (maybe by gluconeogenesis, but that's another story). If the yeast grows, then there is enough protein available to build fermentation enzymes as well.
d. I found some articles about the temperature dependency of alcoholic fermentation:

  Juices fermented at 10°C exhibited ethanol concentrations between 7.4
  and 13.4% and populations of K. apiculata, C. stellata and C. krusei
  in the range 106-108 cells/ml.

1988 - The effects of temperature and pH on the growth of yeast species during the fermentation of grape juice

  At low temperatures, alcohol yield was higher. Secondary metabolites
  to alcoholic fermentation increased as the temperature increased.
  Glycerol levels were directly affected by temperature.

2003 - Effects of fermentation temperature on the strain population of Saccharomyces cerevisiae

  The immobilized yeast showed an important operational stability
  without any decrease of its activity even at low temperatures (1−12
  °C). Specifically, at 6 °C the biocatalyst favored wine production
  within 8 days, which is less time than is required for the natural
  fermentation of grape must.

2001 - Wine Production Using Yeast Immobilized on Apple Pieces at Low and Room Temperatures

It seems like low temperature does not necessary have an adverse effect, but this could depend on strain.
e. Just the same as the previous answer. I think the main fermentation products will be always ethanol in the yeasts chosen for alcoholic fermentation (if the other conditions are right), so it is not temperature dependent in this case. A growing yeast will produce alcohol on both low and high temperatures. The ratio of ethanol and the byproducts can depend on the temperature, but not the presence of the ethanol itself. By too low or too high temperature the yeast will die or will stop to grow. (My experience that CO2 production is faster by high temperature, so it is because everything is faster or because the ethanol/CO2 ratio is lower.) An example of temperature dependence by wine making:

  Temperature control is vital in the production of fine table wines as:

  High temperatures encourage the loss of alcohol and aroma and flavour compounds due to volatilisation. If the temperature goes above
  30 -35ºC, the yeast becomes sluggish and fermentation may stop.
  Low temperatures will lead to a poor extraction of colour and tannins in red wines and can also cause sluggish fermentations and the
  production of high levels of ethyl acetate.

Managing the alcoholic fermentation

I think "sluggish" means stop growing in this case, and ofc. stop fermenting due to the death of the yeast cells.


Why do some fruits have a much wider range of acceptable sizes than others? Some fruits such as pumpkins can grow to be 100 lbs. Under different conditions, the same variety of pumpkin can produce a 15 lb. fruit. Both plants are healthy, and look the same except for their size difference. If I took two red apple trees and planted them in extreme opposite conditions, the fruit size would be nearly the same. The fruit quantity would be lowered in the tree grown under poor conditions. Why do fruits have such a variable range of acceptable sizes?

Pumpkins, squashes in general, grow on vines, while apples grow on trees. Vines are fast growing and trees are not. Zucchini can be quite large; cucumbers, too. Pears, plums, peaches and other tree fruits do have a reduced variation in fruit size. While I do not know the answer to your question, my background in plant biology tells me that this is an important part of the reason. For example, a watermelon or pumpkin rests on the earth, but a tree fruit hangs. If that fruit is too heavy it falls from the ground before it is ripe - before the seeds are fully differentiated that is. So, while "evolution" might be an answer, it is important to discuss what aspects are at play.

I think it has to do with vine vs tree, and how the fruit is attached and hangs/lays.


Do human genes get affected by irregular sleep and other factors I'm new here so please go easy on me.

Do our genes-the ones that carry our appearance, intelligence and other traits get destroyed or lost due to irregular sleep, excessive body heat, smoking, drinking and other factors?

Asking cause, I have some relatives of mine with really good genes that are worth passing down but afraid that their children wouldn't get it because of the abovementioned habits.

This is a good opportunity to correct some major misconceptions. I'll be brief and avoid being technical because this is introductory biology.

First, genes are present on DNA, and "store instructions" on building proteins, among other things. Poor diet, lifestyle and sleeplessness do not primarily affect the DNA itself, but rather the reading of it and the production of the proteins. Genes seldom get lost or damaged in a way that affects the next generation, at least in modern humans. Analogy: genes are the recipe in the cookbook, not the prepared dish. Lifestyle choices affect the dish.

This is because the aforementioned "bad habits" must affect cells responsible for the next generation (sex cells) - which is unlikely - unless the effects of the "bad habits" are strong enough to influence the entire system and cause damage to the production or maintenance of sex cells or their DNA. Sex cells are well isolated from the rest of the body. The other foreseeable way these habits can affect the next generation is to affect pregnancy itself. Poor sleep or smoking during pregnancy is obviously not advised. Gestation is a critical period in development.

In short, the expression and action of genes is certainly affected by sleep, diet, and so on, but the genes themselves are much less affected. Mutations may build in the body and contribute to the formation of cancer and other disease, but the sex cells specifically are very likely to remain mostly unaffected; it is these cells' DNA that is passed down to children.

As for the I have some relatives of mine with really good genes that are worth passing down* statement... That's a matter of eugenics and short-sighted opinion, which is strictly not scientific. Let's not address that!


Is there a purpose for nucleated red blood cells in reptile, avian and fish blood? I have read, and read, and read documents on this subject but still have no conclusions.

Everything I have read explains why mammals don't have a nucleus (to make more room for the haemoglobin and allow for more oxygen to bind as well as making it easier for the RBC to fit through capillaries) but the reports don't explain why birds, reptiles and fish may still have nucleus in a red blood cell.

Is there really any other function a nucleus has within a red blood cell apart from being the 'brain of the cell?

It's doing my head in, all I've gained from this research is the understanding that birds have a far more advanced respiratory system and their capillaries are bigger than mammals, this still doesn't explain the need for a nucleus, it's actually suggesting they don't need one!

Any enlightenment will be great,

Thanks.

http://onlinelibrary.wiley.com/doi/10.1002/iub.490/pdf

It's difficult for vertebrates to aquire/evolve enucleated cells, that's why they are very rare previous to the mammalian adaptation. Salamanders have evolved enucleated cells. Research suggests that it may be due to a salamanders big genome and big cell nucleus, compared to the salamanders small body size.

Mammals may have acquired the trait because they evolved from small animals with miniaturized capillaries and blood cells and large genomes, and the advantage was kept afterwards. Large genomes inhibit flow and flex of nucleated blood cells.

The smallest bird genomes are found in the most miniturized clades of birds at 1 Gb. Mammals of a similar size can have carry 2-3 Gb of chromosomes.

Lizards have lower energy than mammals.

Fish are most active in highly oxygenated water, i.e. salmon, which allows them to be very energetic, water is a more efficient breathing medium than air, hence the small size of gills. fish and humans both contain 6-7 percent blood by volume.

Birds have smaller haemoglobin including the nucleus, and have a different kind of capillary size and structure with advantages and disadvantages, and lighter hollow bones with less marrow. Birds didn't radiate to new shapes as well as mammals did.

Enucleate cells are fairly rare in the plant and animal world, so they perhaps have a hidden expense. Maybe it's not just a factor of shedding the nucleus, and in fact there is a cost of adapting the primary circulation system's immunity against paramecia and pathogens without a nucleus. various viruses can take advantage of enucleate cells.

Perhaps that is the reason why birds did not evolve backwards into dinosaurs. some factor made their genome comparatively small. It could be the lack of enucleated bloodcells that forced them to shed genes as an alternative. Perhaps that's why they lost the dinosaur genes which held code for quadrupeds, arms, jaws, horns and teeth and the things that birds don't have.


How effective is water purification by boiling? Does boiling water kill all harmful bacteria, fungus etc from water, or it is just a myth and removes only few of microorganism?

To be precise, boiling water would not remove all bacteria as there are certain extremophiles that thrive at higher temperatures.

However, boiling of water is known to get rid of harmful pathogens. Boiling of water is a method of pasteurization, which means killing those organisms that can cause harm to humans.

Quoting from New York State - Department of Health >>

  Boiling water kills or inactivates viruses, bacteria, protozoa and
  other pathogens by using heat to damage structural components and
  disrupt essential life processes (e.g. denature proteins). Boiling is
  not sterilization and is more accurately characterized as
  pasteurization.

  Cooking food is also a form of pasteurization. For pasteurization to
  be effective, water or food must be heated to at least the
  pasteurization temperature for the organisms of concern and held at
  that temperature for a prescribed interval.


What is accumulation and release centre of neurohormones? What is accumulation and release centre of neurohormones?

Is it hypothalamus?

The neurohormones in most mammals include oxytocin and vasopressin, both of which are produced in the hypothalamic region of the brain and secreted into the blood by the neurohypophysis (part of the pituitary gland).

A second group of neurohormones, called releasing hormones, also originates in the hypothalamus. The members of this group, however, are transmitted within the neural cells to a second locus in the brain, from which they pass in the bloodstream to the adenohypophysis, which also is a part of the pituitary gland. There they either stimulate or inhibit the release of the various adenohypophysial hormones.

A third group of neurohormones includes the enkephalins and other endorphins. The endorphins are effective in relieving pain, a property apparently related to their function as neurotransmitters, passing nerve impulses from one neuron to another. Their neurohormonal activity is manifested by their stimulation of the secretion of somatotropin and vasopressin by an indirect process involving a site (other than the secretory neuron) in the central nervous system.


Do wolves bury food like dogs? Many breeds of domestic dogs seem to like burying food, presumably in preparation for leaner times.

Assuming that dogs evolved from animals similar to the modern wolves through a mix of natural and artificial selection, is this burying behavior novel in dogs, or inherited from wild wolves? Do wild wolves also habitually bury food, and return to their caches when hungry?

The habit of burying food in modern dogs is an instinct that came from the grey wolf (Canis lupus) long ago, and originates from a phenomenon called surplus killing, where a carnivore would kill more than it could eat, and often use it at a later time.

  Many, if not all, carnivores possess behaviour patterns which allow utilization of a kill at a later time, or allow other members of the same social unit or offspring to use the food.

When the prey is small enough to transport, and there are pups, it is often returned to the den.

  Pups will usually remain in their den for the first three or four weeks of their lives before mother allows them to venture forth into the light. During this time the mother is quite dependant on her mate and other pack members to bring her food in the form of meat that is often regurgitated for her.

It is then fed on by the litter, and the excess buried for later use.

This is called 'caching', and is still seen today in the domestic dog (Canis familiaris).


What is an organism? The definition of an organism Wikipedia gives is

  An organism is any contiguous living system.

I understand that these are not organisms according to this definition:

A bird and a tree it's perching on are living and contiguous, but they don't form a system.
All humans are living and form a system, but they are not contiguous.

But some things are unclear to me. My veins and my skin are contiguous and living. Do they form a system? I think so, at least according to what I read about systems in Wikipedia. They are definitely interconnected; they have behavior; and I believe they have structure, though I'm not really sure what structure is. Perhaps if we carefully define what we want "structure" to mean, we can save the definition from allowing (skin + veins) to be an organism?

Is (mother + her unborn child) an organism? I think it definitely is according to the definition. Is the unborn child an organism?

Is an apple that's just fallen off a tree an organism? Was it an organism before it fell?

Is (human + their microbiome) an organism? Is a human without the microbiome an organism?

I think the part of the definition that the least clear to me is the word "system", and in the definition of the word "system", it's the word "structure".

I think the definition in Wikipedia is simply bad because it depends on another debatable definition.

I prefer something which follows from an observation made by Ricard Dawkins in The Extended Phenotype (the following is my definition, but I think Dawkins had something similar in mind):

An organism is any system of components which depend on each other for survival and cooperate in proliferating potentially unboundedly.

A single-celled organism is by this definition an organism since it proliferates by coordination of its components.

A single-celled organism with organelles deriving from endosymbiosis (think mitochondria) is an organism: even though mitochondria do proliferate on their own inside the cell, they don’t do so outside of the cell, hence have a bounded proliferation only; and they depend on the cell as a host. On the other hand, they cooperate with the cell division.

Endosymbionts, on the other hand, are organisms because even though they depend on a host (and the host on them), they may theoretically switch host or even survive a limited time without a host.

Similarly, the cells in a multi-cellular organism can sometimes divide independently (in organs) but they cannot survive without the rest of the organism, and the unbounded reproduction of any organ in fact requires going via the germ line of said organism.

A virus which depends on a host to proliferate does not form an organism with the host since it doesn’t use the host’s germ line; if, on the other hand, it does use the host’s germ line (consider virally derived pseudo-genes on our DNA) then, yes, it forms a common organism with its host.

  Is (mother + her unborn child) an organism?

I wouldn’t say so, since the child is only temporally part of the host.

  Is an apple that's just fallen off a tree an organism?

Interesting; I’d say yes, as long as it retains the potential ability to proliferate (it’s a separate organism from the tree though).

  Is (human + their microbiome) an organism?

No. Humans can survive (albeit only shortly) without a microbiome; in the same vein, the bacteria of the microbiome can change their host.

Unfortunately, this definition also has a drawback: there are organisms which cannot reproduce because they are sterile, yet they are clearly still organisms.

Note that other definitions (e.g. “an organism is a collection of components sharing common genetic material”) also don’t work universally since they also break down – the example of genetic commonality would preclude mosaicism and organelles derived from endosymbiosis.


Why are dolphins so smart? It seems that dolphins have (among?) the highest encephalization quotients found outside of humans, higher even than chimpanzees. By the "use it or lose it" principle this indicates that intelligence must be particularly valuable in their niche. Why is that? They are predatory and social, and both of those are associated with intelligence, but why are dolphins smarter than other predatory pack animals? For example, is there something about being an air-breathing organism living in water that makes having a high EQ particularly adaptive?

It might not fully answer your question…

Cost of having a heavy brain

Generally speaking, having a heavy organ is an important cost for flying animals, a medium cost for terrestrial animals and a low cost for marine animals. Loosely speaking, the principle "use it or lose it" does not apply with the same strength in all animals in regards to brain weight. If you create a regression between "intelligence" and "need of being intelligent"(supposing it means something!) in terrestrial mammals and add the dolphin on your graph, you might be surprised that the dolphin does not fit on the regression but it might only be due to the fact that they live in water which is much more dense than air so that it is less costly to carry a big brain. So, yes there might have something to do with "living in the water".

Indexes of intelligence

EQ does not mean intelligence! It is just an index. And we have to understand that people first were happy to think that humans are very smart because they have a big brain but they were terribly confused when they've learned that sperm whales brain weight 8kg! So they tried finding other indexes. EQ is one of them and we're quite happy to use it because it places humans at the first position. But it does not mean that this index is a good representation of intelligence. Some small birds with their tiny brain were shown to be have a spatial memory that is much more efficient that the one of humans for example.

Something else. When looking at these indexes one should not forget that size (or weight) does not equals efficiency. Let's make an analogy with computers. You can have a good software or a good hardware. Big brains are not necessarily very efficient!

Now, it is still true that dolphins are good at performing many tasks that we link to the concept of intelligence. Dolphins have complex social organization that is probably link with their intelligence. I would tend to think (just a guess) that there are many social factors involved into the evolution of their cognitive abilities. Because the social structure changes as cognitive abilities evolves, it seems to me quite hard to know what factors made that clever individuals were more fit than stupid ones at every moment during the evolution of dolphins. But I might overlook the complexity of the problem. And I honestly never learned any article concerning the role or the evolution of cognitive abilities in dolphins.


Is there selection against long proteins and long genes? Background thought
Titin and TTN
Titin is the largest protein in the human genome with 33423 amino acids. Titin is coded by the gene TTN that must be at least $3 \cdot 33423 \approx 100kb$ long. Looking at NCBI entry for the gene TTN indicate that TTN is actually about 240kb long.
Transcription rate
The average transcription rate (Ref.) is around 1.5kb per minute. It therefore takes about $\frac{240k}{1.5k * 60}$ 2.5 hours to transcribe TTN in mRNA. This mRNA then need to be spliced before being available for being translated. Per consequence, I don't think it is possible for translation to happen in the same time as transcription but might well be wrong.
Translation rate
The translation rate is about 8.4 amino acids per second (Ref.). It therefore takes about $\frac{ 33423} { 8.4 \cdot 3600}  \approx 1$ hour to translate the protein. Sure, several ribosome can translate the mRNA in the same time but it still remain that it takes 1 hour to synthesize at least one protein.
Transcription + Translation rate
Assuming translation does not occur in the same time as transcription, the total time to create the first protein of titin is about 3.5 hours.
Half-life
The half-life of a typical human protein is 6.9 hours (Ref.). Intuitively I would expect a negative correlation between mRNA size and mRNA half-life.
Half-life and Transcription + Translation rate
Because the time to produce the first protein is about half the half life, it means that a quarter of every single mRNA that is being produced would never give rise to even a single protein because it would degrade before either before or after translation has started.
It sounds like an important cost and would be surprised if a gene or a protein could be any longer.
Question
Is there evidence of selection against long proteins and long genes?
Are there proteins that are much longer than Titin in other species?
Do I exaggerate the cost it represents, either by not considering that an average rate (such as transcription rate) is not representative of the actual rate for typically long gene/protein or by assuming that it is costly to create tons of mRNAs that won't never be translated?

Is there evidence of selection against long proteins and long genes?

I am not aware of any such evidence and cursory googling did not reveal studies that researched a correlation between gene selection and gene size. However,  the larger a gene, the larger the probability of a deleterious mutation within said gene so I expect that there is some limit to the size genes can reach and be stable through evolution.

  Are there proteins that are much longer than Titin in other species?

To date, titin is the largest known protein

  Do I exaggerate the cost it represents, either by not considering that
  an average rate (such as transcription rate) is not representative of
  the actual rate for typically long gene/protein or by assuming that it
  is costly to create tons of mRNAs that won't never be translated?

I really like how you estimated the time cost of producing titin. However, as you already suspect, I believe that you have several flaws in your assumptions.

First of all, the stability of mRNA and proteins varies a lot and depends strongly on their sequences. The half life of proteins can vary from minutes to Years. The Titin protein has a half life of ~70 h.

Similarly, mRNA stability varies from minutes to > 12h. Especially household and structural genes were identified to have mRNAs with long half lifes.

Both protein and mRNA stability is not simply governed by random decay but rather by tightly regulated degradation. For proteins, an example is ubiquitinylation which is a process where certain amino acid sequences are recognized and cause the protein to be ubiquitinylated which in turn triggers the degradation via the proteasome. For mRNA, the secondary structure is crucial since certain loop structures can be recognized by RNAses. Thus average protein/mRNA lifetimes do not help to estimate the actual turnover of a specific protein.


How many water molecules will be generated when single nucleotides are used to make this RNA: 5’-UUAACCGUCAG-3’? Based on what we learned on condensation reactions, how many water molecules will be generated when single nucleotides are used to make this RNA: 5’-UUAACCGUCAG-3’

I had an online biology quiz with this question, and I thought it would be one molecule for each nucleotide, for 11 total. The answer I have been given is 10. I feel like I am missing something obvious.

It's one for every phosphodiester bond formed. 11 nucleotides, but only 10 bonds needed to join them into an oligonucleotide:

1  2  3  4  5  6  7  8  9  10 11
N--N--N--N--N--N--N--N--N--N--N
 1  2  3  4  5  6  7  8  9  10


How do proteins get into the blood stream? So I'm asking this in reference to the injection of insulin, which is commonly done subcutaneously (in the hypodermis, a fatty part of skin). Now I know proteins usually get into the blood when digested through the stomach/intestines - but I was wondering how they manage to get into the blood when injected into muscles/fat? I know there are capillaries pretty much everywhere, but from what I've researched proteins are too large to get through capillary walls.

That begs the question then, how do proteins manage to get into the blood stream when injected? I can't really envisage large capillaries, because surely they'd have huge holes in them or whatever to allow large proteins like insulin in. Any help on this one? Cheers

Found the answer - the lymph capillaries. I've not researched them too in depth but from what I've read thus far, their job is to essentially pick up fluids not picked up by the blood capillaries. They have walls that allow proteins to enter but make it very hard for fluid to flow out.

Wiki states that an average of 20 litres of blood gets processed each day by the blood, with roughly 17 litres through the blood capillaries/system (1), with the remaining 3 litres through the lymphatic system.

These are also prevalent around skin. 70% of lymph capillaries are found near the skin (2).

1) http://en.wikipedia.org/wiki/Lymphatic_system
2) http://www.lymphnotes.com/article.php/id/151/


Questions on DNA structural motifs In the recent Nature Chemistry paper I-motif DNA structures are formed in the nuclei of human cells (open access link in LATimes) figure 1a shows "Schematic of i-motif and G4 structures."

I'm not a biologist, nor a chemist, so please forgive if the answer to my  questions seems obvious. I've looked at Wikipedia's Structural Motif article but there's little there about nucleic acids.

The length of the unlinked strand seems shorter, is this just because it is a schematic, and in reality the two branches would have the same number of bases?
What does the presence of the dual left and right arrows in G4$\ce{<-->}$ iM in the figure mean in this case? Does it suggest that a single molecule can change configuration back and forth between two distinct structures, or something else?

To answer point 1: The length of the unlinked strand is not represented accurately, it is shown shorter only because this is a schematic. In reality, the unlinked strand should be the same length, and would have the same number of bases as you have guessed.


What could cause no pain but sense of touch? What could cause a mammal to have and respond to a sense of touch with only isolated numbness but not feel pain?

I think Congenital insensitivity to pain with anhidrosis might be what you are looking for, it is the closest thing I can think of right now.


How does Iota-Carrageenan achieve an antiviral effect? "Cold Defence" nasal sprays are recommended to be taken either preventatively or in the early stages of a cold.  The active ingredient in these sprays is Carrageenan.  After some research, the active compound is Iota-Carrageenan (ι-Carrageenan).

This study by Eccles et al[1] shows that this drug is clinically effective.  The study was only designed to test efficacy rather than to explain the mechanism, however. A fleeting mention is provided in the discussion section:

  The above results suggest that the treatment with Iota-Carrageenan reduces the viral replication. Consequently fewer cells are infected, the immune reaction against the viruses is less pronounced and fewer symptoms occur.

How does ι-Carrageenan produce an anti-viral effect?

Eccles R, Meier C, Jawad M, Weinmüllner R, Grassauer A, Prieschl-Grassauer E. 2010. Efficacy and safety of an antiviral Iota-Carrageenan nasal spray: a randomized, double-blind, placebo-controlled exploratory study in volunteers with early symptoms of the common cold. Respiratory Research, 11:108, doi:10.1186/1465-9921-11-108.

Through two different pathways, one relying on a non-specific (innate) response, and another through a reactive oxygen species, the level of NF-kB(**) is amplified, as such a response would have happened as a result of the presence of the virus anyway.

  In thousands of experiments, carrageenans have been used to
  induce inﬂammation, since inﬂammation is a predictable effect of
  exposure to carrageenan in animal and cell-based models. For the
  most part, these experiments were designed to test the effectiveness of anti-inﬂammatory agents or to study the mediators of inflammation

  The innate immune pathway is mediated by toll-like
  receptor (TLR)-4 and B-cell leukemia lymphoma (BCL)10, leading
  to increased Interleukin (IL)-8 secretion by both canonical and noncanonical pathways of NF-kB activation. The ROS-mediated
  pathway of inﬂammation does not involve TLR4-BCL10, but
  requires Hsp27 and IkB-kinase (IKK)b, leading to increased phosphorylation of IkBa, and thereby enabling the nuclear translocation
  of NF-kB.

From the intro to:

  Yang B, Bhattacharyya S, Linhardt R, Tobacman J. (2012) Exposure to common food additive carrageenan leads to reduced sulfatase activity and increase in sulfated glycosaminoglycans in human epithelial cells.  Biochemie, Mar 5,epub ahead of print, doi

(As an aside, the direct conclusions of this study are that these changes in GAGs may further influence transcription and play a role in determining cell fate, and perhaps may influence cell/cell interactions)

  (**)NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls the transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens  wiki


Biological meaning of taking zero as coefficient of the Laplacian in mathematical models of cell motility Several mathematical models from theretical biology deal with various forms of cell motility (for example, cancer growth) or evolution of populations.

The equations that make up such models usually contain (among others) a Fickian diffusion term of the form $$- \delta \Delta u(t,x),$$ where $u$ is the cell (or population) density.

To fix some ideas, consider the following examples.

A chemotaxis model:

$$\partial_t u(t,x) = \delta \Delta u(t,x) -  \nabla \cdot(uK\star u),$$
where $K \star u = \int_\Omega K(x,y)u(t,y)dy$, for a certain kernel $K$.

A model arising in population dynamics:

$$\partial_t u(t,x) = \delta\Delta u(t,x) + u(t,x) \left(\lambda - a\int_\Omega u(t,y) dy\right).$$

  Biologically, what is the meaning of a situation where $\delta = 0$ (that is, where there is not Fickian diffusion governed by the Laplacian term)?
  Is there any interest in studying such situations?
  Can you point out some references on this topic?

Just so we're on the same page..

$u(x,t)$ is a concentration/density function that describes the number of particulate species (bacteria, gas molecules, etc.) at point-in-space $x$ and time $t$. And although it may be an obvious statement to make.. with $u$ having the parameters $(x,t)$, this indicates that particulate concentration values are dependent upon both position and time.

$\delta$ is the diffusion coefficient of the particulate concentration, defined as a proportionality constant between particulate diffusion and the overall particulate concentration gradient. Particulate diffusion can be regarded as local behavior, whereas the overall particulate concentration gradient describes the behavior of distribution for the entire particulate concentration, and of which may be affected by forces other than the particulate's response to an attractant/repellant gradient, including temperature, pressure, and/or other environmental variables. An in depth understanding of this coefficient can be obtained by reading sections 2.1 & 2.2.

Your questions

Biologically, what is the meaning of a situation where $\delta = 0$?

Well, if you did in fact read the recommended sections, you may already have realized that it's just not possible for $\delta = 0$, unless you're considering concentrations of mass that simply can't diffuse throughout one another, but even then $\delta$ would be considered as $DNE$.
To reference a portion of 2.1 & 2.2:

Molecular diffusion, strictly speaking, cannot occur under conditions in which both the net flux and the [concentration gradient] are simultaneously zero. If the [concentration gradient] is uniform, then in general fluxes are different for different species, and the net flux is not zero. If the net flux is zero, a small [concentration] gradient must exist in order to counter the tendency for the different species fluxes to be different.

That being said, the diffusion coefficient can be an extremely small value - of which is based on the nature of the particulate(s) undergoing diffusion, and the medium for which they travel throughout - but it's never zero. See here for a series of tables that contain diffusion coefficients for common substances at standard conditions.
And as for the biological meaning to $\delta = DNE$.. the only conclusion that could be made is that the mass concentrations under consideration can't diffuse with one another, for whatever reason. Whether or not there's meaning beyond this, I believe that would be dependent upon what's specifically being studied.

.. that is, where there is not Fickian diffusion governed by the Laplacian term?

This statement however, does have biological meaning to it. When $\delta \Delta u(t,x) = 0$, this means there is a zero net flux occurring at point-in-space $x$ at time $t$. Which is to say that - the number of particulates of a given species entering a given region of space over a given time interval is the exact same as the number of particulates of the same species leaving that exact same region of space over the exact same time interval. When this is true for all regions of space within the [biological] system, it means that the system is in a steady-state, and/or has reached equilibrium.
Note: Equilibrium and steady-state systems are not the same, however, the differences involved aren't relevant to the scope of this discussion, and so nothing further will be said about this.
When a biological system is in a steady-state, and/or is in equilibrium, that can carry significant implications. Perhaps the most ubiquitous example that also first comes to mind are the steady-states of ion channels, with the effects of cell activation/non-activation being the implications. Another example could be pretty much any chemical reaction that reaches equilibrium.

Is there any interest in studying such situations? Can you point out some references on this topic?

Yes, there are many occurrences where these states are studied, of which you may already be aware of. Regardless, here are a few that seem worthy enough for me to provide in this response:

Steady-state Distribution of Bacteria Chemotactic Toward Oxygen

Equilibrium of Two Populations Subjected to Chemotaxis

The Hodgkin-Huxley Model

In summary
The biological meaning of $\delta \Delta u(t,x) = 0$ usually deals with scenarios where the region(s) in space experiences a flow of mass that has equal incoming & outgoing rates for a given particulate species. Most of the time, this is indicative of a steady-state, and/or equilibrium, and this can be confined to local regions, or globally throughout the system.
And I'd also like to offer a slightly different perspective. Normally, the diffusion coefficient is a temperature & pressure dependent function. However, if you're considering situations with STP/NTP, the diffusion coefficient can truly be treated as a constant. When this is the case, the Laplacian term is analogous to the heat equation. By taking this perspective, the Laplacian term [being zero] is stating that there is no loss or gain in heat (species-specific particulate motion) when considering a region of space over a defined time interval, and the overall model would describe the change(s) in motion (heat) for the entire system. From there, biology could explain as to why the "heat" behaves the way it does, of which would involve the mechanisms & behaviors of an organism with respect to its reaction(s) to an attractant/repellent.
And lastly, for the sake of inclusivity, the other terms in these models generally represent behaviors that are external to local interactions, and each may carry differing effects, such as birth/death rates in population dynamics, or particulate concentration movement that's perpendicular to the axis to which the concentration gradient moves upon, as is the case with the second term in the chemotaxis model. So then, when the Laplacian term is not contributing to any change, i.e., when there is a zero net flux, these other terms will then be the only candidate contributors to any potential changes in the system, whatever those changes may be.

References

A Mathematical Model For Chemotaxis
Keller-Segel Models for Chemotaxis
Gaseous Diffusion Coefficients
Fick's Second Law


How does the brain know what to remember and what not? People remember some information for example when learning for an exam, or remember to go to a shop after work etc., but we don't remember usually much other stuff like people passing us, what was the weather some days ago etc. How does the brain know what to remember and what not, how does it filter important information from not important?

The body of work on this topic huge, so I'll just try to mention a few things.

On the cognitive level, one possible answer is salience (also see here for an article specific to the visual system). You can think of this (in a somewhat circular answer) as the thing that makes certain stimuli stand out from others. Salient stimuli capture bottom-up attention. Another possible answer is top-down attention. This is where you actively/deliberately pay attention to something.

In terms of mechanism, we have to think about different types of memory. For example, there are separate long-term and short-term memory systems (among many other distinctions). In general, there are hypothesized gating mechanisms that determine the information that can enter memory. The gating systems are controlled by some signal that says 'store this information' or 'ignore this information'. Different memory networks can have different gating systems.

There's a lot of work looking at neuromodulators as gating signals. Dopamine and acetylcholine are some prominent examples. For example, people have found that dopamine can modulate synaptic plasticity (the strengthening and weakening of connections between neurons, which is thought to be a primary mechanism of long term memory storage). It can also cause cortical remodeling. For just a couple examples, see:

  Zhang et al. (2009) Gain in sensitivity and loss in temporal contrast
  of STDP by dopaminergic modulation at hippocampal synapses.

  Bao et al. (2001) Cortical remodelling induced by activity of ventral
  tegmental dopamine neurons.

  Froemke et al. (2007). A synaptic memory trace for cortical receptive field plasticity.

On the behavioral level, stimulating the dopamine system can induce particular forms of learning (which you can think of as a form of memory). For example, if you stimulate the dopamine system, an animal may tend to repeat the behavior that led to the stimulation. A pathological version of this is thought to be what happens during addiction with certain classes of drugs that stimulate the dopamine system (e.g. cocaine, but not lsd).

Interestingly, many of the same mechanisms appear to work across species, from sea slugs to humans). Although,sea slugs can't remember going to a shop after work.


Enzyme kinetics at the chemical level I am stumped by two questions:

Why do we take only the initial 10%(or may be 9.99999....%) of S conversion as the rate of the enzyme reaction. why not more than 10%?
Why doesn't the velocity keep on increasing linearly until the Vmax is reached (as all the S molecules get exhausted)

Research and attempts to answer:

Why v0's 10%?

Steady state kinetics apply when the [ES] is constant, on reaching 10% [P] (for a uni uni reaction) the backward reaction increases, increasing the [ES]?
On reaching 10% conversion the rate decreases, so we measure the optimum activity.

Why doesn't the velocity increase linearly until all the molecules are used up?

Since an enzyme's turnover number (kcat) is constant...
...

Disclaimer :

'have put two Qs together.
Didn't find relevant Q on BioSE.

The answer to the first part of your question is that we don't take the initial 10% of a progress curve (velocity vs time) as a measure of activity, but we measure the initial rate of the reaction.  We do this by drawing a tangent at the origin.

It is merely a 'rule of thumb' that progress curves are practically linear provided that not more than 10% of substrate has been used up. If there is significant slowing down before 10% is used up - and there may be if the substrate concentration is way below Km value - then it is not valid to draw a line through the points: we must draw the tangent to the curve. That is, it is not acceptable to take the average rate during the first 10% of the progress curve.

For this reason it is desirable to use as sensitive a method as possible when measuring an enzymic rate, and to never rely on a single time point (as is common in radioactive assays) without sufficient controls to justify that it it is the initial rate, and not the average rate (or something else) that is being measured.

The reason we measure initial rates is that is makes things simpler on two fronts.

Firstly, the decrease in rate with time of an enzymic reaction may be due to many factors: product may be inhibiting the reaction, the reverse reaction may become important, the enzyme or substrate may be unstable. It is only during the initial rate period that conditions are accurately known, and such  effects may be legitimately ignored. It was Michaelis and Menten that first realized the importance of measuring initial rates, and of the great simplification principle that ensued, in enzyme kinetics. (see Cornish-Bowden, 2004).

Secondly, the rate laws themselves are greatly simplified.  Provided that eo << So (the initial enzyme concentration is very much less than the initial substrate concentration), we may take the So as being equal to the substrate concentration and 'plug in' this value into our rate law (such as the Michaelis-Menten equation), and ignore the effect of time on the value of S.  In addtion, we can set all product terms to zero. This can greatly simplify things.

For example, the rate law for a reversible single-substrate mechanism (see here) is the following:

$$ v = {
  {{{V_{max}^f}\over{K_{m}^s}}\ S\ -{{V_{max}^r}\over{K_{m}^p}}\ P }\over{1 + {{S}\over{K_{m}^s}} + {{P}\over{K_{m}^p}}}}\ \ \ \ \ (1)$$

This one is not as complicated as it looks: we have just defined a Km and Vmax for the forward and reverse directions. But let's set product to zero:

$$ v_i = {
  {{{V_{max}^f}\over{K_{m}^s}}\ S_o\ }\over{1 + {{S_o}\over{K_{m}^s}} }}\ \ \ \ \ = \ \ \ {{V_{max}^f S_o}\over{{K_{m}^s} + S_o}}\ \ \ \ (2)$$

We now obtain the familiar Michaelis-Menten Equation (where $v_i$ is the intial velocity).

The second part of your question is more fundamental. I'll take it to mean the following. Why does an enzymic reaction not follow second-order kinetics at all substrate concentrations? Why doesn't doubling the substrate always double the rate (as is often the case in chemical kinetics)? A. J. Brown in 1902 suggested that the reason for this is the formation of an enzyme-substrate complex and that at sufficiently high substrate concentration all the enzyme would exist in such a complex and the enzyme would become 'saturated'. The formation of an enzyme-substrate complex, of course,  is now a cornerstone of enzyme kinetics. One of the early key pieces of evidence for an enzyme-substrate complex was the observation that an enzyme is much more heat-stable in the presence of its substrate than in its absence.

Finally, it is probably worth pointing out that some enzyme operate way below Km values and at 'physiological' concentration of substrates do obey (to all intents and purposes) second-order kinetics. Catalase, for example, has a Km for hydrogen peroxide of about 1 Molar (Ogura, 1955), and one assumes that physiological concentrations never reach this level. (We need to be a little careful about catalase, however: it is one of the few enzymes that is inactivated by substrate).

A great reference on enzyme assays is the following:

Principles of enzyme assay and kinetic studies by K. F. Tipton in Enzyme Assays: A practical approach

For an introduction to enzyme kinetics, and the early history of enzymology, I like the following:

Cornish-Bowden (2004) Fundamentals of Enzyme Kinetics 3rd Edn. Portland Press, London.


Why do most animals never seem to evolve over millenia? People often say, including those with extensive knowledge in biology, that a certain species of animal will evolve in one way or another:

From changing environments.
Mutations.
Possibly even genetic engineering from human animals.

My question lies in the fact that, aside from the latter option, why haven't any differences in animals'(except humans) markup, morphology, intelligence, DNA, behavior, or any habits changed over thousands or (possibly millions) of years?

A cockroach has had the same behavior it has today more than 10 million years ago, and there have been no advancements in the species in the slightest bit.

It makes you question evolution, because why don't other animals (like cockroaches) have any changes over 10+ million years, yet humans, like me and you somewhat, have, in a relative period of time similar to the linked geological period above, evolved from spear tossing hominids into someone brilliant enough to even ponder this question.

If modern humans are the result of mutations in genes, why has no one species over the course of hundreds of millions of years been fit enough, or advanced mentally as we have, or even in any slightest bit?

How come most animals never seem to evolve over millennia?

The word "seem" in your question should not be disregarded. You seem to assume that cockroaches (or most animals as you say) did not change much the last tens or hundreds of thousands of years. But what do you know about that (no offence here)? Have you actually reviewed many kinds of research that estimate the rate of evolution of different randomly chosen lineages in the past 500,000 years? I think you assume that other species evolved slower than humans rather than know it. And you will certainly put much more importance to the evolution of the gene FoxP2 (involved in language) than to a gene allowing cockroaches to have a better sense of smell. This is a biased view of what is a rate of evolution. It would be much wiser to consider a rate of evolution as something like the number of newly arising mutations that succeeded to get fixed in the population. See Haldane's rate of evolution and the Darwin unit. Please don't make the mistake to think that being smart (or complex) is some kind of the goal of evolution and those that are not smart (or complex) are "less evolved" or that they evolved more slowly.

You also seem to want to point on the evolution of DNA and evolution of habits. I guess you might be appreciative of the evolution of human knowledge and culture. But this is obviously something that does not have to do with genetic evolution but is rather a matter of cognitive capacity. You cannot compare the change of culture and traditions of insects and humans as insects have mostly no traditions.

Now, this is obviously true that different lineages evolve at different rates. Many things influence this rates such as the population size, the mutation rate, the generation time, the selection pressure (which itself might depend on social structure or the rate of environmental change for example). In these terms, I would rather believe of Homo sapiens as a lineage that should have a rather slow evolutionary rate.

Homo sapiens is quite a recent species. And speciation is often linked with phenotypic divergence, with niche competition and niche complementarity and therefore with a high rate of evolution. In these terms, I would believe that humans are a lineage with high evolutionary rate.


Parameters for Fitzhugh-Nagumo model of Action Potential I'm a high school student who's currently in AP Biology, so my background in biology is quite limited. I'm interested in mathematically modelling action potentials.

Doing a quick google search, I discovered the Fitzhugh-Nagumo model, a simplified case modelling the voltage of the cell during an action potential as a second order differential equation $ C \frac{d^2V}{dt^2} + \epsilon(V^2-1) + \frac{V}{L} = 0$. I want to solve this equation numerically, but I can't find the numerical values of $\epsilon$, $L$, or $C$ online. What are some reasonable parameters for this model for a human neuron?

This is actually not the Fitzhugh-Nagumo model of the a neuron, however it is highly related to it. I believe the the Equation you have there, is capable of oscilations for any positive values of $\epsilon$, $C$, $L$. I generated this graph with the parameter values all set to 1.  Note how it is very similar to a sine wave.

I believe you where trying to write Van der Pol's equation here:
$$C\frac{d^2V}{dt^2} +\epsilon (V^2-1) \frac{dV}{dt}+ \frac{V}{L}$$
Note the subtle difference of multiplying by the first derivative.
Here is again a image with all parameters set to 1

The Fitzhugh-Nagumo equation can be found on wikipedia here and on peer reviewed  scholarpedia here. For reference it is a two state model described by the equation:

$$ \frac{dV}{dt}=V-V^3/3-W+I$$
$$ \tau \frac{dW}{dt}= V + a -bW$$

A common value for the parameters are $a=.7$,$b=.8$,$\tau=12.5$ $I$ can be anything really, I used $I=.5$ to generate the graph below. Also note that the model wont spike if I below a certain value. The Fitzhugh Equation is is slightly more general, but does simplify to the Van der pol under the assumption $a=b=0$. Here is the graph of it with the constants I described.


Why is yawning contagious? Why does yawning seems to be contagious?
Is this similar to laughter being contagious or does it has a different reason?

Yawning is contagious in humans, which means that, in general, it is more likely that a person yawning after perceived (by sight, hearing, or both directions) yawning issued by another person. The frequency of infection varies throughout the day, with a peak in early morning and late evening.

A recent study conducted by Ivan Norscia and Elisabetta Palagi (University of Pisa) has provided the first evidence that the behavioral contagion of yawning is associated with the empathic bond between people. The study showed that the infection follows the same gradient of empathy: is greatest in close relatives (parents / children / grandchildren, brothers, stable couples), decreases in friends, then acquaintances in (people connected only by a third, external, ie work or a friend in common) and reaches a minimum in the unknown.

Various studies of clinical, psychological and neurobiological suggest and support the link between the yawn contagion and empathy. For example, the infection begins to occur at 4-5 years of age, when children develop the ability to identify, in a proper way, the emotions of others. In addition, the infection is reduced or absent in people who have problems related to empathy, how people with autism, and is positively related to subjective scores of empathy based on tests of psychological type. Finally, the areas of the brain related to the emotional sphere overlap, in part, with those involved in the response to yawn, with a possible involvement of mirror neurons.

Yawning has been observed among various primates. In these cases the yawn is a threat gesture, a way of maintaining order in the primates' social structure. Specific studies were conducted on chimpanzees and stumptail macaques. A group of these animals was shown a video of other conspecifics yawning; both species yawned as well. This helps to partly confirm a yawn's "contagiousness".

In animals, yawning can serve as a warning signal. For example, Charles Darwin, in his book The Expression of the Emotions in Man and Animals, mentioned that baboons yawn to threaten their enemies, possibly by displaying large canine teeth.

see yawn

autism

Gordon Gallup, who hypothesizes that yawning may be a means of keeping the brain cool, also hypothesizes that "contagious" yawning may be a survival instinct inherited from our evolutionary past. "During human evolutionary history, when we were subject to predation and attacks by other groups, if everybody yawns in response to seeing someone yawn the whole group becomes much more vigilant and much better at being able to detect danger.

Personally, I can make an observation. Cats yawn as specific means to calm people, and especially to reassure the other cats and the pups. In order, they stretch, yawn, lie down, half close theyr eyes as if they start to sleep. When the whole group repeats the gestures, the majority of them (now calm) actually falls asleep.

EDIT @kmm

Norscia & Palagi
The Pisa Group in cooperation with CNR Consiglio Nazionale delle Ricerche =
Friends and loved ones yawn together - Science Daily
The Pisa Group/ Elisabetta Palagi, Ivan Norscia, and Daniela Antonacci - University of Michigan - Dearborny
Gordon G. Gallup


How can green algae be both multicellular and unicellular? How can green algae be both multicellular and unicellular? What are the cases in which it can be both uni and multi cellular?

Because Algae are represented across four kingdoms, namely Bacteria (unicellular prokaryotes), Plantae (multicellular eukaryotes), Chromista (multicellular eukaryotes), and Protozoa (single-celled eukaryotes).

For example, I. Chlorophyta is unicellular:

I. Chlorophyta. Source: University of Wisconsin

While kelp can become huge and can form underwater forests:

Kelp. Source: Nature

Reference
Guiry, J Phycol 2012; 48, 1057–63


Why estimate linear and full (linear, quadratic, and correlational) selection coefficients separately? "We then fitted a linear regression including all three life-history
  traits to estimate the vector of linear selection gradients, β, for
  each sex (Lande and Arnold 1983). A quadratic regression model
  incorporating all linear, quadratic, and cross-product terms was then
  used to estimate the matrix of nonlinear selection gradients, γ, for
  each sex. "

This is from the paper Evidence for strong intralocus sexual conflict in the Indian meal moth, Ploida interpunctella. I am not sure why they estimate these gradients separetly rather than taking them just from the one full model - any suggestions? Is this normal or have they done it for a reason?

For some similar work see these two papers:

Gosden et al which seems to use only the linear gradients from one model with sex as an effect.
Stearns et al which uses linear, quadratic and correlational estimated from one multiple regressions model per sex (similar to the main paper I cite first but not using a linear terms only model for the linear coefficient).

I have mailed the corresponding author on the quoted paper to ask why, I will let you know what he says if he replies

This is directly following the advice of Lande & Arnold (1983), saying:

  Linear multiple
  regression can be used first to estimate the forces of directional selection, $\beta$, and their standard errors. Then a quadratic multiple regression (16) or (Al), can be used to estimate the forces of stabilizing selection, $\gamma$, with their standard errors. The regression (16) provides the best quadratic approximation to the selective surface (although valid estimates of $\beta$ can be obtained
  only from a purely linear regression, or by using the orthogonal regression (Al)).

The reason is that the estimates of direction selection is influenced by the higher order terms in the full model that includes quadratic and correlational selection, and the linear model therefore has the best estimates of the change in mean value over a generation of selection ($s = \bar{z}_{after} - \bar{z}_{before}$). However, the full model is the better representation of the fitness surface. There are also other methods to approximate the fitness surface.

For the record, I used the same approach in my master's thesis many years ago.


Is the poison from Stink Bugs dangerous? I just went to kill what I thought was a moth on the wall, and instead it fell on the floor and it sounded like dropping a coffee bean (because of the hard shell)

I live in the UK and have never seen one of these things before, I thought maybe it was a variant of a woodlouse, so I just crushed it in some kitchen roll I had over my hand and saw a little stain on the paper, but I assumed it was just blood.

When I looked on the internet and discovered what it was, I smelled my hand and it stank (I'd literally washed my hands like a minute or two before killing this thing). Since I've touched my laptop keyboard and stuff, is that a problem? If I use my laptop and now eat something will it poison me or leave an awful taste in my mouth?

P.S. If this seems OTT I do have slight OCD when it comes to hygiene and bugs.

Apparently there are no poisonous species (see this website), and some species are even eaten (website). No worries.


Mathematical relationship between membrane conductance and conduction velocity? By what factor would the myelin need to decrease membrane conductance (gm) if you wanted conduction velocity in a 10 μm myelinated mouse axon to be 100 times faster than in a 10 μm unmyelinated mouse axon?

This is a question from a homework set. I understand WHY myelin decreases membrane conductance, and WHY decreasing membrane conductance would increase conduction velocity. I just do not understand how to calculate what factor specifically the myelin would need to decrease membrane conductance by.

The conduction velocity is inversely proportional to the membrane time constant $\tau_m$ and proportional to the length constant $\lambda$. Membrane time constant is proportional to membrane resistance (inverse of membrane conductance), and the length constant is proportional to the square root of membrane resistance.


Does the brain always think of an appropriate response when reacting to a stimulus? Does the brain always think of an appropriate response when reacting to a stimulus?

For example, when seeing things, does the brain have to think of an appropriate response to the eyes?

Well, not always but most of the time; reacting to stimuli is what defines the nervous system and the part of the nervous system that includes the brain is called the 'central nervous system' or CNS. Reactions to stimuli (nerve impulses) don't always have to pass through the brain as the CNS consists of the brain and the spinal cord. This means that in the case of thinking, if what you see (or sense) is something harmful (a man with a knife, feel extreme heat) then you will react without the nerve impulse having to pass through your brain (instead it will simply pass through your spinal cord). This is because the body does not need nor want to waste time thinking about an obvious and protective response. This reaction that requires no conscious thinking is called a 'reflex reaction' or an 'automatic reaction'. If you want to know more about this you should probably look into the nervous system.


Beta-diversity for data with zeros Background
I am looking into enterotyping the gut microbiome data, obtained by shotgun sequencing. This essentially means performing the Principal Coordinates Analysis (PCoA) of the beta-diversity matrix (distance matrix), based on the abundance table of species/gene-counts for all possible species/genes in all samples: for sample $i$ the counts of species/genes are $\mathbf{x}_i=(x_{i1}, x_{i2},...,x_{im})$. Such a table necessarily contains many zeros, whenever a species/gene is not present in a sample. Some of the possible beta-diversity measures are listed in table 1 of this article.
Problem
Statisticallys peaking, such data are considered to be an example of compositional data, i.e., the meaningful information is contained only in the ratios of the counts, which makes log-based distances the most suitable ones. These are used in many statistical methods (see, e.g., here). However, the log-transofmation is meaningful only when all the entries in the count table are strictly positive $x_{ik}>0$. One thus faces a problem of dealing with zero entries.
Possible solutions

Using metrics not sensitive to zero entries (excluding alr, ilr and other similar log-transformations, highly recommended by statisticians - this limits the choice of statistical methods)
Imputation of zeros: this requires a principled/biologically-sound way of imputing the zeros, since the results may be potentially very sensitive to this choice.

Question
What are the commongly used imputation methods? What is their advantages/disadvantages and justification for their use?
Some references

Here is a statisticians' view on imputation in compositional data: the methodology may get rather involved, but does not have any specific biological basis.

I would recommend using a Bray-Curtis dissimilarity matrix since it accounts for abundances and can handle the so called double zero problem. I'm on my commute now and so must return to this for a complete answer later


Why are oceans carbon sinks? Building on this question,
I understand pretty clearly why forests are carbon sinks (trees grow, and there is carbon stored in soil and biomass).

What about the oceans, though? Are underwater plants the real actors here?

Check out the excellent Wikimedia picture of the carbon cycle:

All the numbers are in billions of tons of carbon: white = stored, yellow = natural flux, red = human contribution. Notice that the deep ocean stores much more accessible carbon than any other carbon cycle source, and is only surpassed by the lithosphere* in overall quantity of carbon stored on the planet. Some is stored by algae/sea plants, but the vast majority is stored as dissolved CO2.

*The lithosphere (crust and upper mantle) is not involved in the carbon cycle, and is therefore not shown in the above image.


Tryptophan side-chain structure, how should it be orientated? I would like some clarification on whether it matters where the NH and double bond are placed in these two structures of tryptophan (W) that I drew. I marked the right side as correct and the left side as the incorrect one, but suddenly I am thinking that where you place the double bond and NH don't matter as long its placed in either orientation of the structure it should be tryptophan right?
Simply put, I took my chemistry classes a few years ago and don't remember if this changes the structure if I changed the position of the NH and double bonds, that is all, and would some clarification on it.

EDIT / UPDATE:
I noticed a mistake and re-drew the structure, but am still not clear about the so called "trivial" rotation mentioned. Does the new picture reflect whether or orientation not mattering? I am still confused if I drew it correct.

Good question, this regards rotamers!
Basically, the side chain of amino acids can rotate as shown in the figure below for glutamate (Glu; E). The various option for side-chain rotation is called rotamers! Some amino-acids side chains have the potential of many rotamers (such as glutamate) while some can only adopt a few (such as tryptophan) due to steric restraints. You can read about it here on FolditWiki or in the article 'Rotamers: To be or not to be?: An Analysis of Amino Acid Side-chain Conformations in Globular Proteins'.

The set of amino acid side-chain conformations in globular proteins
cannot be considered as normally distributed around some rotamer
points. Outliers occur systematically. The rotamericity of an amino
acid depends essentially on the different environments the amino acid
meets in real protein structures. Factors such as the backbone torsion
angles of the residue itself, the secondary structure and tertiary
contacts influence the rotamericity. (...)

When solving a protein structure, scientists spend a lot of time on placing the amino-acid side chains into their correct rotamer position. Which rotamer a particular side chain should adapt, depend on the surrounding environments. Some amino acids side-chain are also very flexible and will move around the various rotamer position that they can adopt. In the example of glutamate (figure above), it would most likely adapt a rotamer position pointing either out towards solvents (if the the side chain is on the surface of the protein), or perhaps towards a positively charged amino acids side chain such as Arginine (R) or Lysine (K) to form salt-bridges or H-bonds.
In the case of Tryptophan (W), it is often involved in pi-stacking and would therefore be found in a rotamer position that stacks with other aromatic amino acids side chains. It is also a very bulky amino acid, and might therefore only have space in one particular conformation. Note that tryptophan (W) only has two rotamers, which are similar to the two that you drew in the updated figure, and again shown below. Note that both of these are correct, and that my hand-drawn bond angles are a bit off. These two rotamer options for tryptophan are even found in enzymes catalytic site, where the 'flipping' from one confirmation to the other is the key-mechanisms the allows substrates into or out of the active site!

These structural arrangements are a lot easier to understand in three-dimensions, if you are still struggling then it could be a good idea to use a visualisation program (e.g. PyMol or Coot) and take a look at tryptophane's and other amino acids side chains by downloading some protein structure from the PDB database.
Here are also some related questions

Protein Structure Parameters
How to convert PDB file of Amino Acids to rotamer tuples list of all AAs instances


DNA or enzymes — which came first? Considering that the DNA needs enzymes, to be formed, however enzymes need DNA to be formed too. What biomolecule was created first?

If one is scientifically rigorous, the answer to this question is:

  Nobody knows.

If one accepts the most commonly accepted (although not proven) view of the evolution of genomes and catalysis, the answer is:

  Enzymes

Explanation

The ‘RNA world’ hypothesis, mentioned by @vkehayas, postulates that the first genome was RNA, not DNA, and the first enzymes were also RNA. DNA genomes arose later (as did protein enzymes, although the timing of that event is irrelevant to the question as originally written).

Alternative Question

If one was not aware that RNA is thought to have preceded DNA as genome, and had not been aware of catalytic RNA, then one might have asked:

  Which came first, RNA or protein?

And in fact, this question was originally asked by Francis Crick in the restricted context of  the synthesis of proteins by ribosomes on mRNA and led him to remark.

  “It is thus not impossible to imagine that the primitive machinery had
  no protein at all and consisted entirely of RNA.”

The later discovery of catalytic RNA provided a mechanistic basis for an original world in which RNA was a self-replicating genome.

(So the answer to the alternative question is that ‘RNA’ preceded protein.)

Supporting citations

I have kept this answer brief and only provide a single general reference because @vkehayas provides links to other questions about this topic on this list.


Neurons during Numb feeling We become numb when there is short supply of blood to some parts, as mentioned here.

If that is the reason, why don't neurons and other cells die at that part if they don't receive oxygen and other things needed?

A lower supply of blood does not mean no supply of blood, so my guess is there's generally enough to keep stuff alive for some time. But if the supply is restricted for long periods (think frostbite), then stuff starts to die.

Also, the sensory neuron endings in the skin are normally just one long projection from a cell body, the major components of the neuron are protected by being located in e.g. The Dorsal Root Ganglion.


How can a child be blood type AB, if both of the parents are blood type A? Basically, both of my parents are blood type A (both are confirmed and it's also certain both of them are my biological parents). I recently found out my blood type is AB. How is this possible? I tried reading about different mutations in blood type, but I couldn't find anything that was similar to my case.

Blood type A has a variety of subtypes, which have different features in terms of their antigens. This leads to people with different A subtypes having somewhat different kinds of antibodies in their blood (for a technical article, see here). I don't know the population prevalences well, but I read somewhere (can't find it now) that as many as 20% of blood type A people actually have one of the subtypes. And these are themselves going through their own mutations. It is possible that you have an A subtype of some kind.

Testing blood types usually consists of testing which antigens and antibodies are present in your blood (see e.g. here). So if you have some kind of A subtype that didn't fit well into the blood test's expectations, you might have shown up as AB. I'm not a hematologist or physician, so I'm not sure how plausible that is.

But if you are really interested, you might consider getting a DNA test that will identify which type/sub-type you have, as this will add a different source of information on top of the standard blood test. In the jargon, the standard blood test is for "phenotype" (what are your blood cells actually doing), whereas DNA tests are for "genotype" (what is your DNA sequence). Often genotype and phenotype have less to do with each other than you might expect, or they don't fit in all that well with the cut-and-dried tests. In particular, a lot of medically underserved populations have variation that isn't really accounted for by standard medical typology.

Hope that helps.


How do cone cells underneath capillaries receive light? Came across this image of retina's cross section:
1) How do the cone cells directly underneath the blood vessel ('demarcated in the picture') receive a spectrally correct representation of the incident light? Wouldn't the blood absorb most of the spectrum, leaving only red behind. Is it because the blood vessel is too thin?

2) The fovea region seems to be void of any such capillaries, how do the cells then receive nutrition and oxygen?

1) The photoreceptors in fact don't receive all the light because some of it is absorbed by the blod vessels and nerve cells above the photoreceptors. The Wikipedia article on the retina states:

  Although the overlying tissue is partly transparent, and the accompanying glial cells have been shown to act as fibre-optic channels to transport photons directly to the photoreceptors, light scattering does occur.

Here is the direct link to the article describing the fiber-optic effects.

The red blood cells in the capillaries do absorb some light but the brain corrects for the color distortion. The most notable effect of the capillaries is that you can actually see white blood cells moving across your retina when looking into the skye:

  The white blood cells in the capillaries in front of the photoreceptors can be perceived as tiny bright moving dots when looking into blue light. This is known as the blue field entoptic phenomenon (or Scheerer's phenomenon).

However, our eyes are still extremely sensitive:

  A rod cell is sensitive enough to respond to a single photon of light.

Furthermore, the inverted retina actually protects the light sensitive cells from overexposure and damage by UV light.

Interestingly, cephalopods (e.g. squid, octopus, nautilus) have their photoreceptors on top of the retina, making their eyes more sensitive and better adapted to the low light conditions of the deep sea.

2) While blood circulation is necessary to maintain nutrient concentrations in large tissues, small distances can be covered pretty well by diffusion of the nutrients through the tissue. The fovea is only 5.5 mm in diameter which is small enough for diffusive nutrient supply.


Are all genetic disorders inherited? I know that genetic diseases such as cystic fibrosis are often passed down through generations and are therefore classified as genetic disorders, but if a mutation occurs spontaneously, which for example leads to cancer, is this then classified as a genetic disorder?

Are all genetic disorders inherited?

Not all individuals with a genetic disorder inherited that disorder. Some genetic disorders are caused by spontaneous mutations.

  Is cancer a genetic disorder?

Yes. The seminal paper by Hanahan and Weinberg, the Hallmarks of Cancer, is a good place to go to get a sense of what we understand cancer to be. This paper is quite influential and has its own wikipedia page. These authors wrote an updated review in 2011. Re: your question as it relates to cancer, yes, genetic changes result in tumorigenesis. Cancer is a genetic disorder of cell populations. One can view cancer diagnosis and treatment from the framework of cancer as a metabolic disease, but this adds to, rather than subtracts from the framework of cancer as a genetic disease.

  Are other diseases caused by spontaneous mutations genetic disorders?

Yes. Achondrodysplasia is one illuminating example. It is a form of dwarfism caused by a mutation in the FGFR3 gene. It does follow mendelian autosomal dominant inheritance patterns, but in 80% of cases, the mutation is, in fact, acquired spontaneously (that is, not present in either parent). As noted by @Eff in the comments, Down syndrome, Trisomy 21 (and other chromosomal abnormalities, e.g., Turner, Kleinfelter, Patau, Edwards) are other common examples.


What kind of beetle is this? (Black and yellow) Found this in my house in Colorado. I took this picture before releasing it. I didn't measure it, but the diameter of the cup it is trapped under is about 5.5 cm, so that makes it about 1.1 cm long. It easily climbed up the side of the glass cup.

This shield bug belongs to the species Perillus bioculatus, and has the nickname "two-spotted stink bug". They're native to the United States, and come in a variety of colors.

You mention that its colors are yellow & black, however, from the image you provide, it seems more of a pale yellow/off white. Because of that, I think it your found insect more closely resembles the first of the following images, whereas you may think it's closer to the second.

And then, a few other colors:


Getting PCR amplification at annealing higher than Tm! I am amplifying a gene where in a gradient pcr i am getting amplification at an annealing temperature about 5 degrees (67) higher than Tm (62.5)? What is wrong here? Also, I am getting a very strong intense band at wrong size for all the temperatures tried below Tm. Pls help

It is very common to get annealing at higher than predicted Tm.  If it's a problem in your case, especially if you're getting mis-annealing at lower temperatures, consider using touchdown PCR to find an optimal temperature.  Or, pragmatically, if you have any flexibility in primer design, simply order a set of primers and try them all.  Primers are cheap today, and you'll often find a set that work even where the design programs claim they won't.


What is the evolutionary reason behind human preference for salty foods? It's been established that food palatability is related to it's caloric density. This hypothesis is used to explain why humans are partial to sugar and fat. But it is also said that humans are partial to salt.

Given that salt has no calories, are there evolutionary reasons that explain why humans have a preference for salty foods?

The body needs more than energy to survive.

Salt is vital to the body's function. Ions of sodium and calcium perform numerous vital functions, but are particularly related to the function of the nervous system and contraction of muscles. Accordingly, seeking out sources of salt makes sense in a natural environment in which salt is relatively unavailable.


What is this small black spider found in NY? I found this small, black, spider with a yellow mark at the top of its abdomen, crawling on my desk in my office (located in the Lower Hudson valley in NY). I have never seen a spider like this before.

What is this spider, and is it native to NY, or is it an invasive species?

It resembles a juvenile Phidippus audax, of the family Salticidae.

Image Source: SpiderZule

According to Wikipedia >>

  They are typically black with a pattern of spots and stripes on their
  abdomen and legs. Often these spots are orange-tinted in juveniles,
  turning white as the spider matures.

Phidippus audax is a common jumping spider in North America and definitely not an invasive species.


What processes are responsible for focusing on an image only seen by one of the eyes? When a person is spying from around a corner with only one eye, it's rather easy to ignore the other eye's image, since it's probably much darker, because one usually spies around a corner standing close to a wall.

But if both eyes get equally bright visual input, it takes some effort to try and stay focused on just one of them. What processes in human body allow such action?

Short answer
Image blur on the retina is the most important monocular cue for lens accommodation.

Background
Focussing of an image on the retina is mediated by the lens. Re-shaping of the lens to focus the image on the retina is called accommodation. In general , the main cues for focussing are retinal disparity and blur, and to a lesser extent proximal cues such as looming, motion parallax and overlay of contours.

When looking with two eyes (binocularly) at an object, retinal disparity is by far the most important depth cue for accommodation. The two eyes look at an object from slightly different angles, so they get slightly different views of it. This difference is the disparity (imperfect match) between the two views. The visual system normally fuses these two images into a single perception and converts the disparity between the two images into perception of depth (Source: Indiana university).

When only one eye is available (monocular focussing), use of retinal disparity isn't possible, and retinal blur becomes the most important factor for lens accommodation. When an image is out of focus, its representation on the retina is blurry. By adjusting the shape of the lens the visual system adjusts the image projection to bring it into focus such that blur is minimized (Horwood & Riddell, 2008). Looming (incoming object becomes apparently bigger), motion parallax (objects further away move slower across the field of view) and overlay of contours (objects closer by obscure things further away) also provide monocular cues for accommodation.

Reference
Horwood & Riddell, Vis Res (2008); 48:1613–24


Insect identification request. Long anteni. Grasshopper legs Found in solo cup used to catch drips from toilet valve. East coast of U.S.

That is a camel cricket, Rhaphidophoridae. https://www.pestworld.org/pest-guide/occasional-invaders/camel-crickets/
Likely some species of Ceuthophilus


Is there a Pharmacology Textbook that Satisfies the Conditions listed in the Body of this Question? The conditions are:

As extensive and explanatory as Goodman and Gilman's The Pharmacological Basis of Therapeutics, Twelfth Edition
With additional extensive and thoroughly explanatory information on drugs (e.g. flupirtine, piracetam, nefopam, etc.) that are used elsewhere in the developed/semi-developed (like Russia or China) world (e.g. European countries) but not in the US.
Additional information about the medically recognised (in some of the world at least) herbs cannabis sativa and hypericum perforatum (St. John's wort; recognised in Germany).

If there is no such book then the European (or a European, like for instance the British equivalent. So long as said equivalent comes in English) equivalent of Goodman and Gilman's will be accepted.

A title called Essentials of Medical Pharmacology fulfills these criteria and is quite popular in India.

Reference to the current edition:

Tripathi KD. Essentials of medical pharmacology. 8th ed. New Delhi: Jaypee. 2019; 1064 p.


All flowering plants gives fruits. Why does jasmine flower plant not yield fruits? My question is actually my long term doubt. I have seen most of the flowers turning into fruits. But why not this jasmine flower?

Flower gives rise to seeds and fruits which are the ways through them the plant distributes the seeds.

Here, one should differentiate botanic term "fruit" and general common meaning of the word "fruit" which are not the same.

Botanic fruit can be subtle, not fleshy and come as a grain or pods.

Jasmine fruits are black berries.


What are some uses of oxidative/reductive power inside cells? I know respiration and photosynthesis are based on oxidation and reduction, and the formation of NADH and NADPH in them is very important for many cell processes. I know that NADPH, for example, is used in the CBB cycle to fix carbon. However where else are oxidation and reduction reactions needed in cells? I can think of an example for oxidation: getting rid of toxic products. For example, alcohol dehydrogenase in the liver oxidises alcohol to acetaldehyde. However I can't think of much else, and i'm especially stuck on ehy reductive power is useful in cells.

This topic is quite broad, excluding energetic metabolism, there are still many reactions that use redox equivalents, whether NADH, NADPH, or FADH. Here are some paradigmatic illustrations.

Xenobiotic metabolism

Oxydation of substrate : as you mentioned, alcohol to aldehyde to carboxylic acid. Generate reducing power. (The alkane oxydation shown below occurs in bacteria)

Mono-oxygenation : hydroxylation of a substrate with $O_2$, with the other oxygen atom reduced to water. This proceeds as follow with CYP450 enzymes :

Regeneration of oxided gluthatione

Anabolic metabolism

Basically every time there is a need to create/remove a double bond, or move from carbonyl to aldehyde to alcohol and back, redox equivalent are used.

Fatty acid elongation : as this proceeds with acetyl-CoA as carbon source, intuitively one sees the need to reduce the carbonyl to obtain an alkane chain.

HMG-CoA Reductase (HMGCoAR) catalyses the commited step in cholesterol synthesis.

Synthesis of prostaglandins from arachidonic acid. (More generally, any lipidic mediator)

There are many, many more examples. You may want to check out the Wikipedia page for NADH, NADPH, FADH, or the list of enzyme that use them (1, 2, 3)

All illustrations from Biochemical Pathways, G. Michal & D. Schomburg, 2nd edition, Wiley


Problem on Probabilty of a restriction enzyme cutting a random DNA sequence I think its a silly question to ask here. When I came to this site all I could see were the questions which asked detailed explanation behind a phenomenon and reasoning was there at first place. I am bringing quite math here!!!

First, I am a beginner.

Second, I would like to mention some problems..

Genomic DNA is digested with AIU I, a resrtiction enzyme which is a four base pair cutter. What is the frequency with which it will cut a DNA assuming a random distribution of bases in genome?
Eco RI and Rsa I restriction endonucleases require 6 bp and 4 bp sequences respectively for cleavage. In a
10 kb DNA fragment how many probable cleavage sites are present for these enzymes?

These questions were solved by my teacher using some probability results or rules.
I would like to mention it here.. [you know already...!!! ;-)]

(1/4)^n *10,000 or simply (1/4)^n. By putting n = number of base pair cut by enzyme.

I get the frequency with which enzyme will cut a DNA assuming a random distribution of bases in genome by using (1/4)^n and I get probable cleavage sites are present for Eco RI and Rsa I in 10 kb DNA fragment.

But why do I do that? I mean why that formula? How to understand how it was derived? Can you explain me that?

Please suggest some good books containing concepts and numerical problems like these so that I can work on it.. [Please let me know your source]. Thank you.

EcoRI recognizes, binds to, and cleaves the hexamer 5'-GAATTC-3'. In a completely randomized DNA sequence, with 25 % A's, 25 % C's, 25 % G's, and 25 % T's we would expect to randomly discover the sequence GAATTC, once every 4,096 base pairs, on average. The actual distribution of EcoRI fragments (a fragment where each end contains a cleaved EcoRI site) in our random genome will vary and yield a normal distribution, or curve, with some fragments longer and some shorter. The mean value should be 4,096.

The expectation of 1 site per 4,096 bp is indeed (1/4)^6.

1/4 = 25 %

6 = the number of contiguous base pairs in the recognition site.

In a model like this it is important to keep in mind that the probability of one base occurring in the sequence is completely independent of the sequences before that base, and the sequences after that base. In other words, for each and every position the probability of getting a base that will contribute to an EcoRI site is 25 %, or 1 out of 4 = 1/4.

75% of the time, the next base will not contribute to an EcoRI site (and a quarter of the time it will).

Let's start with your 10 kb fragment, and go through from one end to the other, and mark every time a 'G' occurs. Theoretically those could all be the beginning of EcoRI sites, right? There will be approximately 2500 such 'G's. Now to match our pattern, we need an 'A' in the second position, so let's mark all those sites that contain the dinucleotide 'GA', there will be about 2500 x 0.25 = 625 of them. The next match we need is position 3, another 'A', so in a similar fashion, let's go through the positions of all those GA dinucleotides, and just mark the ones that have an 'A' at the next position. So that will be about 625 x 0.25, or approximately 156 'GAA's distrubuted randomly along the 10 kb fragment.

If we continue, essentially filtering out more and more of those 'G' sites in our initial list then we will find, on average, that there are

39 sites with GAAT

10 sites with GAATT

2 sites with GAATTC

If you don't believe me just pick a sequence and try it yourself.

10,000/4,096 ~ 2.5