What is the advantage of not having cytokinesis after karyokinesis?

The absence of cytokinesis allows the two nuclei to remain in the same cell. If a cell has 2 nuclei instead of 1, it can transcribe DNA to mRNA at double the maximum speed, and so produce the desired proteins at double the rate. It's almost as if the cells become tetraploid, or hexaploid, and so on.

Learn more: http://www.nature.com/scitable/definition/cytokinesis-100

Why is it more desirable to have 1 cell with 2 nuclei than actually do cytokinesis and have 2 cells with 1 nucleus each (still 2 total)?

Because it is unfavorable to create two cells, which needs an extra investment in energy and nutrients to maintain, and is also harder to coordinate, and so it becomes more desirable to just have one single cell with the capacity of producing double the proteins.

Then why don't all cells adopt this strategy? What is the reason for such partiality?

First, because most cells don't need the extra transcription speed, as they don't produce a lot of proteins. Second, because of cell differentiation - to have cells doing different things they have to transcribe their genetic material differently, and so must be separate. Third, a lot of times it is desirable to have extra cells. For example, skin epithelial cells: their main purpose is to serve as a barrier or protection, and so there has to be a lot of them. That's why the basal cells are in constant mitosis.


How does an embryo know where to grow limbs etc

You may want to look into "Evolutionary - Developmental Biology", which deals with how an embryo develops into a grown organism.

  Thus, by combinatorial specifying the identity of particular body
  regions, Hox genes determine where limbs and other body segments will
  grow in a developing embryo or larva. A paragon of a toolbox gene is
  Pax6/eyeless, which controls eye formation in all animals. It has been
  found to produce eyes in mice and Drosophila, even if mouse
  Pax6/eyeless was expressed in Drosophila.

In short, there's a sequence of gene activations that progressively map body into different regions. At first, there are just 3 regions (head, body, tail), then these get broken down into more and more finely defined sections.

You can think of these sections as GPS coordinates for the body. A gene combination at a certain point means that a limb will grow there.

You can look into "Sonic Hedgehog" gene, which allowed scientists to produce fuzzy growth on a fruit fly head.

The most interesting thing is that every living creature is mapped/built using the same toolbox of genes. The genes that define where a fruit fly wing is also define where a human arm is.


What's the technical terminology for call-and-respond type behaviour?

if you are referring to call and response in rapid succession, ethologist use the terminology "turn-taking" or "antiphonal calling".
Many species do it with different degrees of precision.
A rapid research on google scholar will give you several results.
I do not know whether it would apply specifically to your case, which might be more general and it could be simply "contact calling".

Regarding the hypothesis you formulated ("(...)presumably to confirm they haven't been silently snatched by a predator"),   it would be nice to know if actually everyone respond, who is calling first (always the same individual?) and if they would behave different if someone does not reply.

Hope it helps and have fun with your observations.


In what does Genetic clustering and Cline sharpness differ?

Clustering and Clines are two fundamentally different approaches to target the population structure problems. Because many results in classical population genetics are derived from a panmictic population, it is natural to extend them to multiple panmictic populations with some degree of gene flow in between, such as Wright's Island model and Kimura's Stepping stone model. In these discrete models, we view each subpopulation as a breeding group and hence the clustering algorithm can be used to a large number of individuals to classify them based on which subpopulation they belong to. It is 100% valid if the real population is actually discrete (such as in Galapagos), but not so if the real population is distributed continuously in space. In the latter scenario, cline may be more appropriate to describe the spatial variations of the population.

You can check Montgomery Slatkin and Nick Barton's papers on cline theory back in 1970s and 1980s to get the details, but the general property of a cline is that if divergent selection is the primary cause of the cline, then the cline steepness is proportional to the selection differences, but there is a characteristic spatial scale of variation $\sigma/\sqrt{s}$, below which any spatial structure will likely to be swamped by dispersal ($\sigma$ is the mean dispersal distance of an individual, and $s$ is the selection intensity).So Even if the cline is a step function, which is not realistic at all, the cline will still be of finite steepness. As long as $\sigma$ is not zero, you will not get a clear-cut boundary between the two sides of the population, thus invalidating the assumption of clustering algorithm. However, although clustering is not very rigorous in a continuous population, we can still use it to make qualitative explorations of our genetic data and population structure, in fact many people prefer to use that because they are conceptually clear and easy to manipulate in a computer.


Basically you would rot from the inside out, as bacteria and viruses destroy your cells.

Fever is your body using heat to denature the viral proteins (viruses don't have chaperone proteins like us so they are more vulnerable to heat) Sore throat is you body killing infected cells before the virus can reproduce inside them, normally the virus will reproduce inside the cell until the cell bursts or simply runs out of resources and dies both release huge numbers of the virus.

Check out the virus life cycle. https://en.wikipedia.org/wiki/Viral_life_cycle


How can I tell if a protein has been denatured?

In my experience, when protein denatures, it typically aggregates and precipitates from solution. I would expect a denatured protein to create a cloudy solution, or actual precipitates in the form of little globs or fine wisps. A solution where protein is correctly formed and solubilized in the solution should be clear.


It looks very similar to Cephalaria gigantea.


Needing help in order to infer the statistical hypothesis tests performed in an old paper

Someone else can probably elaborate on how "peripheral lymphocyte culture" works, but this is what the statistical results suggest to me:

  The results suggested that the SCE in occupational workers was significantly higher than that in controls (11.31 vs 6.37, P < 0.001).

This is a two-sample t-test. Occupational workers were pooled into one group and the mean value of SCE for those workers (11.31) was compared to controls (6.37). The null hypothesis is that the means are not different. They reject the null hypothesis. It would be nice if they included the standard errors for the means, so that you would have a sense for the amount of variation within the groups.

  The SCE in workers exposed to CTP and to COV was higher than that of control (10.27 and 12.58 vs 6.37) respectively.

This is likely an ANOVA with three groups (CTP, COV, and control). This test is kind of redundant with the first test, since the appropriate post-hoc test will tell you that CTP and COV are both significantly higher than control. But since they report only one P-value, then this is probably the overall F-test for the ANOVA. So all they can say with this test is "at least one group is different." You don't know if, for example, CTP and COV are different from one another. It's not clear from the text that they did a posthoc test (Tukey's HSD, for example), but I doubt it.

  In workers exposed to CTP and COV, there were no differences of SCE for smokers and nonsmokers (P > 0.05).

Considering only the occupational groups, the sample is divided into smokers and non-smokers. There was no significant difference in mean SCE between the groups. This is a two-sample t-test like the first one. The null hypothesis is that the means are not different. They fail to reject the null hypothesis.

It's also possible (but impossible to determine from the abstract alone) that they did a single, larger multiple regression. Properly coded, they would be able to, at once, test for occupational vs. control, CTP vs. COV vs. control, and smoker vs. non-smoker. It would be pretty dicey with such a small sample, so they probably didn't take that approach.

Why do we perform t-tests?

The null hypothesis of a two-sample t-test is that the means of two groups are not different from one another.

How do we know that our data follows a normal distribution? Shouldn't we perform tests in order to decide whether our data follows normal distribution and is of equal variance?

Assumptions of t-tests include normal distributions within groups and equal variance between groups. These should be checked prior to carrying out the test. We can assume that the authors did these tests, but they are very rarely reported.

In case the criteria needed to perform a t-test are not fulfilled should we choose a non parametric equivalent?

Non-parametric alternatives should be considered when the assumptions are not met. That being said, t-tests are pretty robust to violations of these assumptions.

Also the anova mentioned in the answer above is an N-way anova?

ANOVA in general is a test of equality among N groups. So you could think of a t-test as just a special kind of ANOVA on two groups (indeed, they are numerically equal).


Why is the chordate nerve cord described as hollow when it appears to be solid?

Your book is talking about an embryonic structure, the neural tube. This structure forms from an invagination of the neural plate, a collection of cells on the dorsal surface of the early embryo. The process forms a hollow neural tube that will eventually develop not only into the spinal cord but also into the entire CNS.

(image from https://commons.wikimedia.org/wiki/File:Neural_Crest.png)
There is still a lot of development to happen at this point: the cells making up the neural tube will divide many times and proliferate to create the central nervous system. Within the section that becomes the spinal cord, hollow part remains and becomes the central canal, contiguous with the fourth ventricle in the brain and containing cerebro-spinal fluid:

(image from https://commons.wikimedia.org/wiki/File:1313_Spinal_Cord_Cross_Section.jpg)
(note: I had a bit of trouble finding an image showing stages of spinal cord development with a license suitable for posting here, but you can find a bunch if you image search for "spinal cord development". Some examples: https://www.medicalimages.com/stock-photo-illustration-of-spinal-cord-development-within-the-embryo-atweeks-five-a-eight-b-and-ten-c-image22427030.html https://www.brainkart.com/article/Development-of-the-Spinal-Cord_18920/ )


Trying to understand reduction of color dimension in colorblind case

Let's start with a quick overview of the different types of dichromats in man:

Protanopes have no functional red cones. Red appears as black. Certain shades of orange, yellow, and green all appear as yellow.
Deuteranopes have no functional green cones. They tend to see reds as brownish-yellow and greens as beige.
Tritanopes have blue-yellow color blindness and lack blue cone cells. Blue appears green and yellow appears violet or light grey.

Now color vision can be modeled with the Hering model, where there are two opponent channels, namely red-green and blue-yellow. These opponent channels determine color vision. Because of these two limbs, color space is often represented as triangles, rather than cubes as in your post. Fig. 1 shows the color space in trichromats. In Fig. 2 the same is shown, alongside the three types of dichromatic deficiencies.

Fig. 1. Color space in trichromats. source: Lighting Analysis

Fig. 2. Triangles in trichromatic and dichromatic vision. source: Chartlr.


How is the activation energy lowered in an enzyme by just orientating the reactants closer to one another?

The activation energy is not only lowered by orientating the substrate but by stabilizing the transition state.

According to the induced fit model many enzymes show a higher binding affinity to the transition state of a substrate.


You are looking at a protein here, which is mutated in the higher host specificity, so glucose is not involved here. What is written here are the amino acids in the three-letter-code, the notation Pro→Glu means that Proline (Pro) is replaced by Glutamic acid (Glu).

The notation Pro16 means the proline on amino acid position 16 in the protein. You often find this replacements noted as Pro16Glu or P16E (in the 1-letter-code)


What is this beetle looking fly creature?

It is of course it is difficult to tell exactly from the quality of the image, but with mandibles of that size relative to the body (approx. 20-25% of total length) it is very likely to be a male Stag Beetle Lucanus cervus, the mandibles will grow much larger. The antenna sticking out from the side of the head just in front of the eye matches your photo (note: in the image below it looks like two on each side, but it is just the shadow in the photo)

Picture from Wikimedia commons https://commons.wikimedia.org/wiki/File:Lucanus_cervus_1922.png

They can be found flying at dusk, and are found in the SE of England from late May to August.

If you are looking for a good insect ID book, I can recommend "A comprehensive guide to Insects of Britain & Ireland" by Paul D. Brock, published in 2014


Is it possible to have sleep paralysis while sleepwalking?

While it is hard to completely rule out this convergence ever happening (perhaps cases haven't been reported), it is highly unlikely due to the specific stages of the ultradian sleep cycle at which sleep walking and sleep paralysis occur [Ref. 1]. Sleep walking during non-REM sleep would have to continue through the REM stage in order to see intrusion of sleep paralysis that occurs at the exit of REM to wake [Ref. 2].

A key feature of REM sleep is deep muscle atonia that paralyzes the body and prevents among other things one from acting out dreams [Ref .3]. Thus, if a person sleep walking were able to enter REM before returning to bed, the sleep walking / other unconscious motion itself would cease.

I do question your reasoning that the combination of these two parasomnias would result in being:

  consciously aware of yourself and
  your surroundings while you are also unconsciously moving about,
  outside of your conscious control.

because the intrusion of sleep paralysis would in fact lead to muscle atonia and prevent one moving about. This is not to say that terrible things have not occurred where muscle atonia has failed while the subject remains asleep/unconscious; this falls under the fascinating category of REM-behavior disorders (where people act our their dreams - including violently hurting themselves and their partners), which judging by your question I think you will find interesting! [Ref. 4].

References:
[Ref. 1]: sleep stages
[Ref. 2]: sleep paralysis
[Ref. 3]: muscle atonia
[Ref. 4]: rem-behavior disorder


Why are many anti-malaria drugs gap junction antagonists?

I wasn't sure when I first read this, but this is actually a very interesting question.

Right now there seem to be two completely divorced lines of inquiry that researchers are pursuing with respect to the antimalarial drugs.

One group of researchers is working on working out the mechanism by which say, chloroquine and its ilk bind to and  interfere with the formation of hemazoin (a parasite-friendly form of red blood cell proteins) in the vacuoles of the plasmodium (the parasite that causes malaria). Some folks have recently gotten some pretty reasonable crystals of chloroquine interacting directly with hemazoin. This all provides strong evidence for the view that, as regards killing plasmodium, the most significant interaction for an antimalarial is the one between it and hemazoin.

In (probably) unrelated news it was discovered that many of these antimalarials are also potent channel blockers of various kinds. I haven't dug into this too deeply yet, but most antimalarial people seem to view the channel blocking activity as a side effect. There are a number of other studies underway right now evaluating the psychological effect of the channel blocking activity of the antimalarials. There's one out of Iran that says that the blocking activity of Mefloquine can be used to ease the symptoms of morphine withdrawal.

Another thing to keep in mind is that Mefloquine fell out of favor not due to a decrease in efficacy, but was instead mostly taken out of circulation due to it's (justified) reputation for causing psychotic episodes in patients. So maybe this gap junction blocking stuff could be used to explain Mefloquine psychological side-effects. That would be neat!


One important point that you might not be considering is the heat of vaporization.

You may be aware that while it normally takes 4.18 J (1 calorie) of heat to raise 1 gram of water 1 °C, it takes around 2250 J of heat to raise 1 g of water from liquid at 99.5 °C to gas at 100.5 °C, due to the energy needed to go from a liquid to a gas. - What you may not know is that the enthalpy of vaporization isn't limited to vaporization at the boiling point. Any conversion of water to water vapor requires heat of vaporization, though exactly how much is temperature dependant.

So when water evaporates, it cools things much more than one might expect from the "average" energy (or even statistically above average energy) a water molecule may have in the liquid state - several hundred times more. All this is driven by the entropic benefits of having water molecules in the gaseous state rather than the liquid state.

Wind makes the process more efficient because it removes the water-vapor laden air, unbalancing the equilibrium of the process in favor of further evaporation. More water makes it more efficient (to a point), because there's more water to evaporate and the rate of evaporation increases, increasing the removal of heat.

This is not just a physiological perception effect - one can actually measure the temperature drop when water evaporates. Evaporative coolers make use of this effect, and traditional wet-bulb hygrometers (psychrometers) use exactly this effect to measure the humidity -- in some cases you can get a temperature differential of 20 °C or more between a dry bulb thermometer and a wet bulb thermometer.

There is a small perceptual effect in that the evaporative cooling is happening on your skin, where a large number of temperature receptors are located. Therefore, your skin (and temperature receptors) feel a cooling effect even if your core temperature doesn't change detectably. Local cooling produces a larger temperature change than might be expected if you calculated for a whole-body heat change.


Synaptic strength is defined as the average amplitude of postsynaptic potential evoked following a presynaptic action potential.

This is a correct definition. Synaptic strength is a fairly abstracted measure. It can be influenced by both presynaptic (for example: number of vesicles/concentration of neurotransmitter per vesicle) and postsynaptic effects (for example: receptor number and composition). So yes, changes presynaptically such as the character of an action potential can influence synaptic strength, but that isn't a problem: we still represent this as part of the synaptic strength if it affects the average postsynaptic potential.
Biologically, action potential amplitude in the axon does not really matter much for synaptic release, but local conditions in the presynaptic terminal that influence calcium influx do. The section on presynaptic inhibition in the answer here may help a bit.


How does cancerous tissue break down radioisotopes faster than normal tissues?

Cancerous tissues break down glucose faster, not radioisotopes. Doctors use PET technique to detect breakdown of glucose, and "hot spots" are investigated as potential tumors.

Glucose can be labeled with radioisotope to show up on PET scan. Normal glucose is "invisible".

Hence, candidate for tumor will breakdown any glucose, but radioactive glucose will show up on scan.


Speciation in sexually-reproducing organisms can be identified as the inability to produce viable offspring. In other words, when two suspected sub-species are not able to produce viable offspring, they can be considered to be two species. In this case it is not so much determined at the molecular level, but at the organismal level.

This mating procedure does not work in asexually reproducing species. In this case molecular techniques are needed. Navarro & Barton (2003) investigated what the molecular differences were induced by evolution by comparing the genomes of humans and chimpansees. These two species diverged relatively late in evolution and their DNA differs by about 2.1%. It turned out that the main differences between the two genomes were clustered around regions where chromosomes were rearranged. Although indicative of the cause of speciation, it can nonetheless also be the result of it. We can never be sure.

Reference
- Navarro & Barton, Science (2003); 300: 321-4


My guess is that some people (likely Jennifer Doudna, Emmanuelle Charpentier and Feng Zhang) will eventually be awarded a Nobel Prize for the discovery of CRISPR and the development of its applications for genome editing, because it really is a major advance. But for now, the University of California Berkeley and the Broad Institute are still legally fighting over patent conflicts, and the patent situation worldwide is generally complicated. I think this is a possible reason why the Nobel committee decided to wait.


I think this may be a male of Trichocnemis spiculatus (Cerambycidae, subfamily Prioninae). This species is known from Western USA/Oregon, based on this key: Screening Aid for the Cerambycidae of the Western U.S.A. (from Oregon Department of Agriculture). By overall appearance, this species fits well. However, females have more pronounced spines at the sides of the pronotum, which points to a male for the individual in your picture.

(picture from http://cerambycidae.org/taxa/spiculatus-(LeConte-1851), also more pictures at bugguide.net)


Should I use RNAseZAP on my bench and pipettes before RNA extraction?

The common practice in my lab is to work in a laminar flow cabinet and clean it with alcohol, then spray it with the RNAseZAP. I've always heard from my professors that, while DNAses are more uncommon, "RNAses are everywhere". So, zap it early, zap it all.


What is the function of the polar bodies produced during oogenesis?

"In other animals and some plants, polar bodies give rise to vital tissues that protect and nourish the embryo " ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164815/). This could be the same fucntion to humans since we are all eukaryote.

Polar bodies are not waste. They sacrifice themselves after giving their energy to the embryo, completing development and differentiation into a baby.


Gene perturbation, what is it used for, explain to computer scientists?

Here are 3:

1) gene knockout.  Just delete the gene from the genome.  The function is gone - useful for demonstrating a direct involvement of the gene in the phenotype.  As a phenotype, the microarray will register all sorts of reactions to the loss of the gene in addition to the RNA in question being gone.

2) use selection to find mutants for the gene.  Expose the organism to a mutagen or high amounts of UV radiation.  Useful mutants vary by what the function of the genes are.  Temperature sensitivity - the gene doesn't function above 30 deg C is an example of a phenotype for a mutant that has been used classically.  In this case the functioning of the gene itself is a phenotype.  This is an example of a weaker perturbation.  Can be used when knockouts are fatal or when the system is too sensitive for a knockout.

3) change the environmental conditions. increase the concentration of a substrate or lower the availability of nutrients.  Phenotypes can be rate of growth/division, production of a given metabolite from the cells, but it goes on and on.

The affect on whole genome microarray data can be quite complex in such perturbation experiments because the coupling of many genes, even in bacteria can be broad and significant.


Could random male-only-offspring mutation wipe out a species?

It has happened the R2D2 mutation in mice is famous for it, the mutation prevents or drastically reduces female offspring.  It can wipe out entire populations when it shows up, it doesn't wipe out the species becasue there are frankly too many mice, separated by too much distance, while breeding too fast for the gene to spread fast enough before the population crashes. If mice happened to live on only one island however they would be gone. These events are called selfish sweeps or selective sweeps that result from a transmission bias in a gene.

the opposite can also occur (female only) however this is slighly less likely to lead to instant extinction since a possible out exists. Lepidodactylus lugubris(a gecko) being a famous example and is a female only species that reproduced through parthenogenesis. These types of species are exceedingly rare and have problems however as they are very vulnerable to disease since they have low diversity. Species like this are driven extinct indirectly by the mutation that led to a female only species as their diversity sufferers drastically so disease or environmental change can wipe them out more easily.


What makes a protein structure discernible?

There are two main methods for discerning a protein's structure; x-ray crystallography, and more recently cryo-electron microscopy. Both methods work by firing a high-energy beam through the sample and observing how the path of the beam has been changed by passing through the sample. The data obtained by measuring the beam includes "signal" information on the structure of the sample, but also a lot of random data, or "noise". If the signal from large numbers of copies of identical proteins can be averaged together coherently, it can be separated from the noise and the positions of the atoms that make up the protein can be determined. In crystallography, this is achieved by getting the proteins to arrange into a crystal, and in cryo-EM by a computational process after data has been collected. Either way, if the many copies of the protein are not quite identical, the signal averaging will not work, and the positions of the atoms cannot be determined as accurately, or at all. In some cases, the protein has two or a few distinct structures that it switches between, and these can be separated and determined accurately. In other cases, the protein only takes a specific shape when it is bound to another molecule, and just flops around randomly when nothing is bound. Here is the abstract of a review on this second type of protein:

Many gene sequences in eukaryotic genomes encode entire proteins or large segments of proteins that lack a well-structured three-dimensional fold. Disordered regions can be highly conserved between species in both composition and sequence and, contrary to the traditional view that protein function equates with a stable three-dimensional structure, disordered regions are often functional, in ways that we are only beginning to discover. Many disordered segments fold on binding to their biological targets (coupled folding and binding), whereas others constitute flexible linkers that have a role in the assembly of macromolecular arrays.

Finally, some proteins will not crystallize unless a portion of their sequence is removed. These portions may have a consistent structure, but it can't be determined by crystallography.


Genetic pros or consequences of children born to parents of mixed nationalities?

Did you read the rest of that article? The authors suggest many alternative possibilities for the effects they observe:

  Several hypotheses have been postulated, including the idea that fathers with social disability potentially due to a genetic mechanism associated with autism may be less able to find a spouse from their own country and may therefore find a wife from a foreign country with whom to have children91. More likely, Gillberg et al.91 suggested that women born in another country may not be immunized against the common infectious agents in the country in which she gives birth and may therefore be more susceptible to relatively innocuous infections which may increase the risk for autism. Other possible explanations include a potential role of maternal stress due to the demands of residing in a new country, particularly with limited social support, or stress resulting from the experience of emigrating, perhaps due to economic or social factors. These hypotheses do not explain the relationship with maternal place of birth seen in a cohort study of children born in California between 1989-199416, which showed a 40% decreased risk of autism among the children of women born in Mexico as compared to California. The association between maternal immigration and autism risk requires further examination in other areas of the world to examine whether the relationship can truly be generalized.
  Gardener et al., 2009

(emphasis mine)

In addition to these factors, note that p-value for that trend was only .06, and although there are a lot of problems with basing conclusions on fairly arbitrary p-values, a p-value of .06 suggests that differences of the magnitudes observed would often occur by chance. I'd say it's an area of open study, but it is quite a leap to jump to a conclusion that mixed nationalities result in higher incidences of things like autism from 1) the observation of a very small cohort of 12 children and 2) this other study which suggests many alternative possibilities for what is a small and possibly insignificant effect.

There are two main benefits for populations to avoid becoming inbred. The first is that there may be many deleterious alleles with low-incidence across a whole population, but you have a very high likelihood of producing a homozygous recessive offspring with a close relative. The second is overall maintenance of genetic diversity across a population, which could be important if suddenly exposed to a new disease, for example.

However, it is also possible for outbreeding depression to occur, which is a reduction in fitness after mating genetically distant individuals. However, outbreeding depression usually occurs either when fitness of some variable is low at intermediate values: for example, high fitness for small or large animals, but not for medium-sized animals, perhaps due to slightly different niches within the same species. Outbreeding depression can also occur when there is sufficient genetic separation between two individuals such that their whole protein milieu has evolved on a different background, such that alleles that cause no problems in either population alone are incompatible with alleles in the other population.

This previous answer here on Biology.SE talks about the lack of evidence for outbreeding depression in humans and a bit about why. Briefly, there is simply not the type of disparity in fitness conditions or sufficient genetic variability within humans for either of those situations to occur.


This is a question that is not as straightforward as it may seem.

One could make arguments, some better than others perhaps, for several different answers. The way it is worded, one could defend answers from 0.000 and 1.000 and many of the intermediate numbers as well.

  After four generations, what is the expected percentage of mitochondria from the original population of females that will still exist in the population’s children?

0.000; the original women died; THEIR mitochondria died as well. None of the original mitochondria still exist.

That may seem, and it largely is, a matter of semantics, but in some ways, it is true without word games.  Every time the mitochondria split, the copies are not EXACTLY the same.  The changes may be so minute they are not always detectable with the current technology, but that does not mean they do not exist.

Some changes occur to the underlying genome; they are rare and may not be readily observed, but that does not mean they do not exist as well. When one of these changes occur, all subsequent mitochondria will have the new genome assuming, of course, that the genome is viable.

If the change will not allow the cell to function properly, this will undoubtedly affect whether the child, as a whole organism, is able to survive.  Depending on the severity of the malfunction that results from the new genome, it may make it more difficult, perhaps impossible, for the offspring to thrive, to mate, and to produce their own offspring which can accomplish the same.

It is also likely that some of these genetic mutations will result in change that is too minute to have an effect on the mitochondria or how it functions. By the same token, it is likely that eventually there will be a mutation in the mitochondrial genome that will have a marked effect on cell function. The change may even improve the overall function of the organism to an extent that will enable the offspring to thrive, to mate, and to produce their own offspring at a greater rate than organisms that do not have this change. Needless to say, the 'improved offspring' will pass on their 'improved genome' to the lucky offspring that will be more likely to thrive and pass it on to the next ..... etc.

There are many factors influencing how well the new genome is going to spread. The population in this particular question was somewhat isolated; this will encourage the genomic change to spread through the general population more quickly. The rate of the spread, however, is affected by many variables.

So in a world with no mutations or any other factors that can result in changed mitochondrial DNA, it would be 1.000 as every offspring gets its mothers, who got it from hers, who got it from hers, so the four types, on an isolated island, would remain four types.

However, in reality, changes do happen. An error(s) in transcription would be one of the most common, but certainly not the only, process that could result in any DNA being changed in a heritable manner.

There is an average rate of mutations. In fact, one can look at the mitochondrial DNA of two individuals and calculate how long ago the genomes were essentially the same. In other words, one could look at a mitochondrial genome from some ancient fossil and tell how many generations it likely took for it to evolve in to the genome of a particular modern individual.  However, as these changes start as mistakes, it can take several generations for a change that is adaptive and will spread to occur.

The only way humans can observe these changes are in animals with very short life spans, such as fruit flies.

There would be very little change likely in only four generations; therefore, unless you had a very large sample size, any prediction would have little more than a theoretical chance to be correct.


It probably is somewhat genetic.  A good example is pigeons.  When you approach them, they turn their back to you so that if you get close enough they can escape / fly away.  I'd be surprised if this is only a learned behavior, but I also note that pigeons who have been fed let you approach to a closer distance than other birds, so in this example a distance is not completely hard wired.

Such behaviors are more likely a combination of learned and genetic, especially as the animal becomes more complex (has a larger brain).  This is a major concern of 'ethology'.

I think few inherited behaviors are completely inflexible.


A person infected with a strain of a pathogenic virus will have copies of that virus in their body.

Virus particle genomes could contain a number of substitution, insertion, and deletion mutations. The surface proteins on enveloped and non-enveloped virus copies could contain mutations. Most mutations are deleterious and those particles will not be infectious.

But the genome sequence of that virus will be largely identical, these mutations aside, and copies will be packaged so as to attempt to reinfect and reproduce.

Actual mutation rates depend on the virus type (RNA, DNA, single- or double-stranded, sense; see Figure 12.1 about the Baltimore classification of viruses), and how it uses reverse transcriptase, RNA, or DNA polymerase to make copies of its genome for use in expression (to make viral proteins) and reproduction (to make viral genomes).

For instance, RNA-dependent RNA polymerase has a lower fidelity rate — makes more copying mistakes — than DNA polymerase. Reverse transcriptase can also introduce mutations when turning the viral RNA genome into DNA, and vice versa. These processes can also introduce errors in expression of membranous or capsid proteins in enveloped and non-enveloped viruses.

The RNA virus family Orthomyxoviridae contains the strains of influenza that infect humans. These are enveloped, negative-sense, single-stranded RNA viruses. They use RNA polymerase to turn their genome into forward-stranded RNA molecules that can act as both mRNA (messenger RNA that is translated into viral proteins) and as a template (again, using RNA polymerase) for making copies of the influenza genome, itself.

Errors introduced at these two steps will result in copies that are different from the parent.


How can both strands of DNA code for proteins with similar functions?

You are confusing the the forward and reverse strands of DNA as two alleles. They are not. Remember you have a double stranded DNA from each parent. Each of those two pieces of double stranded DNA represent alleles for a given locus.

For the example you gave, you can have different genes that overlap the same region of DNA. One is on one strand and a different gene is on the other. The DNA is read 5' to 3' so we think of one strand as forward and one strand as reverse.

See embedded pic for examples from this publication about different kinds of overlap and whether they are conserved across species.


Does GABA enhance or inhibit negative effects of glutamate?

Glutamate causes an EPSP (Excitatory Post Synaptic Potential,) thereby making the neuron less negative depolarize) and closer to voltage required to cause an Action Potential (AP)  and thus fire.  GABA causes an IPSP (Inhibitory Post Synaptic Potential) making the neuron more negative (hyperpolarize) and further away from the voltage required to fire and cause an AP.  GABA & Glutamate receptors  are generally on different neurons that synapse with other interneurons & oppose each other, although neither one is generally the end neurotransmitter of the locus,  nor the only neurotransmitter of the neuron, so basically act as neuromodulators on the post-synaptic neuron. Glutamatergic receptors generally affect Sodium Channels &  GABA-ergic neurons generally  affect Chloride Channels. In theory, inhibiting an inhibitory neuron would be the equivalent of exciting an excitatory neuron, but since they primarily affect  post-synaptic neurons, the effect is cumulative, so the post-synaptic interneuron is basically adding up all the EPSPs & IPSPs to get a RMP (Resting Membrane Potential) & some additional stimulus must occur to get the neuron to fire (AP)


Drowsiness is caused by the chemical adenosine binding to a nerve cell's adenosine receptor. A compound that binds and elicits a response, in this case a slow down of nerve activity, is called an agonist.

Caffeine is also capable of binding to the adenosine receptor. However, it does not elicit a response and no drowsiness is experienced. This type of compound, binds with no response, is called an antagonist.

When caffeine is in your system it blocks the nerve cell from "seeing" any adenosine, causing the cell to increase activity. This increase of neural activity is interpreted by the brain as an emergency resulting in the release of adrenaline, the "fight of flight" hormone.

Caffeine stops you from being drowsy, speeds up your nerve activity, and gives you an adrenaline rush. All of these interfere with sleep.


What kind of spider is this? And is it dangerous? (photo)

I would think this is a European garden spider (or cross spider). See here and here.
It can bite humans but it is not dangerous for them.


This is a prototypical case of evolution by natural selection. Any trait that prevents the organism from being eaten or destroyed will probably make that organism more likely to reproduce* than similar organisms that do not have that trait**. This results in self-preservation traits becoming more prevalent in the population and eventually ubiquitous.

* Or they reproduce more, or are able to provide for their offspring better, etc. Self-preservation behaviors that reduce reproductive success are not selected for and generally aren't common (unless they are a special case of some general trait that has a net reproductive benefit).

** Assuming that the trait is reproductively favorable after considering any trade-offs such as increased energy expenditure.


Do all kind of unicellular asexual reproductions let mutations happen, resulting in evolution?

It is not essentially asexual reproduction that causes mutations. Mutations can be caused because of errors in DNA replication which can happen during both mitosis and meiosis.

Mutations can also be caused because of error-prone DNA repair mechanism.

Other than these intrinsic factors there are physical and chemical mutagens that alter the DNA or accelerate the intrinsic mutagenesis mechanisms.

These mechanisms are universally common for all living organisms (that we know of :P ), however, their tolerance to mutagens and rates of intrinsic mutagenesis may vary.

Have a look at this post too.


Why use RRBS (reduced representation bisulfite sequencing) instead of general BiSeq?

The use of RRBS instead of WGBS is mostly about coverage vs. cost.

To confidently call methylation status at a cytosine residue, you need to have at least 10x sequencing coverage at that particular residue (ENCODE standards require at least 10x coverage for RRBS and 30x coverage for WGBS). To perform whole-genome bisulfite sequencing (WGBS) on large genomes (e.x. mammalian genomes) is very expensive if you are trying to achieve the 10x coverage requirement.

The principle behind RRBS is to improve the sequencing depth of cytosine-rich areas by enriching your sequencing library with CpG-dense regions of the genome. This is accomplished through the use of CpG-specific restriction enzymes like MspI, which recognizes 5'-CCGG-3'.

In RRBS, the entire genome is cleaved using MspI, leaving at least two cytosines per cleaved DNA fragment (one cytosine at either end of the MspI-MspI fragment). Sequencing libraries are constructed from size-selected MspI DNA fragments, bisulfite conversion is performed, and the converted library is sequenced. Specialized software is needed for alignment and analysis of the converted genome (e.x. Bismark, methylKit).

One of the major limitations of RRBS is that you will sequence only CpG-rich regions of the genome. Also, since the library is size-selected after MspI digest but before adapter ligation, you will never sequence any MspI fragments outside of your size-selection range (~40-250 bp).

I have analyzed both types of data and found that the RRBS data was very unsatisfying and didn't answer our research question. WGBS, though extremely costly, is a better option for a comprehensive cytosine modification profiling. There are publicly available RRBS and WGBS datasets at https://www.encodeproject.org/.

I must mention a critical limitation of both techniques in that neither RRBS nor WGBS can distinguish between the type of modification (methylation, hydroxymethylation, carboxylation, etc) present at a particular cytosine residue. RRBS and WGBS, which rely upon the ability of certain modifications to protect cytosines from deamination, can only be used to determine whether cytosine residues are modified or not.

Further reading:

I would suggest following this link for an exceptional technical and practical article in which the authors compared RRBS to WGBS: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026711/

A more technical guide to RRBS: http://www.bioinformatics.babraham.ac.uk/projects/bismark/RRBS_Guide.pdf


What is a phospho-protein binding domain?

This is a very large topic but I will try to partially provide an answer. Now your question has three parts as far as I understand it.

Do phospho-protein binding domains only bind to phosphorylated proteins i.e. is that their sole (observed) function.
What roles do phospho-protein binding domains mediate.
Function of BRCA1 phosphorylation/phospho-protein binding

Just to get some basics out of the way, there are three amino-acid residues in a protein that can become post-translationally modified by phosphorylation, including serine, threonine and tyrosine. Now the purpose of protein phosphorylation ranges from activation/deactivation signals to binding and changing cellular localisation i.e. recruiting a protein to different part of a cell. Now tyrosine phosphorylation, which I know by far the most about is capable of all the above. So if you think about a receptor tyrosine kinase (RTK) such as epidermal growth factor receptor (EGFR), once a ligand such as EGF binds to it, it becomes tyrosine phosphorylated (activated) through its intrinsic tyrosine kinase activity. Once tyrosine phosphorylated, many proteins are capable of binding to tyrosine-phosphorylated RTKs such as Grb2 to induce a signal downstream of RTKs. So as you can see, phosphorylation of RTK affected cellular localisation of GRB2. Excellent Ras signalling review by Karnoub & Weinberg, 2008 Nature reviews (Fig 5). Grb2 binds to phospho-RTKs through a specific domain called Src-homology 2 (SH2) domain, which provides a platform for other proteins such as Son of sevenless (SOS) which is a GEF to bind to it and induce RTK signalling through Ras. So in the above case the role of phospho-protein binding domain (SH2) is to change cellular localisation of multiple proteins and mediate signalling.

Now I'm no expert in BRCA1 but just had a quick look and it seems serine phosphorylation of BRCA1 may be responsible for its recruitment to the DNA site of damage and if serine residues in BRCA1 are mutated, the protein will no longer get phosphorylated, which may effect its recruitment to the DNA sites of damage, which may affect its DNA damage response function (Clark et al 2012 Comput Struct Biotechnol J). Now BRCA has a phospho-protein binding domain called BRCT, and that is also thought to mediate DNA binding and binds to phosphorylated and non-phosphorylated proteins. So BRCA1 phosphorylation and phospho-protein binding is though to be important in its function (Clark et al 2012 Comput Struct Biotechnol J). So to answer your question in short, phospho-protein binding domains such as BRCT do not necessarily bind to their target proteins through phosphorylation.

Hope this helps.


From where does the oxygen in glucose come in photosynthesis?

RuBisCO attaches one molecule of CO2 onto Ribulose-1,5-bisphosphate (RuBP). RuBP gets split to two molecules of 3-Phosphoglyceric acid (3-PGA). Via reduction to Glyceraldehyde-3-phosphate (GAP) the link to glycolysis is established. By doing the Glycolysis reactions backwards, you reach Glucose.

This is the reaction of RuBisCO (from humboldt.edu):

EDITED to correct: One molecule of RuBP, one molecule of CO2 and one molecule of water are converted to two molecules of 3-PGA. This compound then is either used to refill the Calvin cycle by production of new RuBP, or is inserted into glycolysis, where it can be converted to Glucose. So, as David correctly points out, the oxygen comes from water as well as from CO2.


When to measure resting heart rate and blood pressure for following day-to-day trend?

I would be very surprised if the time of day made a difference.  I've personally never heard mention of such a phenomenon in discussions with intensive care practitioners (where of course HR and BP are measured constantly).  However this is only the case during rest, this paper (on horses) suggests that there is some difference in HR and BP after exercise depending on time of day.

You are right to attempt to control it however, I suppose.  It doesn't matter when you take your measurements, as long as you take them at the same time each day.

I would say that one of your first suggestions of taking the measurements almost immediately after waking.  Of course you would have to be relaxed as you assembled your equipment then rest for a few minutes in the posture you have chosen (this will matter) before taking the measurements but otherwise I can't see you having too great a problem.


What is the name of this plant with many purple blooms with orange inner parts?

This looks pretty much like Buddleja davidii to me. They are available in a range of different colors, see this image from the Wikipedia:


Does it make sense to classify all humans in a single species?

Actually, we not only consider that all human beings belong to the same species (Homo sapiens) but even that we belong to the same subspecies (Homo sapiens sapiens). So, does it really makes sense?

Concept of species

First, please note that the concept of species is more arbitrary than the most layman would think. I wrote my opinion about the concept of species in this post.

Concept of species in sexually reproducing lineages

In sexual lineages, the existence of different species is generally defined by the existence of a reproductive barrier (see reproductive isolation and see UnderstandingEvolution > biological species concept).

A reproductive barrier can be caused by either pre-zygotic or post-zygotic isolation. I will mainly disregard potential case of pre-zygotic reproductive isolation in this answer because such isolation depends highly on the culture and not only on human genetics. I do not mean that pre-zygotic isolation does not matter or are irrelevant, I just decide to focus on post-zygotic isolation because, as being very independent of the culture, it makes its study much easier.

Reproductive isolation might be partial typically leading to cases of outbreeding depression (when it comes to post/zygotic isolation).

If we had many documented cases of outbreeding depression, it would suggest that we should reconsider the decision of considering all human being. So the question is really: Do we have documented cases of outbreeding depression?

Do we have documented cases of outbreeding depression?

Many cases of inbreeding depression have been documented in humans (McQuillan et al. 2012, Strauss et al. 2013, Lettic et al. 2008, Gellera et al. 1990) but cases of outbreeding depression seem much rarer if any!

I spent some time screening through the literature searching for potential evidence of outbreeding depression. The only paper I found is Udry et al. 2003.

Udry et al. 2003:

First, note that they do not place their results in the context of our present discussion and do not talk about outbreeding depression.
They report that children of "mixed-race" in US colleges report having more behavioral troubles. One would obviously note that there could well be true that "mixed-race" children experience a different environment (incl. social environment) than "non-mixed-race" children. Such results, therefore, does not suggest the existence of any outbreeding depression.
They also report more skin problem in mixed-race children. Unfortunately, 1) their p.value is only slightly significant and 2) they track tens of variables without correcting for multiple comparisons and only one came out significant causing the expected family-wise false positive rate to be higher than the observed family-wise positive rates (see false positive and related concept in statistics).

So, in short: No, there is little to no evidence of outbreeding depression in humans

Potential publication bias and taboo

It is not impossible that there is a publication bias in which researchers looked for inbreeding depression more than for outbreeding depression. One would note also that it would probably be quite taboo to attempt to suggest that there are several species of humans for social reasons and such taboo could cause a publication bias too.

I personally doubt it would be the case that such publication bias exists. Note also that if the evidence of outbreeding depression were obvious and common, then we would not have a problem telling that there are several species of humans. In essence, if there is a publication bias that is causing us to fail to see existing outbreeding depression, it must mean that existing outbreeding depression would be relatively rare and with small effect anyway.

Other definitions of species and taboo

Well, the issue is that there is no other commonly accepted definition of species. Typically, above I only considered outbreeding depression and I did not consider a potential pre-zygotic barrier that would result from geographic isolation or from cultural reasons (e.g. maybe on the ethnic group does not like the appearance of people of another ethnic group and vice versa). I don't doubt that for social reasons, we tend to be quite happy that our only definition of species support the idea that all humans belong to the same species.

It is hard (for me at least) to tell whether we might tend to be more permissive in other lineages and naming two sister lineages as belonging to different species.

Why same subspecies and not only species?

Under the biological species concept, H. sapiens and H. neanderthalis should belong to the same species. This is why we now rather call them H. sapiens sapiens and H. sapien neanderthalis. I suppose it would feel painful to many to not highlight our differences with H. neanderthalis and so, we decided to discriminate.

Again, it is hard (for me at least) to appreciate how this subspecies discrimination in the Homo lineage compares to discrimination among potential subspecies in other lineages.

Related posts

Do humans have enough biological differences to be grouped into races or subspecies?
Is there a consensus on whether or not race exists on a biological level?


The question could be rephrased

Can a measle virus be created anew and not via reproduction from another virus?

The answer to which is "no".

The falsified idea that new life forms can jump pop up out of nowhere is called spontaneous generation. Spontaneous generation do not occur.

Note however that sometimes it may look like as if a new epidemic came from nowhere. The reasons is due to natural reservoir.

  A natural reservoir  or nidus (the latter from the Latin word for "nest") is the long-term host of a pathogen of an infectious disease.

An asymptotic carrier can be used as a natural reservoir

  An asymptomatic carrier (healthy carrier or just carrier) is a person or other organism that has contracted an infectious disease, but who displays no symptoms.

These reservoirs can keep the viruses (or other pathogens) alive in while from the outside it looks like the disease has been eradicated. At some point the virus can spread again making it feel like it came out of nowhere.

[..] my confusion is on how a population gets the first instance

There is no clear first instance. Modern day measle viruses evolved from an ancestor that was not the modern day measles. Just like there was no sudden first human (or any other species). There were just ancestors that evolved to become what we now call modern day humans.

You might want to have a look at an intro course to evolutionary biology such as understanding evolution by UC Berkeley for example.


You would be mistaken to assume that a computer program that is predicting, or classifying, the biological features in a nucleic acid or protein sequence is infallible.

Different programs use different algorithms and will have different parameters for their models of what a gene looks like. Typically they are tested on a learning or training set of features, and optimized to yield the highest score on that training set.  Then when you feed in your novel sequence and ask the program to predict where the genes are it will hopefully give you a list of predictions along with an estimated probability of the confidence of that prediction. However there will always be outliers, actual protein-coding genes that have atypical features not contained in the training set.

In other words, each program is only as reliable as its underlying model, and nobody has a perfect model.


What is the difference between Molecular and Cellular tolerance?

Personally, I find these distinctions a bit silly but I also understand they have some use.

People sometimes divide neuroscience into molecular, cellular, and systems levels of understanding. Molecular covers all the "one cell" phenomenon: expression of particular receptors or related proteins, for example. Cellular is one step above of molecular and considers the collection of all "molecular" entities and also considers a circuit level, recognizing that neurons exist among other neurons. Systems level neuroscience sometimes ignores these low-level interactions and sometimes embraces them, but overall is more connected to the behavior and state of the whole organism, approaching psychology.

The reason I think this separation is a bit silly is because, well, none of these levels of understanding are independent. That said, it's a good framework especially for novices to drive home that stuff happens at different levels of explanation. This is true for drug abuse as it is for many other concepts in neuroscience. It also lets someone that is writing a textbook focus on these different levels of explanation in sequence, in a way that is easier to process. A professional in the field is unlikely to draw the same boundaries, but they also have enough background to consolidate knowledge at all levels of interest.

I included a reference that makes the same distinctions I'm making here, but it's likely to be hard to find a canonical one. Different textbooks are going to draw different boundaries as they explain what we know in their own ways, and that's okay. I hope students recognize that A) There are different levels of explanation for neurobiological phenomenon, and B) These levels are interconnected. It's important to recognize that it's possible to study addiction at these different levels of abstraction; it shouldn't be important to draw boundaries between them, however.

Pietrzykowski, A. Z., & Treistman, S. N. (2008). The molecular basis of tolerance. Alcohol Research & Health, 31(4), 298.


How long does it take for a hard clam (Mercenaria mercenaria) to reach sexual maturity?

According to Ebersole 1987, Mercenaria mercenaria reaches sexual maturity at two years of age although some individuals can reach maturity at 1 year of age under certain growing conditions.  The mean size of individuals reaching sexual maturity is 33 mm with males somewhat smaller than females.

Ebersole cited a few studies that estimated fecundity of M. mercenaria. The results were highly variable. Individuals of about 60 mm in size released between 2 million and 6 million eggs.  Other estimates were as high as 25 million eggs.  Ebersole also cited a paper by Bricelj and Malouf (1980) where they found a general association of increasing fecundity with increasing clam size.  I don't have access to that paper but a book called The Great South Bay edited by Schubel et al. 1991 discussed the results of Bricelj and Malouf. Scroll to page 45 of the Google Books preview.  They show the mean fecundity and size as follows:

Seed (<48mm): 1.6 million eggs / individual
Little Necks (48-70mm): 2.9 million
Cherrystones (70-79mm): 5.9 million
Chowders (>79mm): 6.3 million

However, the figure on page 45 of Schubel et al., and taken from the Bricelj and Malout (1980) paper, shows a lot of variability in fecundity at different size classes.  Hopefully, the citations in the Ebersole paper will point you to other useful studies. If you don't have ready access to the book, your local library may be able to get it for you on loan.

Literature Cited

Bricelj, V.M. and R.E. Malout. 1980. Aspects of reproduction of hard clams (Mercenaria mercenaria) in Great South Bay, New York. Proceedings of the National Shellfish Association 70: 216-229.

Ebersole, 1987. Species profiles: Life histories and environmental requirements of coastal fishes and invertebrates (South Atlantic). Hard clams. US Fish and Wildlife Service Biological Report 82 (11.75).

Schubel, J.R. et al. (editors) 1991. The Great South Bay.  State University of New York Press, Albany, New York, USA.


Did some senses evolve from other senses or are they considered independent?

Hearing and touch are both examples of mechanosensation, i.e. touch receptors are activated by pressure changes and sensory hair cells (hearing) are activated by fluid motion initiated by sound waves. Therefore, I think it makes sense that they evolved from similar origins.

Vision on the other hand is due to photosensation, which has a very different physiology, so I don't think there's any evidence of a similar evolutionary link, but there may be (almost certainly are) similarities in the way our brains have evolved to respond to the different senses.


How to Diagnose this hepatitis A, B and C case?

The last sentence of the question doesn't make it clear what's being asked. But it seems to be asking: What version of Hepatitis did he get from the contaminated blood?

To that end...

  Serum antigen of HB tells us about the levels of IgM and IgG. If vaccinated, then IgG should be positive, I think? What does HBsAg tell you?

HBsAg gives you the knowledge of whether or not there's an acute infection of Hep-B. Hep-B IgM antibodies indicate an acute infection, whilst IgG antibodies would show up due to his previous exposure/immunization. If the patient has Hep-B IgM, the icteric illness was probably a re-infection of Hep-B.

  Why do we need to detect anti-HCV? If they are found, what does it mean? I think that then it means if found that he does not have hepatitis C then.

That would my assumption as well.

You run the HBsAg and can get two outcomes: IgM(+)/IgG(+) or IgM(-)/IgG(+). The former indicates the icteric illness was probably a reinfection of Hep-B.

You run the anti-HCV and get two outcomes: (+) or (-). The former indicates a present infection, the latter indicates no Hep-C.

What might throw you off is the wife's anti-HepC antibodies. If she was formerly infected and infected the patient (or vice versa) then you'd expect to find a (+) anti-HCV result.

I might come back to this after thinking on it a bit more, but that's the best I have for now.


Why would diffusion be faster across a non-specialised tissue?

There are several issues here:

1) Any mucous membrane is a specialized tissue for absorption.

Mucous membranes are indeed not so good for passive diffusion, that makes them absolutely perfect tools for active absorption of certain substances, almost independently from the membrane type. To provide some examples: many drugs like cocaine are inhaled and absorbed in nasal cavities, whereas the rectum is also known and favorite delivery way for medicines.

Generally the absorption force of the mucous membrane is dependent upon how well it is vasculated, for after going through the basal membrane the substance directly enters the blood flow and quickly travels away, thus the concentration gradient on both sides of the basal membrane -- the main barrier in mucosa -- remains relatively high.

See  Bhat P. 1995. The limiting role of mucus in drug absorption: Drug permeation through mucus solution for an experimental model for this statement.

2) Mouth mucosa can absorb many substances.

There is a special term called "oral absorption" to describe the rapid drug absorption into blood flow from the mouth cavity. The mucous membrane is not specialized here, but small molecules are able to permeate here through all barriers.

3) Advantages of oral absorption.

There are some:

The mucous membrane in the mouth cavity is very highly vascularized. The whole mouth can be seen as a bundle of skeletal muscles and every muscle requires a lot of energy and oxygen, therefore they have one of the highest vascularity rates, having much less distance between single capillaries.
Blood flow is higher in the mouth cavity walls than in other inner organs. This is mostly because muscle contractions (during chewing) lead to increased propulsion of blood through capillaries and small vessels here.
Any substance that enters blood flow here bypasses the hepatic-portal system. This means that the substance does not have to wait until it is filtered by our liver, it is immediately distributed through the whole body.
There are special reflexes from oral mucosa to inner organs. Even not so important in case of aspirin, this is very important for some placebo drugs like methyl valerate (known as "Validol" in many countries) used a lot for treating angina pectoris whose only action is to activate the cold receptors in mouth and thereby leading to reflectory dilating of cardiac vessels.

This is why many drugs, like for example loperamid, are administered only as sub-lingual tablets. And this also explains why in emergency medicine many remedies are injected directly into the tongue.


How does a virus take control over the host cell?

A virus does not typically destroy its host's DNA. Rather, the virus makes the host cell express viral proteins at an elevated rate compared to the host's own proteins. This is usually achieved because the viral genome contains a strong constitutive promoter, possibly coupled to an enhancer sequence. The virus may also preferentially insert itself into transcriptionally active sections of the host DNA.

As I said earlier, expression of the host's own genes as a whole is not directly regulated by the virus, though specific genes may be up- or down-regulated (immune-system related genes are often primary targets). However, the host's genes will usually be expressed at a reduced level because of the resources being diverted to make virions.

Remember however, that the virus relies totally on the host's machinery to make viral proteins. So, anything that kills the cell before sufficient viral particles are assembled is going to be selected against. This doesn't mean that the cell is healthy though. A significant chunk of the cell's resources have been hijacked by the virus, and a virus infected cell is typically just limping along, clinging to life, as it were.

Depending on the virus, once sufficient virions have been assembled inside the cell, the virus may enter a lytic phase, where the cell literally bursts to release the virions into the surrounding environment to infect new cells. At this point, the cell is obviously dead.


Would Bubling Oxygen Through "Dead Zones" Like A Fish-Tank Make Much Difference?

Actually, if you could get the oxygen in there, you would probably turn the dead zone into a "feast zone," because all that algae would be food.  But I think it would be prohibitively expensive.  Fish tanks aren't deep, so it doesn't take much pressure to force air bubbles into the bottom.  And they're not large in volume, so you don't need huge amounts of air bubbling.  Oceans, or even rivers or harbors, would be another matter.
Also, some of the algal blooms are poisonous "red tides."


From DNA data, is it easier to conclude that chimpanzees are our close relative, than it is to do a paternity testing?

The answer is complicated. In the early days of molecular phylogenetics, it was extremely difficult to demonstrate whether chimps or gorillas are our closest relatives. This is because the common ancestor of chimps and humans lived between 5 and 8 million years ago, and the common ancestor of gorillas and humans (and chimps) lived around the same time, just a little older. This means that there was a rapid split of three lineages, and it was difficult to disentangle them. As molecular phylogenetics advanced, we could generate larger datasets, and it because clear that chimps and humans were sister taxa. The smoking gun that demonstrated that chimps and gorillas were not one another's closest relatives was found when sequencing across the chromosome region in humans that corresponds to where two of our ape ancestors chromosomes merged. Orangutans, Chimps and Gorillas have 24 pairs of chromosomes, humans have 23. Sequencing across this region shows the exact splice site, which can be associated with the same regions on two chimp or gorilla chromosomes.
To answer your specific question, if you sequence any two genes between chimps and humans, you will find that the sequences are almost identical, with perhaps 1 in 100 nucleotides being different. If you sequenced a human and a gibbon for the same gene, you would find more differences. But finding that the sequences are similar is not the same as finding relationship, which requires sequencing multiple genes from multiple animals. For example, some genes between humans and rabbits would be extremely similar. So inference of relationships takes a lot of data from a lot of different animals. As for paternity testing, these practical tests are based on a different technology, targeting many DNA repeat regions or single nucleotide polymorphisms at specific sites that vary among human populations. But since the test is prescribed, and established, they are cheap, quick, and easy.


Trying to identify a baby bird seen in Palermo, Sicily

It looks like the chick of a Moorhen (Gallinula chloropus) or Coot (Fulica atra), probably the former. Both species are common on ponds.


Why might you NOT observe a tradeoff between two life-history traits?

The simple explanation is that there are three (or more) traits drawing from the pool, and you're only looking for trade-offs between two of them. The unobserved third may show the effect of a trade-off.


Do invasive species cause long-term damage to ecosystems they invade?

The answer really depends on how you think of invasive.  One extreme answer is to say that all things are relative, and that the concepts of local and invasive are all relative.  This matters to a certain extent because ecologists draw a fuzzy line between invasive and naturalized.  You could start with some basic species that we all think of as either good, local, or neutral.  Take the earthworm.  Most people think of it as a common native species, but the earthworm is actually an invasive species that has radically changed much of North America that came over with the Europeans.  Similarly, brown trout are also invasive, coming to the US in the 1800's.

As far as why invasive species succeed, it's still an open question.  What you reference is the enemy release hypothesis, but there are others such as disturbance, diversity of the new community, and just the traits.  Here's a good review of biological invasions and a second one.

To answer your question about adapting, I wouldn't trust your memory. It's important to keep in mind that most likely your memory is flawed, and you are only observing a very limited number samples with an incomplete sampling methodology.  For instance gypsy moths undergo wild population fluctuations, and have for over 100 years.  How well do ecosystems bounce back from invasions depends on lots of factors.  Often time the ecosystem can survive, but the some species won't.  An easy example would be Norther Hardwood forests.  Chestnuts (extirpated by an invasive fungus)are mostly gone from the wild, but the forest persists, as well as many of the species that rely on them.  So in part the answer to your question depends on scale.  The forest survived, but an individual species was nearly destroyed.

Ecological economists have tried to put a value on the destruction that invasive species have caused too.


Why does the gc content deviate from 50% in prokaryotes

Interesting question. I think that bacterial GC content diversity boils down to a mix of mutational biases, such as using different polymerase and replication/repair gene isoforms, and environmental pressures, such as temperature and salinity, that have placed different selection pressures on the various microbes.

I would read over the linked papers for more detailed info, but at least in broad strokes, I think that the two mechanisms listed above account for most of the observed variance.

NB: This isn't my main field, so you might get a more detailed answer if an actual microbiologist weighs in. :-)


This spider has a roughly globular abdomen, (actually kind of egg-shaped, and pointed, which is a good clue), and is hanging upside-down in a 3-dimensional web which (if we could see it) would look pretty tangled instead of a nice, 2-dimensional orbweb.  It doesn't have any noticeable pattern other than the banded legs, and the greyish-brown abdomen looks like it has some darker blotches.  It's made its web near the top of a doorway in a house.
These clues all point to a very common Theridiid spider which goes by the name of House Spider.  It's not the House Spider that spins a flat sheet from a funnel retreat - that's the Tegenaria House Spider.  This House Spider is the Theridiid House Spider Parasteatoda tepidariorum.  It's a harmless (to us) spider that eats almost anything it can entrap in its web.  I've seen them happily eat Gypsy Moth caterpillars, centipedes and other arthropods that aren't very popular choices among household spiders.
Here's a link that you can browse to see the wide degree of variation that this spider can show - but always a kind of smudgy, blotchy greyish brown abdomen, banded legs and the tangled web in which it hangs upside-down.  You'll note that the legs of this Theridiid, like most of its relatives, aren't as burly and sturdy-looking as those of its cousin the Black Widow.  These Theridiids kind of totter along on their relatively spindly legs when out of the web, while the Widows go striding along like small Mecha-Spiders.  I always expect to hear the Imperial March from Star Wars when I see a Widow walking on the floor.

https://bugguide.net/node/view/6919


When mosquitos feed on blood they release water droplets, this is so they can condense the amount of nutrients from the blood but dispose of the unnecessary water weight. This act of releasing excess water is often mistaken as 'pooping', a clearer view of the process here. Actual footage of fecal excretion however, is harder to come across.

Mosquito defecation is more like iron pellets, to maximize their meals they excrete water during or after feeding (in case they need to make a quick get away). Iron is toxic in high doses, so the mosquito excretes it after absorbing the nutrients in the blood, resulting in dark pellets, containing iron and uric acid.


Filamentous algae - what exactly am I looking at?

It looks indeed like a Spirogyra, or at least a member of the Zygnematales.
And yes, the green things are the chloroplasts (or one long chloroplast?), and they are arranged in spiral.

The "empty" space in the middle is likely the nucleus, and the darker circles within the chloroplast(s) could be the starch accumulated at the periphery of pyrenoids.


General transcription factors vs. DNA Binding transcription factors

When we say trans we mean that a diffusible factor, or agent is involved. So a molecule synthesized at one location, that can have a regulatory role in another location in the cell is said to be a "trans-acting" factor.

When we say cis we mean physically linked to, in such a way that the biological regulation only affects other molecules that are attached (in other words, something that is "cis-acting" cannot be freely diffusible).

So prokaryotic operators or promoters, and eukaryotic enhancers and promoters would be examples of cis-acting sequences, or elements.  All protein transcription factors, or even DNA-binding proteins, are therefore trans-acting.


What chemical test can be used to tell apart meat and plant-based meat?

There are a lot of things you could test for.  The thing that come to mind off the top of my head is cholesterol.  This will be present in all animal meat, since all animals muscles contain cholesterol, whereas meat substitutes usually do not.
That said, there are other options as well (such as starch vs. glycogen levels, for example), and even molecules such as collagen differ between plants and animals, so a careful analysis (provided the proteins have not been too altered by the commercial production process) should be able to reveal thousands of differences, even in molecules found in both plants and animals.
Further reading

Marzetta CA, Rudel LL. 1986. A species comparison of low density lipoprotein heterogeneity in nonhuman primates fed atherogenic diets. Journal of Lipid Research.  27: pp. 753-762


Why do stranded marine mammals die so quickly?

In the case of whales, I always thought that it was something to do with the fact that they rely upon buoyancy to support their weight and this seems to support that view:

  When whales, including small whales or dolphins become stranded on beaches
  they suffer from the pressure of their own weight on their organs,in the
  water they are weightless.  They also suffer from overheating as they have
  blubber that insulates them in the water and outside of the water causing
  them to overheat.  This is why we place wet towels and cold water on their
  fins and flukes when do they strand to help keep their body temperature
  down.  Unfortunately most stranded whales do not survive once they have
  beached themselves.


Obvious phenotypic inheritance markers in humans

No. To determine the genetic relationship (if any) between two individuals requires molecular evidence based on genetic markers in their somatic DNA. Using phenotypes could be misleading because a genetic marker (an allele) can have variable penetrance (the percentage of carriers who actually have the phenotype) and variable expressivity (the severity or degree of the phenotype). Some of this variability can come from gene-environment interactions, and some could come from epigenetic effects (ie non-heritable).


What do we call this adjustable platform used to ensure that something is positioned strictly level in a lab?

I remember using those for agarose gels as an undergraduate, though using them for PAGE doesn't make a lot of sense unless your bench is seriously out of level. Anyways, they can be called levelling tables and are used to promote uniform migration across the gel. Casting table also seems reasonable.


If you are interested it from the point of view of "chemical computations", you probably want literature which looks at signal transduction in detail. I would suggest Marks' et al textbook on signal transduction. I have not yet read it through (it is on my list), but I liked the clear writing style of the introduction, and, as you can see from the table of contents, it does have chapters which address synapses and their neurotransmitters specifically.

I doubt that it will contain a complete list (there are several hundreds of compounds which can be considered to be neurotransmitters), but as an introductory textbook, it is likely to contain the major ones.


What is the best way to clean immersion oil from the microscope lens?

In my experience, any microscope worth using has a minder. I would strongly suggest finding that minder, their opinions about cleaning practice should be respected. Objective lenses can be very pricey so they should be handled with care.

Detergent or water are inappropriate for an oil immersion lens. Detergent is likely to damage anti-reflective coatings on the lens. Water doesn't mix with oil.

My standard procedure with oil objective lenses is to wipe oil off with a good quality lens tissue (Kodak). Do not use facial tissues or a lab tissues, such as kimwipes. They are too abrasive and may sractch the lens. If someone has allowed oil to dry on the lens, I take care to know what solvents are correct for the lens and oil that are being used.


How valid is the theory of human's chimp-pig origin?

Briefly, the "theory" makes no genetic sense. Pig and human genomes have both been sequenced, and their sequences are completely incompatible with this model.

The "theory" is completely idiotic in many other ways -- debunking it almost becomes difficult because there are so many ways it fails to make sense -- but the genetics alone make it impossible.


The reason for the decay are ever evolving bacteria, which happen to be very hard to overcome, even nowdays. There is a lot of research centered towards protein interactions, even mapping whole interactomes, which would help us get rid of decay, yet naturally our system wasn't able to evolve as fast as technological advances, but bacteria did.


Either; they're identical to the units of $N(0)$.  In $N =N(0) e^{kt}$,

$t$ has units of time (days, minutes, whatever you have chosen)
$k$ has units of (1/time) (inverse of $t$'s units)
$kt$ is thus unitless, as is $e^{kt}$
$N$ and $N(0)$ have the same units.


Substitute 25mM dNTPs mix with 10mM dNTPs

Yes, you can do this. As long as the final mix has the proper concentrations of everything, its fine. Just make sure you compensate the by adding 30 uL (the extra volume) less of water to the master mix.


Could alpha-numeric taxonomy of fungi make things simpler?

This is actually already done in some contexts.

For instance: yeast (a fungus) is a pretty extensively studied organism, and this means that there are a vast number of yeast strains which are know/used by biologists.  Many of these strains are referred to simply by an alphanumeric string rather than a "verbal" name.  (some examples in link 1)

This is also the case for bacteria, and maybe most of microbiology.


What is this giant insect that just bounced off a second-floor glass door?

Searching the Internet again this morning, I think I may have identified it as a California (Giant) Root-Borer Beetle (https://www.insectidentification.org/insect-description.asp?identification=California-Root-Borer-Beetle). Yes?

They fly, and are active at night.

The disturbing serrated appendages are antennae (whew!).

It looks like I have nothing to fear from it unless I or others panic at its appearance, but it or its progeny may be bad news for nearby deciduous trees.


Why do predatory mites have to be introduced multiple times?

You are right that ideally it should be enough to apply them once, but predatory mites seem to be quite sensitive: If it gets too cold or too hot or the moisture is too low, they might die.
I applied several rounds of predatory mites in non-optimal conditions without any success. They just kept disappearing without any effect whatsoever. Funnily, some small type of Heteroptera came to save my plants. (from nature without my doing)
Next time I would try some Chryson instead.


Where does the initial action potential come from?

The very first evoked spike is most likely triggered by spontaneous activity, as even neurons with no synaptic connections are able to fire action potentials (Luhmann et al. 2016). Later in life neurons can be excited by the external environment through sensory stimulation. At some point the central pattern
   generators also mature and, either by network synchronization or tuning of intrinsic neuronal properties, are able to maintain a self-sustained activity pattern.

The question is then what triggers spontaneous activity during development? It has to do with calcium signaling, both exogenous and from internal stores. The exogenous trigger is paracrine release of GABA and glutamate before the formation of synapses (Rosenberg and Spitzer 2011).


Which brain regions are D1 dopamine receptors expressed, and which brain regions are D2 dopamine receptors expressed?

As to your main question, I imagine the Paul Allan Brain Atlas has what you're looking for. In 3D even.

Human Brain Map
D1 Receptor
D2 Receptor
Also comes in mouse flavored.

Offhand, I cannot be of assistance for the second question.


Cause of short sightedness/ far sightedness

The physical shape of the eye and lens are as @RoryM points out, the reason we become near/farsighted.

The most common cause of farsightedness is pretty well known.  The lens of the eye allows us to focus as a ring of muscles pulls outward and flattens the lens, allowing it to focus on closer objects.  As we get older the lens of the eye becomes stiffer and inflexible, which means that the muscles that pull on the lens can't flatten it as easily and focusing on nearby objects becomes difficult or impossible.  This is why we need to get bifocals or reading glasses as we are older.

The reasons for nearsightedness are 'natural changes in the shape of the eye'.

Mentioned briefly in the WebMD link above is that close work (e.g. reading, web surfing, phone videos, reading and reading, etc) tends to cause nearsightedness.

25% of adults in the US and 40% of adults in Asia are myopic and it does look as if there is a strong genetic component to myopia.  If neither parents have myopia, the incidence is only about 7%.

I'm probably going to get ding-ed for this, but I am going to offer alternative explanation, which makes good scientific sense to me, so hear me out.

This seems like a poor adaptive phenotype for humans who are otherwise so optimized for survival.  Why would we naturally lose our ability so young (often before the fifth grade)?  So many people who have myopia are so impaired that they can't find their way around their own house (or legally drive) without glasses/contacts/corrective surgery.

This is supported by studies which show that non industrial societies have almost no natural myopia compared to industrialized ones.  This is just one example reference, not a survey of all evidence.

Physiologically the explanation for myopia is this: in the relaxed state, the eye is focused at the horizon (infinity).  If one habitually focuses on a book or screen within 1-2 feet from your face, the muscles might well adapt to a set point that is closer than infinity.  This would make myopia an adaptive response to modern life.

Eye exercises are proposed as a way to correct myopia.  This is a bit controversial - some say they help, others say they do not. I would not be surprised that myopia developed in youth (8-15 y.o.) when the eye and body are developing can't be overcome by eye exercises when you are 25-30, but the jury is still out.

There are enough free descriptions of eye exercises out there that you don't really need to pay for them.  Getting young students outside to look around once in a while doesn't sound like a bad idea either, given this.

If you are going to down vote or complain, I would appreciate it if you please cite counter reasoning other than 'this is not a popular explanation'.


This is basically metagenomics.
Congratulations, you already did the most time consuming step.
There are several ways to go from there, but I will talk about the one I know best.
There is the metagenomic analysis tool MEGAN. It can read your Blast Output, if it is in the correct format (normal XML or tabular) and will automatically do what you want.
For a start, just use the default values, for more help you an then go to the Community Website of MEGAN for help.

Analysing your data may take a little, depending on how many contigs you have. But if you were able to blast them in reasonable time it should be no problem. As I said, you are through the most time consuming step already.


What would life expectancy be in the western world in the absence of Ischemic heart disease?

This paper from 1991 is intervention-based, so it reports the effects of behavior modification on lifespan in people who turned 35 in 1990.  The authors report the gains for each individual behavior and then say:

  Eliminating coronary heart disease mortality is estimated to extend the average life expectancy of a 35-year-old man by 3.1 years and a 35-year-old woman by 3.3 years

Which they feel is a modest increase but I rather disagree.  This report estimates the that reduction in death due to heart disease of over 50% between 1950 and 1995 gained around 3.5 years, although most of that is probably due to better medical treatments.  This 2004 study used 1998 data from the UK and estimated that:

  The average gain in life expectancy from the elimination of cardiovascular disease risk as a cause of death was 4.0 years for all the 35 year-old men in the sample (n = 24), and 1.8 years for all the 35 year-old women in the sample (n = 32).

Although I would note the low sample size.  I didn't expect to find much, so I was surprised to find these... and with similar results!  One big issue is that a lot of the more recent research has focused on smoking, weight/BMI, and blood pressure reduction, rather than all IHD/CHD/CAD; I found tons of those.  As a side note, simply reducing TV watching to less than two hours a day can lead to a gain of almost 1.5 years.


This is a nymph of a shield bug in the Tessaratomidae family, commonly called tassarotimids (or sometimes "giant shield bugs" due to typically being 1.5 - 4.5 cm long).

According to Wikipedia:

  They are mostly found in tropical Africa, Asia, and Oceania though a few species can be found in the Neotropics and Australia. There are about 240 species known

Of the subtaxa, only a few genera are even found in India:
Empysarus, Neosalica, and numerous in the subtribe Eusthenaria (e.g., Asiarcha, Aurungabada, Carpona, and Dalcantha). A key (Leston (1955)+)to this group of insects is available for purchase or institutional subscription on Wiley

Specific Taxa:

Similar to a comment under the OP's post suggests, this page appears to suggest that the nymph of a Eusthenarian called Eurostus validus (shown below) appears quite similar to the OP's specimen. However, I cannot find definitive record of E. validus being in India.

 Source: Vic wicked on Pinterest

the availability of useful information (keys, reputable websites, etc.) for this group of insects (especially for India and in English) are extremely limited, so I will just leave you here with the understanding that your insect is a tassarotimid nymph that is closely closely related to Eurostus validus, Eusthenes femoralis or some other member of the Eusthenaria.

 + Leston, D., 1955, April. A KEY TO THE GENERA OF ONCOMERINI STÅL (HETEROPTERA: PENTATOMIDAE, TESSARATOMINAE), WITH THE DESCRIPTION OF A NEW GENUS AND SPECIES FROM AUSTRALIA AND NEW SYNONYMY. In Proceedings of the Royal Entomological Society of London. Series B, Taxonomy (Vol. 24, No. 3‐4, pp. 62-68). Oxford, UK: Blackwell Publishing Ltd.


Are there any half-evolved animals alive today?

I know that there are animals that are "simpler" than other animals but are there any that are half-evolved? Why aren't there living half ape and half humans?

Oh come on. You know if Australopithecines or Homo habilis still existed you would be asking "Why aren't there living half Homo habilis and half humans"? And when the other Great Apes go extinct you'll be wondering why there are no transitional forms between humans and monkeys. The answer to that question is, humans are apes; chimpanzees and we are pretty much as close as two species can be; we could have closer forms that survived but we could also have a much bigger gap between us and our closest relatives than we currently do. In other words, any ape is a valid example of something "half-human half-ape". It's like asking for a vehicle that's half-car, half-volvo.

  Are there animals that are just starting to evolve arms and legs?

You mean, modifying fins into limbs in a general movement from water-living to land-living, like the first tetrapods are thought to have done? I like mudskippers.

  Saying that every species on the planet is "transitional" because there are no ultimate or final species is an unacceptable answer because it only works on the assumption that macro-evolution is true.

Not quite, it is an explanation of what "macro-evolution" is and what things it predicts.

There are two aspects to the theory of evolution that are often confused; one is how it works to generate diversity and change in living organisms, and the other is how it works to adapt living organisms to their environment and create what we humans see as "design", "function". Both things are results of evolution, but the latter is much less important than we'd think, which leads people who explain evolution to de-emphasize it, which then leads people to be confused as to how it can happen at all.

The thing is, both "design" and "goals/purposes" are concepts that are meaningful in considering evolution, it's just that the words are dangerous because they imply an conscious intention that isn't there. You could replace "design" with "optimization"; random mutation combined with natural selection can form an optimizing process, i.e. a process that will over time generate forms that have specific properties. In the case of life, whatever properties promote the spread of the organism we're looking at.

As for "goal", that's just the physical fact of the world that some arrangements of matter have different effects from other arrangements of matter; meaning that if some arrangements of matter will lead organisms to reproduce better, the optimizing process of evolution will predictably lead to organisms having that arrangement of matter. So we can talk about, say, eyes being "designed" by evolution "for seeing"; the difference between that and a rock "being designed" "for having its shape" is that "seeing" (i.e. that organisms ancestors surviving and reproducing based on how well they interpreted light signals) had a causal influence on the organism's eye's structure.

So in that sense we can think there are "goals" in evolution; seeing, flying, swimming, breathing... and many lineages can be retrospectively seen as evolving "in the direction" of those goals. But the important thing is that those "goals" are completely dependent on the environment; as long as there's selective pressure for improved sight a lineage will evolve to have better eyes, but the second the selective pressure disappears or reverses, the lineage will evolve to maintain its current eyes or to lose them. And of course different lineages may have different selective pressures on them and "evolve in different directions". That's why there isn't a single overriding goal in evolution, just millions of lineages under different selective pressures that might change tomorrow.

That's why we can say every species is "transitional" (because they'll all be something different tomorrow, or not) and at the same time not be able to say transitional towards what (because the environment is complicated and we usually can't tell under what sustained selective pressure a given organism is under, and even if we could we couldn't be sure it remained the same over the next thousand or million years).

Having said that, when our human brains say "half-evolved" we often have specific goals and images in mind - like "halfway towards flight", "halfway towards eyes", "halfway towards limbs", "halfway towards dolphinhood". And there are plenty of "transitionals" by that definition - I brought up the mudskipper; there are also plenty of gliding animals, a plethora of eyes (or "eyes") at every point on the "good at seeing" continuum (more of a state space than a continuum really), aquatic mammals that may remind one of what the ancestors of cetaceans were like and might evolve to be more aquatic in the future...

  Saying that all the transitional animals just died off also doesn't seem quite right. If all the previous transitional animals just went extinct, then wouldn't we just have a few specialized species alive today? This wouldn't allow for the diversity we see today.

Ah, but what diversity do we see today? What we observe in the fossil record is the constant extinction of some forms and diversification of others, that nevertheless remain more like each other in important ways than they were to their earlier aunts and uncles - meaning while at some point you might have forms A, B, and C, a million years later you have A1, A2, A3 and A4. To illustrate, the earliest tetrapods had a wide variety of number of digits on their limbs. Of course they all basically looked like fish. Most of those early tetrapods went extinct; the only line that survived had five digits. And millions of years later we have a stunning variety of organisms descended from that lineage, most of which look nothing like fish or each other, yet they all follow the same basic skeletal plan, down to the five digits. So which is more diverse?

Basically your question accurately describes the biosphere as the fossil record shows it, you just missed one thing: diversification. Meaning the "few specialized species" are actually a "few specialized families/orders/classes/phyla that themselves contain many species".

When thinking of evolutionary change it's better not to think of a line from A to B, but something like self-spawning fireworks. One group expands, a lot of its elements fizzling out but some of them spawning their own subgroups that expand in turn while still being recognizably part of the original group, and so on so forth with the fizzling of the most and spawning of the few, at some point the older groups might be so large and full of different subgroups that they start losing their definition, and basically at some point you realize the whole big mass of elements that now cover the sky includes both A and B, meaning if you roll back the tape you can certainly track how something that looked like A changed over time into something that looked like B, but it's really a very small part of the whole show.