Besides fruits and milk, what other things in nature are "intended" to be eaten?

There are plenty of examples! Here is a short list

Defence ("Eat that so that you don't eat this")

Evisceration. It is the ejection of internal organs so that predator eat them but not the prey entirely. (sea cucumber does evisceration)
Lizard's tail being fragile on purpose

Parental care

Milk
Regurgitation
Sexual Cannibalism (as it is often hypothesized as benefiting the male also as he indirectly nourish his offspring)
In haplo-diplontic species, one of the two generation can be much bigger and can transfer its nutrient to the other generation (offspring), such as in moss for example.

Mutualism

Nectar
Fruits
Honeydew produced by aphids to attract ants which protect them from predators
Ant breeding fungi

Symbiosis

Lichen
Root nodule

Social behaviour

Honeypot ant (if we are happy to consider the honey stored in the ant for a long being part of the ant biomass).

Human related

The researcher in parasitology that feed his mosquitoes with his own blood!
Crops (and other things) under artificial selection. It is here just cases of mutualism where humans is involved.


Can microdialysis be made in Drosophila melanogaster?

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


What is the space between -10 promoter sites and start sites (+1)

By "start site", do you refer to the "start codon"?

I think the spacing you are referring to is the 5' UTR.

  The 5′ untranslated region (5′ UTR) (also known as a Leader Sequence or Leader RNA) is the region of an mRNA that is directly upstream from the initiation codon. This region is important for the regulation of translation of a transcript by differing mechanisms in viruses, prokaryotes and eukaryotes

Have a look at the wikipedia article for more information about its roles.

The 5' UTR is typically 3 to 10 nucleotides long in prokaryotes but can be much longer (up to several thousands of nucleotides) in eukaryotes. On which species did you notice this spacing of about 10 nucleotides?


With AIDS, the whole immune system is not non-functional. The condition results in a severe drop in CD4+ T-cells, which is what primarily predisposes AIDS patients to secondary infections.

Fever can be an immune response to infection, but it is not directly affected by the loss of CD4+ T-cells. Rather, fever occurs due to a complex cascade of events triggered by pyrogens, which causes a release of prostaglandin E2 (PGE2). In the hypothalamus, PGE2 signals a systemic response for the body to generate heat. More on the pathophysiology of fever can be read here.

AIDS patients still produce PGE2 in response to pyrogens (such as compounds produced by bacteria). Therefore, AIDS patients can certainly get fevers. In fact, AIDS patients may be more likely to get fevers because they may produce more PGE2.


Breeder's equation and equivalent expressions for narrow-sense heritability

I found my mistake, which is where I said "To get the terms to cancel, we want to write $E$ as $\alpha E$ where $\alpha E$ has the same distribution as $G$." What we actually want is to find a constant $\alpha$ such that $\mathbb E[\alpha E\mid X=a] = \mathbb E[G\mid X=a]$. In my question, I assumed that this was the same thing as finding $\alpha$ such that $\mathbb E[\alpha E] = \mathbb E[G]$; hence I was trying to find $\alpha$ to make the distributions of $\alpha E$ and $G$ the same (the means are both 0, so I just needed to get the variances to equal each other). But actually, conditioning on $X=a$ shifts the distributions so the $\alpha$ I found in my question doesn't work.

Since my previous strategy doesn't work, I ended up skipping the step of finding $\alpha$ entirely. I realized that the random vector $(G, X)=(G,G+E)$ is a bivariate normal, because we can write $$\begin{pmatrix}G \\ G+E\end{pmatrix} = \begin{pmatrix}\sigma_G & 0\\ \sigma_G & \sigma_E\end{pmatrix}\begin{pmatrix}Z_1 \\ Z_2\end{pmatrix}$$ where $Z_1,Z_2$ are standard normal random variables.

Now Wikipedia gives the conditional distribution for bivariate normals, which in our case is $G\mid X=a$. We only need the mean, which is $\mu_G + \frac{\sigma_G}{\sigma_X}\rho (a - \mu_X)$. Both $\mu_G$ and $\mu_X$ are zero, and $\rho$ is the correlation which is $$\rho = \rho_{G,X} = \frac{\mathrm{cov}(G,X)}{\sigma_G \sigma_X} = \frac{\mathrm{cov}(G,G) + \mathrm{cov}(G,E)}{\sigma_G \sigma_X} = \frac{\sigma_G^2}{\sigma_G \sigma_X} = \frac{\sigma_G}{\sigma_X}$$ Thus we end up with $$\mu_G + \frac{\sigma_G}{\sigma_X}\rho (a - \mu_X) = \frac{\sigma_G^2}{\sigma_X^2}a$$ which is exactly what we want.


Why will tissue from identical twin be rejected in some cases?

This was too long for a comment, but I have absolutely no evidence for what I'm about to say :)

It looks like that sentence was a little bit of hand-waving, as the author didn't want to categorically state that identical twin tissue would never be rejected. I suspect that in the early days there may have been reports of organ failure (esp. kidneys) in the recipient that were incorrectly identified as rejection episodes. I suppose there's also the slight possibility that one twin could have a mutation event very shortly after the separation of the twins in utero (when all the cells are still pluripotent) that could somehow change or (more likely) silence one or more of the HLA or other surface antigens involved in transplant rejection. This would almost certainly have to happen when the separated twin was a single cell. The mutated twin would therefore not express an antigen the non-mutated twin did, and if the non-mutated twin donated a kidney or other organ to the mutated one, its immune system wouldn't recognize the silenced antigen and could potentially result in rejection.

Like I said earlier, all pure conjecture :)


Are some people more 'attractive' to mosquitos? If so, is that a hereditary trait?

There is a genetic component to mosquito's attraction to humans.

  Female mosquitoes display preferences for certain individuals over others, which is determined by differences in volatile chemicals produced by the human body and detected by mosquitoes. ... Overall, there was a strong narrow-sense heritability of 0.62 (SE 0.124) for relative attraction and 0.67 (0.354) for flight activity based on the average of ten measurements. The results demonstrate an underlying genetic component detectable by mosquitoes through olfaction.

--Heritability of Attractiveness to Mosquitoes

  However, analysis of a comparative rating variable "compared with your twin, who is bitten by mosquitoes more often?" indicated a strong genetic influence on frequency of being bitten by mosquitoes, with no significant differences observed between males and females.

--Twin study of adolescent genetic susceptibility to mosquito bites using ordinal and comparative rating data.

There are many other influences on how attractive people are to mosquitos, including diet, alcohol consumption, and various disease conditions.


Reason for conversion of glucose to fructose in glycolysis

Avoiding diffusion is one reason to phosphorylate glucose, the other is that it is removed from the osmotic balance between inside and outside of the membrane, so it can be transported at a high rate.

The Glucose-6-phosphate can then be used as a substrate for different pathways, namely glycolysis and the pentose phosphate way, and (depending on the organism) also be converted into glycogen and starch for further storage.

The reason for the phosphorylation lies further downstream in glycolysis: The isomerization by the glucose phosphate isomerase and the subsequent second phosphorylation into Fructose-1,6-biphosphate make the conversion and dedication of the molecule into the glycolysis irreversible.

Fructose-1,6-biphosphate is then cleaved by the aldolase into two C3-units: Dihydroxyacetone phosphate (DHAP) and Glyceraldehyde 3-phosphate (GA-3-P). GA-3-P is converted into DHAP, so that downstream only one metabolite needs to be processed.


Learning tensors for evolutionary or developmental biology

The field of tensor decompositons has been discovered in many fields simultaneously, each with their own notation. Many modern notation in fields like CS or STAT have originated from the work of Tamara Kolda
http://www.kolda.net/publication/koba09/
However, this is restricted to the CP and Tucker decomposition, and we have many others now. See
https://arxiv.org/pdf/1609.00893.pdf
and
https://arxiv.org/abs/1708.09165


Fast standing and the heart's insufficient accommodation of the increased venous return

Raoul's gives sensible comments:

ventricle overloading not sensible
retrosternal pain $\to$ myocardial ischemia
other cause reminding retrosternal pain such as celiac disease:

Posterior 1/3 of the septum is supplied by the following artery where any ischemia can weaken the isovolumetric contraction (TODO this has to be discussed much more carefully):

ischemia coronariaea posterioris created by problem in ramus interventricularis posterior arteriae coronariae dextrae


Species identification. Is this a leech?

Yes this is a leech. It appears to be a species in the family Glossiphoniidae, or the freshwater jawless leeches. This family of leeches is relatively flattened with a poorly defined anterior sucker.
According to The Canadian Encyclopedia, there are about 45 species of leeches found in or around Canada.
Langer et al. (2018)1 provide a more limited selection of Glossiphoniidae leeches they ascribed to Ontario. Of the ones they list, yours most looks like a specimen from the genus Placobdella.
See, for example, this image of Placobdella phalera from de Carle et al. (2017)2 found in Ontario, Canada:

 Source: Figure 1, de Carle et al. (2017)

1  Langer, S.V., Vezsenyi, K.A., De Carle, D., Beresford, D.V. and Kvist, S., 2017. Leeches (Annelida: Hirudinea) from the far north of Ontario: distribution, diversity, and diagnostics. Canadian Journal of Zoology, 96(2), pp.141-152.
2  de Carle, D., Oceguera-Figueroa, A., Tessler, M., Siddall, M.E. and Kvist, S., 2017. Phylogenetic analysis of Placobdella (Hirudinea: Rhynchobdellida: Glossiphoniidae) with consideration of COI variation. Molecular phylogenetics and evolution, 114, pp.234-248.


Binding BSA to silver surface via large difference in isoelectric points of the two materials

Concerning the apparent discrepancy between your first and second citations, the difference in values is addressed by the authors in the more recent work:

Perusal of the literature yields few IEP values for silver metal. Chau and Porter reported an IEP of 10.4 for an evaporated silver film as determined by contact angle titration.(6) The method employed in their investigation used only neutral and basic liquids, and the maximum contact angle achieved on the silver films was ∼35°, in contrast to the maximum we observe of 52° at pH 3.2 (Figure 1d). This dichotomy may be indicative of the amphoteric behavior of the native oxide at the surface.

Concerning your third citation where the authors bound BSA to silver via a 2-mercaptoethanesulphonate linkage monolayer, the authors give their reasoning in the abstract:

The direct adsorption of proteins on metal surfaces usually leads to loss of their enzymatic activity

So, to answer one of your questions

Why the need for this if the silver should attract the BSA electrostatically?

BSA here is a proxy for other proteins.  The purpose of the research was to examine how the structure of the linkage monolayer changed in response to protein adsorption, not how BSA specifically binds a silver substrate.


Why didn't the polar bear change its color from white to black during evolution to absorb heat?

Polar bears do not have white fur - they don't have pigments in their fur hairs which makes them clear and translucent. The outer fur consists of hollow fibres, which shatter a part of the incoming light (the visible part) which makes them look white. This gives a very good camouflage in a white environment.

It was initially thought (see reference 1) that the hollow fibers work in the same way as fiber optic cables and direct the UV part of the light (the visible was thought to be shattered) towards the black skin of the bears where it generates heat, but this hypothesis has been disproved. The UV part of the light is simply absorbed by the bears outer fur and doesn't reach the skin (see reference 2 for details).

The hollow hair helps with the insulation of the skin and can change the color due to environmental influences. The tend to get yellow after feeding on seals due to the fatty substances from the animals. There have also been reports from zoos that algae lived inside the hollow part of the fur making the animals more grey and sometimes even green (see reference 3).

Reference:

Light collection and solar sensing through the polar bear pelt
Is polar bear hair fiber optic?
The greening of polar bears in zoos


Sleep deprivation relation to growth rate and mental health in adolescence

A couple of papers (from the same group, it seems) defines sleep deprivation in adolescents as less than 6hr of sleep within a month. They found that sleep deprivation increases health risks, importantly depression (which in turns increases sleep deprivation).


You can use 3 or 4 dilutions- 1:1, 1:5, 1:25, 1:125

Purpose of doing this is to calculate the primer efficiency. Ideally primer efficiency should be 2 i.e. two molecules of DNA are formed in a round of PCR. So after n-rounds of PCR there should be $2^n$ DNA. However, this may not be the case always. You calculate primer efficiency like this:

Plot $Ct$ vs $log_2(Conc)$
Get the trendline (in excel) or use a linear regression command for other applications
Get the slope ($s$) of the trendline
Efficiency in this case would be $2^{-s}$.

Some people use base of 10 in the log instead of 2 (for which you have to do $10^{-s}$ instead.

This, you can directly use to find out how many copies are produced after n cycles i.e instead of $2^n$ it will be $x^n$  where $x$ is the calculated efficiency. This is particularly useful when you are calculating the fold changes using the comparative Ct method. For details see this article.


How are cardiac cells stimulated by an action potential?

If you go to probably any physiology textbook and look at the chapter on cardiac action potentials, you'll find a number of diagrams of the different ion permeabilities and channels in the heart (e.g. fast sodium channels, calcium channels, etc) that lead to the depolarization of the cardiac myocyte. As you alluded to in your question, there is one cell, or group of cells, that is part of the sinoatrial node (or SA node) that is referred to as the "Pacemaker of the Heart". It is these cells in the SA node that have the leakiest ion channels and thus most frequent spontaneous depolarizations that set the rate of contraction for the heart.

For the cells in the atrium, the depolarization of the sinoatrial node spreads almost instantaneously across the atria because of gap junctions (see that link for more info...Michela et al. Role of connexin 43 in cardiovascular diseases. European Journal of Pharmacology, 2015) between the cardiac myocytes. Gap junctions are small communicating junctions that link all the cells of the atrium and "electrically-couple" the cells to contract in synchrony. There are typically no gap junctions between the atria and the ventricles, which is why the atria contracts before the ventricles. However, there is the bundle of His that slows the electrical conduction just enough before it rapidly spreads through the purkinje fibers and then to the remaining ventricular myocytes through gap junctions in those cells as well.

**For more information on gap junctions go to any basic cell biology text or Wiki. The picture below is a simplified diagram of gap junctions. For this question all you really need to appreciate is that the electrical depolarization (i.e. the positive charge) spreads quickly across cells connected by gap junctions because they are 'sharing' a common cytoplasm due to these channels. When ions flux during depolarization that current flows through the gap junctions and nearly instantaneously depolarizes the next cell... and so on, and so forth.


What would happen if nerves didn't have refractory period?

Refractory period returns the repolarization period to the nerve's resting potential . it's the time taken for recovery of a neuron to generate another impulse being excited by another stimulus . so if nerve doesn't have refractory period they wouldn't be able to return to its resting potential & generate new impulse . moreover the repolarization potential further exceeds its value and cause hyperpolarization , so its badly necessary to restore to resting potential by expelling na+ and taking k+ in . unless it would be impossible to restore the resting potential & be ready to get excited to transmit another impulse via the electrochemical pathway . one more benefit of refractory period is that it causes unidirectional impulse conduction.
I didn't get the 2nd part of your question. What are you trying to mean , make it more clear.


This is fundamentally a teleological argument.

The error is in assuming that the intermediate steps were a precursor to the present functionality. For example, interpreting an 'intermediate' bird wing as a fully functional wing, intended for flight. In fact, there is no prerequisite that present characteristics or functions have evolved from intermediates that were intended FOR that characteristic or function.


Why don't mosquitoes target the visible blood vessels under the skin?

For a mosquito, there is really no benefit to targeting those visible blood vessels. Mosquitoes take only a small amount of blood, and their proboscis is going to be a limiting factor anyways.

However, mosquitoes also aren't just blinding sticking their proboscis into the extracellular space. They actually do target individual vessels, and scientists have actually been able to video the process. Capillaries are good targets because they are found in all the tissues, so the mosquito doesn't need to find a surface vein.

See the videos with the original paper here: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050464 (in the "Supporting information" section)

There are also versions on YouTube, like here:
https://www.youtube.com/watch?v=MbXSPacvuak

Choumet, V., Attout, T., Chartier, L., Khun, H., Sautereau, J., Robbe-Vincent, A., ... & Bain, O. (2012). Visualizing non infectious and infectious Anopheles gambiae blood feedings in naive and saliva-immunized mice. PLoS One, 7(12), e50464.


qPCR : Cross-contamination while sealing plate

I can't say this happened to me before (but also don't do qPCR all the time).

In principle it should be fine to add the template to the side of the well, since this also lets you visually confirm that you did add the template. However, if you are having problems do consider adding the template to the liquid.

As another way to avoid this problem I would try to first put the adhesive foil lightly on top and then push it down/fix it with something sturdy that has a straight edge (there are special plastic things for this, but a tip-box can also work).


What is the genetic distance where linkage can be ignored?

I think you must have misremembered what you heard.

The cut-off distance for genetic linkage is 50 centimorgans which corresponds to 50% recombination. In the human genome 1 centimorgan is approximately 106 base pairs, so the 'unlinked distance' is 5 * 107 base pairs.


Is it possible to Breed an Animal to have more Females than Males?

Yes.
 What you are looking for is a meiotic drive, it's a genetic factor that favors its own transmission. Sex linkage is very common in these due to sex chromosomes not undergoing recombination. Once such driver, R2D2 (I shit you not) is a Y linked gene that drastically increases the number of male offspring in a mouse that carries it, to the point it can cause a population collapse from lack of females.
Several such drives are known, none quite as drastic as R2D2.


Example of invertebrates that are attracted to heat?

The tendency to be attracted toward heat is called thermotaxis.

Documented cases

Thermotaxis has been documented in

C. elegans

Ploff and Sokut 2010

Slime molds Meloidogyne incognita

Pline et al 1988

Drosophila

Rosenweig et al. 2004

Mosquito Aedes Aegypti

Patterson and Brown 2009

Lake sculpin (Cottus extensus) larvea

Wurtsbaugh and Neverman 1988

Mammalian sperm cells

Bahat et al. 2003

The best documentation is on C.elegans. There are probably many undocumented species that display thermotaxis but above are the only documented cases I could find.

Many of these species are easy to find in biology labs. Mammalian sperm cells are very easy to find if you are a male but it may take complex methodology to observe thermotaxis on cells. Bigger organisms are of greater interest. Drosophila might be the way to go.

Do you really need to test with another species?

Whether the test is a good idea was not part of your question but I thought I would comment on it anyway!

I am wondering whether testing your device on a different species is of much interest to you. Testing that your device creates a thermal gradient is sure of interest but one species may react very differently to a specific gradient than another one and it feels a priori to me that you'd be waisting your time by testing it on a different species.

I think it would be more interesting to just place thermometers (if you have access to good accurate thermometers) along space and measure temperature to ensure that a gradient exists and make sure that the temperatures and steep of gradient are within the range of what schistosome may experience in nature.

I am not involved in this research and you may have good reasons of yours of testing your device on a different species.


That is a blue parrotfish (Scarus coeruleus):

(photo: Marc Tarlock via Wikimedia Commons)


Is there term for thermophilic-halophilic plants and if so, what is it?

Well, at least in other biological contexts, such organisms are often simply referred to as being thermohalophiles (or as being thermohalophilic).
Examples of the use of these words:
Bacteria:

Mavromatis, K., Ivanova, N., Anderson, I., Lykidis, A., Hooper, S.D., Sun, H., Kunin, V., Lapidus, A., Hugenholtz, P., Patel, B. and Kyrpides, N.C., 2009. Genome analysis of the anaerobic thermohalophilic bacterium Halothermothrix orenii. PLoS One, 4(1).

Denger, K., Warthmann, R., Ludwig, W. and Schink, B., 2002. Anaerophaga thermohalophila gen. nov., sp. nov., a moderately thermohalophilic, strictly anaerobic fermentative bacterium. International journal of systematic and evolutionary microbiology, 52(1), pp.173-178.

Pereira, M.M., Antunes, A.M., Nunes, O.C., da Costa, M.S. and Teixeira, M., 1994. A membrane‐bound HIPIP type center in the thermohalophile Rhodothermus marinus. FEBS letters, 352(3), pp.327-330.

Biochemistry:

Amoozegar, M.A., Salehghamari, E., Khajeh, K., Kabiri, M. and Naddaf, S., 2008. Production of an extracellular thermohalophilic lipase from a moderately halophilic bacterium, Salinivibrio sp. strain SA‐2. Journal of basic microbiology, 48(3), pp.160-167.

I'll note that I haven't found evidence of plants being referred to in this specific manner, but read the example papers below for use of the related phrases "thermohalophyte vegetation" and "thermohalophytes", respectively:

Accogli, R., Nutricati, E., Famà, L., Medagli, P., Manno, D., De Bellis, L., Marchiori, S. and Colasante, M., 2008. Iris revoluta Colas., natural hybrid origin species: characterization and preservation problems. Plant Biosystems, 142(1), pp.162-165.

Vekhov, N.V., 1996. Thermal and freshwater springs of the Chukchi Peninsula: Unique subarctic ecosystems. Part ii. flora. Polar Geography, 20(3), pp.209-220.

Is this word-blending approach the best or most appropriate? Couldn't say, but there is certainly prior  precedence for combining the habit adjectives into "thermohalo-".


What does it mean to have a Y-DNA Haplogroup "R-M512"?

Normally Humans inherit from each parent one sex determine Chromosome. If you have a XX chromosome pair you are female. If you have a XY pair you are male. Therefore the Y-Chromosome get only passed on from father to son. The Chromosomes itself consist of DNA. The DNA consists of base pairs in which an A only pairs with a T and a C only pairs with a G. The Y-Chromosome has about 57 million of these base pairs. DNA is normally relative stable but from time to time only one of these base pairs randomly changes from a C-G base pair to an A-T base pair. This phenomenon is called a pointmutation. So imagen two brothers. One has the unchanged Y-Chromosome of their father the other has one this pointmutations. So the descendants of the one Brother have the same Y-Chromosome, with exception of the pointmutation, the same Y-Chromosome. This is called a Single Nucleotide Polymorphisms (SNP). In the millennia the Y-Chromosomes acquire more and more of these SNPs. One combination of these SNPs is called a Haplogroup. By the amount of SNPs and the kind of them you can reconstruct which Haplogroup descended from which one. You have the Haplogroup R-M512 which is a rather old one (https://upload.wikimedia.org/wikipedia/commons/d/d4/R1a._Info-19.05.2014.jpg) and could be found in great area. M512 is actually the name of the last SNP that defines your Haplogroup. Here some people had write down which Haplogroup they belong to. By the ethnicity of the name you can assume how far it is spread ( https://www.familytreedna.com/public/R1a?iframe=ysnp ).
Another Name would be R1a1a. Maybe these papers help you more to understand the nomenclature ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155271/  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1288547/ ).
Short tandem repeats (STR) are small DNA sequences that repeat multiple times.  On the Y-Chromosome these STR can be referred to as DNA Y-chromosome Segments (DYS).  DYS448 has the sequence AGAGAT  with 20 to 26 repeats. Here ( http://cstl.nist.gov/strbase/ystrpos1.htm ) is visualized where actually  it is located on the Y-Chromosome.  In your case the laboratory was not able  to measure any repeats.


What is the number of influenza strains occurring at a given time?

Antigenic drift in the coding portions of the genes that involve antibody binding sites accounts for the seasonal variability of flu strains, i.e. they mutated enough that the antigens require new antibodies, hence a new strain. The process is as you said constant, like evolution, and in an analysis of pandemic H1N1 the authors are able to note 1 - 18.1 mutations per genome per replication cycle (ref). Because of this, flu vaccines tend to have more A strains than B strains due to the greater mutability of influenza A, at approx. 30% more mutations per site per infectious cycle (ref). At current It will take me time to research the remaining questions.

Interestingly enough, however, and I've never looked at this but CDC offers weekly influenza reports that detail by region what they're finding (CDC):

Source: CDC's so-called FluView

Beyond that, I'm pretty sure they take this weekly data, see what strain is on the rise in hospitals, and manufacture the vaccine to mirror the "popular" cocktail of strains.


What happens if an IV drip with a saline solution slips out of the vein, but keeps dripping into the body?

The most common IV drip that would be sent home with a pet owner is Ringer's solution. This fluid is also commonly injected as a subcutaneous (between muscle and skin) bolus into both cats and dogs. Although IV administration is more efficient, this fluid is completely harmless if an IV catheter were dislodged allowing it to accumulate in the surrounding tissue.


How does permanently modifying human DNA work? And how does it impact procreation?

It seems this therapy is targeted to liver cells. Cells that are affected will continue to express the inserted gene as long as they last, and any dividing cells will spread it to their daughter cells.
Genetic information is passed on to the next generation through germline cells: eggs and sperm. There won't be any effect on the next generation unless these cells or the cells that give rise to them have the inserted gene.


I would recommend The selfish gene by Richard Dawkins. It is targeted at a scientifically interested audience, but well written and recognized by the scientific community.

http://amzn.com/0199291152


Do we consume DNA and proteins of other organisms?

Yes, we are eating the DNA and proteins of an organism when we consume and digest its cells.

However, consuming the "raw flesh of hen or fish" in your example would not cause harm strictly due to the consumption of their DNA.

DNA has two basic components - a structural 'backbone' of alternating phosphate molecules and sugar molecules (called deoxyribose) and a nitrogenous base (a group of atoms that includes nitrogen) on each backbone unit. These basic components of DNA are common to the all organisms that contain DNA, like the hen and fish in your example.

When you digest the DNA in your food, specialized molecules (in this case nuclease, which digests DNA) produced by your digestive system break down DNA into its components. These components can then be rearranged to create 'human' molecules, such as human DNA.

In other words, you don't integrate fish or hen DNA directly into your human DNA; you break it down and rearrange it into human DNA, then integrate it into your body.

To answer your second question, we get energy by breaking down the proteins, carbohydrates, and fats (known as macromolecules) of other organisms. Much like DNA, these three macromolecules are broken down into their singular components. For carbohydrates, this would be glucose.

These components are then further broken down into energy (as a force) which powers cellular machinery to 'recharge' ADP (the 'discharged' version of ATP) back into ATP, a specialized molecule which can 'bring energy' to other parts of the body to power your body's processes.

ATP is not energy per se - energy is defined as the "capacity to cause change" (Campbell Biology, pg. 160) and do work. Energy is therefore a property rather than a distinct molecule.

Summary:

When we consume DNA of organisms, it does not inherently damage us as we break it down and rearrange it into completely 'humanized' molecules.
Glucose and ATP aren't energy per se - they are just molecules that contain lots of energy. ATP 'brings energy' to other parts of the body; glucose is broken down into energy to 'recharge' ATP. Energy is not a molecule - it is a property.


There is no standard notation called Q (matrix).

However in this case I think the matrix that they are referring to is the state transition matrix (similar to the adjacency matrix as mentioned by Justas in the comments, but with rates instead of just the connections). Basically you have three states (lets call them A, B and C) and there is a rate for transition from one state to the other. You can also represent these rates in the form of transition probabilities.

You just represent this as a 3×3 matrix. Put zero where there are no such transitions (for example there is no transition from A to A or A to C):

$$\begin{array}{|l|c|c|c|}
\hline
 & A & B & C \\\hline
A & 0 & 10 & 0 \\\hline
B & 100 & 0 & 50 \\\hline
C & 5 & 0 & 0 \\\hline
\end{array}
$$

You can then calculate the eigenvalue for this matrix. How to calculate eigenvalues and what is their significance is off-topic in this site. You can easily find out how to calculate eigenvalues. Their significance is something that is not that easy to understand but you can read more about that and can perhaps ask a precise question in Mathematics Stack Exchange. Basically, they tell you how the system proceeds in different directions (denoted by eigenvectors).


Mathematical models of gene editing using CRISPR

There are several probabilities that you need to take into account.

The efficiency of DNA transformation of CRISPR encoding DNA and
target DNA into the host cell (varies between cell types and
transformation agent).
Efficiency of cutting by CRISPR at target site. (varies by DNA compaction - which varies by site and cell type, and guide RNA)
Number and cutting efficiency at off targeting sites.
Efficiency of degradation of free DNA by cellular antiviral systems
(varies between cell types)
Efficiency of DNA repair machinery to fix dsDNA breaks. (thus removing CRISPR cut sites. Varies by cell type)
Efficiency of recombination machinery (homologous
recombination and microhomologous recombination) (which is used to
insert new DNA sequence).
Probability of NHEJ damaging target site. (which can delete the CRISPR cut site)

Too many things to count.

However to give you some idea. The efficiency of CRISPR making a correctly targeted knock in for DT40 (chicken lymphoma) is  ~1% of all resistant colonies (ie colonies that have taken up the DNA seq used to make the knock in), when lipofectamine reagents are use. Lipofectamin trasfromation efficiency varies depending on the size of the transformed DNA, host cell type and plating density. So for a 5kb construct that transformation efficiency varies between 30%-50%.

CRISPR is nearly 100% efficient in yeast cells, ie all knock in cells are correctly targeted. This is likely due to the high levels of HR in yeast


Expanding on the comment by @Chris:

Short Answer

Overlapping sequences imply evolutionarily conserved regions, i.e. preserved by evolution through time due to theirs having some important function.

Long Answer

Assuming the sequences are homologous, overlapping regions of similarity reveal "evolutionarily conserved regions".

These are regions in the protein sequence that are shared by the ancestors through ancestral history due to that shared sequence bearing some important function at the phenotypic level. Evolution acts to "preserve" the sequence through natural selection if that function was important for fitness (see Negative selection).

E.g. Perhaps the shared sequence codes for an active site for an enzyme that is shared by all the ancestors you are using in the multiple sequence alignment - natural selection will then prevent changes to that sequence from occurring.

Look at this online lecture for finer detail.


Why is this the equation for the fitness of cooperators?

As Bryan Krause points out in the comments, looking at the units gives you the answer. The correct form of the equation is $f_{c}=\frac{b(i-1)}{N-1}-c$, where $f_{c}$ is the fitness of cooperators, $N$ is the total population size, $i$ cooperators, $b$ is the fitness benefit of cooperating and $c$ is the fitness cost of cooperating. It doesn't make sense to subtract $c$, which is a kind of relative cost in terms of offpsring production, from $N$, which is population size. It would be like subtracting the cost of a car from the speed of an aeroplane. It also makes sense from the viewpoint that we expect the the fitness of cooperators, $f_{c}$, to reduce as the cost of cooperating increases, but independently from the number of defectors in a population.
Also, in the paper, it gives the equation with square brackets:

then the fitness of cooperators and defectors, respectively,is given
by fC=[b(i−1)/(N−1)]−c


A calorie is a measure of energy. In nutrition, we usually mean the kilocalorie (kcal), which is the same as about 4.2 kJ (kilojoule). A average person needs about 2,000--2,500 kcal per day, but this of course varies quite a bit between people, depending on size (muscle mass, particularly) and level of physical activity (physical work, exercise).

Nutrition guidelines found on the labels of food products give a pretty good summary of the amount of energy they contain. I'm not sure what applications you have been using, but they most likely rely on the same basic data, so the values should be similar. You can use these values to figure out roughly what your calorie intake is, and to spot very calorie-rich foods. But counting calories exactly is actually quite difficult --- you need to carefully weigh everything you eat and keep track of lots of numbers, and it's easy to make mistakes.

Burning calories does not always mean burning fat. Fat is a long-term energy storage form in the body. When exercising, the body tends to burn stored carbohydrates (glycogen) first, and turns to burning fat when carbohydrates are exhausted. Therefore, prolonged, low-intensity exercise like long walks are usually better for burning fat than short "sprint" type of exercise. The body also burns fat during normal daily activity if your energy intake is lower than the daily need (when dieting). But it is also possible that some muscle mass is degraded (to amino acids) and used for energy as well.

See also Wikipedia articles on food energy and exercise. Please note that "how to burn calories" is a heavily debated issue, there is an entire industry of weight loss methods, and various claims about "easy" methods or products to lose weight quickly are generally not true. The only reliable method to lose weight is to reduce food intake and increase exercise, for a long period of time.


Reaction centre in Photosystems of higher plants

Someone else too had asked your question no. 2. here Photosystem 1 and 2; P680/P700; Chlorophyll a/b

The answer basically quotes Molecular Biology 4 ed. by Lodish as follows.

"The chlorophylls in the two reaction centers differ in their light-absorption maxima because of differences in their protein environment."

[I could've just commented this but I can't locate add comment option on your post. Am new here.]


It's an  elephant hawk-moth, Deilephila elpenor. Here is an image from Wikipedia to compare with:


Why is inhibition of inhibition (reciprocal inhibition) such a common motif in cell signalling?

This feels like a my philosophical question...

Direct regulation of proteins would have to have biological utility - such a gene has to be driven by positive selection to adapt that ability.  The question is more about learning what might be driving its role.

I would hazard that protein deactivation and degradation would be important to make sure that these inhibitors could be down-regulated fast enough - if they were left to degrade via a general pathway, the specific signal would not be available for too long a time.


There are dozens of cell marker genes. The number refers to antigen protein from one of those specific genes. The number itself can be a result of any of a variety of things, from the order in which the protein was discovered to the corresponding antibody being the 125th antibody produced against the cell line or organism. These are often used as biomarkers of various cancers. CA-125, for example, is sometimes found at high levels on the surface of blood cells in women with ovarian cancer.


Are mitochondria transferable between cell types, individuals and species?

There is evidence that cells can exchange mitochondria. There are some donor cells that transfer mitochondria to recipient cells via cytoplasmic nanotubes (within the same species). This happens endogenously and triggering factors may include stress.

References:

Pasquier et al. 2013
Ahmad et al. 2014
Wang and Gerdes. 2015
Hayakawa et al. 2016

On interspecies mitochondria transfer.

In a study by Yang and Koob, the feasibility of mitochondrial transplants was studied. Mitochondria isolated from donor cells were initially injected into mouse oocytes/embryos. Then mitochondria, along with a chunk of cytoplasm and membrane was taken out; these cell-like structures were called  mitocytoplasts. Then, these mitocytoplasts were fused with recipient cells (mouse rho0 cells - these lack mitochondria) with the help of a viral fusion protein.

They found that the recipient cells supported mitochondria from the same species (donor species include mouse, rat, Mongolian gerbils and Golden Syrian hamsters).

The success of the "mitochondrial xenograft" depends on how different the species are and as shown in the abovementioned experiment, a donor cell (mouse) would not support the mitochondria from even a closely related species (rat). This incompatibility would primarily be based on the dependency of mitochondria on the nuclear genome which may be different for different species. It is possible that "mitochondrial xenografts" may be accepted; the impossibility of it has not been exhaustively verified.


Basic understanding of cell cycle (mitosis) phase

# DNA molecules
A chromosome can have either 1 DNA molecule or 2, this depends upon what stage the cell is at that moment. It actually might help to know what chromatids are:

  A chromatid (Greek khrōmat- 'color' + -id) is one copy of a newly
  copied chromosome which is still joined to the original copy by a
  single centromere. (wiki)

This means that the number of chromatids is directly related to the number of DNA molecuels.

  Before replication, one chromosome is composed of one DNA molecule.
  Following replication, each chromosome is composed of two DNA
  molecules; in other words, DNA replication itself increases the amount
  of DNA but does not increase the number of chromosomes.(wiki)

We can now add another row which indicates the DNA molecules, chromatids are directly related to the number of DNA molecules thus from left to right:

 46        92         92        46

These are the basics, now in some more detail about mitosis:

So based on the number of chromatids and your chromosome number you can figure out the nubmer of chormatids and thus the number of DNA molecules:
Thus before replication (G1) = 6, then after S phase (G2) = 12, then metaphase = 12 and after cytokinesis = 6. Just as in your table so that part is correct!

# of chromosomes
You can read these from the table, however I think it's important to understand what is happening. In simple words chromatids and chromosomes are related in this sense:

  It is only when sister chromatids separate – a step signaling that
  anaphase has begun – that each chromatid is considered a separate,
  individual chromosome (source)

The phase in which the chromatids seperate is called anaphase, so after this seperation:

we consider the previoulsy chromatids as chromosomes. Thus anaphase and telophase contain the double number of chromosomes as the amount you started with. However anaphase and telophase are not mentioned in your table. So let's go back to the phases in your table. During metphase the chromatids are still connected to each other, meaning that we consider them as one chromosome (the same is true for G1 and G2, because we did not seperate anything). So that part of you table is correct too.

# genome copies

  The human genome is the complete set of nucleic acid sequence for
  humans (Homo sapiens), encoded as DNA within the 23 chromosome pairs
  in cell nuclei and in a small DNA molecule found within individual
  mitochondria.(wiki)

However read this question and the answers,  some say 1 genome per cell and some say two genomes per cell, this confuses me too so I'm not sure about this one, however based on the wiki it would say that 2n = one genome, which would make sense because the two pair of chromosomes are not equal and when saying you have two genomes per cell you are actually counting mitochondrial DNA twice.


How could be the "Eurasian magpie" bird won the "Mirror Test" where Gorillas failed

I think this website provides a pretty surprisingly thorough breakdown of avian brain anatomy, including historical contexts and debate around what exactly is homologous and what is not, and whether 'homologous' is a useful bit of information.

In short: It was thought until recently that the bird brain was just the core of the mammal brain with some layers peeled off, but it turns out to be more like a scale model, with many of the same parts. Roughly. Sort of.

So birds do not technically have a neocortex. They have a structure that looks like a neocortex, but it also looks like some other things. Gorillas do have a prefrontal cortex etc (even if they are smaller than in humans). The knowledge that structure X performs function Y in an organism generally implies little about a second organism, with or without structure X. Even features like 'wings are for flying' and 'fins are for swimming' have exceptions.


There is no color code for the leafs - the color results from biochemical reactions. Basically there are three colors: Green, yellow and red.

Green color is caused by the chlorophyll inside the chloroplasts,
when the leafs are active in photosynthesis.
Yellow color is caused by Carotenoids, which are present in the
leafs all the time, but are masked by the chlorophyll. The
carotenoids become visible when the amount of chlorophyll in the
leafs is reduced, which usually happens in the fall.
The red color is caused by Anthocyanins, which are usually not
present in the leafs. They are made during the late summer and can
also mix up with the carotenoids (color mix) to get intermediate
colors.
Brown color is caused by the cell wall of dry leafs which have no
other color.

For further reading these articles are interesting:

Unravelling the evolution of autumn colours: an interdisciplinary
approach.
The Science of Color in Autumn Leaves

There is also the hypothesis around, that the bright colors are a warning sign to insects, this is called the co-evolution theory of autumn colors. The color should warn the insects that the tree has a high level of defense and thus reduce its parasitory load. You can read more about this hypothesis here:

The coevolution theory of autumn colours.
The shared and separate roles of aposematic (warning) coloration and
the co-evolution hypothesis in defending autumn leaves.


DNAse-seq is the most obvious choice. It uses the same idea as DNAse footprinting but measures output using high-throughput sequencing, so it can be done on a whole genome in one shot.


Why are the grey matter structures of the inferior medial frontal lobe not directly (not via white matter) connected?

Could anyone offer an explanation as to why these structures are distinctly NOT continuous at this point?

The crista galli physically separates the straight gyrus.

Click to zoom

Click to zoom

  ... that would, presumably, permit grey matter from the left hemisphere to be directly continuous with grey matter from the right hemisphere. However, no such connection exists.

They are not physically touching in that location, elsewhere the two hemispheres are not connected (even though physically touching) by gray matter.

  Further, if anyone could confirm whether any part of the cortex exhibits grey-matter-continuity (i.e. not via white matter tracts) between the left and right hemisphere, that would be greatly appreciated.

Except in rare cases, for example agenesis of the corpus callosum (ACC), communication between the hemispheres is via the anterior commissure and the corpus callosum.

The two halves are separated by a deep longitudinal fissure, see this animation:


Risk factors for dizygotic twinning are related to multiple follicular development, and include maternal family history, ethnicity, geography, maternal parity, maternal age, and, of course, use of assisted reproductive technology. There may be a genetic component to monozygotic twinning as well, but that rate is fairly consistent across populations. Other risk factors, such as diet and supplementation, have been proposed, but the data are less robust. There are some interesting studies demonstrating geographic clusters of twinning, but these tend to be demographic clusters that are associated with other risk factors.

Though a higher risk of twinning can be transmitted from a father to his daughters, the father's family history of twinning is not a significant risk factor (for his own children to be twins). To clarify -- if a man has a family history of multiple births, his children are no more likely to be twins than the general population, but his daughers are more likely to give birth to twins. This study is one example of the studies that have shown a significant independent association between maternal family history and twinning, with no significant independent association with paternal family history.

As far as the case of Feodor Vassilyev is concerned, many people have lived on this earth, making very unlikely events in a single instance more likely to have ever occurred. I would say this case is either a hoax or a rare chance event. There is no modern data I'm aware of that would support a paternal genetic reason that this particular man produced so many multiples.


Disclaimer: Assumes you know how flow cytometry works.

You've done a flow-based AnnexinV apoptosis assay here.

Annexin A5 (AnnexinV) protein binds to phosphatidylserine (PS), which is typically in abundance of the inner leaflet of live cells. Upon the initiation of apoptosis, PS is known to flip to the outer leaflet. Thus, you can use AnnexinV conjugated to a fluorescent molecule such as fluorescein isothiocyanate (FITC) to look at externalized PS.

7-Aminoactinomycin D or 7-AAD is a fluorescent intercalator that can be used to detect DNA and is excited on the 488nm laser (emits on a 650nm longpass filter or the like). The dye is not permeable to live cells, and so for dead or dying cells with compromised membrane permeability, it binds freely to DNA.

The problem with either alone is you cannot say a 7-AAD+ cell is apoptotic and you cannot say an AnnexinV+ cell is apoptotic, because we know that you have early apoptosis and late apoptosis, and in either the cell isn't wholeheartedly dead, yet. You also have necrosis.

And so on a dot plot of 7-AAD and Annexin V, you can create 4 quadrants based on the mechanism of the two components:

Double-negative: No external PS or DNA binding means these are viable cells.
Double-positive: Both external PS and membrane instability means late apoptosis.
AnnexinV single-positive: Undergoing early apoptosis, nucleus isn't yet permeable.
7-AAD single-positive: Completely dead or necrotic, membranes have probably disintegrated.

The basis of the assay is you're trying to determine at what stage of cell death your cells are in.

The unstained control is a way of looking at your cells alone, and allows your to correct for autoflorescence, florescence generated by your cells just from excitation alone. You also want to run single-stain controls to see where your positive, and negative populations lie. Without FMO (fluoresence minus-one, basically your full staining panel minus a color) controls, it's hard during gating to confidently say where your positives and negatives are delineated, due to the effects of spillover and noise.

A note about the AnnexinV single-stain control: You can see that in the untreated sample, there's basically no AnnexinV, but in the control it's 22.0% of the cells. Single-stain controls where you assume positives exist have to have positive and negatives. Without positives, where do you set the gate for them? What if the population shifts during acquisition? They probably used cells that were dying on purpose to generate confident controls for that sample.

That's the left half of your data. The right half are treatments. Basically you've stained the cells for both markers and then treated them with Torin2, Rapamycin and Mitomycin to see how those compounds affect the viability of the cells. There's a control where you added nothing.

Based on the gates set with the controls, you can see that the mitomycin sample has the greatest effect: The cells are 6.54% AnnexinV positive, undergoing early apoptosis, and 14.3% are double-positive, undergoing late apoptosis, and 8.09% are dead or necrotic.

The conclusion you'd derive is that mitomycin, but not the other compounds, has a profound effect on the viability of the cells.


If fever is a natural immune defense, why do people take drugs to lower it?

Personal comfort is the primary answer. Quite a bit of research has gone into fevers, and the current consensus is that Fevers less than 105F (40.5C) shouldn't necessarily be treated.

The primary reason the body raises its temperature (via the Hypothalamus in this case) is that bacteria and viruses tend to optimally thrive at 98.6F, which is also your body's optimal operating temperature. By raising the body's temperature, the bacteria/viruses become less efficient, allowing your body to "catch up" since the body's immune response takes time to ramp up before it reaches its peak (which is a bit after peak viral/bacterial load). Here's an example for Hepatitis (HBxAg = the virus, Anti-HBx = antibodies against the virus):

Along with the Fever, joint inflammation (part of the Innate Immune system's primary response) is also a coinciding symptom. So when your body begins to fight an infection you get a fever (which can make the environment uncomfortably hot/cold) and the tissues around your joints swell (which makes movement and relaxation uncomfortable). NSAIDs like Ibuprofen reduce those symptoms, making the duration of the infection more bearable. They do not reduce the length of the infection by any measure (and might increase it, though the research is not particularly conclusive), but can make the day go by better if you've used up all your sick days or have a child to take care of.

Basically, people take NSAIDs to reduce fevers for the same reason most take any over-the-counter pain medications. To make life a little easier in the meantime.


What is the mechanism of folic acid deficiency and neural tube defects?

You are having difficulties finding the mechanism because it is as of yet unknown.

Now of course comes the hard part where I need to prove that statement. Often, it's just apparent by papers not saying anything about the mechanism, even though you'd expect then to include a brief section if it was known, for example Folic acid supplementation for pregnant women and those planning pregnancy: 2015 update or the various Cochrane reviews on the topic of how much folic acid supplementation is optimal, or the WHO and CDC documents on the topic

Here's a few relatively recent ones that state it outright:

Folic Acid Supplementation and Pregnancy: More Than Just Neural Tube Defect Prevention, 2011

  The mechanism by which folic acid prevents structural anomalies in the fetus is not known, but may involve the regulation of homocysteine metabolism

Folic acid supplementation in pregnancy and implications in health and disease, 2014

  as FA deficiency may be a risk factor for NTDs additional studies will be required to determine the mechanistic role of the FA pathway in the onset of neural tube defects

FA = Folic Acid, NTD = Neural Tube Defects

Neural Tube Defects, Folic Acid and Methylation, 2013

  To date, animal studies have not provided
  sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs.

There are some putative mechanisms to do with folic acids effects on the homocysteine metabolism and its effects on methylation. I can't really tell how well-established those are yet, but maybe this can be a starting point for you.


What is the mechanism by which bactericides kill bacteria?

Each bactericidal agent has a different mechanism of action. For example:

Alcohol denatures proteins necessary for function and the lipids in the plasma membrane dissolve into the alcohol.
"Iodine can penetrate the cell wall of micro-organisms quickly, and the lethal effects are believed to result from disruption of protein and nucleic acid structure and synthesis." [CDC]
other mechanisms include tampering cell metabolics, tampering DNA replication, and more.

See also:

The 2008 CDC guidelines for sterilization and the such for healthcare settings. Each method will contain a comprehensive description along with a statement of "mode of action," i.e. how the method actually kills the bacterium.
Another good link here from the CDC examines factors affecting the efficacy of sterilization.

Otherwise, it would be best therein to split the specific mechanisms you perhaps don't understand into separate questions. But an important take-home message in the efficacy link above just adds to just how broad this question is:

  Microorganisms vary greatly in their resistance to chemical germicides and sterilization processes.


Why does absorption (at 260nm) of ssDNA increase with temperature?

It seems canadianer's intuition is correct --

Base stacking still occurs in ssDNA, so I suspect that is why you see a temperature dependence

-- based on this paper:
Conformational Changes in Single-Strand DNA as a Function of Temperature by SANS
Motivation --
UV absorption-based measurement of DNA melting temperature is reliant on the assumption that the DNA duplex dissociates into the same single-stranded DNA (ssDNA) random coil conformations at all temperatures.  However, calorimetry studies (citations 2 and 3 quoted below) have suggested that temperature-dependent conformational changes occur in ssDNA, too.

Early results from calorimetric studies on the dissociation of a 13-mer DNA duplex have shown, however, that the conformation of the single complementary ssDNA does depend on temperature (2). This was evident in the absolute difference between the heat of dissociation of a 13-mer DNA duplex of 490 kJ mol−1 determined at 74°C determined from differential scanning calorimeter (DSC) measurements and the heat of association of the duplex of −236 kJ mol−1 directly determined at 25°C from batch calorimetry measurements (2). This difference was attributed to the additional thermodynamic contributions from conformational changes in the complementary single strands implied from UV absorption changes upon heating solutions of each of the complementary strands from 25°C to 74°C.
...
More recent results also show a large disparity between the free energies of the dissociation of 10-mer duplexes extrapolated from DSC measurements at high temperature to 25°C and the free energies determined directly from isothermal titration calorimetry measurements on the binding of the single strands of the duplex at this temperature (3). This was again attributed to free energy contributions of the change in the single-strand random coil conformations as the temperature increased from 25°C to the melting temperature of the duplex (3).

Methods --
The authors used a 2 μM solution of 10-mer ssDNA (5′-ATGCTGATGC-3′) in 10 mM sodium phosphate buffer, pH 7.0, containing 0.1 M sodium chloride and 0.1 mM ethylenediaminetetraacetate.  Temperature-dependent changes to this solution were measured by three methods:

Small-angle neutron scattering (SANS) at 10°C increments from 25°C to 80°C.  Normalized scattering data were used to compute the geometry of the ssDNA using the LORES algorithm (PDF).
Optical density measurements (260 nm) between 20°C and 90°C, with a heating rate of 1 K per minute and measurements taken every 30 seconds.
Differential scanning calorimetry with continuous measurements from 5°C to 105°C at 1°C per minute.

Findings and Conclusion --
Taken together, the SANS and calorimetry data suggest that the change in shape of the ssDNA with increasing temperature is due to unstacking of bases, corresponding to an endothermic transition.

... [the ssDNA] undergoes an expansion in the diameter direction that causes a slightly shortened length as the temperature increases from 25°C to 43°C. Then, as the temperature increases further from 43°C to 53°C, it expands in the length direction as the diameter decreases. Finally, the ssDNA increases dramatically both in length and diameter as the temperature is further increased from 53°C to 80°C.
...
These conformational changes correspond to the unstacking of the A and G purines as well as the T and C pyrimidines in 5′-ATGCTGATGC-3′ as the temperature is increased. The unstacking is manifested in molecular motion of the nucleotides in and out of the cylindrical axis (an increase in diameter) and in the stretching of the helix or cylinder (increase in pitch). The increase in the optical density upon melting of the single-strand substantiates the SANS results since the optical density changes indicate exposure of the purine and pyrimidine bases to a more polar (water) environment.

And, as with liliae's figure, the results of the ultraviolet absorbance scan show density increasing with increasing temperature.

Figure 6. Normalized UVM scan of a 2-μM ssDNA solution. The solid line is the least-squares fit of a two-state, A↔B transition model to the data points. The broken horizontal lines are the extrapolated pre- and post-transitional base lines and the broken vertical line indicates the temperature at the midpoint of the transition.


Microscope recommendation for an amateur?

Higher magnification is definitely NOT always better. Indeed, the microscope you are considering is designed for maximum magnification of 1,000x. The 2,000x is achieved by adding 20x eyepieces BUT it creates what is known as 'false magnification'. 2,000x is beyond the resolving power of a light microscope so what happens is that the image is magnified 2,000x but without a corresponding improvement in resolution. In fact, you will notice a degradation in image quality....it's like magnifying a pdf on your computer....it gets bigger but you still can't read it! And in any event, you will never use 2,000x let alone 1,000x! Read this article http://www.microscope.com/education-center/articles/false-magnification/

Second, I advise against buying an integrated digital microscope. Far better to buy a standard trinocular microscope and add a microscope camera. The reason is that the camera will be obsolete within about one year while the microscope should last a lifetime. If anything goes wrong with he camera, you will have to buy an entirely new microscope. Moreover, with separate scope/camera, you can switch cameras on the same microscope or use the camera on a different microscope. For more info read this article http://www.microscope.com/education-center/articles/digital-microscope-options/

Look for a lifetime warranty. A mechanical stage is standard and helps move the slides on the stage.

In full disclosure, I own www.microscope.com so give me a call if you would like any further assistance. You will not find false magnification or false advertising on our website!


Does opening of ion channels alter the membrane potential directly?

Not in any substantial way from the perspective of the overall membrane potential; it could be possible to measure the charge moving as a way to study channel gating, but that's a completely separate issue (and the scale of measurement would have to be incredibly precise, way more precise than is relevant for neural function).

Although very few ions have to move across the membrane to change the membrane potential, this "very few" is in relationship to the total number of ions present in a solution, which is massive and difficult to imagine. A single ion channel can flux millions of ions per second.


How many nutrients do trees process daily?

I don't know much about trees, but I was very skeptical about this post at first. If this web page is correct, then the post is actually not so far-fetched.

Trees are amazing. According to the page, the average tree absorbs 10,000 gallons of water and uses 1000 gallons, evaporating the rest. 24 gallons of water contains one pound of dry matter. That means that the average tree would accumulate almost 42 pounds of dry matter in a single day.

Now, I certainly cannot vouch for the credibility of the website, but it was difficult to find a page that showed the numbers, so take it with a grain of salt and try to find other sources that back it up or counter it.

Here's the link: https://www.thoughtco.com/process-of-using-water-by-trees-1343505


The typical name for this technique is "corrosion casting" - if you search for literature on corrosion casting you will find many many papers detailing the technique. Another answer mentions "plastination" but I don't think this is really what you are looking for; plastination is a technique for preserving the tissues themselves (though the "Body Worlds" exhibit that post references also uses corrosion casts extensively).

Briefly, in corrosion casting, you gravity or pressure-fill the vasculature with a plastic, typically acrylic. It is best if the vessels are flushed free of blood before injecting the plastic, with saline/PBS, for example. (Organs from a butcher will work fine but you will get better results if you can administer heparin premortem to prevent clotting, which of course is not possible for a meat animal.) The acrylic cures, and then the tissues that remain are digested with a basic solution, ranging from 0.5 M NaOH to 6M KOH depending on the protocol (lower concentrations or NaOH will digest more slowly, higher concentrations or KOH will digest more quickly), often at elevated temperature (~37C). Note that this solution technically digests all of the vasculature as well, but you have already filled the vascular lumens with plastic, so that is what you are left with.


In the context of Darwin's Variation under Domestication, "true breeding" is a phenotypic characteristic rather than a genetic one.  True-breeding organisms produce offspring that are identical to themselves, concerning some trait -- i.e. white fantails, when bred with white fantails, produce characteristically white offspring.  For diploid organisms, true-breeding typically implies that the parents are homozygous at the locus conferring the trait of interest.


Evolution of diversity and extinction resistance

The topic you describe is very interesting and known as "species selection." Some traits exist that not only affect the reproductive success of individuals, but also affect the diversification rate of the entire species, either through affecting the extinction rate, the speciation rate, or both.

To give you an example, I'll summarize this paper by Goldberg et al 2010. Self-incompatibility (SI) in plants is the ability of a plant to reject its own pollen to prevent inbreeding. This mechanism is expected to increase the genetic diversity of the plant's offspring. Self-incompatibility has been lost many times in the history of flowering plants, yielding self-compatibility (SC), which allows a plant to breed with itself. A plant that can breed with itself has an advantage in that even if the population size is low and it can't 'find' another individual to breed with, it can still breed with itself to produce offspring. However, this trait is expected to result in decreased genetic diversity in the offspring due to inbreeding.

The transition from SI to SC is a common transition that cannot easily be reversed. One might expect, then, that SI would be very uncommon as lineages would lose it to SC. However, it turns out that SC lineages have a lower diversification rate than SI plants in the Solanaceae due to the fact that SC lineages have a higher extinction rate than speciation rate. This difference in diversification allows SI to persist. This is an example of trait-dependent net diversification rate. It is not known exactly why SI lineages have a higher net diversification rate, but it could be related to the higher effective population size which results in "increased polymorphism,
lower linkage disequilibrium, more
efficient response to purifying selection, more
extensive geographic distribution of genetic diversity,
and lower rates of extinction".

If you want to read more, I can suggest a few more papers:

The Units of Selection by R.C. Lewontin

Darwainism and the Expansion of Evolutionary Theory by S.J. Gould

Species Selection: Theory and Data by D. Jablonski


Is there a period after you have had a cold when you cannot get a cold again?

The short answer is no, there is no minimum time between two colds. The reasons for this are different.

Mostly it has to do with the viruses which cause the common cold. There is a bunch of them causing what we call a cold, including rhinoviruses, coronacviruses, adenoviruses, human parainfluenza viruses, human respiratory syncytial virus, enteroviruses other than rhinoviruses and metapneumovirus. As much as 200 different virus serotypes are connected to this disease, alone 99 from the rhinoviridae. See the references 1-3 for more details.

Different serotypes means that two viruses of the same family (a rhinovirus for example) have different surface antigens on the virus and are not recognized by the same antibody. And this is what makes it difficult for the immune system. When it has learned to recognize and defeat one virus which causes a cold, it still has to learn how to do this with another (serotypically different) virus. So the adaptive immune system has to make highly specific antibodies every time it is faced with a new virus (which is of course not limited to cold viruses).

Once you have been infected with a virus and developed a sufficient immune reaction to develop antibodies, you are usually immune against this specific virus (with its specific serotype). Cold viruses live in communities, so when you move or travel, you will most likely encountered with different viruses, which your immune system doesn't know...

Finally there is another point which adds to the problem: Mutations of the viruses. The viruses are mutating constantly (RNA viruses at high rates) which changes their appearance and also their surface molecules (which are important for the recognition through the immune system). This leads to new serotypes, which are unknown to the immune system. See reference 4 for some more details.

References:

Understanding the symptoms of the common cold and influenza.
Sequencing and analyses of all known human rhinovirus genomes reveal
structure and evolution.
Common cold
Mutation rates among RNA viruses


databases for plant growth temperature and altitude

You might find these maps useful. I am not sure where you live, but most plants will list what region they will grow in on their seed packet or online.

You might also find luck by searching ESRI or ArcGIS maps to find more information.

http://www.ahs.org/gardening-resources/gardening-maps


I don't think this answer answers the post given the discussion and new edits. I will leave it here nevertheless just in case I still misunderstand the OP's question.

  [..] introducing cancer or radiation [..]

A cancer is not a transmissible disease (except very few cancer last the facial tumor in Tasmianian devils). A radiation is not even a pathology, it is a physical phenomenon which include light. Did you rather mean something like a virulent flu for example?

  If we introduce any disease or deadly effect to a large group of living things, will such a group be able to develop a resistance?

The population may or may not survive. It depends upon many parameters such as how virulent is the parasite, how large is the population, whether individuals in the population have already encountered the parasite before, whether there is already genetic variants resistant in the population or whether de novo mutations will be needed, etc... There is no way to answer to this question in the general sense.

Note by the way, that an individual may be resistant or tolerant to a certain disease.

Most of the time, the population survive well. The population will likely decrease in size a little bit though.


What is the most basic organism to respond to Classical conditioning (capable of learning)?

Very simple nervous systems are capable of learning  C. elegans, with only 302 neurons, is reportedly capable of both learning and memory.  There is a fairly large literature on the subject, as C. elegans is a popular research subject - a Google Scholar search gives about 40K hits, e.g. http://learnmem.cshlp.org/content/17/4/191.long

We have to remember that small is not necessarily primitive: the C. elegans nervous system (like every other one in existence today) has been optimized by millions of generations of evolution to do what C. elegans needs in order to survive.

Actual evidence of learning in nervous systems in the distant past is rare.  It's behavior, and behavior doesn't fossilize well :-)  Actual nervous systems apparently don't fossilize all that well, either.  The earliest well-preserved example I could find was this http://www.cam.ac.uk/research/news/520-million-year-old-fossilised-nervous-system-is-most-detailed-example-yet-found from 520 million years ago.  But since learning would give a creature a survival advantage, I'd guess that it evolved fairly early.


Help me identify this caterpillar looking insect

They look like the caterpillars of Alope sphinx (Erinnyis alope)

There is a webpage on a dedicated website here:
https://www.butterfliesandmoths.org/species/Erinnyis-alope

Among the pictures in the linked website you can find one with the green and brown morphs/stages of the caterpillars.


Is this how female and male gametes look like in plants?

The comments are very unclear and your interpretation of the figure seems very wrong (no offense). You should have a look at an intro course (such as this one by Khan Academy) as asking such intro questions here will require for one to rewrite an entire course.

The pink and blue thingies on the image are chromosomes, not gametes. A gamete is a haploid cell (we can see 4 of them at the bottom of the figure). One chromosome (say the pink one) has been inherited by the mother of the individual and the other chromosome (say the blue one) has been inherited by the father of the individual.

Let's assume that the segregation we see on the figure happens in a female individual. So, on the figure we see female diploid cells and female haploid cells. The female haploid cells are called ovules (there is a bit of oversimplification here). You can imagine the same process of segregation could occur in a male individual. The male haploid cells are called spermatozoid (there is a bit of oversimplification here). The male and female gametes might fuse to become a zygote which will develop in a new fully grown individual. The colors of the chromosomes in this scenario indicate whether the chromosome originally come from the grandmother or the grandmother of the zygote.


Depth perception consists of what are called monocular cues and binocular cues. As you mention, binocular vision has a lot of advantages for depth perception, but it is not completely necessary.

Many animals, particularly those that don't need especially precise vision, have little to no binocular vision, opting instead for visual coverage in more directions by having eyes on the side of the head.

The Wikipedia page I linked at the beginning has a whole list of various monocular cues, but I will mention a few of them here as well that I think roughly outline the different "categories" of monocular cues.

Relative size is a simple one: you expect certain objects to be a certain size. You can use that information to approximate distance.

Motion parallax: moving relative to objects gives you more information. Nearby objects move very quickly across the eye when you move, far away objects do not.

Accommodation: when you focus on a nearby object, you can estimate the depth by how much the lens needs to be deformed to bring the object in focus. The brain gets a copy of that muscle signal that it can use to estimate distance for nearby objects.

Although monocular depth perception is actually quite good out in the natural world, it is possible to trick the system with sufficiently clever strategies, like many other types of optical illusions. The Ames room is one of these.


A critical step in meiosis is the formation of tetrads. In diploid organisms like donkeys, they have a paternal version and a maternal version of each chromosome. Two chromosomes 2, for instance. During prophase 1, these two "matching" or homologous chromosomes form a tetrad and cross over, swapping alelles. There is no recombination and no tetrad formation in mitosis, which is used for growth and daily living.

  How is the meiotic process disrupted?

In a hybrid, there are no matching maternal and paternal chromosomes. In the zebroid testes or ovary, a lonely donkey chromosome 2 is wandering around, looking for another donkey chromosome 2, and there isn't a homologous chromosome. This mucks up Prophase 1, and the first division pulls crazy numbers of chromosomes to each daughter cell, and the gametes from this division are likely full of extra chromosomes and missing some critical ones.

  Apparently this difference doesn't obstruct producing (infertile) offspring. How comes the process of recombination of such vastly
  different number of chromosomes in gametes is viable?

An embryo needs a solid set of genes to grow up, but chromosomes don't have to be homologous for mitosis, and organisms use mitosis for growth and living, not meiosis. As long as the crazy mis-matched chromosomes in a zebroid have everything needed for a healthy organism, the hybrid will be healthy. It isn't until the zebroid starts to make gametes via meiosis that a problem occurs, as the homologues ONLY form tetrads in making eggs and sperm. The inability to recombine only occurs in the making of gametes.

  54 is an even number. How comes zebroids can't just normally produce
  fertile offspring with other zebroids of the same number of
  chromosomes?

Because even chromosome number doesn't help if they are not each homologous with another chromosome.


How to calculate extent of Sequence similarity

Well. You perhaps need not use the bioinformatic algorithms of string matching. These algorithms were primarily developed because of the extensive search space.

In your problem you just need to compare two recording experiments and you should use mathematical metrics for it. You have a 60x4 i.e 240 dimensional random variable. Moreover this variable is not discrete, it is continuous. For similarity measurements you have to use statistical tests or otherwise define a cutoff either on each element of the vector or the total magnitude defined by any norm.


The question is a bit unclear, it should be reframed as suggested by AliceD. To simply answer the question,

Glucose is the substrate, and in the first step it is converted to Glucose-6-phosphate.

Only the Phosphate group is added which originates from ATP, your notes also are a bit misleading because it tends to suggest that Hydrogen is released, which is not the case, the phostphate group in ATP loses an OH and Glucose loses an H in an SN2 reaction giving rise to Water in the process.

Always remember that ATP is categorized as an energy donor which drives chemical reactions in your body by breaking chemical bonds. ATP or Adenosine Triphosphate has three phosphate groups. The last Phosphate in ATP produces the highest amount of energy in any given chemical reaction where ATP is involved.

This is an ATP molecule.

The first P that you see is the Phosphate which gets released, and the ring that you see is a five member ring called a ribose sugar, while glucose is a six member ring.


Can swallowed fingermails, hair, or skin get caught in your appendix?

Skin is safe to chew, and digestible. Fingernails are not digestible, so really shouldn't be swallowed if avoidable. In the medical literature, there are at least 225 cases of foreign bodies in the appendix. They include:

a metal drill bit that was ingested unintentionally 3 months earlier
pins (81  cases)
lead shot (81 cases)
seeds (34 cases)
bones (16 cases)
eggshell
glass
teeth
nails (hair causes problems with bezoar formation)
a die (dice)
the clinical end of a thermometer.

Most (71%) patients were symptomatic, typically with intermittent abdominal pain for months or years. Pins were most likely to elicit symptoms (93% of cases).

So it seems there is some truth to this nugget of folk wisdom.

The above were found over many, many years. Since most cases are asymptomatic, it's likely there are many cases that never come to light, but not remarkably so (lots of appendices are removed and examined every year!).

Foreign Bodies in the Appendix


Book for artists' renderings of extinct species?

With a quick search I was surprise that I could only find

Animals of a Bygone Era: An Illustrated Compendium
Extinct Species
Extinct Animals of the British Isles
Extinct Birds

It looks like there is an open niche to someone who like biology of extinct species and illustrations!

Note all will be of interest to you. None of them seem to offer good quality computer based illustration but rather pencil drawings.


You are right in a sense. The processes which generate mutations in an organism are stochastic (not quite exactly random, but in most organisms they are effectively random for all intents and purposes). In terms of population genetics, it is considered that mutations occur randomly across the genome and have an equal probability of occurring at a given base pair.
The environment is also random/stochastic in the sense that it occurs mostly independent of mutations which have occurred. Whether or not it is cold one year is independent of the mutations which have occurred within an organism. (Actually that's not quite correct since organisms can generate their own environmental niches and evolve according to them, but I think that is beyond the scope of this question).
What is not random is how the frequency of genetic variants respond to different environments. This is natural selection. Over the long run, we expect genetic variants which increase the fitness of an organism within a given environment will increase in frequency and vice versa. There is a large body of theory and evidence which predicts how a particular variant may change in frequency in response selection of a particular pressure.
As @jamesfq correctly points out, a nice example of selection being non-random on the macro-scale is convergent evolution. For example, aquatic animals such as fish, certain mammals (e.g. Dolphins) and Amphibians and Dinosaurs have independently evolved streamlined bodyplans in order to conserve energy when moving through the water.


Can both the overlapping genes (in opposite strands) produce proteins?

While overlapping antisense RNAs are quite well known, there are very few examples in which both the RNAs from the pair can code for proteins. However, it is not impossible. I can cite one validated example: RU2S (DCDC2) and RU2AS (KAAG1) pair.

While RU2S is constitutively and ubiquitously expressed, RU2AS is specifically expressed in kidney, bladder, liver, and testis. It is also expressed in certain tumours (Peltz and Dougherty, 1999).

 Peltz SW, Dougherty JP. Antisense Translates into Sense. The Journal of Experimental Medicine. 1999;190(12):1729-1732.


Do DNA viruses have their own DNA dependant DNA polymerase?

Probably I won't be able to answer all of your questions satisfactorily, but let's begin one by one.

Does the pox virus also have its own DNA-dependant-DNA-polymerase?

Yes. See this article from Wikipedia:

The replication of poxvirus is unusual for a virus with double-stranded DNA genome (dsDNA) because it occurs in the cytoplasm, although this is typical of other large DNA viruses. Poxvirus encodes its own machinery for genome transcription, a DNA dependent RNA polymerase, which makes replication in the cytoplasm possible. Most dsDNA viruses require the host cell's DNA-dependent RNA polymerase to perform transcription. These host DNA are found in the nucleus, and therefore most dsDNA viruses carry out a part of their infection cycle within the host cell's nucleus.

If yes, is it unique in having so?

Actually no. Hepatitis B virus also has its own DNA polymerase. And there's also the classic example of retroviruses: they have an RNA-dependent-DNA-polymerase (but yes, you can't consider it since it isn't a DNA-dependent-DNA-polymerase). See this wikipedia article:

Some viruses also encode special DNA polymerases, such as Hepatitis B virus DNA polymerase. These may selectively replicate viral DNA through a variety of mechanisms. Retroviruses encode an unusual DNA polymerase called reverse transcriptase, which is an RNA-dependent DNA polymerase (RdDp). It polymerizes DNA from a template of RNA.

Another example, as mentioned by @David in comments, is the Herpes simmplex virus (HSV) which contains a bunch of its own enzymes for DNA replication on its own. See this article:

Herpes simplex virus (HSV) encodes seven proteins necessary for viral DNA synthesis—UL9 (origin-binding protein), ICP8 (single-strand DNA [ssDNA]-binding protein), UL30/UL42 (polymerase), and UL5/UL8/UL52 (helicase/primase).

The rule that they need to get into the host nucleus - is it for making protein using the host DNA-dependant-RNA-polymerase or for replication using the host DNA-dependant-DNA-polymerase? Or for both?

Umm, both. Viruses (generally; there might be exceptions) need to reach to the nucleus of host to replicate as well as transcribe their DNA. See this article (emphasis mine):

Most DNA viruses replicate in the cell nucleus, which is where cellular replication and transcription proteins are localized. After infection, the nucleocapsid of DNA viruses is therefore usually delivered to the nucleus where uncoating occurs. An exception is poxviruses, which replicate in the cytoplasm of infected cells.
The first stage in the viral replication cycle is expression of the viral early genes. Transcription of these genes occurs using cellular RNA polymerase II and cellular transcription factors. These proteins bind to the viral DNA in regions called early promoters/enhancers, and promote synthesis of the early pre-mRNAs.
Once the viral early genes have been expressed, and the cells have been induced to enter S phase, viral DNA is replicated. This occurs in the nucleus of infected cells, and gives rise to new viral genomes. Many hundreds or thousands of new viral genomes can be produced in the nucleus of a lytically infected cell.

Are there instances where the host DNA-dependant-DNA-polymerase is expressed at times other than the cell's S-phase?

I think it has already been answered in your 2nd question. No, and the exception is the poxvirus itself. Again see the same article (emphasis mine):

Most DNA viruses replicate in the cell nucleus, which is where cellular replication and transcription proteins are localized. An exception is poxviruses, which replicate in the cytoplasm of infected cells.

Are there viruses that replicate inside the cell's nucleus without being integrated into the genome?

Wait! There's a difference between being inside the host cell's nucleus and being integrated into the host genome. Integration of the viral genome into the host genome requires a special enzyme called integrase and, you know, DNA viruses don't have integrase because they don't need it. So your question can be changed a bit to Are there viruses which replicate inside the cell's nucleus by getting integrated into the genome? Now, I could find only one such example i.e. Ectocarpus siliculosus Virus (EsV).

Ectocarpus siliculosus virus-1 (EsV-1) is a lysogenic dsDNA virus belonging to the super family of nucleocytoplasmic large DNA viruses (NCLDV) that infect Ectocarpus siliculosus, a marine filamentous brown alga...the EsV-1 and FirrV-1 genomes encode a large putative integrase/recombinase for which no counterpart exists in current protein databases. Only the Tyr-recombinase domain at the carboxy terminus of this enzyme is similar to phage integrases. Therefore, this enzyme might be involved in the integration and/or recombination of the integrated viral fragments.

References:

Pox virus

Hepatitis B virus DNA polymerase

Herpes simplex virus

Herpes Simplex Viruses: Mechanisms of DNA Replication

Wikigenes: UL9, ICP8, UL30, UL42, UL5, UL8, UL52

Reverse transcriptase

Viral Life Cycles in Cells

Integrase

Ectocarpus siliculosus Virus-I


Why does the mass increase in this question?

The reason that dialysis bag A and B will get heavier is due to water diffusing into the bags in order to bring the sugar concentration on both sides of the membrane to an equilibrium. Likewise bag C and D will get lighter as water will diffuse out of the bags in order to bring the system as close as possible to equilibrium. Water diffusion is also called osmosis and can be studied closer here: https://en.m.wikipedia.org/wiki/Osmosis


Cerebral activity during exposure to non - visible light

Vision is based on a protein interaction with a molecule called retinal from vitamin A.

Wavelengths of light in the visual range cause a photoisomerization of retinal (a cis- to trans- change), which is sensed by the protein that is "holding on" to the retinal.

Wavelengths that do not cause this photoisomerization cannot be sensed by the photoreceptors of the retina, so there isn't any signal produced to transmit to the brain.

However, there is some filtering done by the lens of the eye. Without the lens, humans (and other animals) can see further into the UV range. That UV light is also damaging to the retina, though, so it's best to keep the lens intact.

Note that the image in the answer by @Remi.b is actually from a psychometric experiment, so the lens is intact. The responses there are actually human perceptual sensitivity to light for each cone. The blue curve would go off to the left quite a bit further into the 300nm range if the lens were not present. The research subjects probably prefer the experiment as-is, however.

You wouldn't perceive that UV light much differently than a far violet color, however, because differences between different cones are necessary for color vision, and by that end of the spectrum only the cones responsive to the shortest wavelengths are responsive at all.


What does microglia process length tell us?

Part of this question is due to the function of microglia in the healthy brain (as we currently understand it).  The general idea is that microglia in a healthy brain are in "surveillance mode," and have long, thin processes that extend of the cell body to monitor the environment.  It would be like beat cops splitting up and walking the streets when no crime is reported, they're just monitoring one large area by spreading everyone out.  However, when some insult occurs and microglia are activated (which just means they get into a mode responsive to some insult or injury), which results in them having shorter processes and enlarged cell bodies to focus on the damage done in their immediate vicinity.  This would be like one of the beat cops seeing a crime, then calling for back-up.  Now the focus is on the scene of the crime or site of damage.  Therefore, if your microglia have long, thin processes, everything is pretty much normal because these microglia are not activated.  However, having a lot of microglia with short, thick processes indicates that they are activated in response to some injury or insult.  This is why a common practice is to use microglial process length as an indicator of microglial activation and, in turn, some form of damage to the brain.

In shorter terms:

Long, thin processes = lack of microglial activation and little to no brain injury
Short, thick processes = microglial activation, indicative of brain injury

My source is just my experience in neuroscience and reading these types of papers, but there's more information on microglial activation here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5431479/ which includes some discussion of process length and morphology.


Yes, just planting seeds from the tallest plants would already do great. You could just chose an arbitrary size threshold under which you discard the seeds and above which you plant the seeds. Or you could plant all the seeds of the largest plant, almost all the seeds of the second to largest plant, all the seeds of the third largest plant etc... If plant height is a heritable characteristic (and it certainly is) then you will see a result after a few generations only.

You might want to ensure you understand the definition of heritability and the basics of quantitative genetics by reading the post Why is a heritability coefficient not an index of “how genetic” something is?.

Now instead of picking a random threshold for selection, you could be smarter and make some calculations. If you were to perform too a strong selection pressure (such as growing the seeds of the tallest individual only), then you will very quickly reduce genetic variation for height to zero and therefore remove all heritability. If you are using not a strong enough selection pressure, then you might barely see any changes even if you go on for many generations. Estimating the right type of selection pressure depends on the specific population you are facing (typically population size) and to its evolutionary history (typically previous selection on height or correlated traits and past population size).


If evolution is true, how do all organisms have varying amount of chromosomes?

A mutation is a general term referring to any alteration of a nucleotidic sequence. It includes small mutations like indels (insertion or deletion of a single nucleotide) and substitutions, or bigger mutations such as e.g. chromosome fusions, whole chromosome duplications, whole genome duplications and gene deletions. So yes, some mutations do change the number of chromosomes (and ploidy number).

If you are interested in a very short and very introductory course to evolutionary biology, consider having a look at Understanding Evolution by UC Berkeley


They look like lacewing eggs, though related insects can have similar-looking eggs. Lacewings are beneficial insects; their eggs are laid on stalks, like this:

Edit to point to other questions and answers here:

Is this some sort of fungus?
What are these (eggs?) ? ( Location - India )


What is the point at which abiogenesis is complete and evolution begins?

I think it's a mistake to assume that there is such a point. All plausible seeming models of abiogenesis currently under consideration involve evolutionary processes long before they reach the stage we'd consider alive.

Evolution will occur whenever there is (a) replication-with-error and (b) selection (simplifying slightly). This is the case with a self-replicating RNA. It is replicating, but those replicates can be imperfect. Imperfections in replication that improve its ability to replicate will be favoured. That's evolution.


Data are usually binned in broad age groups partly because that's all the detail that's useful in some context, and because access to more detailed data often involves access to strongly controlled, personally identifiable information.
This preprint (full disclosure: I'm a co-author) gives information in 2-year bins for COVID in Ontario, e.g. this graph of the fraction of known infections (KI) hospitalized, and fraction of hospitalizations that resulted in survival, by (2-year) age group.
It looks pretty smooth, although if you squinted hard you might be able to convince yourself there were some breakpoints, e.g. between [60-61] and [62-63] in hospitalization or between [62-63] and [64-65] in survival (although I doubt these impressions would stand up to a formal statistical analysis ...)


A lot of mammals do have eyespots. Specifically "mid-guild" predators such as raccoons, coatimundis, ringtails, foxes, raccoon dogs, many opossums, skunks, red pandas, civets, etc. It's thought to be an anti-predator defense, with the eyespots or face mask being places further back on the head. A predator might mistake these eyespots for its actual eyes, and because they're placed further back they create the optical illusion that the animal's head belongs to a much larger animal than it actually does.

This is a photo of the gray four-eyed opossum (Philander opossum). It's called "four-eyed" because of the two eye spots it has just above it's eyes. It's thought that the position of these spots mimics the position of the eyes on a much larger predator, so if a predator like a raccoon or a coyote sees the opossum they'll mistake it for a much larger predator and they'll leave it alone.


Why are embryonic germ cells considered stem cells?

The difference in designation is the timing of the foundation of the cell line and the tissue that it was sourced from.

Embryonic Stem Cells are harvested from the inner cell mass of a Blastocyst around day 5 post fertilization. This is the first or second generation of cells to have started to differentiate, but they still have Pluripotency, which means that they can differentiate into any one of the three germ line cell types. [1][2]

Those  three germ cell types are:

Endoderm
Mesoderm
Ectoderm

Embryonic Germ Cells are "cultured from primordial germ cells obtained from the gonadal ridge and mesenchyma of 5- to 9-week fetal tissue...." [1] These cells are multipotent, meaning that they will usually only be able to give rise to mesenchymal derived cell lines.[3][4]

There are also differences in replicative ability. ES cells are for the most part immortal cells able to be maintained in in-vitro culture for long periods of time, while EG cells have a life cycle of about 70 to 80 cell divisions before they reach quiescence.[1] If I had to venture a guess as to why this was the case, I would say that EG cells have likely already reached a stage of differentiation where they are repressing or down regulating the expression of Telomerase. ES cells will be expressing telomerase, so they will not experience telomere shorting due to the 3' end replication problem during DNA synthesis in S phase of mitosis.

There are other cell types of Adult Stem Cells other than Hemopoietic Stem Cells, so I am not sure why your course is making the distinction. It could be that in practice, we have only really successfully used Hemopoietic Stem Cells in treatments for diseases by doing bone marrow transplants. You would likely have to have your instructor clarify this point for you.