Better population models than the logistic equation

It is not complicated to make your own model of population growth

You can make a model with any kind of function, it is not super hard. It just happen that logistic growth offer quite a good match to observations. You can have exponential growth, linear growth, quadratic growth, ...

However, there are more possible behaviours behind those models than what you think!

The behaviour that you describe is totally possible with a discrete time logistic model. In short, consider the recursion equation $n_{t+1} = f(n_t)$. Consider also $\hat n$ as being an equilibrium of your system (typically n=0 or n=k, where k is the carrying capacity). In other words, $\hat n$ satisfies the equation $\hat n = f(\hat n)$. And finally consider the statistics $\lambda$ which is equal to the derivative of $f(n)$ over $n$ evaluated at the equilibrium $\hat n$. If $\lambda < 0$, then you have oscillatory behaviour (and therefore overshoot) at the vicinity of the equilibrium $\hat n$. Using the correct parameters, the logistics equation gives you a lambda smaller than 0 (typically between $-1 > \lambda > 0$), and therefore you can have the oscillatory behaviour you describe.

If you have any trouble to make these basic analyses of those models, I strongly recommend that book.


Technical term for water entering a semipermeable membrane?

This is not imbibition, as water molecules don't get absorbed in the semipermeable membranes commonly found in biological structures like Membrane around cells and cellular organelles (I took this example as you asked it in Biology forum). The water molecules pass through biological membranes via protein channels, that may be an active, secondarily active or passive process. Percolation and permeation are also inappropriate.

If the membrane doesn't hinder a particular solvent it can be said to be permeable to that solvent (e.g. Permeable to water etc.). "Osmosis" is also applicable. As osmosis is only a type of diffusion, you can use the term 'diffusion', but it would be too broad or generalized.


Extinction of species with extant descendants

You are right. Consider a population at some point back in time and ask how many of the individuals left descendants that are still alive today?, the answer will be between 1 and N (inclusive), where $N$ is the population size. We call this process coalescence

A tiny introduction to coalescence

Consider a population of constant size $N$ and to the previous generation and ask the question What is the probability of two random individuals to be siblings?. This probability is $\frac{1}{2N}$ (assuming no selection and diploid population). The probability of them not being siblings is $1-\frac{1}{2N}$. We can say that, with probability $\frac{1}{2N}$, two randomly individuals coalesce in the previous generation. What is the probability that 2 random individuals coalesce $t$ generations ago? It is the probability that they don't coalesce for $t-1$ generations and then coalesce, that is $P(t) = \left(1-\frac{1}{2N}\right)^{t-1} \frac{1}{2N}$. In words, the coalescent time follows a geometric distribution with parameters $t$ and $\frac{1}{2N}$.

Because coalescent times are independent variables (and I won't prove it here), one can extend this to not only 2 individuals but $n$ individuals. There is therefore, a point in time where all individuals of the modern day population coalesce into only one individual. At this time, this one individual was not alone in the population of course.

Coalescent theory: Usages and book recommendation

The simple calculations I just made are the very basis of coalescent theory. Coalescent theory is a very powerful set of mathematical tools that one can use to make detailed predictions of the genetic patterns to expect in a population. Statistical test such as Tajima D test is based on results from coalescent theory. Coalescence theory can be extended (through approximations) to structured population (structured coalescent theory), non-neutrality (selection) and recombination.

coalescent theory: an introduction (by John Wakeley) is a good book on the subject. However, it requires from its reader some basic knowledge in mathematics and problem some knowledge in population genetics.

What is the percentage of people living in England in 1500 AD whose lineage is still alive? is a recent post on Biology.SE that is relevant to the kind of question that could be answered with coalescent theory.


Can 5 alpha reductase inhibitor drugs work for life or do they lose effectiveness?

As noted in a comment, a truly thorough answer to this question would require one or more books (1,2) or scientific journals (3), but a simpler, necessarily incomplete answer can be provided.

The short answer is: transmembrane drug transporters of the ABC family (4)

But what are those? Well, you should read the wikipedia article for a detailed description, but essentially they're proteins that burn energy in order to remove a broad range of drugs from the cytoplasm, making them less "bioavailable". The answer to why some drugs (or broad spectrum treatments with multiple drugs) are more or less susceptible to export by ABC family proteins is much more complicated (buy books from (1) and (2) or similar texts(5)), but the broad spectrum HIV regimen prevents resistance by a completely different mechanism (6).

Briefly, ABC transporter-mediated resistance involves no evolution, simply a "transcriptional response" to the presence of harmful drugs, while HIV actually evolves to become resistant or immune to antiretroviral drugs. However, it's difficult or impossible to be virulent (fast replication) and hardy (drug resistant and/or immune system resistant) at the same time, so mutations which increase resistance to one drug also decrease virulence - if you treat HIV with enough drugs then the mutations required to be resistant to all of them will result in a virus that has very poor virulence.

(1) http://www.wiley.com/WileyCDA/WileyTitle/productCd-0470927941.html

(2) https://www.amazon.com/gp/search?index=books&linkCode=qs&keywords=9781782620693

(3) https://scholar.google.com/scholar?q=human+drug+transporters&hl=en&as_sdt=0&as_vis=1&oi=scholart&sa=X&ved=0ahUKEwjVh6-a8aPPAhVK1B4KHfxABSsQgQMIGjAA

(4) https://en.wikipedia.org/wiki/ATP-binding_cassette_transporter

(5) https://www.google.com/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=human+drug+transporters&tbm=bks

(6) https://en.wikipedia.org/wiki/HIV_drug_resistance


In theory how fast could nerve signals travel if the nerve fibre was perfectly insulated?

For some background on saltatory conduction: https://en.wikipedia.org/wiki/Saltatory_conduction

I feel that a "perfectly insulated" neuron couldn't actually allow the signal to travel. Insulation (which, in neurons, is basically layers of fat wrapped around axons so ions cannot pass) allows the electrical signal to move further along axons (less ionic leakage) and faster (due to decreased membrane capacitance-it takes less charge movement to generate the same potential difference across the membrane; see this question: How is membrane capacitance related to the increased speed of saltatory conduction?)

Also, you should check out wikipedia's page on cable theory of neurons:
https://en.wikipedia.org/wiki/Cable_theory

This is why myelination increases conduction speed, as you may or may not already know. The increased length of the ionic signal (due to the inhibited leakage) allows voltage-gated ion channels which are further away to be activated as a result of any given local membrane depolarization. This all happens faster due to the lower capacitance.

However, the only way the action potential can actually "travel" at all is due to the sequential activation of voltage-gated ion channels along the axon. This is the case in both myelinated and unmyelinated axons, it's just that the spacing is greater when myelinated. In the insulated, fat-wrapped regions of axonal membrane, there are no ion channels, voltage-gated or otherwise. If there were, the layers of fat would not allow ions to pass through anyway at this point. Thus, the "perfectly insulated" axon could never actually propagate a signal, because the signal still requires the chain reaction of voltage-gated ion channel activation and sodium influx at some point. Myelinated conduction is faster because the spacing is increased, but increasing the spacing to infinity would not allow the action potential to be passed on.

I suspect that there is a certain threshold in the extent of myelination where the spacing between nodes of Ranvier becomes to great to have effective propagation of action potentials. I wouldn't be surprised if evolution has resulted i a relatively optimal spacing of nodes. I suppose a better question might be: what is the speed of conduction between nodes?

I suppose it would be possible to send current through a perfectly insulated axon and potentially activate a voltage gated calcium channel at the terminal. However, This would be different than an action potential and would be effectively reducing the neuron to an electrical wire. Sometimes it's better to keep things simple.


Are rods/cones rejuvenated periodically?

The answer can be found in the excellent lecture from 1983 The Life History of Retinal Cells which also has gorgeous microscope fotos. The renewal time of rod outer membrane proteins is less than two weeks. Cells stay indefinitely, as I understand, but are periodically rebuilt in a logistical nightmare/wonder.


There isn't a fixed value for the human exome AFAIK, nor would it be a good idea to have a fixed value for the exome because different regions and genes can be under different selective pressures.

The norm is to compute the ds/dn ratio and then test against a null hypothesis of the ratio being 1 to infer if your region is under selection or not. If it is greater than 1 it indicates positive selection and if it is less than 1 purifying selection.

You can find a  decent introductory treatment here.


It is a Hoya Carnosa Krinkle Kurl flower. It is native to Australia and East Asia. Hoya Carnosa links to wikipedia and Krinkle Kurl links to plant rescue in case you want to read more on it.


In the future, it is plausible that we can change the physical appearance of a living animal by editing DNA?

This article explains that scientists managed to change the DNA of adult laboratory mice with an inherited liver disease, thereby curing them of the disease.

Yes, Read about CRISPR-CAS9 method of gene editing. This is not the only method which can achieve this. There are many others like TALEN or Zinc Finger.

  If we used this same method to edit our hair follicles, could we alter our hair color?

Yes, similar studies like this has already shown this potential but using different method as mentioned in article you linked.

  The new hairs would have altered DNA, and come out a different color depending on what the cells have been altered to.

For this you need to express such constructs in cell specific manner. Drosophila geneticists are doing such things for long long time.

  And then, is it possible to change the physical size and shape of a living animal by editing DNA? For example, if an animal has porous and small bones, is it plausible that we could edit its DNA so that its bones start to become more dense and thick? The physical appearance of the living animal would be changed, since the bones are larger than before.

Plausible but remember such characteristics are controlled by many factors which will be hard to control. Plus there will be age/environmental/epigenetic factors which you can't control with such techniques.

  Along these lines, could we then edit DNA of an adult human to change bone structure so that we have sharper noses? Larger eyes?

Most of these techniques required change in germ cells. Hence it will be difficult to implement such techniques in adults. However 'ideally' you can use techniques like RNAi which can be triggered by specific inducers at any stage of life (like temperature sensitive UAS-Gal4 system used in fly genetics).


The pixels in a TEM image are whiter or blacker based on the dose of electrons that impact that pixel in the whatever detector is being used to form the image, be that photographic film, a scintillation screen, or a direct detector camera.

As for how the image that reaches the detector is formed by the specimen being imaged, there are two different mechanisms.
Amplitude Contrast is relatively simple - denser parts of the specimen scatter electrons strongly enough that some electrons do not make it to the detector at all, so pixels below these parts of the specimen will receive a lower dose than pixels below less dense parts of the specimen.
Phase Contrast is more complex, and is responsible for most of the contrast in high-resolution cryo-TEM. Briefly, the specimen is illuminated by a parallel beam of electrons and every "pixel" of the specimen scatters some electrons but lets most of them pass straight through without interaction. The scattered electrons go off in a different direction than the main beam but are focused back by the lenses to the same point on the detector as the unscattered electrons. Because the scattered beam took a different path from the unscattered beam, and because electrons are waves as well as particles, there is a phase difference between the two beams which causes them to interfere. Typically, areas of the specimen that scatter electrons more will cause destructive interference, so darker pixels. If there is no scattering, then there is no interference, so brighter pixels. There are many resources explaining the technical details of this mechanism (1, 2, 3), but these tend to focus on crystalline specimens.


Does learning increase the number of neurons in the brain?

Short answer
Training increases white and gray matter densities in the brain. This may reflect increases in neuronal cell counts especially in the hippocampus. In the cortex, however, such observed changes are probably more reflective of other processes, such as synaptogenesis.

Background
Gray matter is generally viewed as being the neuronal cell bodies, while white matter corresponds to myelinated fiber tracts. Changes in both can be reflective of changes in cellular content, but changes in gray matter are generally more directly related to changes in cell numbers, which you are after.

A striking example of the effects of learning on the brain is observed in subjects that start to learn to juggle. These people have been shown to have increased gray matter density in the occipito-parietal regions (the visual motion areas). These changes are apparent after as little as 7 days of training. Such experience-dependent changes are also observed in white matter. Occipito-parietal regions are involved in visuo-motor coordination, reaching and grasping. There have been a host of other studies that showed similar changes in the brain. For example, taxi drivers were shown to have increased hippocampal volumes.

There is good evidence for adult neurogenesis occurring with learning in the hippocampus. Adult neurogenesis also produces thousands of new granule cells in the dentate gyrus every month, but this is a relatively small increase in total number of hippocampal neurons. Furthermore, although there have been reports of neurogenesis in the mammalian adult neocortex, this is controversial.
Thus, neurogenesis is likely a minor factor in MRI changes, particularly those found outside the hippocampus.

Instead, other factors such as increase in glial cell numbers, synaptogenesis, changes in dendritic structures, axonal sprouting and re-routing and even vascular changes may underly the observed changes in imaging studies.

Note: there is a host of imaging studies available on effects of learning on structural changes in the brain. The referenced review article cites many.

Reference
- Zatorre et al., Nature Neurosci (2012); 15: 528–36


What does the number after Vitamin B signify?

It appears to be fairly arbitrary, but they were originally numbered chronologically by discovery. However...

From Gizmodo:

  These Bs are not necessarily designated in chronological order, as B12 (Cobalamins) was discovered in 1926, B5 (Pantothenic acid) and B7 (Biotin) in 1931, B6 (Pyridoxine) in 1934, B3 (Niacin) in 1936 and B9 (Folic acid) in 1941. The missing Bs are substances originally thought to be vitamins, but later reclassified.

Wikipedia explains that certain numbered B vitamins were originally classified as other vitamin letters when discovered and only later reassigned as a B vitamin.

In conclusion, B vitamins were numbered in order as they were assigned as a B vitamin.

missing numbers are due to specific vitamins being reclassified as either different letters or as non-vitamins.


What are the differences and similarities between fimbriae and adhesins in microbes adherence factor?

Fimbrae is a catch all term to denote the hairlike projections on many gram-negative and some gram-positive bacteria, but exludes flagella. Adhesins are a subtype of fimbrae that serve as organs of attachment to cells or mucosal surfaces. Another type of fimbrae are pili, functioning in conjugation, the transfer of DNA from one bacterial cell to another  (Koneman, I can't even find the year on this crazy book. Used to be the bible of determinitive bacteriology. So many hours.)


By what mechanism does elevated homocysteine level accelerate thrombin formation?

According to a heavily-cited paper (below), homocysteine reduces the expression of thrombomodulin on the surface of endothelial cells.

Thrombomodulin binds to thrombin, and the resulting complex does not promote coagulation, but instead activates protein C. Protein C has an anticoagulant effect. Thus reduced levels of thrombomodulin will result in increased levels of free thrombin (promoting coagulation) and in reduced levels of protein C (also promoting coagulation).

I haven't found any evidence that homocysteine has an effect upon thrombin formation directly.

  Lentz,SR and Sadler, JE (1991)Inhibition of thrombomodulin surface expression and protein-c activation by the thrombogenic agent homocysteine. J. Clin. Invest. 88:1906-1914

  Abstract Elevated levels of plasma homocysteine are associated with both venous and arterial thrombosis. Homocysteine inhibits the function of thrombomodulin, an anticoagulant glycoprotein on the endothelial surface that serves as a cofactor for the activation of protein C by thrombin. The effects of homocysteine on thrombomodulin expression and protein C activation were investigated in cultured human umbilical vein endothelial cells and CV-1(18A) cells that express recombinant human thrombomodulin. Addition of 5 mM homocysteine to endothelial cells produced slight increases in thrombomodulin mRNA and thrombomodulin synthesis without affecting cell viability. In both cell types, thrombomodulin synthesized in the presence of homocysteine remained sensitive to digestion with endoglycosidase H and failed to appear on the cell surface, suggesting impaired transit along the secretory pathway. In a cell-free protein C activation assay, homocysteine irreversibly inactivated both thrombomodulin and protein C in a process that required free thiol groups and was inhibited by the oxidizing agents diamide or N-ethylmaleimide. By inhibiting both thrombomodulin surface expression and protein C activation, homocysteine may contribute to the development of thrombosis in patients with cystathionine beta-synthase deficiency.


Is the mutation rate in organisms in general consistent over the genome?

Well, for start, there are "mutational hot spots", regions that are more prone to mutation than others.

As for immune system genes, first of all, lung cells and heart cells and retina cells don't need to mutate those genes, because they don't use them.

But you are right that in immune cells there is a lot of DNA futzing in the sequences for the heavy and light chains, in order to generate diversity in T and B-cell receptors.  Those receptor sequences are built in a mix-and match fashion, like building an outfit from a closet with a few pairs of pants and a few shirts.  Add in some messiness in cutting out the specific sequences, and you have a fair bit of diversity in receptor sequences possible from a single genome.

Later, once a B-cell or T-cell meets a matching antigen, the cell multiplies, and each descendant cell is subject to somatic hypermutation, in the hopes that one of the tweaked sequences will better match the antigen.

But none of that is going to be very evolutionary relevant, since only mutations in gametes or gamete stem cells are passed on to the next generation.


Is DNA a single molecule or 46 separate pieces (out of 23 chromosome pairs)?

Unbroken strands of DNA are single molecules. So Yes, DNA is a molecule. However, the sequence of nucleotides allow for a near infinite variety. So unlike other molecules, like collagen, or water, they cannot be characterized with a unique descriptive name, other than by their sequence. I think this is the cause for confusion, because in this sense, DNA is a class of molecules, and we don't generally give them names. Each chromosome has two unique DNA molecules in diploid organisms (except in rare cases of highly inbred individuals where the two molecules might be identical). So if you have 23 chromosomes, you have 46 DNA molecules in each cell nucleus.


Workers cannot become "queens" because the development of a larvae into a worker or a queen happens during the larval stage, depending mainly on the food that the larvae is given. That being said, once the queen is removed from a colony, in many ant and other social hymenopteran species, workers are no longer inhibited by the pheromones produced by the queens that prevent the growth of the worker's ovaries. So in some species, removing the queen can lead to workers laying eggs but these will most often be parthenogenetic and lead to the production of males only. In a very few species, workers can produce female eggs by parthenogenesis or mate with males after the removal of the queen. Such traits are usually associated with large body size and small colony size, so they are unlikely to be the ones you have in buildings.

  Bourke, A. F. (1988). Worker reproduction in the higher eusocial
  Hymenoptera. The Quarterly Review of Biology, 63(3), 291-311.

  Page, R. E., & Erickson, E. H. (1988). Reproduction by worker honey
  bees (Apis mellifera L.). Behavioral Ecology and Sociobiology, 23(2),
  117-126.

  Wenseleers, T., Helanterä, H., Hart, A., & Ratnieks, F. L. (2004).
  Worker reproduction and policing in insect societies: an ESS analysis.
  Journal of evolutionary biology, 17(5), 1035-1047.


What is the most common way of administering loop diuretics and what is their time course of action?

I know that furosemide (there are more types of loop diuretics) can be given intravenously (but can be orally given as well (furosemide info sheet)). Effects of i.v. furosemide are pretty much immediate as it is carried quickly to the kidneys via the blood. After i.v. administration the effects wear off in about half an hour. t1/2 is about 2 hours, but likely depending on route of administration.


From what I can tell, marine mammals can't dynamically control buoyancy during a dive. They ease the beginning of the dive by starting with a small lung volume to reduce buoyancy.

Pinnipeds like seals do this by exhaling half their breath before diving.

Deep-diving whales actually breathe in before diving, but their lungs are small relative to body size to begin with. This makes their surface buoyancy weak enough to swim against without great difficulty (unlike humans).

As they dive their lungs compress rapidly with depth:

V = Vs / (1 + D/10)

V is lung volume, Vs is lung volume at surface, and D is depth in meters.

At 90m, the lungs are already at 10% original volume. Pretty soon they've shrunk enough that their effect on buoyancy is negligible compared to the density of the incompressible tissues. Presumably, these are close to neutrally buoyant (though the fact that dead whales sink suggests that they're slightly negatively buoyant).

Thanks to @souvik-bhattacharya for the ucsc.edu link.


Was lactose present in the environment before the evolution of mammals?

Preamble

This is an answer to the motivation expressed in the question:

  “…whether lactose-utilising enzymes in bacteria evolved only after the appearance of mammals”

rather than that in the title. The presence or absence of lactose elsewhere in Nature will not decide this question.

Answer

The name lactase is applied to the mammalian enzyme that is able to catalyse the hydrolysis of the disaccharide, lactose, to glucose and galactose, allowing the digestion of this milk sugar by the suckling infant. However bacterial and plant enzymes that are normally referred to as β-galactosidases can also catalyse the same reaction.

The role of the β-galactosidases in bacteria such as Lactobacillus lactis that are found in a dairy environment may well be to hydrolyse milk lactose, as may be that of Escherichia coli, found in the human gut. However this is unlikely to be generally true for all bacteria. This is because β-galactosidases are found in a wide spectrum of bacteria, including extremophiles† which cannot possibly have had access to milk lactose.

β-galactosidases are generally members of a group of enzymes termed glycoside hydrolases and have been categorized into a number of families on the basis of sequence similarity. The enzymes in these families differ in their substrate specificity. To explain the existence of such enzymes in bacteria which do not have access to lactase it has been suggested that their natural substrates may be other disaccharides. This is actually the subject of a PhD Thesis by S.A. Shipkowski, who suggests that some β-galactosidases may actually hydrolyse β-1,4 galactobiose:

The significance of this is that the polysaccharide, pectin, found in certain plant cell walls, could be broken down by by other enzymes in the bacteria, yielding galactobiose.

Conclusion

Although the β-galactosidase in certain bacteria may be optimized to hydrolyse milk lactose, the gene encoding it is almost certainly derived from an ancestral glycoside hydrolases gene, the product of which predated the appearance of mammals and was used to hydrolyse other disaccharides derived from polysaccharides originating from various sources.

† It should be emphasized that the β-galactosidase from extreme thermophiles such as Thermus thermophilus KNOUC114 — isolated from a hot spring — hydrolyses lactose well. Indeed, its thermostablity has attracted interest in its development for use in the food industry (Ahn et al. 2012).


Theoretical Rules Governing Life in the Universe

On Earth, many animals only have one locomotory organ (such as the tail of a fish or a legless lizard). Some have five limbs (starfish). It just happens that the presently dominant group of large animals has bilateral symmetry (a distinct head and tail, underside and back, and medial and lateral, but usually no left and right distinction, except in internal organs), and hence often has paired anatomical features.


Evolution: One big population vs. many small populations

Note: This is not an area where I know the litterature well

Where are many counteracting processes to consider for this question. For instance, the rate of evolution will be affected by the rate of mutation, the distribution of positive and deleterious mutations, strength of selection, whether the fitness effects are small or large, if fitness effects depend on interactions between multiple mutations or single mutations with large effect, asexual vs. sexual populations, and processes such as genetic drift.

A recent review that is useful for your question is Lanfear et al (2014). They focus on how substitution rate is affected by effective population size, and go through both theoretical and empirical evidence. They conclude that in most cases, most mutations are deleterious, and that drift and selection are the most important effects in determining rates of evolution. They also state the effect of effective population size (Ne) is likely to depend if mutations are dominated by deleterious or advantagious mutations, and they expect the rate of evolution to be negatively correlated with Ne when deletious mutations dominate evolution and a positive correlation to Ne when advantagious mutations dominate.

A paper by Rozen et al (2008) indicates that while large populations are more effective in fixing mutations with large positive effects, small populations can be more effective in complex "rugged" adaptive landscapes.

  While such determinism speeds adaptation on the smooth adaptive landscape represented by the simple environment, it can limit the ability of large populations from effectively exploring the underlying topography of rugged adaptive landscapes characterized by complex environments.

However, this does not deal directly with the rate of evolution, but mostly about attaining the highest possible fitness in a particular fitness landscape. Another interesting paper is Desai et al. (2007), but I haven't looked through this yet.  However, they find (for asexual bacteria) that the speed of adaptation scales less than linearly with population size, and similar results have also been found in studies from Lenski's group. Their interpretation is that evolution is driven by multiple concurrent mutations of small effect and not one-by-one fixation of single mutations (which would favour large populations more).

For your case of evolution of resistance, I think one crucial thing is if you expect resistance to be driven by a few single mutations or combinations of many mutations that interact (related to whether resistance is "easy" or "hard" to evolve). From what I understand, the first case should favour a single large population (since they will fix mutations for resistance more quickly), while the second case might favour many smaller populations (since you might get more effective exploration of combinations of mutations)

These are just a few starting points in a very large field, and I hope that you find them useful.


What's the difference between reading and synthesizing RNA?

What's the difference between reading and writing a book? Synthesizing RNA means producing an RNA based on a sequence in DNA. Reading it means processing RNA that is already produced. Reading also implies that protein will be produced based on the sequence in RNA.

  What's the difference between synthesizing and transcribing?

"Synthesize" means to produce any chemical molecule. "Transcribe" is specifically the synthesis of RNA form DNA via a polymerase (as opposed to for instance inorganic synthesis of RNA de novo, as might be done in a chemistry lab).

  Didn't this just contradict sentence 2?

It's just saying that genes can be oriented forward or in reverse. Reverse genes are on the opposite strand, so they are still 5' to 3' (the 5' ends of the two strands are on opposite ends of the DNA). But every gene must still have a promoter on its 5' side.

And actually, that bit is not quite true: There are bidirectional promoters that will cause transcription in both directions.

  If RNA polymerase is recruited at a site to and directed to "move along" the DNA, what is it doing when it "moves along" (reading? synthesizing? transcribing? wtf?).

Usually, it will transcribe (so it will also synthesize, or "read"). But technically, RNA pols belong to a family of proteins which are "molecular motors", meaning that their fundamental activity is to move along DNA step by step like a little monkey climbing a ladder. With RNA pols, RNA synthesis is coupled to this movement, so each step on DNA also causes a letter to be added to the RNA they are making.

Also, technically the RNA pol is not only moving and making DNA, but also unwinding the two strands of DNA and separating them. But this may be outside the scope of your material.

  My understanding is this is the "transcribed strand", not the "coding strand" of DNA, correct?

RNA comes out matching the sequence of the gene (except for T->U), and it is assembled through basepairing to DNA. If it paired with the strand the gene is on, the RNA would come out as the reverse complement of the gene. Instead it is assembled on the opposite strand, which is already the RC of the gene. RC of RC of a sequence is the same sequence. Thus we say RNA is transcribed from the "non-coding" strand, but keep in mind that these coding/non-coding assignments are arbitrary and only used by us humans, the cell does not have a special marking for it (beyond the 5'/3').

  I don't understand this paragraph and the more I read it, the more confused I get. Could someone please clarify (preferable with visuals)?

It's very simple: DNA is a directed (because of 5'/3') string of ACTG. It is coupled to another, complementary string that runs opposite to it. The sequence on either strand may be meaningless, or parts of it may encode genes. Genes consist of a promoter, some sequence, and terminator. RNA pols can slide along either strand, but only in 5' to 3' direction, so they will slide in opposite directions on opposite strands, like cars on a two way street. When RNA pol encounters a promoter, it starts synthesizing an RNA: It separates the two strands, and lets single RNTPs basepair with the opposite-direction strand, when they do so it glues their phosphate backbones together. It keeps sliding and making RNA like this until it reaches another sequence, the terminator, at which point it stops assembling RNA and releases it. The RNA snaps off DNA and goes off on its merry way, the two strands of the DNA that were separated by RNA pol come together again.

Thus for every promoter-terminator pair, whatever sequence is in between them will be transcribed into an RNA. These are basically genes. These genes may be on either strand of DNA, and they must always be oriented along the 5' to 3' of the strand they are on. Thus genes on opposite strands will appear "reversed" with respect to each other.


As I understand from your post, the computer virus you are talking about is modifying database (FASTA files) in genetics. That would have a pretty bad impact on research in genetics and medicine.

If one uses such a database to synthesize/edit sequences and then introduce this DNA into a living organism, then yes the computer virus would have affected a living organism. If the sequence the computer virus has introduced is able to be transcribed into mRNA and go on infecting other cells, and eventually spread, then I guess one could say that the computer virus would have become an actual virus.

However, two things are to be considered. First, I very much doubt such a thing could go unnoticed. Second, anyone could have fun and create novel sequences. The only thing the virus does is corrupting files in a computer. The eventual existence of a man-made virus has no specific relationship with the computer virus and doing too much analogy here would stand little meaning.


Why isn't photosynthesis catabolic reaction?

Catabolic reactions are those that make larger/more complex molecules into those that are smaller/less complex, releasing energy.

Anabolic reactions are those that makes smaller/less complex molecules into those that are larger/more complex, costing energy.

Photosynthesis takes two of the least complex molecules from the perspective of biology, carbon dioxide and water, and forms glucose which is high-energy and complex - this is clearly an anabolic reaction.

The only way I can interpret your question is that you were misunderstanding the definitions of catabolic and anabolic.


Concept of species

First have a look at How could humans have interbred with Neanderthals if we're a different species? to better understand the concept of species.

I will assume that you are using the "biological species definition" which is based on reproductive isolation.

  Can any organism possibly have the capability to create a new species every time it reproduces?

The question is mainly non-sense. In short, if it is true that all offspring are a new species, it means that by definition the lineage is asexual and then the concept of species is typically considered to be of little interest. Let's consider both asexual and sexual lineages separately to maybe clarify what I mean.

Asexual lineages

For exclusively asexually reproducing lineages, either we decide the question makes no sense because the concept of species does not apply to them. Or we decide the concept of species applies and then every individual is necessarily a new species. So, yes, by definition there is no exclusively asexually reproducing lineages where a new species isn't created at every reproductive event.

Sexual lineages

For sexual lineages, the question would make no sense either as if it was the case that every individual was it's own species, then the lineage would be asexual!


When endothelial cells in blood vessels (arteries or veins) are damaged, does atheroma form first or blood clot?

It is unlikely that atheroma would develop as a complication of a thrombus.

Atherosclerosis and thrombosis are two independent disorders and not two stages of the same disorder. Atherosclerosis is a disorder of the arterial wall and atheroma develops in the arterial wall. Thrombosis is a disorder of the blood and thrombus is merely attached to the atheroma or arterial or vein wall.

In veins, only thrombosis, but not atherosclerosis can occur, as mentioned here.

In arteries, thrombosis usually occurs only as a complication of an atheroma or calcification (PubMed, 2017):

  The majority of coronary thrombi are caused by plaque rupture
  (55–65%), followed by [plaque] erosions (30–35%), and least frequently
  from calcified nodules (2–7%).

It is very rare that thrombus develops in arteries that have previously not been damaged by atherosclerosis (PubMed, 2015).

Further evidence that thrombus formation is an unlikely initial event in the development of an atherosclerotic plaque:

Thrombosis is not mentioned as an initial stage or risk factor in development of atherosclerosis in various texts: Textbookofcardiology.org, Pathophys.org
Genetic coagulation disorders are not likely risk factors for atherosclerosis (Atherosclerosis, Table 2 (PubMed, 2010):


How and where, in the human brain, are memories stored?

Unfortunately, we are all still "confuzzled" by how memory works. We are far from a complete understanding of how memory is stored and recalled. Nonetheless, we do know a little, so read on.

Your understanding of basic neural function is almost correct. First, an individual neuron will signal through its single axon onto the dendrites of many downstream neurons, not the other way around. Second, I am not sure what you mean by "focusing them based on their permutations," but it is true that neural information can undergo many transformations as it propagates through a circuit. Third, if there is a behavioral outcome of the network activity like a muscle response or hormone release, those effects are mediated by nerves communicating with muscles and hormone-releasing cells. I'm not sure if that is what you meant by "focused response mechanism."

Finally, as you have discovered, the analogy of neural circuits to electrical circuits is relatively poor at any reasonably sophisticated level of analysis. My opinion is that biological systems are often poorly served by being framed as engineering problems. Others will disagree with that, but I think understanding a biological system on its own terms makes many things much clearer.

The key thing missing from the electrical circuit analogy turns out to be one of the keys to understanding information storage in neural circuits--the synapse, the site where one neuron communicates with another. The synapse transforms the electrical signal from the upstream neuron into a chemical signal. That chemical signal is then converted back into an electrical signal by the downstream neuron.

The strength of the synapse can be adjusted in a long-term way by changing the level of protein expression--this is called long-term potentiation (LTP) or long-term depression (LTD). LTP and LTD therefore can regulate the ease with which information can flow along a particular path. As a basic example (that should not be taken too seriously), imagine a set of neurons that represents "New York City" and another set of neurons that represents "My Friend John." If you then happen to be in New York City with your friend John, both of those groups of neurons will be active and synapses between these two networks will be strengthened because they are co-active (see Hebbian plasticity). In this way, the idea of NYC and the idea of John are now bound together.

Where are these neurons that represent NYC and John? We are still not totally clear on this, and the question is complicated because there are many different types of memory. For instance, your memory of how to ride a bike (procedural memory) is not treated the same as your memory of what you ate for breakfast (episodic memory). However, a best current answer is that the hippocampus and its associated regions are important for the initial encoding of memories and the neocortex is where longer term memories are stored. There is substantial communication between these two areas so that memories can be effectively adjusted over time.

Update

In response to Jule's comment asking for some resources, I realize it is important to make the point that the Hebbian model I outlined hasn't been definitively shown. Like with all aspects of neuroscience, there is a lot of good work at the molecular and cellular level and good work at the behavioral level, but the causal link between the two is not so clear. Nonetheless, Hebb's idea is still the mainstream working model for how memory works. Some reading might include:

1) Neves, G., Cooke, S.F., Bliss, T.V.P., 2008. Synaptic plasticity, memory and the hippocampus: a neural network approach to causality. Nature Reviews Neuroscience 9, 65–75.
 A review on hippocampal memory and its relation to LTP/LTD and Hebbian theory. Notes the general difficulty of proving the theory and some ways for experiments to move forward.

2) Lisman, J., Grace, A.A., Duzel, E., 2011. A neoHebbian framework for episodic memory; role of dopamine-dependent late LTP. Trends in Neurosciences 34, 536–547.
 A review proposing an elaboration of the Hebbian model that includes neuromodulatory influence on plasticity and memory process.

3) Johansen, J.P., Cain, C.K., Ostroff, L.E., LeDoux, J.E., 2011. Molecular Mechanisms of Fear Learning and Memory. Cell 147, 509–524.. An excellent review on fear learning and memory with an extensive section on Hebbian theory.

4) Liu, X., Ramirez, S., Pang, P.T., Puryear, C.B., Govindarajan, A., Deisseroth, K., Tonegawa, S., 2012. Optogenetic stimulation of a hippocampal engram activates fear memory recall. Nature. A research article which is perhaps a realization of some of suggestions in the Neves et al review. They use light to reactivate a fear memory. This suggests that activation of the hippocampal network that was active during memory formation is sufficient to elicit the memory.


Your confusion is caused by the assumption that Na+ always leaves the cell and K+ always enters. The Na+/K+ pump is there to maintain membrane potential and relative Na+ and K+ ion concentrations stable inside. When an action potential (AP) is generated, sodium channels open and sodium rushes inside to depolarize the cell( 1st phase of AP). Next, the sodium channels close and K+ begins to leave the cell (since the inside of the cell contains too many positive charges and the cell would remain depolarized if nothing was changed). Potassium leaves through leak channels. So in summary, Na+/K+ pump and the channels that are part of AP generation result in different movement of Na+ and K+ across the cell membrane.

Here is a nice review of Na+/K+ pump and action potential generation.
https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/v/sodium-potassium-pump


Does increased cell turnover cause cancerous mutations?

Increased cell turnover indirectly leads to cancer. Below is a direct quote from Human Molecular Genetics, 2ed. Chapter 9: Instability of the human genome: mutation and DNA repair.

Mutations can be induced in our DNA by exposure to a variety of mutagens occurring in our external environment or to mutagens generated in the intracellular environment. In the case of radiation-induced mutation, for example, Dubrova et al. 1996 reported that the normal germline mutation rate for hypervariable minisatellite loci was doubled as a consequence of heavy exposure to the radiaoctive fallout from the Chernobyl accident. However, under normal circumstances by far the greatest source of mutations is from endogenous mutation, notably spontaneous errors in DNA replication and repair. During an average human lifetime there are an estimated 10^17 cell divisions: about 2 × 10^14 divisions are required to generate the approximately 10^14 cells in the adult, and additional mitoses are required to permit cell renewal in the case of certain cell types, notably epithelial cells (see Cairns, 1975). As each cell division requires the incorporation of 6 × 10^9 new nucleotides, error-free DNA replication in an average lifetime would require a DNA replication-repair process with an accuracy great enough so that the correct nucleotide was inserted on the growing DNA strands on each of about 6 × 10^26 occasions.
Such a level of DNA replication fidelity is impossible to sustain; indeed, the observed fidelity of replication of DNA polymerases is very much less than this and uncorrected replication errors occur with a frequency of about 10^-9 to 10^-11 per incorporated nucleotide (see Cooper et al., 1995). As the coding DNA of an average human gene is about 1.7 kb, coding DNA mutations will occur spontaneously with an average frequency of about 1.7 × 10^-6 -1.7 × 10^-8 per gene per cell division. Thus, during the approximately 10^16 mitoses undergone in an average human lifetime, each gene will be a locus for about 10^8-10^10 mutations (but for any one gene, only a tiny minority of cells will carry a mutation). In many cases, a deleterious gene mutation in a somatic cell will be inconsequential: the mutation may cause lethality for that single cell, but will not have consequences for other cells. However, in some cases, the mutation may lead to an inappropriate continuation of cell division, causing cancer (see Chapter 18).

Here is another great paper that specifically addresses your question, linking increased cell division with the accumulation of both significant and insignificant mutations, which over time, lead to an accumulation of mutations needed for cancer to develop.


Can suppression of the immune system help cure chronic diseases?

No, this wouldn't happen. The logic of your proposition assumes that chronic diseases are caused by the strength of the immune response being insufficient to kill off the virus, resulting in a long-term equilibrium between the amount of virus particles produced and the amount of virus particles killed.

In reality, this is not how chronic diseases work. Only a small amount of chronic diseases are caused by viruses. There are many which have other causes, not all of which can be defended against by the immune system - e.g. chronic depression is not curable by immune response.

But even if we focus on chronic virus infections such as herpes simplex, they are not sustained by the mechanism you describe. They happen due to the fact that our immune system simply does not know how to get them out of their new home within our body, they are just that good at hiding during latency. So even if you could cause a strong immune response all at once, it wouldn't kill all viruses at once.

Even if we have viruses whose serum presence depends on a constant growth vs. destruction dynamic (I don't know if these exist at all), an overly strong immune response won't be that good for the human host. Inflammation is a dangerous state, most of the unpleasant feeling you get when you are sick is not due to the virus itself but due to your own immune response, which causes the fever, muscle pains etc. associated with many acute infectious diseases. If we were to ramp this up, you'd probably get a fever high enough to cook you alive, or some other undesirable effects.

On a side note, I also doubt the author's argument which suggests that long-ish convalescence times evolved because shorter ones would leave the system in an undesirable equilibrium. Sure, an alternative reality is thinkable where the innate and adaptive responses described by Chris occur much stronger at the beginning, leading to steeper curves and shorter healing times. But the simpler explanation for that is that 1) our immune system is not perfect, and it evolved to the highest healing speed it could achieve, and 2) an immune system with higher acceleration would have been way too costly in terms of resources available to the body. An evolutionary advantage in having a low-acceleration immune system is a strong assumption for which I see no support, especially considering that the residual immunity provided by the adaptive immune system would prevent the dynamic equilibrium suggested in your quote.


About how many covid-19 virus particles is required in the human body before infection and sickness follows?

To the best of my knowledge, we don't yet know the infectious dose of the SAR-COV-2 virus in humans. In theory, it only takes one viulent virus particle to start an infection. In practice, it's pretty hard to measure, Published estimates of infectious dose for any pathogen don't often account for differences in age or sex, per se, so it's hard to address that part of your question.
Most of the estimates of SARS-CoV-2 infectious dose I've seen are essentially experts handwaving based on previous coronavirus outbreaks. I'm not saying they're useless, but they aren't necessarily empirical. For reference, there's a perspective article here, with a section discussing infectious dose. They cite an estimate from the 2003 SARS outbreak of 280 particles to cause infection in 50% of the exposed population (ID50). They also point out that this is similar to the ID50 for other animal corona viruses and the common cold in humans.
There's no guarantee that SARS-CoV-2 will be the same, but it's likely to be in the same ballpark.
Referenced:
Imke Schröder, J Chem Health Saf. 2020 May 11 : acs.chas.0c00035. Accessed via PubMed Central, PMCID: PMC7216769


What is the most condensed form of (stored) energy used in biology?

The best ratio between weight and energy content (and of course also stability) has indeed fat. It's energy content is more than twice as high as for carbohydrates (sugars).
See this table from here on the energy contents:

This is the reason why animals which hibernate or migrate fed up to build up fat resources before the winter or their journey. With carbohydrates they would need more than the double amount of stored carbohydrates to get the same energy. Proteins are approximately on the same level as carbohydrates.

If you look on this problem not by energy per mass but volume per mass, fat still wins. For this we need the density of protein (muscles in this case) and fat. Paper 1 (see reference below) say that the human muscles have an average density of 1.06g/cm³. Paper 2 lists a density of 0.92g/cm³ for fat. So fats (this is practically only valid for the human body, but should be in the same range for other animals) are about 15% less dense than muscles. As the energy density per weight is about double as high for fat, this compensates for the lower density.

Carbohydrates are better, but are still not as good as fat. It's a bit hard to find specific densities for carbohydrates in the human body, so let's use Glycogen (which is a widely found carbohydrate used for mid-term storage of energy) for this purpose. Paper 3 lists a density for Glycogen between 1.40–1.62 g/cm³, so fat has only 55-65% of it's density. Since the energy density of fat is about 2.25x that of carbohydrates, fat is still better.

If you look at ATP in comparison, it has relatively little energy to provide. ATP delivers about 32.3 kJ/mole (with 507.18 g/mole this make around 64 J/gram) per phosphate released from the molecule, which is 128 J/gram if both phosphates are released. This is approximately 300x less energy per gram than fat. This makes sense, since fats are completely oxidized (down to water and carbon dioxide), while in ATP only the phosphate bonds are broken. ATP acts as an energy carrier in the body and not as an energy storage molecule.

References:

Specific Force Deficit in Skeletal Muscles of Old Rats Is Partially
Explained by the Existence of Denervated Muscle Fibers
Association of adiponectin and resistin with adipose tissue
compartments, insulin resistance and dyslipidaemia
Shifts in the Distribution of Mass Densities Is a Signature of
Caloric Restriction in Caenorhabditis elegans


Is there differences in components of saliva among species

It could be better answered if you specified which species you were interested in. Broadly from Wikipedia, snakes have venom, some swifts have gummy saliva to help in the building of nests, spiders produce their web from salivary glands etc. This is too broad a topic. The human salivary composition is found on the Wikipedia page I have linked. Salivary compositions can change with habits which have been detailed in this article. To compare, I am also providing the link to an article on the saliva composition of an assassin bug.


Are ape communities more "anarchist" or "communist" in structure?

Among the great apes, chimpanzees and gorillas live in very hierarchical, male-dominated clans that are often in violent conflict with other clans. Bonobos, on the other hand, lead very peaceful lives, and are female-dominated, using sexual contact as a manner of communication to reduce tension within and between groups. Orangutans are largely solitary animals, with heavy parental investment (7 years, longest among non-human primates), wherein the mother lives separately with her child during the early years of development. Among the lesser apes, gibbons and siamangs are also highly territorial and pair-bonded, though notably, polyandrous siamang groups have been shown to display higher degrees of cooperation.

Though Anarchism varies greatly between different definitions, the most popular form of contemporary Anarchism values non-hierarchical organization, centered around mutual aid, rather than the kind of isolated individualism that you seem to associate with the term. By this definition, bonobos would be more "Anarchist" than chimpanzees. By your definition, orangutans might be the most "Anarchist."

Your definition of "Communism" is closer to the contemporary definition of Anarchism above, due mainly to the historical trajectory of Communism, which in practice, did not work out so well, leaving contemporary utopian thinkers largely in the Anarchist camp. By your definition of "Communism," bonobos may be the most "Communist"; however, if you mean the state-based gulag Communism of popular culture (ie portrayals of the Soviet Union), then you might say that chimps were more Communist. This is because individual chimps sacrifice individual goal attainment for group ends under the coercion of the alpha male chimp. Of course, some people may call that Fascism.

You may want to take a look at primatologist Franz De Waal's research on bonobos vs. chimpanzees. As a pacifist, he has a bit of an agenda, in terms of trying to prove that female-dominated bonobo "societies" are inherently more cooperative and less hierarchical. Another primatologist that agrees with this view is Harvard primatologist Richard Wrangham, who looks at hierarchical organization and violent behaviors in chimpanzees.

Robert Sapolsky's research on baboons may also be of interest to you. He found a clan of baboons, in which all the alpha males had died from tuberculosis due to exposure to an infected meat found in a neighboring human village. He noted, then, that the remaining baboons lived much more peaceably and cooperatively than other observed clans, and furthermore, that this clan retained its "culture" and passed on its more cooperative ways of behaving to new members in the clan, therefore demonstrating that perhaps baboons (and other primates) are capable of having and passing on "culture." - Perhaps a more "Anarchist" culture than nature normally prescribes.

However, as a caveat, I must say: it is tenuous to make direct associations between ape behavior and human societies. Human culture, social intelligence, and symbolic reasoning facilitate human political systems. Though Sapolsky's work suggests primates may also be capable of some form of "culture," biological descriptions of ape social organization is insufficient to explain human behavior.


What is this pink-flowering plant found in Shanghai, China in March?

I think this is the Chinese Redbud (Cercis chinensis), see this image (from here):


(About the tectospinal tract) the tectospinales fibers originate in the superior colliculus, its axons pass ventromedially by the central gray matter and cross in the posterior tegmental decussation. The upper colliculus receives visual information, and the tectospinal tract is believed to act as a mediator of reflex eye movements in response to visual stimuli (Neuroanatomy of Crossman and Neary pg 81).

A relatively small number of fibers leave the optic tract, before reaching the dorsal nucleus of the lateral geniculate body, to terminate in the pretectal area and superior colliculus (fibers involved in pupillary reflex mediation) (Neuroanatomy of Crossman and Neary pg 157).


Why sigmoid curves appear in quantitative analysis of many biological phenomena?

I would suggest following: take any one-dimensional process that is described by gaussian function. If you integrate such process along variable, you will get a sigmoidal curve. For details see normal and cumulative distribution.

Now, the question is: how many biological processes are described/modeled by Gaussian distribution and dependencies? A lot!

Let's take a look at dinosaur growth from Revisiting the Estimation of Dinosaur Growth Rates

This figure describes how size of dinosaur changes with some time (model, I assume). Remember link between gaussian and sigmoidal functions? If you differentiate, that is find how fast aforementioned sigmoidal function changes, you will get gaussian bell-curve! Which tells you: dinosaur grows faster during middle age, and slower before and after that.

DNA denaturation curve is sigmoidal because efficiency of denaturation is again gaussian. At low temperatures very limited amount of molecules will denature, but at high temperature there are no more molecules to denaturate left, so the bell-curve. Anothe explanation goes like that: at low temperature additional heat doesn't change much because it is still too "cold", at higher temperature same amount of heat is just a drop in a bucket, barely noticeable.


Why do cells have an average 'life span'

We refer to the number of times the cells of an organism can possibly divide as the Hayflick limit for that organism. The Hayflick limit serves as a theoretical life span, because telomeres (on the ends of chromosomes) get slightly shorter with each round of division, until they are gone completely. Telomeres are put on the ends of chromosomes by the enzyme telomerase, which is abundant in infants (who are growing and undergoing rapid mitotic divisions) but bodily abundance of the enzyme quickly diminishes with age. Without telomeres, our actual chromosomes would shorten in length during each round of division -- essentially, this is what happens after the telomeres are eroded away at in the later years of life. The Hayflick limit for humans is given to be 120 years -- with perfect self-care, 120 years of life is possible.


Yes, you nailed it!

Adam's apple (aka.  laryngeal prominence) exist in both men and women. It is a piece of bony cartilage called thyroid cartilage that wraps around the larynx (aka. voice box).

The Adam's apple is more prominent in males because males have have a bigger larynx (giving males a deeper voice). In males, the prominent Adam's apple typically appears during adolescence, when the larynx increases in size and the voice becomes deeper.


It probably makes sense to classify mushrooms (fungi) in two separate ways:

symbiotic vs. free-living: symbiotic organisms are those that live in close association with a host (etymologically sym="with", biosis="life"), free-living organisms don't.  So a mycorrhizal fungus that lives within or on the surface of a plant root is a symbiote; a fungus that lives in the soil is free-living.
mutualistic (benefiting from and benefiting a host) vs. parasitic (benefiting from but harming a host) vs. saprotrophic (consuming already-dead material; these are your "decomposers"). (Commensalism [benefiting from, but neither hurting nor harming, a host] is  a fourth possibility.) Mycorrhizal fungi are generally mutualistic. Fungi like chestnut blight or the genus of phythophthora, which includes the organism that causes potato blight, are pathogens; so are the myco-heterotrophs. Fungi such as wood-decay fungi are saprophytic.

To answer your question, species of fungi that are associated with trees may be either mutualistic (e.g. mycorrhizal fungi) or parasitic (e.g. chestnut blight).

Parasitic fungi might also be called pathogenic (i.e., disease-causing)
In popular speech, "symbiotic" is synonymous with "mutualistic" (i.e., organisms that benefit each other); in biology, however, it may refer to either a parasitic or a mutualistic organism. An individual symbiotic organism is often called a "symbiont".
In general, saprotrophs would be free-living (since they don't get their resources from a host, it doesn't really make sense for them to live on a host)
Individuals of a some fungal species can switch lifestyles/categories depending on their environment: these are called facultatively mutualistic/commensal/parasitic, e.g. see Redman et al. 2001.

Redman, Regina S., David D. Dunigan, and Rusty J. Rodriguez. “Fungal Symbiosis from Mutualism to Parasitism: Who Controls the Outcome, Host or Invader?” New Phytologist 151, no. 3 (2001): 705–16. https://doi.org/10.1046/j.0028-646x.2001.00210.x.


Can an infectious diseases come from a plant?

This is a great biological question! I'm glad we encourage such questions from curious people who want to learn more about modern biology.
Much as other animals can be vectors for diseases that infect humans, plants can be vectors for pathogenic infectious agents.
You may occasionally read news stories of disease-causing strains of Escherichia coli which contaminate vegetables and force product recalls. There is currently a CDC advisory to not eat clover sprouts, as an example, because of contamination with E. coli O103, a strain which can cause a variety of health problems (including kidney damage, in severe cases).
This kind of contamination is becoming more common, largely as a consequence of how we produce food:

Fresh fruits and vegetables once were thought to be relatively free of disease-producing pathogens. In recent years, however, outbreaks of foodborne illness linked to fruits and vegetables have become more common. These outbreaks come from produce grown both in the United States and in other countries. Outbreaks have been linked to Escherichia coli O157:H7 and Salmonella on apples, lettuce, cantaloupe and sprouts; Listeria monocytogenes on cabbage and cantaloupe; Shigella on parsley and lettuce; and Cyclospora on imported raspberries.
Changes in microorganisms have undoubtedly contributed to this increase, as have changes in growing, harvesting, distribution, processing and consumption practices. Listeria monocytogenes, Clostridium botulinum and Bacillus cereus are naturally present in some soils. Their presence on fresh produce is not uncommon. Salmonella, E. coli O157:H7, Campylobacter jejuni, Vibrio cholerae, parasites and viruses can contaminate produce through raw or improperly composted manure, irrigation water containing untreated sewage or manure, and contaminated wash water. Contact with mammals, reptiles, fowl, insects and unpasteurized animal products are other sources of contamination.

Wash your fruits and veggies!


How many proteins are in the Earth's proteome?

Current records
According to Uniprot, there are 85,381,808 protein records, and with the UniRef90 filter (i.e removing records that can be represented by an entry with at least 90% sequence similarity), there are 42,424,511. However, these databases are moving targets and will change over time. We will sequence more species, find novel splice isoforms, and various other methods will expand the databases. Indeed, the databases will be truncated also from time to time as some hypothetical proteins may be based on genes that turn out to not code for proteins after all.
In 2007, a study estimated that the earth's proteome would contain around 5 million sequences, and that the majority of these would be elucidated by 2012. I suspect this is a very thorough study, however, a lot has changed in the last 10 years. This estimate is actually less than the nearly 9 million species estimated in more recent studies.
Approximate estimate
So let's do some back of the envelope maths. Let's assume the article estimating nearly 9 million species is about right, and that we've only catalogued some 1.2 million. But UniProt isn't even close to this number.UniProt contains 25477 scientific names in it's controlled vocabulary. So for 25 thousand names, we have 85 million protein records. What if we had 8.75 million names?
Let's assume:
$\frac{Predicted~Proteins}{Predicted~Species}=\frac{Known~Proteins}{Known~Species}$
We can rearrange this to:
$\frac{Predicted~Species~\times~{Known~Proteins}}{Known~Species}= Predicted~Proteins$
Generous estimate (Uniprot, 335527 proteins per species):
$\frac{8750000\times{85381808}}{25477}=2.932413e^{+10}$
Conservative estimate (Swissprot, 41 proteins per species):
$\frac{8750000\times{554241}}{13408}=3.616952e^{+7}$
For the sake of completeness let's assume the number of <90% identical proteins will remain around half that value. We can say that there might be around $1.8e^{+7}$ to $1.5{e}^{+10}$ "unique" proteins, less than a trillion ($1e^{+12}$). Given the absurdly generous 335 thousand proteins and very stingy 41 proteins per species, we can be fairly certain that if there are indeed 8.75 million species, the number of proteins will fall between those estimates.
The biggest assumption here is that the proteins have a linear relationship with species which is unlikely to be the case, and at the generous estimate we are pretending that there are no proteins in UniProt that don't have species annotation. As for Swissprot, this only includes proteins that have been manually curated, so this ignores many proteins that are safe to assume exist and typically only covers proteins that are of interest to scientists.

A minor correction to your question, the UniProt lists ~20 thousand protein coding genes in the human proteome, not millions. Those protein coding genes are subject to various post translational modifications and isoform splicing, so there will be more final proteins than 20k.


In this context crude means naturally occurring or unrefined.

Purified trypsin alone, for example, is usually ineffective for tissue dissociation since it shows little selectivity for extracellular proteins.

Source: Worthington Tissue Dissociation Guide


Is it known how human sweat glands evolved?

I am not sure exactly what you are after when asking "how did these glands came?". It seems that you wrongly believe that similar glands do not exist in other primates. Here is a short answer that will help you to search for more information about the evolution of these glands.

Chimpanzees and Gorilla also have sweat glands. The use of sweat gland in thermoregulation is however quite unique to humans and is thought to have evolved in parallel of hair loss and bipedism. See The evolution of sweat glands (Fold and Semken 1991) for more information.


Changing genetic code of E. coli to accept synthetic amino acids?

This has been done by engineering a synthetic tRNA that can recognize the stop codon. The synthetic tRNA possesses a non-natural amino acid that is processed normally by the Ribosome and incorporated into the growing polypeptide chain.


How long does antibiotic-dosed LB maintain good selection?

This Bitesize Bio article is very informative on this issue.  The 1970 study they cite found negligible reduction in the the efficacy of non-beta-lactam antibiotics (kanamycin, chloramphenicol) over spans of 4 weeks or 60 days.  Ampicillin loses about 10% activity at 4 weeks.

In my lab, we only take care not to use LB/Amp plates that are older then 4 weeks, for LB/Km, we store them at 4 °C for more then a month, sealed in a plastic bag.


Humans, unlike cows for ex. don't have the necessary bacteria in their intestines that make the enzymes(cellulases) necessary to breakdown the 1-4 beta glucose bonds. So we cannot break down cellulose into its constituent glucose molecules as we do with starch. Therefore this is secreted as unbroken down chains of glucose called fiber.


Is the barcode COI sequence the sense or antisense strand of DNA?

When the barcode sequence is generated by Sanger sequencing, it is sequenced in both strands, and presented in sense strand.


Cooperativity of haemoglobin and oxygen dissociation curve of haemoglobin

As you may notice from the graph you provided, there actually is no such thing as true 100% saturation: there is always an asymptotic approach to 100%, regardless of cooperativity.

Let's think, though, of what is actually plotted in that graph: $p_{O_2}$ effectively oxygen concentration, versus number of total percentage of binding sites that have an $O_2$ bound.

However, this also means that as you go up on the y-axis, the number of sites available to bind also goes down. So even if those sites have a high affinity for oxygen, there aren't as many of them open!

That's one big problem with the type of plot you show: it doesn't highlight the cooperativity very well. Therefore, people sometimes plot this information in a "Hill plot", with an algebraic shuffling and log scaling like this:

See Wikipedia

...where $\theta$ represents the fraction of receptors bound to ligand, and $L$ is the (unbound) ligand concentration. $n$ is the Hill Coefficient, i.e., the cooperativity.

When plotted this way, you can easily see the effect of the cooperativity of hemoglobin versus myoglobin (which has cooperativity of 1, because it has a single binding site):

http://cbc.arizona.edu/classes/bioc462/462a/NOTES/hemoglobin/hemoglobin_function.htm via Fig. 7-13, Nelson & Cox Principles of Biochemistry, 3rd ed., 2000


This information is all strictly for Entonox - a brand of analgesic gas comprising 50% Oxygen (O2) and 50% Nitrous Oxide (N2O), Laughing Gas.  This mixture is known as 'Gas and Air' and is in very common use.

The active ingredient in Entonox is of course the nitrous oxide, so the discussion of the mechanism below refers solely to the N2O as you asked for.

Nitrous oxide enters the blood by diffusion from the alveoli whilst it is being inhaled, but does not bind with haemoglobin.  It is fat soluble so quickly moves into cells, including synapse ends in the brain.  Because of the stability of the compound, N2O is not metabolised by the body so has its effect as that molecule, then is eliminated by diffusion out of the lungs once inhalation has ceased (taking roughly 2 minutes for on and offset).

According to the material that BOC pharmaceuticals provide, the exact mechanism of the analgesia is not fully understood.  It is known, however, to induce "inconsistent changes in the basal levels of thalamic nuclei".

N2O inhibits NMDA receptors in the brain whilst simultaneously encouraging the stimulation of the parasympathetic GABA receptors.  This eventually produces an anaesthetic effect.  It is also understood that N2O promotes the release of endogenous opioid neurotransmitters ('natural painkillers' e.g. endorphins) that specifically activate descending pain pathways.  This inhibits the transmission of pain.  In this way the analgesia provided by nitrous oxide is antinociceptive (literally pain reducing) rather than a generalised limbic depressor.

However, nitrous oxide also positively effects potassium ion channels too [ref] - reducing the chance of an action potential being generated in affected neurons.  Research into this area of the effects of N2O is ongoing.

Euphoria is a common side effect of N2O usage, hence the name laughing gas.  This is as part of wider emotional changes that can occur when nitrous oxide is being administered.  For example, some people instead of laughing become scared or in other cases extremely aggressive towards those nearby. The emotional excitement may result in depressive or manic behaviour even to the point of psychosis and hallucinations especially in those who have a preexisting vulnerability to mental illness. The precise mechanism for these disinhibiting is again not fully understood.

Whilst it seems a lot of the answers are missing, the course I'm taking this information from is available online at Discover Entonox - modules 8-10 have relevance to this question.  It's free to register and view the materials, they're all nicely narrated with diagrams etc.


At which temperature is the Tick-Borne Encephalitis Virus destroyed?

A very basic model of virus inactivation is exponential decay.

You can describe exponential decay with the $N(t) = N_0e^{-\lambda t}$ equation, of if you want to use half-time, then with the $N(t) = N_02^{-t/t_{1/2}}$, where $N$ is the value which reduces by time, $t$ is the time, $\lambda$ is the exponential decay constant and $t_{1/2}$ is the half-life (the time required to reduce the actual value to its half).

Exponential decay looks like this on diagrams:

Figure 1 - exponential decay

Figure 2 - exponential decay on log scale is linear

In the case of your TBEV virus, the $N_0$ will be the initial virus titer, the $N(t)$ will be the virus titer by a specific time, the $t$ will be the time and the $t_{1/2}$ will be the half-life, which depends on many things; TBEV strain, temperature, dry/moist heat, pH, etc...

Now real life logarithmic diagrams of TBEV thermal inactivation are linear only by the first 30 mins or so (the inactivation is exponential during that period) as you can see on Figure 3.

Figure 3 - virus inactivation at 60°C
2004 - West Nile virus: recent experience with the model virus approach.
where $TCID_50$ is the tissue culture infective dose

By virus inactivation most of the articles like to use log 10 reduction factors. For example $3 lg$ or $3 log 10$ means in this context, that lowering the initial value to $10^3 = 1000$ fold.

According to this article most of the checked TBEV strains has an inactivation index (the reduction factor difference between two temperatures) around 1.7lg between 50°C and 37°C for 15 mins. So you need 15 mins at 50°C to reduce them at least $10^{1.7}=50$ fold. The reduction factor by this study was around 4lg by 37°C for 15mins (so the virus count reduces certainly not just because the heat, but other environmental factors).

  Thermoresistance (Т50) of TBEV strains was tested by Ovchinnikova et
  al. method [17] using 24-hour cell culture grown in 96-hole plates at
  the presence of СО2. The thermoresistance was determined by
  inactivation index – difference in lg of titers of virus samples
  heated at 50°С during 15 minutes or unheated (4°С). In case of titers
  difference equal or less than 2.0 lg the strain was characterized as
  Т50+, from 2.1 to 3.0 lg – as medium, equal or more than 3.1 lg – as
  Т50-.

  The values of lgTCD50/ml at 37ºС varied from 3.5 to 8.26. According to
  the thermoresistanse feature all tested strains were divided into
  three group: thermostable (Т50+) - nine strains; thermolabile (Т50-) –
  one strain; strains with medium thermoresistance – three strains. It
  should be noted that all strains isolated from I. persulcatus ticks
  collected in Krasnochikoiskiy district of Transbaikalia were
  thermostable.

2013 - Genetic and Biological Properties of Original TBEV Strains Group Circulating in Eastern Siberia

According to another study TBEV required 6 hours of moist heat at 60°C for inactivation of 6.6 lg.

  Vapor heating of a FVII concentrate in another study (which used
  lyophilization, followed by adding water to achieve homogenous
  moistening, then heating at 60°C for 10 hours, followed by heating at
  80°C for one hour in an airtight container under nitrogen gas
  atmosphere) was evaluated for its ability to inactivate HAV, HIV-1,
  TBEV, PRV, and MVM. HAV was readily inactivated within one hour at
  60°C (5.9 log 10 ). TBEV required six hours of this treatment for
  inactivation of 6.6 log 10 , and three hours were required to
  inactivate
  6.2 log 10 of HIV-1 and 6.9 log 10 of PRV.

2002 - Part 3a, Plasma and Plasma Products - Heat and Solvent/Detergent Treatments

According to this study TBEV is considered not heat resistant, so if you are worried for example about raw milk pasteurization, then I think boiling the milk for a few minutes is enough.

  Due to the lipid envelope, TBEV is readily inactivated by heat
  treatment, detergents and organic solvents. Even though a viremic
  phase is common during a TBEV infection in several animal species,
  foodborne infection via contaminated meat or organs is unlikely due to
  the fast virus inactivation at elevated temperatures.

2011 - Scientific Opinion on an update on the present knowledge on the
occurrence and control of foodborne viruses


Assuming that my comment is trivial, I think that there is some literature on this question. I'm assuming that the ccf in question is for the relevant tissue type for the cancer.

You might also consider cross-posting to SE Medical Sciences, where people are more familiar with these subjects.

Of course, naively one would expect that a larger ccf would yield a larger possible population of cancer cells to provide "escape" mutations or resistance to chemo, so high ccf should then be negatively predictive. As an extreme example, a highly metastatic cancer will have a high ccf over the whole body, and will be more resistant to chemo just because that's a highly advanced disease.

However, as usual things are a little more complex. The ccf itself has subpopulations. The following I got by just googling around a little bit. For some of the fundamental thinking on this, see this old paper. In this paper, the author puts emphasis for example on the fraction of cancer cells in each stage of the cell cycle; this results in what the author calls "clonogenic" and "nonclonogenic" populations that respectively yield new clones of cancer cells or do not yield new clones. Probably that terminology is somewhat outdated, but it gives a sense of the problem; related are "tumor stem cells". For a more modern treatment, you can look at this.

For a med school lecture treatment, see here to learn a little bit more. For an example of a recent prediction study which uses omic data to predict chemo response, which might be helpful in reformulating your study, see here.

In other words, not all tumor cells are created equal, some are more likely to resist chemo than others. However, overall I would expect that there is probably some kind of relationship between ccf and response to chemo, because they are both related to the mediator variable "number of clonogenic cancer cells"; it's just a somewhat oversimplified model compared to the actual biology, so it looks like the publications in question don't tend to focus on it.


What if target DNA doesn’t have restriction sites

If you're synthesizing the insert then you just design it with restriction sites that are compatible to the vector. Otherwise, you can design PCR primers that have restriction sites in them. That way when you amplify your insert you'll attach the restriction sites to it. EMBL, Addgene, and NEB all offer somewhat more detailed explanations of this on their sites.


Are surface area or volume conserved during cell division?

Another PLOS One article gives evidence of change both in volume and in surface area, but it is across mitosis phases. It could still be considered constant during cytokinesis only.

It seems that cell shape and size have important function during mitosis, according to this research. It would be interesting to investigate different models from your advisor's paper (constant maximum radius, volume or area) but starting from different shapes and sizes.


I think this question can also be said to be - how can the Atkins diet work?

Atkins and other low carbohydrate diets sound counterintuitive.  They vary in details, but the basic theme is: cut back on carbohydrates - e.g. bread, sugar, fruit, pasta, milk etc etc.  But eat as much fat and protein as you like - e.g. steak, ham, bacon, eggs, cheese etc etc.

These diets really do work.  Our metabolism allows us to draw food from two sources.  Glucose or fat. (there is also something called glycogen, but that is only used short term and not relevant for diets long term).

It was known in the late 50s that our metabolism will to switch over consuming fat, allowing weight loss, only based on the amount of carbohydrates we consume. low carb diets initiate this change from glucose to fat metabolism because our bodies make the switch based only on the amount of glucose available in the blood.  Our bodies think we are starving even if we are gorging ourselves on food which is has little or no glycemic index.

Low carb diets are not a hoax or snake oil - they really work.  They can be a shock to the system and so one should discuss with your doctor before engaging them.

The first link you have is also true though.  Eating fat will usually just make you gain weight.  The low carb response has to be induced by basically removing all carbohydrates from the diet.  If you break the low carb regime and eat a large amount of carbs, the body will switch practically instantly out of starvation mode and also take in all the fats you're eating.  Lots of people on low carb diets can gain a lot of weight rapidly if they break the diet.


This paper uses "ultrafast 2D-IR vibrational echo chemical-exchange spectroscopy" to track switching between different protein conformations and finds that they take place on the order of 50 pico-seconds ($ 1 \times 10^{-12} $ seconds). Another paper finds something similar but notes that full equilibriation can take on the order or nanoseconds:

Although the main conformational change of the backbone is completed after only 20 ps, the subsequent equilibration in the new region of conformational space continues for times >16 ns.


What would happen if blood flow wasn't periodic?

In fact, we see our blood pressure as periodic, and feel our arteries pulsating. But our tissues don't see that. What I mean by that, is that tissues get their blood supply ultimately through their capillaries, where the blood pressure and flow is essentially constant throughout the cardiac cycle, as you can see on this chart:

Image from OpenStax. Article on Blood flow and pressure

As for the second part of your question, what would be the consequences of having constant/non-pulsatile pressure? We can only speculate, I don't think it would have any palpable consequences in principle.

The only "real-life" examples include people who are, for instance: on a Cardiopulmonary Bypass during a cardiac surgery, on Extracorporeal membrane oxygenation (ECMO) in the ICU or have a left ventricular assist device (LVAD) for severe heart failure. It's very difficult to infer anything from these situations, because any on these patients are already very sick, and consequences following these procedures are usually due to insufficient oxygenation, thromboembolism and such, which have nothing to do with the constant pressure.


Can ingesting substances that are produced by the body cause a permanent withering of the organs that produce the substance?

Yes it is possible but in most cases it will not occur as the body simply halts production. The most infamous manifestation of this is in adrenal insufficiency. That's where when we take glucocorticoids (e.g. prednisolone used in management of lots of inflammatory diseases like asthma and autoimmune diseases) for a prolonged period at high dose. This causes the adrenal glands to atrophy (physically shrink) and following this sudden withdrawal can be dangerous for a patient. That's why we always slowly withdraw steroids when a patient has been on them for a long period of time.


You can search on Bionumbers.

Here is what I got after searching action potential:

Speed of action potential along non-myelinated invertebrate axons of ~10μm diameter = less than 1 m/s
Action potential speed in myelinated axon = 50 ... 100 m/s
Velocity of action potential in pyramidal tract at 37°C (in Cat Felis) = 164 m/s

It offers you references for every number.


Are there any side-effects from a mosquitoes extinction?

There was actually just such an article in Nature recently.

"They don't occupy an unassailable niche in the environment," says entomologist Joe Conlon, of the American Mosquito Control Association in Jacksonville, Florida. "If we eradicated them tomorrow, the ecosystems where they are active will hiccup and then get on with life. Something better or worse would take over."


This is Kleinia, a genus from Asteraceae family. It is a succulent  native to  Africa.

I found a number of possible candidates, there may be more:

Kleinia abyssinica

Kleinia fulgens
Kleinia stapeliiformis
Kleinia pendula

P.S. There's not much free information from authoritative sources online about this genus. There are similarities in the blossoms' colour across  the Genus and also differences within a single species so to do a species level ID more information about the plant is needed.


Why they are special?

They are also called Branchial efferent.
They are special because they supply striated muscles derived from Branchial arches.
https://en.m.wikipedia.org/wiki/Special_visceral_efferent

Like Mandibular nerve, nerve of 1st arch supply muscles of mastication and motor nuclei of facial nerve, 2nd arch, supply facial muscles and Stylohyoid.

  Special Visceral Efferent (SVE)
  These fibres innervate certain striated muscles with a special embryological origin.
  They are referred to as the branchiomeric muscles.
  Structures that develop into gill arches in fish develop instead into various structures near or in the head and neck (muscles of the face, larynx and pharynx).
  Although these muscles are identical to normal striated muscle, neurons for branchiomeric muscles have a distinctive location in the brainstem.

..

  Why only visceral?

This term is quite ambiguous. That's why some scientists prefer term Branchial efferents. https://en.m.wikipedia.org/wiki/Special_visceral_efferent

The nerves supply striated muscles(also called skeletal, though most facial muscles have no skeletal support).

These do not supply any smooth muscle of viscera (laryngeal muscles are striated too).

But, still they are called visceral.
Well, that is because the muscles supplied are actually mostly to various viscera.
Larynx is a viscera. Pharynx and palate are viscera too. All these are supplied by 5 , 9 and 10th nerve.(Nuclei - motor nuclei of 5th, Nucleus ambiguus for 9 and 10th)
 Nerve to stapedius is muscle of middle ear, again a sensory organ.

So, the word viscera was added.

Facial muscles and sternocleidomastoid and trapezius are of course not supplying organs(viscera). That is why some say branchial efferent to remove ambiguity.
Branchial efferent represents muscles derived from branchial/pharyngeal arches. That's what is important about these nuclei.


Why is there an extended delay before G.M. liver cells are attacked by the immune system?

The delay in immune attack is common for many viral infectious deceases where auto-immune response plays substantial to significant role in pathogenesis of the decease. The classical example here are the viral hepatitis B, C and D where it is auto-immune attack that causes the massive death of liver cells (hepatocytes).

The delay in immune attack is explained by the following mechanisms:

The immune attack is developed against the surface antigen, in case of hepatitis it is the HbS Antigen. "Surface" means that this antigen has to appear on the cell surface in order to elicit immune response: the virus itself as well as the parts of destroyed cells are not immunogenic enough for this.

The second point explaining why the attack takes so long to develop is that it is primarily cell-mediated attack, the humoral factors play the secondary role here.

So, the usual "workflow" in this case is the following:

Contamination with hepatitis virus.
Virus propagation to hepatic cells and their infection.
Processing of the viral DNA (either as DNA or first reversed-transcripted from RNA) so that it is integrated into cell normal processing pathways.
Expression of viral proteins (=antigenes) and their anchoring in the cell membrane.
Surface antigenes are detected by macrophagues, processed and expressed on their membrane for T-helpers
... (continuation of the usual cell-mediated immune response via T4 and T8 lymphocytes).

Every stage takes some time, the total duration can sum up to 4 to 12 weeks depending upon the viral activity and the immune system status.


Babies are bacteria-free at birth. The meconium (the first stool) contains no bacteria if secured early enough.

  Meconium is a sterile mucilaginous material that accumulates in the fetal intestine and is expelled soon after birth. It contains secretions of intestinal glands, gut constituents (proteins, bile acids, fatty acids, and steroids), and components of amniotic fluid and vernix caseosa.

Bacterial colonization of infants begins at birth - literally. They pick up bacteria from the mother's vaginal canal in passing, which they swallow. This is not seen in infants delivered by C-section. The importance of colonization picked up through normal birth is such, that some hospitals are swabbing the vagina of mothers delivering by CS and colonizing the oropharynx that way.  Breast-milk also contains lactobacilli and bifidobacteria that probably contribute to the initial establishment of the gut flora of newborns.

And, yes, an infection the mother has while delivering must be taken into account. Herpes and Group B strep are both dangerous for a neonate.

  The first microbes to colonize the intestines of newborn babies are the aerobic bacteria Escherichia coli and Streptococci. Later, the gut is colonized with anaerobic bacteria, e.g. Bacteroides, Bifidobacteria, and Clostridia. In 1–2 y, the gastrointestinal tract of infants has developed a natural microflora, which resembles the microflora of adults.

The infant continues to pick up bacteria from all people they come into regular contact with, including nurses.

  The effect of the maternal flora on the initial gut colonization may be less than expected as the fecal flora of infants started to resemble both the fecal flora of the mother as well as that of the first nurse.
  Breast milk may contain bacteria which colonizes the gut as well

Infants aren't overwhelmed by infection due to the presence of  antimicrobial peptides found on their skin, GI tract, and immunity is conferred via breast milk.

  Several AMP have been characterized in vernix and skin of the newborn, indicating a well-developed innate immune system, which may play a pivotal role at the time of postnatal colonization.

Antimicrobial Components of the Neonatal Gut Affected Upon Colonization
Dynamics of gut colonization and source of intestinal flora in healthy newborn infants
Protection of the Neonate by the Innate Immune System of Developing Gut and of Human Milk
Establishment and development of lactic acid bacteria and bifidobacteria microbiota in breast-milk and the infant gut


Why is male balding so common in comparison to female balding?

Let's start off by saying that "baldness" is a very broad term... it includes not only hair loss but also miniaturization, which accounts for the majority of the phenotypic "baldness" associated with alopecia areata.  While alopecia areata is not the only cause of baldness, it accounts for 4 out of 5 cases in men, whereas in women it only accounts for half.
The reason that it's more frequent in males is the presence of 5α‐reductase in the sebacious glands and the dermal papilla - this enzyme mediates the metabolism of testosterone into dihydrotestosterone.  Dihydrotestosterone, in its turn, binds to androgen receptors and affects gene expression, speeding up the anogen phase.  Consequently more hairs are in the telogen phase, and the hair is shorter. In severe cases, miniaturization can become actual hair loss.
Because males higher levels of androgens, there is more testosterone available to be metabolized in the follicles. Therefore, the incidence of alopecia areata (and consequently baldness) is higher in men than in women.

References

Piraccini BM, Alessandrini A. Androgenetic alopecia. G Ital Dermatol Venereol. 2014 Feb;149(1):15-24. PMID: 24566563.

Randall VA, Thornton MJ, Messenger AG. Cultured dermal papilla cells from androgen-dependent human hair follicles (e.g. beard) contain more androgen receptors than those from non-balding areas of scalp. J Endocrinol. 1992 Apr;133(1):141-7. doi: 10.1677/joe.0.1330141. PMID: 1517703.


Consolidating my comments, and taking all the results at face value (though microbiology can be very tricky), the most likely candidates are Moraxella, or Neisseria spp.
Gram negative cocci (spherical cells) rules out a large number of possibilities, leaving just the above 2 and Veillonella as candidates.

The OP said that the culturing was done under aerobic conditions at 30˚C. Veillonella is an obligate anaerobe, and so wouldn't survive this. Both Moraxella and Neisseria are happiest at 37˚C but would no doubt grow at 30. Both are cultivable on blood agar. Neisseria is best cultured in a 5% CO2 atmosphere, so is probably somewhat less likely. Both appear as pale-whitish colonies on plates. The OP's observation of yellowish colouring could be artifactual of the plate colouring, I'm not 100% sure.
Both are positive for oxidase and catalase.
Neisseria on blood agar:

Moraxella on blood agar:

One final comment: both of these are pathogens, so continue with all due caution.
Moraxella, in particular, is a respiratory pathogen, so I would advise working in a biosafety cabinet. I'll assume you already have the relevant paperwork/permission to be handling > BSL1 organisms...


See the manual:

PPrel, in each of these, means protein-protein interaction, so we want to approach these by thinking about what the protein products of these genes can do with eachother.

For the first and second example, the subtype(s) give more information about the interaction. They aren't necessarily mutually exclusive. For example, phosphorylation can result in activation, inhibition, something else, or unknown. For the first one, there is phosphorylation and the effect is inhibition.  For the second one, the interaction is phosphorylation but the effect is not characterized.

When compound is under subtype for a PPrel relation, the value is the entry element ID for the compound (so go look for entry element 4), and it refers to an intermediate of two interacting proteins.


This does in fact look like the flower to the cactus species Selenicereus grandiflorus.

 Source: Wikimedia

According to "Indigenous Cactus biodiversity: A viable genetic resource to fulfill multiform needs under rainfed ecosystems"1, this plant is found in India:

  Different varieties of the cactus are found in India which has immense ethnomedicinal value (Table 1). Selenicereus grandiflorus (with large sweet-scented night flowering flowers) and the Opuntia stricta are found in the wasteland as hedge plants

See here for a good image, and see here for a cool gif of one of these flowers blooming!

1. Rai, M., Singh, R.K., Sharma, P.C. and Singh, L.K., 2011. Indigenous Cactus biodiversity: A viable genetic resource to fulfill multiform needs under rainfed ecosystems.


What species is this orange and black caterpillar from Costa Rica?

Probably it is Cricula silkmoth (Cricula trifenestrata, Saturniidae), in caterpillar stage.