What causes the range of severity of neurological deficits in Down's syndrome?

The symptoms of Down syndrome occur due to overexpression of genes present on the duplicated chromosome.

If possessing an extra chromosome meant an equivalent change in gene expression, one would expect to observe 50% more protein production for having 3 rather than 2 copies of a chromosome. However, due to complexities in regulation at the level of transcription, translation, and protein degradation, the actual expression levels vary substantially. These complexities can arise from alleles present on chromosome 21 or elsewhere on the genome. I will present some examples from three categories of variation that are known to contribute to the spectrum of symptoms in Down syndrome.

1. Complexity of chromosome duplication

Down syndrome is sometimes caused not by a complete, but rather a partial trisomy 21 (Antonarakis et al., 2004). These variations can also partly explain the severity of symptoms because some individuals do not possess a full duplication. You mention this in your question, but as you note, this is a fairly rare occurrence relative to full trisomy, so let us consider other contributions...

2. Variation of expression levels in normal individuals and those with trisomy 21

It turns out that among the genes expressed on chromosome 21, mRNA levels vary between normal individuals by as much as 40-fold! (Deutch, et al. 2005; Stranger, et al. 2005) This expression variability can explain the susceptibility of different individuals to trisomy 21, depending on the expression levels of the alleles they possess.

Among the different genes present on chromosome 21, some expression levels are consistently elevated in Down syndrome across individuals, some have overlapping but significantly different distributions (suggesting some Down syndrome patients have expression levels in the normal range and others do not), and others are indistinguishable between patients and controls (Prandini et al., 2007).

Presumably, genes in the first category contribute most to the shared phenotype of Down syndrome, and genes in the second category contribute most to the variation. Perhaps alleles that produce mRNA transcripts at the low end of normal for those genes are less susceptible to the effects of chromosome duplication.

A case study: Amyloid precursor protein

One protein of interest in particular is the amyloid precursor protein, APP, which is also associated with Alzheimer's disease (which shares some phenotypic characteristics with Down syndrome). APP expression varies widely among tissue types and individuals. Therefore, although APP mRNA levels are significantly elevated in Down syndrome individuals, the distributions between controls and Down syndrome are very overlapping; for example, see Figure 2B from the Antonarakis 2016 review.

3. Interactions with genes on other chromosomes

The third contributor to the variation of symptoms is the interaction of duplicated chromosome 21 genes with alleles located on other chromosomes. Just for an example where some of the genetic basis is understood, Down syndrome individuals are susceptible to certain leukemias, which are also associated with specific alleles on other chromosomes (Antonarakis, 2016). It seems that trisomy 21 affects histone modification in the areas of those alleles (Lane et al., 2014) and promotes proliferation of B-cells. Therefore, Down syndrome interacts with those other oncogenes to produce a greater combined risk. Individual with Down syndrome but not possessing the other alleles are less susceptible to the increased risk of leukemia

Similar interactions are likely with other systems that are influenced by Down syndrome, though the full molecular basis of all of those interactions are not fully understood. The Down Syndrome Genomes Project aims to, among other things, discover these other alleles outside of chromosome 21 that contribute to Down syndrome symptoms, which may also help understanding of the contribution of those alleles to other disorders (Antonarakis, 2016).

References:

Antonarakis, S. E. (2016). Down syndrome and the complexity of genome dosage imbalance. Nature Reviews Genetics.

Antonarakis, S. E., Lyle, R., Dermitzakis, E. T., Reymond, A., & Deutsch, S. (2004). Chromosome 21 and down syndrome: from genomics to pathophysiology. Nature reviews genetics, 5(10), 725-738.

Deutsch, S., Lyle, R., Dermitzakis, E. T., Attar, H., Subrahmanyan, L., Gehrig, C., ... & Antonarakis, S. E. (2005). Gene expression variation and expression quantitative trait mapping of human chromosome 21 genes. Human molecular genetics, 14(23), 3741-3749.

Lane, A. A., Chapuy, B., Lin, C. Y., Tivey, T., Li, H., Townsend, E. C., ... & Yoda, A. (2014). Triplication of a 21q22 region contributes to B cell transformation through HMGN1 overexpression and loss of histone H3 Lys27 trimethylation. Nature genetics, 46(6), 618-623.

Prandini, P., Deutsch, S., Lyle, R., Gagnebin, M., Vivier, C. D., Delorenzi, M., ... & Baldo, C. (2007). Natural gene-expression variation in Down syndrome modulates the outcome of gene-dosage imbalance. The American Journal of Human Genetics, 81(2), 252-263.

Stranger, B. E., Forrest, M. S., Clark, A. G., Minichiello, M. J., Deutsch, S., Lyle, R., ... & Deloukas, P. (2005). Genome-wide associations of gene expression variation in humans. PLoS Genet, 1(6), e78.

(note: the two references I have linked here: Antonarakis 2016 and Prandini et al 2007, are, respectively, a nearly direct answer to the posed question that establishes the current state of knowledge about symptom variability, and an original research paper that provides much more detailed genetic analysis of the variability of expression of many relevant genes than would be appropriate for an answer here; I highly recommend them both for further reading on the subject)


Is the water transpired by plants pure H₂O, or does it contain trace minerals?

It will depend a bit on the specimen of tree / plant that is doing the transpiration. Minerals will typically stay behind during evaporation, but volatile compounds (think the minty smell of Eucalyptus) would evaporate at the same time as the water, and might condense (in some concentration) at the same time as well; this will depend a bit on the temperature of the leaf, the relative humidity of the air (lower will favor evaporation - higher means there is a lot of moisture already in the air, and you don't necessarily know where it came from) and the temperature of the surface used for condensation (lower condensation temperature will trap things besides water).

Note - this is more a physicist's answer than a biologist's... betraying my background here.


What is this plant/creature in my freshwater aquarium?

That is a hydra.
They are a kind of jellyfish, and as such they do technically have stinging tentacles. However, they're also very small, so they're not a danger to most fish or shrimp. If you're planning on breeding your fish they will eat fish fry if they get a chance. On the other hand some fish species will eat them, so it's a bit of a wash.
Generally they only thrive in tanks with extra food hanging around, so you may consider feeding a little less than you have been.


How many dinosaur genes are in a chicken genome?

Be careful when reading media as they tend to exaggerate. That Abzhanov paper is interesting; it will be better when it's published and the figures released. He does a lot of evo-devo work surrounding beak development. What they did in this paper was to inhibit in chick embryos two signalling pathways (which are actually conserved amongst all animals, not just birds and reptiles) so that their expression domain more closely matched that of extant reptiles (which lack medial activation, as opposed birds). They found that doing so results in premaxillary and palatine bones which resemble ancestral archosaurs. While incredibly interesting, this is a far cry from creating living chickens with dinosaur snouts.

To somewhat answer your question, chickens do not contain all of the genes that dinosaurs once had. They will have both gained and lost information. There will be much conservation in the same way that there is conservation between all organisms. For example, the Wnt pathway studied in this paper is conserved across all animals, from chickens to humans to placazoans to, presumably, dinosaurs. It's impossible to say how much has changed since we do not have any whole dinosaur genomes, but it's also important to note that it's not only which genes an organism has but also when and where they are expressed and how they interact.


How to make sure a stem cell culture is cancer free?

It would not be possible to differentiate CSC from normal population non-invasively and select them out. You may do a single cell expression analysis to say if a CSC is present in a population or not but there is no magic bullet method for eliminating them. Also there are several oncogenes and some of them are also required for usual stem cell function. HAT kind of methods will not be able to eliminate potential cancer cells. Also, usual cancer chemotherapeutic drugs also affect other actively growing cell.

Bottomline: Not possible with the current level of knowledge and technology.


Why does this plum/apricot hybrid look like brains?

It is difficult to say, but it is likely due to disease. Many plant diseases have the effect of convincing plant tissues that they are some other organ than what they actually are, which leads to deformations.

I was not able to find anything that looked as dramatic as the image that you show, but there are similar diseases in stone fruits that deform fruit:

Plum pox potyvirus: http://download.ceris.purdue.edu/file/1424
Plum pocket fungus/"Bent banana disease": https://pnwhandbooks.org/plantdisease/host-disease/prune-plum-prunus-spp-plum-pockets, http://shropshireprunedamson.com/a-bad-case-of-bent-banana-disease/

I hope that this is helpful.


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

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


What does fluorogenic mean for fluorescent probes?

The usage of "fluorogenic" is typically applied to probes that are not currently fluorescent but can be, typically by some enzyme action or other reaction. For example, see here, here, or here. Essentially they are precursors to the fluorescent molecules of interest.

As one example, you could get a higher signal to noise ratio if you only "activated" the fluorogenic compound in one area, perhaps inside cells vs in the extracellular space, for example, so you aren't dealing with stray light from that "unwanted" signal.

References:

Shieh, P., Hangauer, M. J., & Bertozzi, C. R. (2012). Fluorogenic azidofluoresceins for biological imaging. Journal of the American Chemical Society, 134(42), 17428-17431.

Lukinavičius, G., Reymond, L., D'Este, E., Masharina, A., Göttfert, F., Ta, H., ... & Blaukopf, C. (2014). Fluorogenic probes for live-cell imaging of the cytoskeleton. Nature methods, 11(7), 731-733.

Friscourt, F., Fahrni, C. J., & Boons, G. J. (2012). A fluorogenic probe for the catalyst-free detection of azide-tagged molecules. Journal of the American Chemical Society, 134(45), 18809-18815.


This has been studied this in Drosophila, and a lot of development hinges on where the cell is in the body.  An initial asymmetry of mRNA in the pre-fertilized ovum leads to the establishment of the anterior-posterior axis (which end is the head, which is the tail)  So cells are told what to develop into based on what mRNA signals they receive which depends on where they are along that axis.

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


Which surfaces contain no epithelial tissues and which epithelial tissues are vascular?

I think you're talking about two different things.  I assume Rafique is referring to vascularized epithelium, but user4693 is referring to vascular epithelium.  Although the terminology is very similar, the difference is important.

vascular epithelium = endothelium of a blood or lymphatic vessel.

vascularized epithelium = epithelium with a blood supply, meaning that small vessels invade the epithelium (pass between epithelial cells) rather than simply occurring in the underlying basement membrane or connective tissue.

Most epithelia are avascular (lack blood vessels).  As far as I know the only vascularized epithelium in humans is found in the inner ear (1).  I've been told that the lips have vascularized epithelium (which is why they appear reddish), but I don't completely trust that source and I cannot find anything online to support it.

Also, some pathological conditions can cause vascularization of certain epithelia, like the cornea (2).


Would somebody born 'reversed' (e.g. heart on their right side, etc.) be completely healthy?

Yes, such a conditions exists. It is called "situs inversus" (literally "inverted sites"). All major organs are placed on the opposite site, the condition is relatively rare with an incidence rate of 1:10.000. There are some even rarer forms occuring, when the organs are flipped, but the heart is still on the left side (levocardia) as opposed to the case when it is also on the other side (dextrocardia).

While some  of the patients are phenotypically normal (besides having their organs on the "wrong" side), congenital heart disease and ciliary disorders (also known as Kartagener syndrome) can occur. See the linked paper below for an overview.

For more information see here and here and the article:

Situs inversus and ciliary abnormalities: 20 years later, what is the
connection?


Does a theory exist for the formation of thylakoid structure?

I think I found a reference.  Most of these papers are behind paywalls - its a pretty obscure topic in biology, though not because it isn't interesting...

For those not familiar with the question, the thylakoid membranes are an organelle structure in the chloroplast, which contains all the photosynthetic machinery in the plant cell.  The chloroplast is though to be a symbiotic cyanobacterium captured to make eukaryotic plants.  Like mitochondria, the chloroplast maintains its own chromosome and some ribosomal machinery.

The stack (grana) and extended (stromal lamallae) structures of the thylakoid no doubt help optimize light/energy capture by distributing the light gathering proteins in an advantageous way.  It was previously believed that the electrostatic charge of the thylakoid membrane helped make the stacks, but this Trends in Plant Science review article (Allen and Forsberg, 2001) discusses how the distribution of photosystem (PS) I and II are more concentrated in the stroma and grana respectively.

They put forth that Light Harvesting complex II (LHC II), which gathers photons for PSII tends to cluster in a trans fashion - forming contacts with LHCII in membranes above it, specifically forming the grana stacks enriched in PSII.


Is there any evidence of causation for breathing rate to affect blood pressure in a human?

Interesting question, it has been studied because sleep apnea is associated with hypertension in humans.
It's not my field of research, so I read a few sources to give you an answer.
There is a open-access review here (https://doi.org/10.1152/jappl.2001.90.4.1600) on the topic of episodic hypoxia, which is similar to the experiment you conducted. Two studies in dogs (https://doi.org/10.1152/jappl.1996.80.3.773 and https://www.jci.org/articles/view/119120) showed that neural reflexes, but also arousal, explain a part of the acute increase in blood pressure but here caution has to be used, as acutely holding breath may have different mechanisms on blood pressure elevation than the chronic hypoxia induced by sleep apnea.
Finally, a review (https://doi.org/10.1038/ajh.2009.43) in 2009 summarizes the evidence between sleep apnea and hypertension.

Overall, there seems to be multiple mechanisms. First, there is a sympathetic discharge during asphyxia, releasing catecholamines which can induce elevation in blood pressure by activating the baroreflex.  These are supported by studies of denervation in multiple organs. Secondly, there is activation of the renin-angiotensin-aldosterone system, a central player in blood pressure regulation. Thirdly, the animals studies show that arousal is an important factor in the acute blood pressure elevation ; in other words, being conscient of holding your breath itself induces blood pressure elevation. I cannot find the exact mechanism linking arousal to blood pressure elevation, though.


Can we change our dopamine baseline levels?

Feelings of pleasure and reward are transient in nature. Similarly, the dopamine release in the reward centers (the limbic structures) is transient, namely in the order of seconds (Rebec et al., 1997).

One way to chronically elevate dopamine levels is by administering certain drugs. A notable/notorious example is methamphetamine, which elevates mood and generates euphoria for 8-12 hours. However, after chronic use, people may report a lack of motivation and anhedonia when they stop taking the drug. Anhedonia is an absence of pleasure in response to acts that had previously been pleasurable. Anhedonia may be reported as long as 2 years after the last use of methamphetamine in addicts. Chronic use of the drug overstimulates the dopamine neurons in the limbic system (and elsewhere), and destroys the dopamine receptors, explaining the anhedonia.

Hence, even with hard drugs like meth, the effects on dopamine levels are transient, just less transient as with physiological reward responses.

Reference
- Rebec et al., Brain Res (1997); 776(1–2): 61–7


Random Mutagenesis vs Directed Evolution as Strategies to boost expression

Well, you already mentioned it. Random mutagenesis (with UV or chemical mutagens) targets the entire genome and you select the organism for certain traits.

In a directed evolution experiment, you are just targeting a gene or a group of genes. With the progress of synthetic biology, it might be possible to synthesize small genomes (already shown by Craig Venter and group) and apply directed evolution methodology genome wide. This would still not be considered directed, as the mutations are actually random over the genome.

The pros and cons depend on what exactly you aim to do.


These are very likely mites (notice their small size and 8 legs). Based on their size, appearance, and abundance, I'd guess they're bird mites (family Macronyssidae). Since they're near your window, I assume you either have a bird nest outside your window or frequent bird visitors to your window.

 Credit: user Aewills on bugguide.com

you can find existing posts about bird mites on Bio.Stackexchange below:

Help identify this mite?
Bug Identification: Tiny Bugs
Tiny white very hard cell bug! Please help to identify!


Why do Centipedes always have an odd number of pairs of legs?

Centipedes are part of the group of insects that utilize a short germ-band mode of embryonic development.1  One feature of this type of segmentation is that new segments are added sequentially to the end of the developing insect (the "posterior proliferative zone").  This is in contrast to insects that undergo long germ-band gastrulation, like Drosophila, where all segments are created simultaneously.
Additionally, Myriapoda demonstrate double segmental periodicity, meaning that segments are always added two at a time.  See the following informative figure from Damen 2004 2 --

Figure 2. Segmentation in the geophilomorph centipedes involves a phase of double segmental periodicity. The drawing shows a schematic model for segmentation in geophilomorphic centipedes. Segments are patterned in posterior tissue that does not show overt segmentation. Segments become molecularly defined in entities (coloured blocks) that eventually give rise to two segments each. Before morphological segments become visible, these two-segment entities are molecularly subdivided into segmental units
(dashed lines), which each eventually will give rise to one segment. For instance, at stage I C represents an entity that is refined into two units (C at stage II), which give rise to one segment each (C′ at stage III). This mechanism of segmentation provides a developmental constraint that only allows the addition of segments in bits of two and in this way only allows odd numbers of trunk segments in centipedes.

One would expect, then, to only see even numbers of leg pairs.  Arthur and Chipman explain this discrepancy in their 2005 essay 3 on Strigamia maritima, the most well-studied member of the Myriapoda subphylum.

Of course, if everything happens in twos, we would expect that there would always be an even, rather than odd, number of segments. But this apparent discrepancy is probably not real. It seems likely that the poison claw segment immediately anterior to the first pair of legs is really a modified trunk segment.

As for how Myriapoda add segments two at a time, I direct you to sources like Chipman and Akam 2008 4, though be prepared for some heavy reading on signaling cascades and morphogen gradients.

Citations

Hughes CL, Kaufman TC. Exploring myriapod segmentation: the expression patterns of even-skipped, engrailed, and wingless in a centipede. Dev Biol. 2002 Jul 1;247(1):47-61.
Damen WG. Arthropod segmentation: why centipedes are odd. Curr Biol. 2004 Jul 27;14(14):R557-9.
Arthur W, Chipman AD. The centipede Strigamia maritima: what it can tell us about the development and evolution of segmentation. Bioessays. 2005 Jun;27(6):653-60.
Chipman AD, Akam M. The segmentation cascade in the centipede Strigamia maritima: involvement of the Notch pathway and pair-rule gene homologues. Dev Biol. 2008 Jul 1;319(1):160-9.


It looks very much like Manulea palliatella, Family Erebidae, Subfamily Arctiinae.
https://commons.wikimedia.org/wiki/Category:Eilema_palliatella
These are present in Spain.


How can I generate a random DNA sequence?

If you want to synthesize a specific DNA sequence chemically, you start by attaching your first nucleotide (one letter in your DNA) to a solid phase. You can then continue adding individual letters to it. Because it is bound to a solid support material, you can wash the whole thing without washing your growing DNA away.

So if you want to synthesize AGC, you would first only add A to your reaction and then wash away all the A that hasn't reacted. Then you'd add G, which binds to your previous A, and again wash away all the G that hasn't reacted. Then you'd add C, and do the whole thing again.

If you want to create a random or semi-random sequence, you simply add multiple letters at once. If you always add all four letters in each step, you'll get a completely random sequence. You can also randomize only specific positions, and only there add all letters.

The result is random, but I don't think it is as random as e.g. a cryptographically secure pseudorandom number generator. There are various factors that can affect the randomness, variations in the concentrations of your nucleotides, variations in the quality or composition of your reactants and probably a lot more.

See also Oligonucleotide synthesis on Wikipedia


What kind of spider has colonised my timber framework?

You've encountered a very common spider, found all over holarctic.
Common names: European garden spider, diadem spider or cross spider
Scientific name: Araneus diadematus
link to wiki:
https://en.wikipedia.org/wiki/Araneus_diadematus

They can bite, but are hard to provoke.
If bitten it will feel similar to a wasp sting.
So nothing to worry about, unless you are allergic.

picture from underneath:

source: http://c8.alamy.com/comp/H45CTY/spinning-network-garden-spider-araneus-diadematus-bottom-side-animal-H45CTY.jpg

picture from above:

source: enter link description here


What are the characteristics of a promising drug?

The specific characteristics sought after will vary widely, but that being said, there are a few key features many groups look for.  I've talked to and heard a number of individuals at a number of different companies, and there are a lot of different techniques and pathways looked for.  In general, however, the single, most important factor is value.  If the drug won't make money, it's almost never considered "promising."  Maybe that's a sad fact of the way the world works, but it's a fact.  The average drug costs around $1 billion (USD) to bring to market so the successful ones damn well better recoup that (Orphan drugs and companies actively pursuing them often have an easier time of this, as the FDA is understandably less restrictive and fast-tracks their progress).

That's not actually so simple.  It's a large, crowded market out there, and there is a lot of intellectual property floating around.  A wise businesswoman told me that her company focuses on the middle-ground.  A target that is too promising is probably already owned by Genentech, so they aim for the ones that are below the attention of the giants but still quite profitable.

After that, it's mainly what you might expect.  High avidity, long half-life coupled with low toxicity (more on this later), small size (if possible), and a realistic time frame.  A month can mean millions of dollars, so working for a decade is not necessarily a possibility.  Often, companies will use high-throughput screens of thousands, even millions of small molecules to look for an effect.  The screening process is usually extremely rigorous, and many potential candidates are eliminated as not good enough.  Sometimes they do some fancy stuff such as 3D modeling but it is definitely a field where brute force can still be successful.

Often those screens are used against primary cells to test for toxicity.  In fact, throughout the entire process, toxicity is a huge factor.  A full 20%-40% of drug attrition is due to safety and liability issues.  It's a constant balance: nothing can risk the health of healthy, control volunteers, but sometimes more risk is acceptable.  The first HIV/AIDS drugs were incredibly toxic, but that was okay because it was still better than the alternative.  These days, the toxicity requirements for HIV/AIDS treatments such as HAART are stricter.  Short-term antibiotics are allowed more risk since you only take them for five/seven days, whereas long-term medication for chronic illnesses are held to much higher standards.

Basically, loss of eyesight might be preferable to death, but it's unacceptable if treating the flu.  The mantra I've been told is three things:

Don’t treat one thing but cause another
Don't cause cancer
Don’t cause birth defects or alter the ability to have children

Toxicologists are conservative, willing to throw the baby out with the bathwater.  In short, Fail Early.


Why don't we consciously know how our bodies work?

We aren't even conscious about most of what goes on in the brain; consciousness is still a poorly understood phenomenon, but we know that lots of brain activity happens without conscious awareness. Most of the regulatory functions of the body are included in that unconscious activity, but so are some processes closer to what we do in day to day life.

For example, if you are experienced driving a car, you are able to do most of the general functions (staying in a lane, for example, or starting to brake at an intersection) without much conscious input, allowing you to have a conversation simultaneously. You only need to be strongly aware of what's happening in an unexpected situation.

Similarly, muscle movements come from executed programs that are learned through experience (especially for humans; some of these movements are innate). When you raise your arm above your head, for example, there are muscles in your arm that move, but also muscles in your back and legs have to adjust to prevent you from tipping over with the new weight distribution, you might lean your head out of the way, all of this is done without you thinking about each one of those individual muscle movements: you are just conscious of the whole general movement.

Regulatory control of things like your heart rate or digestive system is even less out of conscious control.

Brain-computer analogies are often fraught with peril, but in this circumstance I think it is reasonable to use one. Your computer is able to perform all sorts of calculations, it even has software that allows you to communicate with a network of other computers to bring you StackExchange. But even if you download computer science books onto your computer, it has no idea how to assemble a new computer from scratch. It can display the text that could allow someone else to do it, but it is completely unnecessary for its day to day functioning to know how to replicate it.

So back to your original question: why don't we consciously know how our bodies work? Because it's completely unnecessary to know this for normal day to day operation in the context in which animals evolved.


Problems understanding membrane potential

I think this question has more to do with kinetics / transport phenomenons than biology, but that's okay, everything is connected especially my computer to the internet. ;-)

The basic idea behind transport phenomenons is that there will always be a flux of quantitative properties (e.g. charges, particle number, entropy, volume, etc...) where the qualitative properties like (electrical potential, chemical potential, temperature, pressure, etc...) have a gradient in space (note that kinetics of chemical reactions can be described similarly without the space gradient part).

In this case we are talking about electrochemical potential gradient and ion flux. It is very important to recognize that the electrochemical potential is not the same as the electric potential. It has a chemical component, so the result will depend on both charge and concentration gradients. By a single ion channel system (e.g. Na⁺ channel only) you can count the potential of each side of the membrane using the Nernst equation, by a system with multiple ion channels it is more complicated, so in that case you have to use the Goldman equation. So at the end you can say something like one side has a potential of x[mV] and the other side has a potential of y[mV] and so the difference is:  d[mV] = x[mV] - y[mV]

The sign of d depends on x or y has a greater value. By single ion channel systems this expresses an x → y direction so by positive d the cation flow direction is x → y and by negative d it is y → x. By anion flow it is the opposite.

By cells we use the out → in direction by counting the membrane potential. We can count the potentials using the

Nernst equation:
$$E_m = \frac{RT}{zF} \times ln \left(\frac{c_{out}}{c_{in}}\right)$$ or the
Goldman equation:
$$E_m = \frac{RT}{F} \times ln \left(\frac{p_{K^+}.[K^+]_{out} + p_{Na^+}.[Na^+]_{out} + p_{Cl^-}.[Cl^-]_{in}} {p_{K^+}.[K^+]_{in} + p_{Na^+}.[Na^+]_{in} + p_{Cl^-}.[Cl^-]_{out}}\right)$$
where

$Em$ is the membrane potential
$z$ is the ion charge
$[X]$ is the ion concentration
$p_X$ is the relative membrane permeability for the actual ion

and so on...

So for example by an average human cell in blood plasma, assuming that the inside of the membrane has a small negative charge

the Na⁺ has a positive effect (positive charge, high out → in concentration gradient, low out → in charge gradient),
the K⁺ has a negative effect (positive charge, high in → out concentration gradient, low out → in charge gradient),
the Cl¯ has a negative effect (negative charge, high out → in concentration gradient, low in → out charge gradient)
the Mg⁺⁺ has a small positive effect (positive charge, low out → in concentration gradient, low out → in charge gradient)

on the membrane potential. It is hard to find an ion in this case which flow is charge gradient dominated instead of concentration gradient...

  I understand that membrane potential is the difference of the
  extracellular and intracellular ionic charges, due to their
  concentrations.

The (sign and) value of the membrane potential is not determined by the charge gradient because the concentration gradients usually have a much bigger effect on it. The cells maintain these concentration gradients by using up energy.

  We work with a regular cell with potassium 120mM inside and 4.5mM
  outside.

  Say that we increase the intracellular concentration of potassium by
  10 mM, a +1 valence ion which contributes to POSITIVE membrane
  potential.

In your case K⁺ has a negative effect on the membrane potential, because of the high concentration gradient with reverse direction. So decreasing the concentration gradient will increase the membrane potential.

If you want to learn more about how to count membrane potentials, you should read this and its next section instead of wikipedia...


Would it be possible/plausible for a type of spider to fly by weaving web between it's legs to create bat-like wings?

It takes more than wings to fly, just look at the poor penguins. The first problem is that simply weaving webs between a spider's legs would probably not generate enough lift to keep her airborne. Flying creatures have a specific body plan that allows them to fly, if you just add a couple of wings to a hippopotamus it won't be able to fly.

On top of that, the spider would not have the necessary muscles to enable it to flap these wings even if they were capable of producing sufficient lift.

While it is theoretically possible (I stress theoretically) for a spider species to adapt over time (long long time) into a flying form, then it would no longer be a spider. So, in answer to your question, no, it is not possible.


What is the attacking mechanism of RF on IgG?

RF factors comprise antibodies that your body makes that exhibit auto-immunity (recognition of self as an antigen). They often recognize and bind to IgG antibodies as illustrated in this picture:

So the answer to your first question is that the underlying mechanism is inappropriate recognition of self from your immune system.

For your second question, I am not an expert in the type of chemical bonds employed by antibody-antigen interactions, so I looked it up briefly. This article was quite informative for that: Antibody/Antigen Complexes.  The majority of binding seems to be hydrogen and ionic binding.

Hope that gets you going in your own searches.


Mechanism to limit the exponential growth of the number of ancestors that are n-generations away from an organism?

Of course a(n) is limited, and much more tightly than by the number of atoms that exist.  The analysis in the question goes off track with "inbreeding is not germane. Here, all that matters is that each organism has 2 parents. Period."

Consider a person whose parents are first cousins. Then:

a(1) = 2
a(2) = 4
a(3) = 6, not 8

While each of the two parents has four grandparents, together the two parents have only six grandparents because they share one pair of grandparents.  This is due to pedigree collapse.

This table shows the actual collapse for some people with ancestry known to nine generations and with significant inbreeding (from de.Wikipedia):


What is internal symmetry in membrane proteins?

Internal symmetry in this case refers to cases where a part of the protein structure can be superimposed (approximately) on another. It's not a strict mathematical symmetry, more a 'resemblance'

For instance in the 12 transmembrane helix transporters, the first six helices are arranged similarly to the second six, such that if one were to cut the protein in half one would see that the two halves (approximately) superimposed.

Fig 3 of this Nature Micro shows it clearly. http://www.nature.com/articles/nmicrobiol20159 Where the blue helices in 3a could be rotated 180 degrees and then look very similar in arrangment to the yellow helices.


How does receptor downregulation/upregulation work?

Both internalization (sometimes with degradation) and changes in gene expression can occur; the circumstances leading to the down regulation determine which (or both). It isn't necessary for receptors to be bound to their ligand to be internalized, though, and it isn't the internalization of receptors that causes changes in gene expression (I suppose it is possible that happens someplace, but not that I am familiar with). The processes involve activation of second messenger systems and kinases that either phosphorylate/dephosphorylate the receptors to mark them for internalization and/or degradation, or activate/deactivate transcription factors.

Here are two reviews with more information: one is newer but focused on a single class of receptors and fairly in-depth; the other is a bit dated but more broad, but brief:

Williams, J. T., Ingram, S. L., Henderson, G., Chavkin, C., von Zastrow, M., Schulz, S., ... & Christie, M. J. (2013). Regulation of µ-opioid receptors: Desensitization, phosphorylation, internalization, and tolerance. Pharmacological reviews, 65(1), 223-254.

Tsao, P., & von Zastrow, M. (2000). Downregulation of G protein-coupled receptors. Current opinion in neurobiology, 10(3), 365-369.

You can also read about long term depression, which is different from homeostatic responses to ligand concentrations, but it does seem to serve a homeostatic function to keep overall synaptic strengths from growing indefinitely, and the molecular pathways are very similar (and it is a very well-studied phenomenon so you will find a lot of accessible information).


It is more efficient to use fins than feet, hooves, or other similar body parts. It is the same reason that you can swim faster while wearing flippers. Having a larger surface area allows animals to push against more water, so that they have more force when swimming. Here is a picture of the bones in a dolphin fin. They are extremely similar to the bones in a hand, because dolphins evolved from land animals that had individual fingers.

Amphibians like frogs and salamanders have webbed feet, which is a "compromise" between feet and fins. These feet allow them to push against water with more power, since they have webbing instead is separate fingers. It also allows them to grip the ground on land, since their fingers can move independently of each other.


This is speculation, as I haven't done or read of the required experiment. However, I imagine that this would not be a problem.

You're right that the RNA template (TERC) would not hybridize with a poly-G sequence, and so the telomerase would not be able to add more telomere repeats. You can imagine that the poly-G sequence is a cap, preventing telomerase activity.

However, without the telomere repeats other proteins are likely to recognize the chromosome end as a DNA break. Exonucleases would likely chew at the end of the chromosome until they got to the actual telomere sequence, which is bound by protective proteins (namely Shelterin). With the poly-G region degraded, the end of the chromosome would now have the true telomere repeats, and telomerase would be able to add even more repeats.

Even if the poly-G region was bound by protective proteins, the telomeres naturally shorten with each replication cycle, due to the nature of 5' to 3' DNA replication. Therefore, the poly-G region would eventually be removed revealing the true telomere repeats and allowing telomerase to extend the chromosome once again.

In a worst case scenario, rather than degrade the poly-G region the cell undergoes recombination between poly-G regions on multiple chromosomes, leading to either massive chromosomes or circular chromosomes. However, I'm sure these cells would die with some kind of massive mitotic failure.


How many recombinations are required to achieve an active virus?

The FDA has recognised the likelihood that lentivectors can be converted into actively replicating lentivirus if they undergo recombination with wild type HIV in a HIV positive patient. In this case, two recombination events are required to transfer the lentivector sequence into the HIV sequence (the mechanism of transfer is identical to the case of first-generation lentivectors).

This article from VCU describes another mechanism through which this can occur in first generation lentivector systems, which consists of two recombination events between the lentivector and the helper plasmid. Note that the 3 genes gag, pol and env are present on the same plasmid, and that plasmid is flanked by LTRs. Second generation lentivectors, such as the pLKO system, do not suffer from this problem and require wild type HIV to produce actively replicating lentivirus.

To reduce the likelihood of this happening, second and third-generation lentivector systems split the genes into multiple plasmids, which then requires more recombination events to produce replication competent viruses. Additionally, the polyA tail of the 3' LTR is replaced to reduce likelihood of recombination events occurring.

According to Addgene's article on lentivector biosafety, the gene of interest's transfer plasmid (both 2nd and 3rd generations) has a deletion in the 3' LTR region which prevents it from becoming replicatively active. Therefore, the only likelihood for the recombination to occur is for the cell line expressing the virus to undergo replication with an active, wild-type HIV strain. An example is this pLKO transfer plasmid, which contains a truncated 3' LTR, preventing the sequence from replicating outside of E. coli, which replicates it not using the LTR but instead using the plasmid origin of replication.

Are the active viruses produced by recombinations more dangerous in the wild than wild type HIV?

This is difficult to answer, since recombination only allows an active virus to form, but it does not guarantee that the virus will be dangerous. Dangerous viruses are theoretically possible, but require far more recombinations than the minimal 2 for replication competency in 2nd generation lentivector systems.

For example, lentivector systems generally do not encode for the viral proteins vpr, vif, nef and vpu. These proteins are necessary for increasing the infectivity of HIV in different types of tissues (but not cultured cells such as HEK293). The lack of these proteins in a hypothetical replication competent lentivector would significantly hamper its spread in the wild. Incorporation of these proteins is plausible but extremely unlikely, since more crossover recombination events will be required.

To use your example, the env protein coding for the VSV protein coat resides in the envelope plasmid. Since the replication competent lentivector formed by 2 recombination events will be a pseudotype containing only the HIV env proteins, it will need to further acquire the VSV gene to replace its env proteins, since these genes are not present on the same regions. There is no homology between the two DNA strands, which would significantly hamper the likelihood of the VSV gene somehow being incorporated into active HIV.

The addition of various chimeric proteins and LTR regions in 3rd generation lentivectors only complicates the matter.

Overall, I was unable to find any sources comparing the infectivity of these theoretical transgenic HIV versus the wild type. However, even though it is theoretically possible that a transgenic replication competent lentivector can have better tropism than HIV by acquiring the VSV gene, the likelihood of that occurring is far lower than that of it being produced in the first place.

Can a lentivector be detected by a HIV test?

Regarding the final question of whether a lentivector can be detected by a standard HIV test, the answer is that the detection is possible if the person who was infected with lentivectors, has obtained an immune response to the lentivector gag proteins, and the lentivector loads are high enough.

HIV tests are specific to different parts of the virus, but most of them target the viral protein p24, which is a component of the gag polyprotein.

PCR based HIV tests also exist, but these tests would depend on the specific primers produced and whether the RT-PCR would produce an amplicon given the specific sequence of the plasmids.

Since gag genes are encoded for in most lentivector systems, it is therefore very likely that anyone infected with a lentivector would therefore express antibodies towards p24, and therefore result in a positive for the ELISA as well as the Western blot tests assuming that the p24 and antibody quantities are high enough to reach the cutoff point.

I was unable to find publicly available cutoff levels for the ELISA and Western blot levels, but if (hypothetically speaking) a person was injected with a load of lentivectors, they would likely test positive for HIV. However, since the lentivector is not actively reproducing, it would quickly be cleared out by the immune system.


The availibity of -OH groups for hydrogen bonding with polar water molecules is reduced in amylose due to its coiled nature (resulting in part by H-bonds between the glucose monomers).  Amylopectin is even less soluble due to the additional 1-6 glycosidic bonds on the branch chains, further reducing its H bonding potential and therefore reducing solubility in water.


It is probably Holothuria leucospilota

Holothuria leucospilota is a medium-sized sea cucumber reaching a length of up to 40 centimetres (16 in) when relaxed but it can stretch to about a metre (yard) when extended.

Holothuria leucospilota is found in shallow water along the east coast of Africa and in much of the Indo-Pacific region. It is a common species on the north east coast of Australia where it is found on reefs and rocky coasts, often partly concealed under a boulder.

References
https://en.wikipedia.org/wiki/Holothuria_leucospilota


Why does HIV chooses the Macrophage cells to infect first?

Short answer

HIV infects macrophages because macrophages display the CD4 cell surface receptor needed for initial HIV attachment, and also display the co-receptors CCR5 and/or CXCR4 that are also needed for virus entry into the cell.

Cells that aren't good hosts for HIV don't have these receptors.

Addressing some confusion

You ask why HIV chooses macrophages as a virus producing factory. Be careful that you don't excessively anthropomorphise viruses - viruses 'choose' which host cell to infect in the same way that you 'choose' to feel pain when you stub your toe. It is a product of evolution, and not the result of a logical thought process by the HIV virus.

Other viruses happen to infect epithelial cells, or liver cells, or plant cells. HIV infects CD4+ cells. There is no 'best' option that viruses will somehow 'choose'. Anything that allows for successful reproduction and transmission is a viable option, and the rest is down to random mutations and evolution.

Red blood cells as virus factories?

Finally, you ask about red blood cells as a better host for viruses. In fact, red blood cells make very poor host cells for viruses, as they lack the cellular machinery required for DNA replication and protein production. It is this cellular machinery that is usually hijacked by viruses in order to replicate. Red blood cells lose their nucleus early in development, and it is only more complex organisms (such as the Plasmodium species that cause malaria) that can effectively hijack a red blood cell. These Plasmodium parasites have their own nucleus for protein production and DNA replication.


Nope, nope, and nope.  A cursory glance over any page on hematopoesis will reveal that blood cells are replenished from HSC, hematopoetic stem cells, which are self-renewing stem cells.  Telomerase is activated in stem cells.


Does scratched Teflon coated frying pans contain carcinogens which can cause cancer?

Teflon is a polymer of perfluorooctanoic acid (PFOA) and related compounds.  PFOA is thought to be a carcinogen.

I think there's an urban legend that if you really heat teflon up or burn it (it doesn't burn as flouroxides are not stable in air) that you might get some of the constituent chemicals out into the air.

Once the flourocarbons are polymerized into fibers and surface coated a metal pan, they are chemically inert and aren't carcinogenic.  Teflon can be made to burn and some noxious fumes produced, but they are not especially carcinogenic.

Even after all this, this paper reviewed PFOA exposure and points out that most people in industrialized countries have some PFOA in their blood and this does not seem to be related to a strong incidence of cancer as the level of exposure is so low.

Flouro-carbon compounds are terribly inert - thats why teflon is so tough.  If PFOA is dangerous, then Teflon is > 10 million times less dangerous.  If PFOA is dangerous, crossing the street is many more times dangerous.

Even PFOA will be eliminated from Teflon production, supposedly next year (2015).


A question about how the brain determines the source of a sound

If the sources have different locations then they won't reach the 2 ears at the same time, won't have the same loudness and spectral content (although here you describe a pure tone), so your brain will be able to tell them apart. There is a whole field of neuroscience interested in "causal inference", which describes how your brain makes this type of guesses. For example have a click and a flash been produced by the same source of different sources?

But I think this is not exactly what you were asking. If the signals are identical when reaching the ears then it becomes more of a philosophical question. If you place a microphone in the observer's ear and receive a perfect sine, does it matter that it has, in facts, been produced by multiple sources? That's the classical philosophical question of whether a tree falling in a forest produces a sound or not, if no one is around to hear it. Is a sound a physical signal or is it the percept it elicits in an observer? Take the example of color. If you compare 2 lights, one monochromatic red and one complex spectrum that looks exactly the same red. Do they have the same color or not? Due to the physiological limitations of your sensory organs they elicit the exact same response. Yet they are physically different. There is of course no clear or easy answer to this question as on one extreme you will end up arguing that there is no objective reality and on the other extreme you deny the obvious fact that we experience the world differently.

Shams, L., & Beierholm, U. R. (2010). Causal inference in perception. Trends in cognitive sciences, 14(9), 425-432.

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


What is the effect of non-vaccinated people on vaccinated people?

Biology is rarely black or white, all or nothing. Protective immunity is generally not an on/off switch, where from the moment you're vaccinated you're infinitely resistant for the rest of your life. You shouldn't expect that, having received a smallpox vaccine, you could have billions of smallpox viruses squirted directly into your lungs and shrug it off without noticing.

Given that (fairly obvious) fact, you should immediately think of scenarios where vaccinated people are still at risk of disease following exposure to unvaccinated people. What about older people who were vaccinated 20 years ago, 50 years ago? What about people whose immune systems are slightly weakened through lack of sleep or obesity or stress? Any of these vaccinated people might well be protected against a brief encounter, but not against, say, being in an airplane seat for 18 hours beside an infected child shedding huge amounts of virus, or caring for their sick child.

It's all sliders, not switches. You can have a slight loss of immunity (4 hours sleep last night) and be protected against everything except a large exposure (your baby got infected and won't rest unless you hold him for 8 hours). You can have a moderate loss of immunity (you were vaccinated twenty years ago) and be protected against most exposures, but you're sitting next to someone on the subway for an hour. You may have a significant loss of immunity (you're a frail 80-year-old) and still be protected against a moderate exposure, but your grandchild is visiting for a week.


It means that they recorded family information for the traits that they were investigating in the paper, i.e., they had plumage characteristics for siblings or parent-offspring pairs. Look for this phrase in the paper: "phenotypic data usually available for one or two generations, mostly from parent-offspring pairs or siblings."


Can COVID-19 affect a person a second time?

Short answer: Although there are some reports on this, it is pretty unlikely. It is more likely that patients where released too early from hospital, developed further symptoms later on and got worse, was re-hospitalized, tested again for SARS-CoV2, which was positive and counted as re-infected.

Another possibility is that a false negative test happened, when people got re-tested later the test was positive again and the patient was counted as re-infected. Given the rising number of cases worldwide this should become evident pretty soon, if this is a real problem and not an artefact. For the moment, I don't think there is enough evidence for the re-infection of the same patient in such a short time period. If this holds, future will tell.

Long answer: There is now an experimental paper, which infected rhesus macaques with SARS-CoV2, tested if the infection was similar to humans happening in the upper airways (which it was), and re-infected the animals after 28 days with a really high dose of virus (which is much higher than what comes around in our environment), with none of the macaques getting re-infected or showing pathological signs of the infection. See reference 1 for details.
This article has its limitations with small sample size and the general questions if the chosen animal model is really comparable with human.

Additionally it looks very much like that patients who are recovering don't shed infectious virus anymore. The PCR test however does not discriminate between infectious virus and plain virus RNA, so it is most like much longer positive than people are infectious. They also show the rapid appearance of specific antibodies, which would at least temporarily protect against a re-infection. See reference 2 for a nice summary and reference 3 for the original article.

References

Reinfection could notoccur in SARS-CoV-2 infected rhesus macaques
People ‘shed’ high levels of coronavirus, study finds, but most are
likely not infectious after recovery begins
Clinical presentation and virological assessment of hospitalized
cases of coronavirus disease 2019 in a travel-associated
transmission cluster


What are the branches of system ecology?

What are the branches of system ecology that scientists research in nowadays? Or what can system ecology can applied to, or be used?

This field is often referred to as systems ecology or ecosystem ecology. It is the study of ecosystems. Thermodynamic principles are often used to construct food/system webs (networks) to understand cause and effect within the system. But I think systems ecology can be considered beyond just a numerical approach to include social (human) dynamics.

A great primer for systems ecology is that by Howard T. Odum:

Odum, Howard T. "Systems Ecology; an introduction." (1983).

  I have presented this in detail what I understand on my website.

After reading the post on your website I have some recommendations for complex systems science groups/hubs in which you can look for potential mentors/collaborators/ideas:

International Institute for Applied Systems Analysis (IIASA; Austria)
Santa Fe Insitute (US)
National Socio-Environmental Synthesis Center (SESYNC; US)


What is this insect I found in my kitchen?

That is a larva of a dermestid beetle (Family, Dermestidae). https://en.wikipedia.org/wiki/Dermestidae Dermestid beetle larvae feed on dried material, and are the last insects to clean up a carcass. They are the bane of insect collectors, as they will eat a collection right off the pins. They leave nothing but dust and their shed skins behind.


How do I interpret this graph regarding introduced genes and virus-infected cells?

Plus and minus describe what is happening in a specific locus in the genome. When a + sign is shown, the locus contains the natural, fully working gene (wild type). When a - is shown, it means that by natural mutation or lab manipulation, cells lack that natural gene, or make a negligible amount of it, or make a broken variant etc.

These cells are diplod, meaning they have two homologous chromosomes. If +/+ is shown, both chromosomes carry, in that locus, a working gene. If -/- is shown, both copies are not working. If a cell is CatL -/-, both its natural copies of CatL are missing or defective, and the cell is unable to make the corresponding protein. The manipulation through which a naturally occurring +/+ is turned into a defective -/- is called a knock out.

The top part of your chart shows what is happening in the nucleus, on the chromosomes, at the actual places where normal cells store their CatL genes. You don't give much detail, but the bottom of the chart appears to show some manipulation away from the normal locus. There are ways to introduce more copies, to stick them into the nucleus, or even in chromosomes etc, but the main point about introducing DNA is that often it will not work as well as the natural thing.

Optimal infection means something close to the first column, about 25%. By skimming through the chart we are definitely seeing good infection in column 3. Also by comparison with the low levels, we could call acceptable the infection in column 8. The other columns are all clear failures to infect.

The second column is the simplest to interpret: knock out CatB alone, and the infection is gone. Thus, CatB is required for infection. The third column reinforces the same point: restore CatB and infection is back to normal.

The sixth column shows cells where CatL and CatB were knocked out, but then CatB was reintroduced. We know from column 3 that knocking out and restoring CatB should keep infectivity, but in column 6 infection is gone. The only difference between columns 3 and 6 is the knockout of CatL, and its consequence is lack of infection. Thus, CatL is also required for infection. You may say both CatL and CatB are required.

The other columns are control conditions which show that the experiment was well designed and yielded expected results, rather than gibberish. For example, column 5 show that if you knock out both, infection is gone. It would have been very concerning if it weren't gone. Etc.

Your second question is really one of logic: is CatL sufficient? We established that CatB is required, and so there is little CatL could do to supplant its absence. Therefore, logically, CatL should not be sufficient.

But we have a better proof, from the experiments. In column 4, those cells have their natural (endogenous) CatL, topped by some more CatL. But they are still not infected, beause they lack CatB. So CatL, even in larger-than-life amounts, cannot compensate the absence of CatB. CatL is not sufficient.


How is RNA of retrovirus converted into cDNA?

RNA has Uracil instead of thymine and DNA has thymine instead of uracil. So, how can RNA be converted into DNA?

I think you may want to ask a more basic question.  DNA and RNA are extremely similar, with only an oxygen being the difference.  This has vast consequences for organisms, and life as we know it uses DNA and RNA for very separate purposes.  DNA stores the genome providing the instructions for life, and RNA in a nutshell is how that message gets converted into protein for a useful action.  RNA is generally less stable than DNA, so this arrangement works out well.

DNA is regularly and constantly transcribed to RNA, so Thymine is regularly used in favor of Uracil.  There is a fantastic answer here on Biology.SE already dealing with why so I suggest reading that.  The how is pretty straightforward, there are different molecules used!  DNA polymerases incorporate Thymine whereas RNA polymerases incorporate Uracil.  The reverse transcriptase that is encoded by the retrovirus does just this: it transcribes RNA to DNA, using Thymine instead of Uracil.  Both Uracil and Thymine are present in the cell and are thus available for use.


I'm pretty sure that it is a cup lichen from the genus Cladonia. A probable species is Cladonia pyxidata, which is relatively common across Europe. My lichen knowlegde is rusty though, and Cladonia is rather species rich with several species that are relatively similar.

(C. pyxidata, pic from http://fungi.myspecies.info/taxonomy/term/4557/media)


The countercurrent system permits forming a concentrated urine

In the presence of ADH, which increases water permeability, the hyposmotic fluid that enters the distal tubule (DT) from the thick ascending limb (TAL) looses most of its water by osmotic equilibration with the surrounding cortical interstitium along the CNT and cortical collecting duct (CCD). It also continues loosing NaCl through reabsorptive transport along DT, CNT and CCD, until the tubule fluid becomes isoosmotic with plasma, by the end of the CCD.

The relatively small amount of isoosmotic fluid that flows into the medullary collecting ducts losses progressively more and more water to the hyperosmotic medullary and papillary interstitia and is finally excreted as hyperosmotic, highly concentrated urine.

The countercurrent system permits forming a dilute urine

In the absence of ADH, the hyposmotic fluid that enters the DT from the loop of Henle, continues to be diluted by transport of NaCl via NaCl (thiazide sensitive) cotransporters into DT cells and via Na channels (amiloride sensitive) along the CD. Water reabsorption is limited so that the tubule fluid becomes more and more dilute along DT, CNT and collecting ducts (CCD, OMCD and IMCD), until it is excreted as a large volume of hyposmotic urine.

Sources:

Barac-Nieto, Prof. Mario. "Countercurrent System and the Loop of Henle." Countercurrent System and the Loop of Henle. Kuwait University. Web. 08 Feb. 2016.
Wikipedia. Wikimedia Foundation. Web. 08 Feb. 2016. https://en.wikipedia.org/wiki/Countercurrent_multiplication.
"7. Urinary Concentration (countercurrent Mechanism)." 7. Urinary Concentration (countercurrent Mechanism). Web. 08 Feb. 2016.


Need some good resources to learn about Protein function and structure

Given your background (not a biologist or chemist) you would probably find the introductory material in a biochemistry "lite" textbook more accessible/useful than a hardcore text for specialists.  As a co-author of a biochemistry textbook, I can tell you that there are essentially three different classes, or types of texts.

Comprehensive textbooks, of which I think Voet & Voet is an outstanding example, are designed for biochemistry majors who will be taking a full year, in-depth course, typically in the 3rd year of their undergraduate studies.
The general introductory texts are usually thinner, and are designed to whip through the same material in half a year--aimed at life-science students in other majors. Some of these books that I described as "lite" are further targeted to, for example, nursing, medical, or dental school students.
The third category of text tries to be multi-purpose, and appeal to both markets. The current versions of Stryer and Lehninger fall into this class (they are both excellent in my opinion); the instructors can cherrypick the readings if they want to use the book for a half-year course.

Voet, Voet, and Pratt (mentioned in the comments above) is a very good diluted version of Voet & Voet. As you can also tell from the comments, different texts have different flavors, and so which one is best depends on the reader.

It sounds like a more general "concept" based book might be useful for you (to provide background and context). The very thick "Molecular Biology of the Cell" by Alberts et al., has a lighter cousin named Essential Cell Biology which would be well worth looking into.

Keep in mind that when tackling a university-level biochemistry course the instructor has to assume that you have passed university level introductory courses in general chemistry and in organic chemistry. Biochemistry majors typically complete full year courses in both these subjects, as well as a watered-down version of physical chemistry.


Why swordfish aren't put in the same family as Marlins?

Why Swordfish (Xiphias gladius), which are very similar to Marlins, do not belong to the same family as Marlin - Istiophoridae?

The decision about what we call an order vs a family is very subjective. Someone decided that Istiophoriformes was an order containing the families Xiphiidae and Istiophoridae but someone else could have decided to call Istiophoriformes a family (although the name would have ended in -idae, then) and Xiphiidae and Istiophoridae subfamilies.

  [C]an we say that swordfish and marlins belong to the same clade which includes the two families Xiphiidae and Istiophoridae[?]

Yes, you can. This clade is the order of Istiophoriformes. You can hence say that swordfish and marlins are both Istiophoriformes. Or if you prefer, you can say that swordfish and marlins both belong to the order of Istiophoriformes.


Are Night Parrots (Pezoporus occidentalis) really extinct?

As per Wikipedia it is listed as endangered having been downgraded from critically endangered due to the spread in sightings over the years over a large area. Sightings have been rare with a reported sighting on 12th April 2005 and a dead specimen found in 2006 The first photos and a 17 second video of the bird was taken by a wildlife photographer John Young in 2013. Details can be found in this link.

According to Birdlife.org the reason for its population to decrease significantly include predation by feral cats and foxes, altered fire regimes, competition for food, degradation of habitat near water by stock or rabbits, and reduced availability of water as a result of over-use by feral camels.


I took a class in ordination methods a few months ago and found the following books helpful in better understanding the various techniques:

Multivariate Statistical Methods: A Primer by Brian Manley https://www.crcpress.com/Multivariate-Statistical-Methods-A-Primer-Fourth-Edition/Manly-Alberto/p/book/9781498728966

Correspondence Analysis in Practice by Michael Greenacre (this is somewhat more in-depth for forms of CA) https://www.crcpress.com/Correspondence-Analysis-in-Practice-Third-Edition/Greenacre/p/book/9781498731775

Multivariate Statistics for Wildlife and Ecology Research by McGarigal, Cushman, and Stafford https://www.springer.com/gp/book/9780387988917

Numerical Ecology is really excellent, even if it covers a broad number of topics. I focused on the ordination methods and found it to be very straightforward. Check out the McGarigal et al. book if you are interested in seeing examples of application in ecology.


Why does colchicine not affect the source plant itself?

Colchicine is an alkaloid and a secondary metabolite of the plant- a crocus, primarily functioning to protect the plant (like, from consumption by herbivores).

WHY COLCHICINE DOES NOT AFFECT THE PLANT:

It is transported far away from its site of production to the tissue storing it so does not come in contact with normal metabolically active plant cell machinery.
In the storage tissues colchicine is compatmentalised in vacuoles specific for colchicine storage.

The vacuoles are bounded by tonoplast which contains special proteins that facilitate active uptake of colchicine from the cytoplasm into the vacuole protoplast but do not conduct the movement of colchicine from the vacuole to the cytoplasm.

The scientific studies are detailed here.


What is the genomic position of HLA-B*1502 variation?

HLA-B*1502 is not a SNP ID but rather, a name of an allele of HLA-B. This allele is made up of multiple mutations which can be found here.


Which kind of electrical brain activity is associated with consciousness and why?

Gamma band oscillations (GBO) (Wikipedia) (NCBI)  are 30-90 Hz electrical waves generated by the brain and are thought to possibly be associated with cognition and consciousness (Panagiotaropoulos, 2012). Some evidence for this putative relationship can be seen with experiments such as pre-pulse inhibition (PPI), which can describe how our sensations are interpreted by the brain. Also, PPI may be aberrant in Schizophrenic patients (who have altered cognition). Changes to PPI are associated with aberrant GBO, which could imply an association between GBO and an individual's interpretation of stimuli, their cognition and by extension consciousness.

But of course, the counter-argument is that the intrinsic activity of the brain isn't changed, merely how the brain processes stimuli. However, all forms of measuring cognition that I've studied involve investigating responses to external stimuli, so as far as I know, this is a universal problem. Furthermore, there's a lot we still don't know about consciousness and no model or measurement is perfect. This article gives quite a nice overview on neural correlates of consciousness.


Do "non-human" animal like cat, dog, bird or fish think about future while sleeping?

Issue with your question

This question is full of terms that don't have a proper definition in Biology. I don't think there is any clear definition in the verbs "feel" and "think". Also, I don't fully understand what the differences between feeling or thinking (whatever that means) when sleeping matter for the question of whether some animals "think" (and its variants) about future while sleeping. I am not sure either what "thinking about future" really means. One doesn't know the future, he can imagine it and in some cases it is kinda complicated to really know whether a set of thoughts are encompassed within the concept of "thinking about the future". I vote to close for primarily-opinion based. Finally, your question might eventually be a better fit on CognitiveScience.SE.

Theory of Mind

You might be interested in the Theory of Mind (ToM). Having the ToM (I know it is weird formulation, ToM is not a theory per se) means having the ability to 1) be aware (might have various definitions for "aware") of its own existence and 2) be aware that others also think and have intentions and 3) more importantly be aware that others might be aware that you think and have intentions.

It is pretty hard to investigate whether an animal has the ToM. Here is a list of species (and lineages) where ToM has been found (or thought to exist at some level). The list is probably not exhaustive and the difficulty to accurately define ToM and awareness make those pretty arbitrary.

Chimpanzee
Orang-outan
elephants
dolphins
corvids
some parrots
bee-eater

Btw, your list of lineages is funny by the fact that you seem to weight equally two relatively closely related domestic species (cat and dogs) and two gigantic taxa that are fishes (fishes do not represent a monophyletic group) and birds


Why cancer mutations do accumulate sequentially?

TL;DR:

A sixth order probability curve of cancer does not mean six steps. The order of the curve has nothing to do with the number or sequence of mutations.
Causes why ABCD could be more likely than DABC exist and have been extensively studied
Repair and control ("defence") mechanisms are what does the 'ordering' of steps by selecting for mutations which can circumvent them

The sigmoidal shape of the curve thus reflects the slow accumulation of "defence"-damaging mutations, which increase their own probability and thus the slope of the curve. I don't know if the slight decrease in slope towards the end reflects a real limit to the incidence of cancers, or if it's an issue related to the data, its availability or the way it is gathered (but has no basis in substance i.e. there isn't actually a limit).

To elaborate:

There are many biological factors which play into helping you understand the problem you are wondering about, and the fact that different cancers work differently does not make it easier. I would highly recommend that you check out Hallmarks of Cancer, the Wikipedia article also cites the interesting original publication. Basically, certain principles underly all cancers, but different cancers have different tendencies to develop certain hallmarks in a particular order.

Randomness of mutations:

Mutations are not random. The nature of DNA sequences affects their susceptibility to DNA lesions, i.e. damage caused by chemical processes such as a nucleotide losing its base, dimerisation of thymidine, single or double strand breaks and so on. Lesions occur all the time, so there are mechanisms in place to fix all types of DNA lesions. Occasionally however, the circumstances will permit e.g. two lesions to coincide or the repair process itself to make an error, which then leads to a permanent change of the DNA sequence that cannot be fixed anymore because the original sequence has been lost. This is a mutation, and mutations are also not random because the nature of DNA sequences affects the chancefor them to incur lesions that cannot be repaired.

Hence, one reason why certain mutations occur more frequently than others is because they are actually more likely to occur. But this isn't the main reason.

Cell self-control

There are higher levels of control than DNA repair. Various mechanisms in the cell exist to detect malfunctioning proteins (due to mutations in their gene) and degrade them - though sometimes malfunctioning proteins can still escape these mechanisms. Even in this case, there is an additional safety layer created by various mechanisms which lead a cell to kill itself (apoptosis). These are triggered for example if excessive DNA damage is detected, or if the cell-internal signals for and against proliferation are conflicting.

Sequential accumulation of mutations

The result of repair and control mechanisms (which I will now call "defence mechanisms") is on the one hand that we are far more resistant to mutations than we would be without them. On the other hand however, they create selection for mutations which are not affected by them.

This is where multi-hit models of cancer come from. A "first hit", "enabling mutation" or whatever you want to call it would be a mutation which itself is not affected by defence mechanisms - and simultaneously impairs the defence against other mutation(s). The "second hit", "initiating mutation",... would be a mutation which causes cancerous cell behaviour, but would be eliminated by a defence mechanism without the first hit.

This means that mutations do not always occur in the same sequence but rather, they occur in all sequences and sequences other than those that we find in cancer cells are eliminated.

Note that not all cancers have several mutations or a sequence. For example, chronic myeloid leukaemia (CML, a blood cancer) in the vast majority of cases is caused by a translocation from chromosome 19 to chromosome 22 which results in the famous Philadelphia chromosome and produces the BCR-ABL fusion gene. This single mutation is sufficient to cause CML.

Age-dependency of mutations:

Mutations can affect all parts of a cell's machinery, including the lesion repair mechanisms. This means that throughout its life time, a cell can (and will) accumulate mutations which increase the likelihood of further mutations. Mature cells usually have short life spans and mutations to their DNA repair machinery die with them relatively soon (days or weeks). However, pluripotent stem cells (PSC) in the tissues are just as likely to develop these mutations as mature cells - and PSCs are the ones which renew the tissue throughout life by differentiating into mature cells.

Thus, a mutation in a PSC remains for life, and the longer you live, the higher the chance that one mutation will affect the chance for gaining further mutations. This is why for all cancer types, the risk to develop them increases with age (though there are a few which are most likely at young age!)


"Most bacteria have at least one cell wall"

I agree with @Maximilian that the phrase you quote is unclear, and we can't understand if it's talking about the number of cell walls of about the presence of cell walls:

  Most bacteria have at least 1 cell wall, meaning that some bacteria can have more than 1

This is wrong, as @Maximilian explained. But this:

  Most bacteria have a cell wall, meaning that some bacteria doesn't have any

Is correct. Tenericutes, a group of Eubacteria, don't have cell wall:

http://onlinelibrary.wiley.com/doi/10.1002/9781118960608.pbm00025/abstract

Reading the answer, it's clear that the user was talking about the outer membrane in Gracilicutes.

However, it's good to emphasize that all bacteria have only 1 cell membrane, because the outer membrane is not defined as a "cell membrane" (despite being a phospholipid bilayer): http://www.nature.com/nrmicro/journal/v13/n10/images/nrmicro3480-f1.jpg


How many humans have been in my lineage? Is it almost the same for every human currently living?

A quick back-of-the-envelope answer to the number of generations that have passed since the estimated human-chimp split would be to divide the the split, approximately 7 million years ago (Langergraber et al. 2012), by the human generation time. The human generation time can be tricky to estimate, but 20 years is often used. However, the average number is likely to be higher. Research has shown that the great apes (chimps, gorilla, orangutan) have generation times comparatble to humans, in the range of 18-29 years (Langergraber et al. 2012).

Using 7 million years and 20 years yields an estimated 350000 ancestral generations for each living human. A more conservative estimate, using an average generation time of 28, would result in 250000 generations. However, some have argued that the human-chimp split is closer to 13 million years old, which would mean that approximately 650000 generations have passed (using a generation time of 20 years).

The exact number of ancestral generations for each human will naturally differ a bit, and some populations might have higher or lower numbers on average due to chance events or historical reasons (colonizations patterns etc). However, due to the law of large numbers my guess would be that discrepancies are likely to have averaged out. In any case, the current estimates of the human-chimp split and average historical generation times are so uncertain, so that they will swamp any other effects when trying to calculate the number of ancestoral generations.

However, this is only answering the number of ancestral generations. The number of ancestors in your full pedigree is something completely different. Since every ancestor has 2 parents, the number of ancestors will grow exponentially. Theoretically, the full pedigree of ancestors can be calculated using:

$$N_\text{ancestors} = \sum_{i=1}^t 2^i \hspace{1em} \text{or} \hspace{1em} 2^{t+1}-2$$

where t is the number of generations. However, this will yield an unreasonably large number of ancestors (~$2.3*10^{105}$ over just 350 generations), since it assumes that all of your ancestors are unrelated. Basically, you run into something called pedigree collapse, which means that your pedigree will have many overlaps (due to inbreeding, overlapping generations etc), so all of your ancestors cannot be seen as unrelated. In practice, this means that the number of ancestors in successive generations will stop doubling for each generation you go back, and will eventually start shrinking, which will drastically reduce the number of unique ancestors. For more on this, see answers to the question Initial population when i count backwards?. That question is basically asking about the same issue, but less specifically. There might be studies that have tried to calculate the average number of ancestors to living humans, but I haven't seen any. Therefore, I cannot say anything more specific about the average number of unique ancestors for a living human individual.


How dirty are bugs? And is it okay if they touch food?

Well, first of all you should consider that insects and generally animals don't have so much hygiene, like us humans. Some of them, let's say the ants, yes some kind of hygiene is present, but not in the human degree. In fact, most insects are responsible for the most dangerous deseases in the world such as malaria , yellow fiver, sleeping sickness (espacially found in Africa because of the tsetse fly) and many kinds of encephalitis. This article claims that most of insects are carriers of deadly deseases. Also, about the second part of your question, you mentioned " If it is okay for bugs to touch food"... Well the answer is ofcourse no, because you don't know:

1. what the insect was touching before it "lands" to your food

2. If it has dropped any fecesto your food

3. And last but not least if the insect layed any kind of eggs to your food.

4. Some insects carry fungi that if a human being consumes them he might have serious problems, because some fungi are responsible for poisoning or infection.

The third one that I mentioned is responsible for the most cases of Tapeworm infection. This means that the eggs and larvae pass straight to your digestive system and create the infection. To sum up, unknown factors (like bugs) must not touch our food, because there is a chance of infection. To help you here's a wikipedia list that shows the most easily transmitted diseases to humans fron insects: List of diseases caused by insects.


Which hormones/factors affect Calcium absorption in the small intestine and its regulation?

Parathyroid hormone increases intestinal calcium absorption by increasing production of vitamin D, which in turn uses calbindin. It also enhances calcium reabsorption from the kidney and the release of calcium from bone.


If you are in Europe they are juvenile common swift (Apus apus).

There is a website dedicated to them, with a page on how to raise them: http://www.commonswift.org/Hand_rearing_Swifts.html

They are very fragile and with the wrong diet they might develop feather deformations. They also require a continuous effort because they eat very often. I raised them a couple of times and when they take off is magnificent but it is easy to do something wrong. If you have some recovery center or expert nearby  I suggest to hand them over.


Advantage of cup-like shape of blood cells, spores?

The functional implications of the biconcave shape of human red blood cells are not fully understood. Several hypotheses have been suggested as explanations, including bending energy (1) and effects on oxygen transport (2). More recently, it has been hypothesized that the shape is important for the flow properties of the blood cells in capillaries. Uzoigwe (3) states that

  The deleterious nature of turbulent flow on the cardiovascular system
  suggests that the biconcave disc form has evolved out of a necessity
  to maximise laminar flow, minimise platelet scatter which in turn
  suppress atherogenic activity in the large vessels.(...) The biconcave
  profile of the discocyte means that much of the mass is distributed in
  the periphery. This increases the moment of inertia of the cell and
  subsequently renders the erythrocyte less prone to rotation during
  flow in the large vessels. Here it is suggest that this reduction in
  rotation promotes laminar flow and discourages platelet scattering by
  minimising the "Eddy currents" and it thus anti-atherogenic. A number
  of pathological mutations result in the red blood cell adopting a
  spherical shape as opposed to the biconcave disc profile. The sphere
  has a smaller moment of inertia when compared to the discocyte, as
  much of the mass is distributed round the centre. The spherocyte is
  hence much more prone to rotation during flow in the large vessels.

The advantages of various structures do depend on the scale of the system, as you say. For red blood cells, the size of capillaries and veins are of importance. The shape of red blood cells differ in animals that have blood transport systems with different structures than humans. Thus, the red blood cell shape is likely optimized with respect to movement in the human blood transport system, with oxygen diffusion also being a possible factor. To determine what advantages a specific shape of spores would give, you would need to consider the expected environment the spores would live in and their typical lifecycle.


Do viruses pickup new genetic sequences from the host cell?

Yes.  See for example this article, which describes how some viruses can pick up bits of human DNA.  Here's a quote from the article:

...researchers have shown that a large group of viruses, including the influenza viruses and other serious pathogens, steal genetic signals from their hosts to expand their own genomes.


Is it possible to remove one strand of double stranded DNA in vivo?

Both TALEN and ZFN gene editing technologies use a pair of single-strand endonucleases that ultimately lead to a double strand break. Cas9 in CRISPR-Cas technology, however, cuts both the DNA strands (there are some Cas enzymes in certain bacterial species that cut only a single strand [ref]).

  Image courtesy: http://www.xenbase.org/other/static/CRISPr.jsp

So, if you use a single unit of the pair, you can cut one strand of the DNA. You can use another nuclease to impart a cut at another site in the same strand. This will still not lead to the removal of the DNA sequence between the two cut sites. There is no available technology that can do this in-vivo. Possibly (a wild guess), you can use a modified oligonucleotide (or even an IVT synthesized RNA) that can bind to this stretch of sequence and break its interaction with the other DNA strand. In any case, a stretch of ssDNA would not be stable and be repaired quickly by polymerase.


If I cook some food, I get apparently several energetic advantages...

Let's make things a little more explicit. If you are talking of energy within the body, you are talking proteins, alcohols, fats, and sugars. You are not talking Vitamins or Minerals or any of the unique compounds (like specific antioxidants) that are available in the food.

  thermal : the temperature of the food is closer or superior to the temperature of my body or internal organs, so I do not have to produce energy to warm it.

You cannot eat enough to significantly alter the temperature of your body. The average American will eat roughly 5.4lbs of food per day - or roughly 2lbs of food per meal. Given that even raw food is at room temperature, the metabolic requirements to warm food you've eaten is negligible.

What's important is acidity and exposure. Food is generally broken apart and utilized by catalysts and proteins which have specific operating boundaries - which is why your stomach contents is acidic. However, your normal meals will not significantly alter your digestive capabilities either via pKa values or thermoregulation requirements.

What cooking can do is denature the raw food's proteins or compounds so as to make the usable energy sources more readily available. However, it can also just as easily destroy them (the 'char' on barbequed steaks is the meat exposed to high heat long enough to destroy almost everything but the carbon in the tissue). Whether a food gains or loses macronutrients depends upon the specific food and its preparation. A good example is potatoes, which are full of starch (sugars) in their natural state. However, french fries / frites / chips are often blanched before they're fried. The blanching dissolves much of the starch into water, leaving fewer sugars in the end product. However, the process of frying essentially adds fat to the food, and fats have a higher energy density than sugars so you have a net gain in caloric content.

  mechanical : the food may become easier to chew, absorb, conduct in the digestive tract, leading to less muscular force used.

For some foods, this is true. Steaming vegetables often makes them easier to chew/eat. The broth of stews and soups often contains micelles of fat and dissolved sugars, affording them greater and faster exposure to the digestive system. Keep in mind, you are not getting a net gain of caloric content from food by doing so, but merely reducing the time to utilization.

The calories saved by chewing less is going to be pathetically small, so to amend the previous paragraph: Yes, for some foods it's true that cooking will allow easier mastication and thus save energy. However, an extra chocolate chip or sip of spoon of rice could easily cover the energy spared.

  The cooking procedure may involve water immersion, and the water may penetrate the food and improve all three energetic aspects outline above.

If the energy source is water-soluble (that is: alcohols, ketones, and sugars) then water immersion - assuming you are also digesting the water solution after - will offer faster utilization, not necessarily more.

  But what are the respective scale of these advantages, compared to the Joule intake of the raw food?

Negligible in almost all cases. What cooking does is make things more palatable, has the potential to make micronutrients/vitamins more available (not macronutrients), and make the food edible in the first place as is the case with Taro plants, whose roots must be cooked in order to eat.

  Focusing on meat, for instance, is there an optimal cooking duration/temperature and eating temperature for human eaters, independently of personal tastes, for say, beef or chicken meat?

No. Cooking meat makes it safer to eat (unless you end up overcooking the meat and end up with a bunch of charred bone) and more palatable. Properly cooked meat has a very low chance of passing on parasites or other harmful organisms. Beyond that, there aren't compelling reasons to expose meat to heat - although as someone who's picked up stomach flus in his travels, it is a very compelling reason to do so.

*The above is based mostly on sporadically gained knowledge. If there are studies indicating otherwise, please alert me to them and I will rectify my errors.


Hardy-Weinberg applied to three alleles and stimation of allele frequencies

Everybody said it already, but there is none.  The original HWE equation ($(p+q)^2=1$) works because you've got two variables and two equations ($p+q=1$) to work with (in reality, these are just one equation and one variable, since $q=1-p$ so $p+(1-p))^2=1$).  Now you have three variables and still only the one equation ($p+q+r=1$) which is, mathematically, impossible.

You need go out and measure some frequencies.  In particular, you need to measure two of them - I'd choose two of the homozygous types for convenience's sake.

This basically summarizes everything nicely for ya: http://www.bio.miami.edu/dana/dox/trinomial.html


What is the basic structure of the nuclear lamina

Watch this animation and you'll understand the general process of mitosis:

http://www.sumanasinc.com/webcontent/animations/content/mitosis.html


In endochondral bone formation, why does only hyaline cartilage get ossified to form bone?

yes this is correct, i think hyline cartilage gets transformed to bone more quickly due to the fact that is has the matrix which is closest to bone in terms of density, also the cells are located more closely, therefore it is easier to convert this tissue to bone.


The pH profile of an enzyme is not necessarily symmetrical. As random examples, see Figure 7 here, or Figure 5b here. Or if you have access, a pH profile for Magnaporthe grisea catalase can be seen in Figure 7 of http://dx.doi.org/10.1042/BJ20081478

The reasons for this go back to why enzymes are pH dependent in the first place. One of the major reasons for a pH dependence is that key catalytic residues become  (de)protonated as the pH changes. But different residues have different effects and different pKas, so you need to look at the sum of all their effects.

Example:

Imagine that a key catalytic residue must be in a deprotonated form, and has a pKas of 4.0. At any pH above about 5.0, it's all in the deprotonated form, so that residue should work. Any pH below about 3.0 and the enzyme is completely dead.

But an enzyme might have more than one residue that's pH sensitive. So now imagine that there's another residue which in the protonated form helps the reaction, but isn't as critical to catalysis such that the deprotonated still has residual activity. For the sake of argument let's say this residue has a pKa of 9.0.

Now imagine a third pH sensitive residue with a pKa of 6.5, but it's even more removed from the active site and has an even lower effect on catalysis (for example, it's a remote electrostatic effect based on the polarization of the transition state).

What would the pH profile for this enzyme look like? Here's an example:

"Activity" is the estimated total activity, and Residue 1/2/3 are the fractions of "active" form of each residue. - Diagram was made using the Henderson–Hasselbalch equation to determine the fraction of "active" states of each individual residue, and then assuming that the inactive forms are 0%, 80%, and 33% the activity of the fully active form for the pKa 4.0, 6.5, and 9.0 residues, respectively.

Note that the maximal activity occurs at about pH 5.7, but the activity drops off asymmetrically - the enzyme is much more sensitive to low pH than high pH.

A similar thing happens with natural enzymes, except that they may have many more residues which have minor contributions. They also may have $\ce{H+}$ and $\ce{OH-}$ playing a role as reactants (thus affecting the intrinsic reaction rate), and pH may play other effects, such a denaturing the enzyme. That's what leads to the complex pH profiles: multiple small effects all adding together.


Is touching or inhaling 70% isopropyl alcohol dangerous to humans?

If you're interested in the biological or health effects of various chemicals, try to look up the Safety Data Sheet, or "SDS" or "MSDS", for that chemical compound.
Going to your favorite search engine and plugging in your chemical of interest to the search term "SDS" or "MSDS" will almost always get you to some kind of answer — either what you're looking for has a safety data sheet or it doesn't!
In the case of 70% isopropyl alcohol, there are SDSs/MSDSs out there that will tell you what potential health effects are. Here's one example for 70% isopropyl alcohol:

Potential Health Effects
Eye: Produces irritation, characterized by a burning sensation, redness, tearing, inflammation, and possible corneal injury. May cause transient corneal injury. In the eyes of a rabbit, 0.1 ml of 70% isopropyl alcohol caused conjunctivitis, iritis, and corneal opacity.
Skin: May cause irritation with pain and stinging, especially if the skin is abraded. Isopropanol has a low potential to cause allergic skin reactions; however, rare cases of allergic contact dermatitis have been reported. May be absorbed through intact skin. Dermal absorption has been considered toxicologically insignificant. The cases of deep coma associated with skin contact are thought to be a consequence of gross isopropanol vapor inhalation in rooms with inadequate ventilation, rather than being attributable to percutaneous absorption of isopropanol per se.
Ingestion: Causes gastrointestinal irritation with nausea, vomiting and diarrhea. May cause kidney damage. May cause central nervous system depression, characterized by excitement, followed by headache, dizziness, drowsiness, and nausea. Advanced stages may cause collapse, unconsciousness, coma and possible death due to respiratory failure. Aspiration of material into the lungs may cause chemical pneumonitis, which may be fatal. The probable oral lethal dose in humans is 240 ml (2696 mg/kg), but ingestion of only 20 ml (224 mg/kg) has caused poisoning.
Inhalation: Inhalation of high concentrations may cause central nervous system effects characterized by nausea, headache, dizziness, unconsciousness and coma. May cause narcotic effects in high concentration. Causes upper respiratory tract irritation. Inhalation of vapors may cause drowsiness and dizziness.
Chronic: Prolonged or repeated skin contact may cause defatting and dermatitis.

Safety data sheets sound terrible! But in reality, people use rubbing alcohol with common sense, without putting into their eyes, without drinking it, etc.
Mainly the point of this answer is to help you find the answer for yourself, if you want to find out about this or other chemicals you might be worried about.


Is [O2] different in a 5 mL liquid media?

I believe there is. As you can see in the image below, strictly anaerobic bacteria can survive in liquid medium in test tubes, herefore they will migrate to the bodem of the medium to avoid Oxygen. Also you can see that microaerophiles, which require an oxygen percentage of approximately 2-10% (versus approximately 20% in normal air), will be able to survive below the surface of the medium.

So yes, there is a drastic change, seeing as obligate aerobic bacteria can surive at the surface of the medium, and obligate anaerobic bacteria can survive at the bodem.

To this I have one caveat to add. Namely that these tests are normally done in standard test tubes (approximately 9, 22 or 28mL depending on size), which would most likely contain more medium. So I am not absolutely sure, nor have I found any specific information on oxygen gradients in 5mL tubes. You could test this by performing the experiment in described in the figure in your tubes with 5mL medium and see what happens. Then you will definitely know.

Hope this helps!


The long hairy legs make me think that this might be a spider belonging to the Tegenaria genus, or something related.