Why do bacteria produce H₂O₂? I recently read up that people with NADPH oxidase deficiency (Chronic granulomatous disease CGD) have a tendency to be infected by Catalase positive organisms. NADPH oxidase helps produce the $H_2O_2$ via superoxide that is required by other enzymes to kill the bacteria.

Case 1: In the phagoloysozome, when there is a deficiency of NADPH oxidase, catalase positives can clear off the $H_2O_2$ they produce, thereby stopping production of free radicals via Fenton and myeloperoxidase. The bacteria survives and hence causes symptomatic infection in CGD patients.

Case 2: On the other hand, since catalase negative organisms can't clear off the $H_2O_2$ they produce, they remain susceptible to the free radicals produced by other enzymes like Myeloperoxidase and Fenton reaction, which would still kill the bacteria. In short, the bacteria 'lend' the $H_2O_2$ which feeds into these reactions leading to its own death. Hence, CGD patients can fight off catalase negative organisms.

My question is, why do the bacteria produce $H_2O_2$ in the first place? Is it produced only by aerobic organisms? If so, why would there be organisms that produce $H_2O_2$ and still not have a catalase (as had happened in case 2)? Isn't $H_2O_2$ is harmful even in the absence of free radical producing enzymes since the Fenton reaction is a non-enzymatic reaction?

why does the bacteria produce H2O2 in the first place?

It is produced by all organisms as a byproduct of respiration. See this wikipedia article:

  All living cells produce reactive oxygen species (ROS) as a byproduct of metabolism. ROS are reduced oxygen intermediates that include the superoxide radical ($O_2^•$) and the hydroxyl radical ($OH^•$), as well as the non-radical species hydrogen peroxide ($H_2O_2$)....The superoxide anion is formed directly from the one-electron reduction of molecular oxygen. Hydrogen peroxide is then formed from the disproportionation of the superoxide anion. This reaction occurs very quickly in seawater. Next, the reduction of hydrogen peroxide yields the hydroxyl radical, $H_2O_2 \xrightleftharpoons 2OH^•$, which can then get reduced to the hydroxyl ion and water.

 Source

But, it has some useful functions too! One of those, as you mention, is in immunity through NADPH oxidase, but there are some more! From the same above wikipedia article:

  These ROS are important in the normal functioning of cells, playing a role in signal transduction and the expression of transcription factors.

For this line, wikipedia cites 3-4 articles, one of which is this:

  The OxyR transcription factor is sensitive to oxidation and activates the expression of antioxidant genes in response to hydrogen peroxide in Escherichia coli. Genetic and biochemical studies revealed that OxyR is activated through the formation of a disulfide bond and is deactivated by enzymatic reduction with glutaredoxin 1 (Grx1). The gene encoding Grx1 is regulated by OxyR, thus providing a mechanism for autoregulation.

It is not produced by obligate anaerobic bacteria and that is why they are very sensitive to oxygen. See this article:

  Obligate anaerobes are microorganisms killed by normal atmospheric concentrations of oxygen (20.95% $O_2$)...Because molecular oxygen contains two unpaired electrons in its outer orbital, it is readily reduced to superoxide ($O_2^−$) and hydrogen peroxide ($H_2O_2$) within cells. Aerobic organisms produce superoxide dismutase and catalase to detoxify these products, but obligate anaerobes produce these enzymes in very small quantities, or not at all.

If so, why would there be organisms that produce H2O2 and still not have a catalase (when the bacteria is outside, not in the phagosome)?

Logically, no. Producing $H_2O_2$ but not being able to handle it would be like suicide for any organism. Also, I could not find any example of bacteria which lack catalase but still produce hydrogen peroxide. However, if you talk about spontaneous formation of $H_2O_2$ from $O_2$ or spontaneous conversion of $H_2O_2$ to $OH^-$ or $H_2O$, then there could be many examples.

Isn't H2O2 is harmful even in the absence of free radical producing enzymes since the fenton reaction is a non-enzymatic reaction?

I think you have used some inappropriate words here; you probably mean free radical metabolizing enzymes (like catalase or superoxide dismutase) instead of free radical producing enzymes. And you probably want to say that $H_2O_2$ can also affect bacteria through fenton's reaction even in the presence of such enzymes (correct me if I'm wrong here).

You are partially correct. It should damage the bacteria, but, as you know, bacteria are ever-evolving and have already found a way to counteract this. First, lets see how fenton's reaction works. See this:

  After addition of the iron and the hydrogen peroxide, they are going to react together to generate some hydroxyl radicals as it shows in the following equations:

  $Fe^{2+} + H_2O_2 \rightarrow Fe^{3+} + OH^• + OH^-$

  $Fe^{3+} + H_2O_2 \rightarrow Fe^{2+} + OOH^• + H^+$

  The typical range for the iron dose is 1 part of Fe per 5-25 parts of H2O2.

  After that the hydroxyl radicals are going to react with the pollutants to oxidize its. Actually the hydroxyl radicals can react according 4 kinds of reactions with the pollutants:

  Addition: $OH^• + C_6H_6 \rightarrow (OH)C_6H_6$

  Hydrogen Abstraction: $OH^• + CH_3OH \rightarrow CH_2OH^• + H_2O$

  Electron Transfer: $OH^• + [Fe(CN)_6]^{4-} \rightarrow [Fe(CN)_6]^{3-} + OH^-$

  Radical Interaction: $OH^• + OH^• \rightarrow H_2O_2$

  During the Fenton's reaction all the parameters are adjusted to promote the two first kind of reaction between the pollutant and the hydroxyl radicals.

Now, lets see how the bacteria tackles this. See this:

  While E. coli Dps can store iron, it prefers to use $H_2O_2$ rather than $O_2$ as an oxidant (Zhao et al., 2002). This suggests that the primary role of Dps in E. coli is to protect DNA against the potential damage of hydroxyl radical produced by the Fenton reaction, rather than an iron storage function. Although an iron storage Dps-like ferritin was found in the gram-negative bacterium Listeria innocua (Bozzi et al., 1997), recent studies have shown that it is indeed a Dps protein, which attenuates the production of hydroxyl radical by Fenton chemistry: DNA cleavage assays showed that the protein, while not binding to DNA itself, protects it against the deleterious combination of $Fe^{2+}$ and $H_2O_2$ (Su et al., 2005). It seems likely that the principle role of this family of proteins is a DNA protecting anti-redox agent (Chiancone et al., 2004).

EDIT: Now, as you asked in comments:

how catalase negative organisms manage with the H2o2 they produce

read the following paragraph from this article (emphasis mine):

  Under different growth conditions we found that both L. plantarum ATCC 8014 and a catalase-positive strain, T-1403-5, were capable of utilizing $0_2$, particularly during the late stages of growth. This suggested the need for enzymes which would protect the lactobacilli
  from $H_20_2$ and $0_2$ which might be formed. Superoxide dismutase was present at low but constant levels in both catalase-positive and catalase-negative strains. NADH peroxidase was present in strain 8014 and this enzyme increased in specific activity as the cells aged and entered the period of increased $0_2$ uptake. The presence of this enzyme should protect the organism against toxic effects of $H_20_2$ in the absence of catalase production. In strain T-1403-5 this role can be performed by the very active atypical catalase, although this strain may also possess the peroxidase. When growth rates of the catalase-negative and catalase-positive strains were compared, the rates of the catalase-negative strains were greater than that of the catalase-positive strain. Therefore, it did not appear that the possession of catalase conferred any advantage on strain T-1403-5.

Or see another article on Streptococcus pneumoniae:

  Aerobic growth of Streptococcus pneumoniae results in production of amounts of hydrogen peroxide ($H_20_2$) that may exceed 1 mM in the surrounding media...The mechanisms allowing S. pneumoniae, a catalase-deficient species, to survive endogenously generated concentrations of $H_20_2$ that are sufficient to kill other bacterial species is unknown. In the present study, pyruvate oxidase (SpxB), the enzyme responsible for endogenous $H_20_2$ production, was required for survival during exposure to high levels (20 mM) of exogenously added $H_20_2$...Thus, SpxB is required for resistance to the toxic by-product of its own activity. Although $H_20_2$-dependent hydroxyl radical production and the intracellular concentration of free iron were similar to that of Escherichia coli, killing by $H_20_2$ was unaffected by iron chelators, suggesting that S. pneumoniae has a novel mechanism to avoid the toxic effects of the Fenton reaction.

From the same article's Discussion heading (there are actually many points, so I recommend you read them yourself too, I'll add main points here):

  The role of SpxB expression in resistance to killing by $H_20_2$ was confirmed by the demonstration that spxB mutants, which produces no detectable $H_20_2$, had a significant decrease in $H_20_2$ resistance and by demonstrating that complementation of the spxB gene fully restored both $H_20_2$ production both $H_20_2$ resistance. These results showed that SpxB expression is required for wild-type levels of resistance to $H_20_2$ rather than merely correlating with it.
  when cultures of both strains were shifted from anaerobic to aerobic conditions with or without chloramphenicol, a protein synthesis inhibitor, $H_20_2$ resistance was not affected. This confirmed that de novo protein synthesis is not involved in the increase of $H_20_2$ resistance observed during aerobic growth, suggesting that an inducible response is not involved.
  Furthermore, the addition of pyruvate to either mutant or wild-type cultures slightly decreased $H_20_2$-mediated killing, arguing that increased killing of spxB mutants is not due to toxic by-products resulting from the reaction of excess pyruvate and $H_20_2$. Together, this suggested that a product of SpxB activity other than $H_20_2$ acts to increase resistance
  Furthermore, the ability of DF to eliminate the EPR signal caused by $OH^·$ in S. pneumoniae suggests that the inability of this iron chelator to increase $H_20_2$ resistance in S. pneumoniae is not merely due to a lack of permeability.

In the end, what I'd conclude is that different bacteria adopt different mechanisms to tackle this problem, and many of those mechanisms aren't known yet. So, there's no definite or exact answer to this question.

References:

ROS production in marine microalgae
NADPH oxidase
Activation of the OxyR Transcription factor by Reversible Disulfide Bond formation
Obligate Anaerobe
Catalase
Superoxide Dismutase
Iron Metabolism: From Molecular Mechanisms to Clinical Consequences - Robert Crichton
Oxygen metabolism of catalase-negative and catalase-positive strains of Lactobacillus plantarum.
Factors Contributing to Hydrogen Peroxide Resistance in Streptococcus pneumoniae Include Pyruvate Oxidase (SpxB) and Avoidance of the Toxic Effects of the Fenton Reaction


How to name such grouping behaviour? Under which keyword would you try to find out more about the grouping behaviour which looks like this? Does anybody recognizes such behaviour, or know an animal species which uses it?

My tries: threshold group behaviour (threshold here is the group size - if bigger than 5 individuals == stable), or gravitational group behaviour?

After step 6 the group disintegrates (for example due to foraging) and mechanism starts by step 1. Important thing is that the location of forming stable group is always different.

I believe it is a type of fission-fusion society or even some hybrid with agent based modeling.

  In ethology, a fission–fusion society is one in which the size and composition of the social group change as time passes and animals move throughout the environment; animals merge (fusion)—e.g. sleeping in one place—or split (fission)—e.g. foraging in small groups during the day. For species that live in fission–fusion societies, group composition is a dynamic property [fission-fusion society].

A classical example is the Bonobo or pigmy chimp.

Bonobo - Pigmy Chimpanzee
Sociobiology
The Social Behavior of Chimpanzees and Bonobos


During a large forest fire, what is the evacuation behavior of birds? I'm interested in birds' behavior during large forest fires. Do they fly away as soon as they smell smoke, or wait until seeing fire itself? Do they fly away in flocks, or individually? Do they ever try to return to the area later, or just abandon it for good?

Interested mostly in average forest birds like jays, cardinals, finches, etc.

The exact behaviour of birds during a wildfire is unclear and there is little scientific evidence on their exact behaviour. Anecdotal notes from eye witness observations indicate that healthy birds fly away from the affected area before they are in danger. Birds that are unable to fly or move out of danger from the fire such as chicks in nest and indisposed birds are likely to die. Different species are likely to react differently to fire, species that flock normally will probably flock together as they fly and species that are more solitary are not likely to flock. Most fires happen in late summer and fall, just after the breeding season for most birds and during their migration, meaning they can escape the area. If the fire is very widespread, the birds may not be able to find appropriate shelter and food and would likely die as a result.

Wildfires are a natural phenomenon and birds have evolved to adapt strategies to deal with them. Some birds benefit from wildfires as they are a normal part of ecological succession.

  Ecological succession is the gradual process by which ecosystems
  change and develop over time in response to a disturbance or
  colonization of new habitat.

Fire essentially creates a new habitat in which not all the same birds will use. Blue Jays prefer forests, but if a wildfire burns a forest, it will likely become a shrubby field afterwards and may take years to regrow into a forest. The Blue Jays will not likely return in large numbers until the habitat is a forest again.

A remarkable bird that is dependent on forest fires is the Kirtland’s Warbler. They breed in Jack Pine forests that are a certain height, once the forests mature; the habitat is no longer suitable. The jack pines themselves only release their seeds from cones in hot fires as they are serotinous and only open when exposed to intense heat, greater than or equal to 50 °C, the typical case is in a fire. The wildfires then create a succession cycle to always have suitable habitat for the Kirtland’s Warbler. Fire suppression of forests by humans has been listed as one of the reasons that led to large declines of this species.

Additional reading:

How Wildfires affects Birds?

Jack Pine Information


Why does a blood test show ethanol when no alcohol was consumed? Why would ethanol show up in a blood test if a person had not been drinking alcohol in many years. What are other reasons for showing ethanol?

There are some situations when ethanol-like compounds can be present in the blood stream:

  [...] exposure to hand sanitizers, after shave lotions, perfumes, medications, hygiene products, cosmetics, foods [...]  Uncontrolled diabetes mellitus can cause false positive alcohol tests.

Source: Dr. Kokil Mathur. Answer on: False-Positives for blood alcohol content. Available from MedHelp forums.

Other causes as pointed on eHow.com:

low calorie diets
gasoline, paints, lacquers
lower hematocrit values
diabetes mellitus


Why are canines not nauseated by similar foodstuffs/state of decay as human beings? I am continually surprised at the items my pet dog is willing to ingest.

I understand part of the consumption is driven by nutritional instincts (licking salty liquids such as sweat) or nurturing instincts (eating baby faeces to prevent predators) but why does an animal with a sense of smell many thousands of times greater than our own not become nauseated by the same substances, smells or conditions that humans do?

Sweat
Faeces
Decayed foodstuffs
Assorted garbage
Untreated and/or dirty water

I have known my dog to bury a piece of rotting pork only to dig it up several months later for consumption.

In addition I watched dogs refuse to eat certain items (spicy meat etc) until their owner makes a move to take it back at which point the animal will swallow the item causing a gag, hacking couch or nasal clearance.

Is there a biological mechanism that suppresses the gag reflex in canines, is the need to consume overpowering their distaste or do they simply not find such substances unpalatable?

Your dog finds these things palatable, I assure you, and no gag-reflex suppression is needed.

I had a dog that would steal duck eggs from my flock, bury them all over the place, and dig them up when properly rotted to enjoy as a treat, and no, I'm not making this up. I saw her do it, ran across many buried duck eggs while gardening, and could immediately smell when she was enjoying one.

All that to say what smells good to a dog has nothing to do with what is acceptable to you. Many of your "dislikes" are conditioned: living in a society where cleanliness is valued and clean water is available, humans in such societies can afford to snub their noses at less sanitized things.

Manure may well elicit a completely different reaction to a farmer, who saves it carefully before spreading it on his fields to enrich the soil. To him, it might be the smell of a good crop next summer.

Many species exhibit corprophagia. It's not known why dogs (some, far from all) do this. Rabbits, for instance, eat their own feces after their first movement of the day. This is normal and nutritional for them.

Eating the feces of other species, particularly herbivores, is common among dogs and isn’t considered abnormal, just undesirable. My (same) dog followed my goats around like they were Pez dispensers. Since dogs can't digest cellulose, they get some of the advantage of eating plants this way.

Capybara, rabbits, hamsters and other related species do not have a complex ruminant digestive system. Instead they extract more nutrition from grass by giving their food a second pass through the gut. Soft fecal pellets of partially digested food are excreted and generally consumed immediately. Consuming these cecotropes is important for adequate nutritional intake of Vitamin B12. They also produce normal droppings, which are not eaten.

Young elephants, pandas, koalas, and hippos eat the feces of their mother to obtain the bacteria required to properly digest vegetation found on the savanna and in the jungle. When they are born, their intestines do not contain these bacteria (they are completely sterile). Without them, they would be unable to obtain any nutritional value from plants.

Eating garbage and human feces is thought to be one function of dogs during their early domestication, some 12,000 to 15,000 years ago. They served as our first waste management workers, helping to keep the areas around human settlements clean. A study of village dogs in Zimbabwe revealed that feces made up about 25% of the dogs’ overall diet, with human feces making up a large part of that percentage.

Coprophagia
Daily rhythms of food intake and feces reingestion in the degu, an herbivorous Chilean rodent: optimizing digestion through coprophagy
Coprophagia as seen in Thoroughbred Foals


Why are there multiple sequences for the same segment for an individual "strain" of influenza? I am looking at the genome of the influenza virus being used in the flu vaccine 2017-2018: A/Michigan/45/2015.

When I look below at the individual segments, there are 4 sequences for each segment - shouldn't there be only one for a single "strain"? Is this due to rapid mutation rates? Or is it that they are including both positive and negative sense of the virus?

Edit: sorry, link here:

https://www.fludb.org/brc/fluStrainDetails.spg?strainName=A/Michigan/45/2015(H1N1)&decorator=influenza

It looks to me that the website you're looking at is mostly taking publicly available data from Genebank (the NCBI repository for sequence data) an collects it to form an overview.

For your question this means that there are 4 available sequence datasets for the A/Michigan/45/2015 influenza strain - they are likely very similar but based on the reported segment length not quite identical.

  Or is it that they are including both positive and negative sense of the virus?

If you mean the positive and negative strand of the DNA, then no - since the sequence of these two is always complementary the Genebank repositories only stores the forward sequence.

You can also see that the 4 different datasets have similar Acession numbers:
KY117020 - 27 (Passage M1/C3)
KU509700 - 07 (Passage E1)
KU933490 - 07 (Passage E3)
KY090607 - 14 (Passage M1/IR)

You can look up more details for these accessions on the genebank website:

It seems that all 4 datasets came from the same publication
... which apparently was never published (so it's not available online), but it might be part of some WHO program?
The main difference of the 4 datasets I can find is the passage of the strain. I'm no virologist, so I'm not quite sure what it means, but in cell biology passage describes the time a certain cell line has been in (in vitro) culture.


Can inhibition of lymphocytes migration be a direct cause of chronic inflammation? Here is the original slide:

I am thinking about the "cord factor" sentence in a more general case.

Assume you inhibit Leucocytes migration.
How does this lead to accumulation of macrophages in the site of infection?

The mechanism is likely very straightforward. Activated macrophages already in the area are releasing pro-inflammatory cytokines like TNFα, IL-1β, IL-6, IL-12, MIP-2, etc. These are not only important for granuloma formation, but they also recruit other immune cells to the area. However, since cord factor has this anti-migratory effect, once the cells get there they can't leave. This is important because activated macrophages are key antigen-presenting cells (once they kill and break down the antigen, in this case Mycobacteria), and they need to move to the spleen to assist in the upregulation of the adaptive immune response. By preventing this, mycobacteria can evade part of the immune system - part of the reason why TB is so hard to clear once acquired.


How does the body measure dehydration? What, physically, does the body do to measure it? I assume it's measured by how how turgid or plasmolysed certain 'sample cells' are, or water concentration in the blood,

What is the way they use to measure it?
What do the receptor cells that do the measuring actually do that is variable with water concentration, etc.

From Wikipedia entry on thirst:

  In the mammalian brain, the posterior surface of the hypothalamus
  forms the front wall of the third ventricle (a cerebrospinal
  fluid-filled cavity) and clusters of cells (osmoreceptors) on this
  surface, notably in the organum vasculosum of the lamina terminalis
  (OVLT) and subfornical organ (SFO), signal this cellular dehydration
  to other parts of the brain, and thirst is experienced. Destruction of
  this part of the hypothalamus in humans and other animals results in
  partial or total loss of desire to drink even with extremely high salt
  concentration in the extracellular fluids.1

The entry on osmoreceptor says in part:

  When the osmotic pressure of blood changes (i.e. it is more or less
  dilute), water diffusion into and out of the osmoreceptor cells
  changes. That is, they expand when the blood plasma is more dilute and
  contract with higher concentration.

It also describes how the kidney measures chlorine anion flow through some nephrons, which triggers a cascade of messenger molecules resulting in increased blood levels of the hormone angiotensin, which also results in thirst messages originating in the hypothalamus.

1Derek A. Denton (8 June 2006). The primordial emotions: the dawning of consciousness. Oxford University Press. pp. 118–19. ISBN 978-0-19-920314-7.

2Walter F., PhD. Boron (2005). Medical Physiology: A Cellular And Molecular Approach. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 872


Earth's history: The Great Oxidation Event and the 'Boring Billion' From what I understand the 'Great Oxidation Event' occurred around 2.4 billion - 2.3 billion years ago, when cyanobacteria flooded Earth’s atmosphere with oxygen.

The 'boring billion' period was around 1.8 billion years ago, during which it is thought not a lot changed on planet Earth. Low oxygen levels were thought to be 1-40% of modern oxygen levels during this time.

Why did the atmosphere go from 'flooded with oxygen' to 1-40% of modern oxygen levels. Was it because during the Mesoproterozoic era, the rate
of burial of decaying organic carbon matter under marine sediments
flatlined?

Your question probably arises from a misunderstanding regarding the 'flooding' metaphor. I would not assume that 'flooded Earth's atmosphere with oxygen' means a lot of oxygen in the first place ... the metaphor means that oxygen levels rose from basically absent to noticeable.

If you look at the history of oxygen in Earth's atmosphere you see a general trend of gradual increase with a 1GY lasting stationary phase (Holland (2006), picture taken from above linked Wikipedia article - red and green lines are upper and lower estimates, respectively):

After initial atmospheric oxygenation about 2.5 GYa, Earth's oxygen sinks (mainly the oceans, after that landmasses and the ozone layer) were filled and buffered atmospheric oxygen levels, keeping them low. Once those sinks were saturated (approx. 850 MYa), the atmosphere started to oxygenise rapidly.

The constant (or as discussed below: drop in) oxygen concentration is caused by these sinks. The oxygen that is produced by photosynthesis was just not available to Earth's organisms as it was not atmospheric.

As @GerardoFurtado points out in the comment, modalities of the stationary phase are still debated. A review by Lyons et al. (2014) presents evidence that after the initial increase in oxygen levels, a drop in atmospheric oxygen preceded the stationary phase (see their Fig. 1, blue boxes). This does not change much as the newly inferred stationary phase, though probably a more fluctuating stationary phase than suggested by Holland (2006), is still higher than before the great oxidation event and lower than at present.

The major conclusions remains the same: There is evidence that the seemingly slow evolution 2-1 GYa was probably caused by oxygen limitation and oxygen levels were buffered by oxygen sinks. The change of oxygen concentration was determined by both the rate of oxygen production and the rate with which oxygen is stored in those sinks; the interplay of those rates caused the oxygen concentration to remain constant, drop or occasionally even rise, i.e. fluctuated.


Resource for model organism anatomy/physiology for biological experiments I'm looking for a resource that best surveys the anatomy and physiology of common genetic model organisms, and how their characteristics are particularly useful for biological experiments.

For example, I'm studying the eyeless Drosophila gene, but it would help to know that species' specific compound eye anatomy and normal development, so that I can weigh the pros and cons of using that particular model organism over another.

In the Bgee database, you can look at gene expression and anatomy of various model species, e.g. Drosophila. This doesn't give you the full anatomy, but at least an ontology of tissues and cell types.


How do plant cell divide without centrioles? Most plants do not have centrioles, so what organelle enables them to multiply?

There are many different ways to make a spindle in plant cells:

  Mitotic spindles may be organized at centriolar centrosomes (only in final divisions of spermatogenesis), polar organizers (POs), plastid MTOCs, or nuclear envelope MTOCs (NE-MTOCs).

Of these, only the latter has been observed in angiosperms (flowering plants). For more info (and the source of the quote), see Brown & Lemmon, "The Pleiomorphic Plant MTOC: An Evolutionary Perspective"


What microscope/magnification would I need to observe P. Acnes bacteria? I am currently attempting to grow a culture of P. Acnes bacteria.  Right now, my only hope in identifying colonies of the bacteria in the culture is to use a black light to find colonies that glow orange.  I am not sure whether or not this will work since nutrient agar may not provide them with something that helps them produce porphyrins.  It's also entirely possible that another form of bacteria contaminating the culture would produce the same effect.

I would like to entertain the possibility of buying a microscope for this project.  I have never owned a quality microscope(just toy ones in the past), so I don't really know what type of microscope or what magnification I'll need in order to correctly identify and observe the P. Acnes bacteria.

What would be interesting is if I could turn this into a pharmacological project; if I can verify that I have the correct bacteria(to a fair degree of certainty, anyway), I can see how the bacteria reacts to different chemicals and environments.

I agree with canadianer that chemical tests are generally more useful for identification.  However, morphology does help and some staining techniques can be useful for identification (the Gram stain is the obvious one).  If you are looking for a microscope, look for a nice scope with a 100x oil-immersion objective and a 10x ocular lens (12x would be OK too). Zeiss, Nikon and Olympus are some old names that make good scopes - and there are more.


How can a drone be male? A drone bee is male and is the product of only a queen bee. How is it that the drone bee can be male. I know that a drone is produced by an unfertilized egg, but this does not explain where the two X chromosomes come from. To me, this means that the one X chromosome from the queen must some how be duplicated.

The short answer, which has already been pointed out by user137, is that females are diploid while males are haploid. Bees do not have sex chromosomes per se; rather sex is determined by the csd gene on chromosome III (csd stands for complementary sex determination). Diploid bees that are heterozygous at the csd locus (i.e. contain two different alleles (versions of a gene) for csd) are female (workers).

Bees that are haploid at the csd are males. Interestingly, diploid bees that are homozygous at the csd (i.e. contain two copies of the same csd allele) are also males. But in the honey bee, these bees do not survive as they are killed by workers before they mature. In some other haplodiploid species, however, both haploid and diploid males are viable (the bumble bee Bombus terrestris for example). Also note that diploid honey bee drones can be viable if they (somehow) make it to maturity without being killed by workers (e.g. see here).


How do bats survive their own coronaviruses? How do bats survive their own coronaviruses (without showing any symptoms)?

Or, more generically, how can viruses keep reproducing inside healthy carriers without inducing any pathogenic effect?

Are coronaviruses able to replicate themselves without harming bats, or maybe these viruses are just latent like herpesviruses in humans?

Related question: Why are bats the source of dangerous coronavirus pandemics?

It's common for the reservoir host of a zoonotic virus to be tolerant of it. MERS coronavirus appears to cause mild or no disease in dromedary camels ( source ), but kills about 35% of confirmed infected humans. ( CDC ) Sin Nombre hantavirus seems to be mild in the deer mice that spread it, despite ~36% fatality rate in humans. ( source ) Mosquitoes are efficient vectors for flaviviruses like dengue and zika in part because they have adaptations we lack that protect them from the virus. ( source ) Also, human communities are host to several viruses: about 90% of people have a herpesvirus infection ( source ) with similar numbers for polyomaviruses. ( source ) Very few of these infected individuals show symptoms.
The wide prevalence of these asymptomatic infections shows that the virus is successful when it can replicate while the host remains healthy. In general, virus reproduction kills cells, and when cells die faster than the host can replace them, this causes symptoms up to and including death. The host's immune system supresses virus activity, and a virus that can't evolve ways to avoid immune supression will be wiped out. But if the virus gets so good at avoiding the immune system, it will kill the host, which is bad for the virus. So both host and virus tend to evolve to a point where the immune system wins most, but not all of the time. There is a lot more to it, but I'll stop here.

In conclusion, we don't really need to look for special properties of bats to explain their tolerance of coronaviruses, even though, as iayork points out, there are reasons to expect bats might be more resistant.


Value of r (intrinsic rate of natural increase) What is the current value of 'r' (instrinsic rate of natural increase) in India? How do we calculate it?

My book says that In 1981, the r value for human population in India was 0.0205. But this link (https://www.google.co.in/amp/knoema.com/atlas/India/topics/Demographics/Population/Rate-of-natural-increase%3fmode=amp) says it was around 22.50 in the year 1981. Such big discrepancies are a query.

NCERT shows per capita value is divided by 1000, not hundred (%). So the data you see is 22.50 per thousand! So, the per capita rate is 22.50/1000 = 0.02250 that is almost equal to 0.0205 given in book!

To make you understand better, remember that GDP and per capita GDP is different, the same way birth rate or death rate is calculated per 1000 but when we ask per capita we have to actually divide it by 1000.

Now in 2016 , it is 0.01019 i.e. 0.0102

I hope you understand!!


Is monogamy a human innate behaviour? As the question states, got curious and I was wondering if monogamy is an innate human behaviour or is it because of how we built society (religion, traditions, etc.)?

Let's say we go back in time, would we see humans settling down with a single partner at a time and caring for their children as a couple for life or would they reproduce with several leaving the mothers with their children?

Thanks!

Humans are believed to be mostly serial monogamists with a noticeable components of secret cheating. Serial monogamy means most will have a single partner at a time but  will likely have several partners throughout their life, there is however an under current (~15%) of hidden cheating in most studied populations. Also I say mostly becasue human behavior is plastic and nearly every possible combination exists, albeit in small numbers.  Males do have a stronger tendency to seek multiple partners at the same time, which makes biological sense.
 like many social species you really have several mating strategies coexisting, often in the same head. Our large brains allow for more flexible approach to strategies.

In other animals exclusive (one mate forever) monogamy is exceptionally, almost breathtakingly rare, (not counting animals that only ever mate once). The Azara's night monkey is one of the few that has been backed by genetic research. Almost every monogamous species ever studied either has some rate of cheating, or is serial monogamous.


Why is an increase in the amount of oxygen in the atmosphere favorable for life? I have followed the David Attenborough series on 'First life' and heard, that an increase in the amount of oxygen in the atmosphere, as it took place just before the Cambrium, is generally favorable for life and also enables the evolution of larger organisms.
Why is that so? Is it because aerobic respiration had a better conversion rate to energy?

Because it's favorable for the process of aerobic respiration which requires O2 to produce ATP, which is the little power storage unit.

With a bigger concentration of O2, it was possible to produce more ATP, should you evolve in that direction and you needed that constraint to be removed.


Red fox with blue legs On the Wikipedia I found this photo of a red fox, labeled as being taken at Quesnel Lake, British Columbia:

Why would the fox have blue legs? Is that normal for a Red Fox?

Original vs. Adjusted

Adobe Camera Raw Temperature Adjustment +30 / Tint Adjustment +3

The fox has black skin and fur. The blue is just a problem with the White Balance of the photograph. See Adjustments made above.

This is similar to the Blue Dress / White Dress Meme this year.

  I find it kind of hard to believe the legs appear blue because of "white balance". The nose and upper part of the legs are black, so it is not like all the black in the photo is appearing blue. – Imprisoned Rhesus

The reason the legs look Bluer than the Nose is that the nose is mostly black with no white and the front part is in shadow. The top part, which is reflecting some of the sky appears blue in the original.

The reason the legs look more blue is

They are not in shadow
There is a good amount of white fur mixed in with the black

The white fur will look far bluer when the white balance is off and will trick your eyes into seeing the black as blue.


What happened to this seashell? We found this seashell on a Mediterranean beach in the south of France. While most of the shells we found were quite intact, this one caught our attention.
It is light and littered with tiny holes, and thicker than other shells we found.
Is this due to erosion in the water? How did the shell look like before the ocean changed it? Was the shell simply exposed to the water for a longer time?

The holes are probably caused by one of a family of parasitic sponges.  The holes, as you'd expect, kill the oyster, and the sponge then takes up residence in the shell. A number of species of this family live in the Mediterranean, with Cliona apparently being the most common genus (e.g. Cliona celata and C. viridis).  Images of oyster shells after a Cliona infestation can be seen here and here; these images are more dramatic than the one you found, but show the same general pattern.


How can a pathogenic bacterium be avirulent? Streptococcus pneumoniae R6 is a pathogenic bacterial strain but it is avirulent. How can a pathogen be avirulent. What does it mean if a pathogenic bacterium is avirulent?

Streptococcus pneumoniae is a pathogenic species. Streptococcus pneumoniae R6 is an avirulent strain of this species. Presumably this means that specific virulence genes that are present in virulent strains of Streptococcus pneumoniae are missing or mutated in the R6 strain. In fact the most likely difference would be that virulence factors are encoded by a plasmid that has been lost in the avirulent strain.

The use of avirulent strains is a common strategy for studying pathogenic bacteria, although obviously it precludes studying mechanisms of pathogenicity directly.


Is this a grass cell? I found this picture online claiming it was a grass cell. Clearly it is a cross section image but I was hoping you could tell me if this is actually grass, or something else if anything.

It's not a single grass cell, but this does indeed appear to be a micrograph of a leaf of grass—so it actually contains numerous cells. Here's another image I was able to find with a much more clear description of exactly what you're seeing:

  Marram grass leaf. Light micrograph of a cross section through a closed (unravelled) leaf of Marram grass, Ammophila arenaria. The deeply grooved leaf is thrown into folds (seen here) and it uncurls when mature so that the folds do not face the centre. The folds conserve water and withstand salt, and prevent excessive evaporation. Round vascular bundles are visible inside each fold, serving to transport food and water through the leaf. Spines on the surface discourage animals from eating the leaf. Marram grass is important in coastal ecology, since it is one of the commonest grass species in Britain to stabilize sand dunes. Magnification: x22 at 35mm size. (Emphasis added)

  Source: http://www.sciencephoto.com/media/30161/view

And here's another:

  Transverse section of Marram Grass leaf , showing adaptations to prevent water loss; outer thick cuticle, curling by means of hinge cells to protect inner epidermis, stomata
  sunken into surface to maintain high humidity

  Source: http://www.eplantscience.com/index/principles_of_horticulture/minerals.php

The coloration yielding the yellow 'happy faces' is artificial, either due to staining or direct post-processing of the image.


Can RNases/DNases survive in strong acid/base solutions of around 10M? This might be a very stupid question, but I am worried about RNase/DNase contamination of my samples. Since I use 37% HCl and 10M NaOH to pH almost all my buffers, this is a potential source.

I have read however, that both NaOH and HCl should hydrolyze the peptide bonds in amino acids at high concentrations. For HCl, however, I have read that a heating step is required to facilitate the protein hydrolysis, so am a bit confused. Perhaps someone with a better background in chemistry could help?

Thanks a lot!

You are safe here.
RNase is much more stable than DNase (of any flavor). Extreme pH would destroy even RNase, especially considering time (it has to sit in the bottle with all that acid/base..)
Also, consider this: it is highly unlikely that high-tonnage chemicals like HCL or NaOH could be contaminated with organic enzymes.
If you have a problem with RNase/DNase contamination I would look elsewhere for the source of it.


What type of tree is this? I photographed this group of trees a couple of years ago at the northern tip of Prudence Island in Narragansett Bay. Any idea what species these are?

Although it can't be said definitively because of the picture quality, these are actually very likely maple trees. It's possible that they are either Red Maple (Acer rubrum) or sycamore maple (Acer pseudoplatanus) trees in spring leafout.

Source

Evidence:

The branches have an opposite arrangement. Very few tree are opposite (see MADHORSE)
The Rhode Island Wild Plant Society claims that red maple is abundant on the northern part of the island.
The Virginia Cooperative Extension provides an incomplete but detailed list of trees that can tolerate salt spray.

Two maples, Acer psudoplatanus and Acer campestre, (which are tolerant of salt spray) are both present as an exotic plant in that region of the country (see BONAP range map 1 and 2)
The Prudence Island flora mentions that A. pseudoplatanus is a common escaped cultivar on the island.

I'm leaning toward Red maple because of the red leaves appearing -- this is more typical of A. rubrum compared to the often more yellowish spring leaves of A. pseudoplatanus.

Note: The salt spray and windy environment will cause these trees (and most vegetation along a coastline) to develop "strange" (often gnarly) tree shapes.


What are mutator genes which cause copying errors in other genes? Reading Dawkins' book "The Selfish Gene," I came across this line: "There are even genes--called mutators--that manipulate the rates of copying errors in other genes." (The context is his argument that such a gene is looking out for its best interest by killing off the competition.)

What are these "mutator" genes, and how do they function?

Most obvious examples are the genes directly involved in DNA mismatch repair (MMR) such as mutS, mutL, mutH, MLH1 and MLH2.


Is there any completely Computation Drug ever launched in market? I am working in bioinformatics(part of it in Drug Designing) for years, still if I have no idea about it. As it is too hard to prove (Pass all Clinical trials) and get FDA Approvals.

So, My question is there a drug available in market, which is actually designed computationally?

Yes, there are a few. Mostly they are designed in combination with X-ray crystallography of the target which should be inhibited. Then molecules are designed which fit specifically into these targets.

The oldest example I could find is Dorzolamide which acts as a carbonic anhydrase inhibitor. See here: "Application of the three-dimensional structures of protein target molecules in structure-based drug design."
Some more examples are names in the Wikipedia article on drug design.

While looking for an example, I found these articles, which also look interesting:

Molecular Modeling and Computer Aided Drug Design. Examples of their
Applications in Medicinal Chemistry
Computer-based de novo design of drug-like molecules
Recent advances in computer-aided drug design

I am also not sure, to what extent the modern small molecule inhibitors like Vemurafenib (PLX4032) and others are designed using computers. At least to some extent this should be true.


Medical term for "holding urine for a long time" Sometimes I get/feel pain in my stomach because of holding urine for long time. Is there any medical terminology describing: "holding urine for a long time", or pain associated with this activity?

A swollen organ may be described as distended if the swelling is symptomatic of a medical disfunction.
The purpose of most bladders is to collect and retain a fluid; if that fluid needs to be discharged periodically, and is not able to do so, then there is usually pain as a result of the distension.

Inability to urinate is known as ischuria or urinary retention, and could be the result of obstruction to the urethra, could be a failure of the bladder to fully contract during urination, or could many other possible causes.


Action potential: why called "depolarization" when polarity is reversed, not removed? During an action potential, the voltage shifts from the resting potential of -70 mV, to +30  mV, to then fall return back to the resting potential again of -70 mV. This reverse of the polarity, what is the reason it came to be called "depolarization", as in, removed polarity?

While the cell is polarized (in the positive direction) at the height of the action potential, it has been depolarized from its resting, negatively charged state, meaning the original polarity has been lost or reversed. In my mind, the slight (30mV max) positive polarization for that brief period of time is kind of an "overshoot" of neutral charge, just like during recovery the potential exceeds -70mV for a period of time before coming back to the resting state.


What do firebugs do when they "connect" by their rear? See this image for example.

What are they doing? What is the name of this process?

They mate!

These matings can be very long

  When copulating, firebugs (Pyrrhocoris apterus) form tandems for prolonged periods. Half of the copulations of marked individuals in the field lasted longer than 12 h, and some lasted up to 7 days. (Schöfl and Taborsky (2002))

The likely reason for such a long mating is for males to guard the female to prevent future matings and therefore to prevent sperm competition

  males prolong copulations as a form of ejaculate-guarding under high competition with other males. (Schöfl and Taborsky (2002))


Is protein folding symmetric with respect to reversing the sequence order? Suppose that I have two proteins, protein A and protein B, and suppose that the sequence of amino acids of protein B is exactly the reverse of the sequence of protein A.

For example (these are made-up proteins):

protein A = [G,A,L,G,M,F,R]
protein B = [R,F,M,G,L,A,G]

Will the 3D structure of protein B be somehow identical, or perhaps the mirror image, of the 3D structure of protein A?

No! Although there is a relationship, the protein would not fold properly since the C and N terminals are reversed consider the following:

H(NH)-A-C(=O)(NH)-B-C(=O)(NH)-C-C(=O)(NH)-D-C(=O)(NH)-E-(C=O)OH

as appose to :

HO(C=O)-A-(NH)(C=O)-B-(NH)(C=O)-C-(NH)(C=O)-D-(NH)(C=O)-E-(NH)H

These are completely different molecules!

http://www.ncbi.nlm.nih.gov/pubmed/1604320 http://www.pnas.org/content/95/13/7287.long http://www.pnas.org/content/111/32/11679


The genotype of a hybrid plant from a cross and its determination? Question

I know about crosses Inheritance and this question is about Test Cross.
I want to know if we can determine the genotype of hybrid plant by crossing with a pure recessive parent from Filial generation 1 or if we require more generations to know the genotype?

My thoughts

if the plant is homozygous then no need if it is dwarf as we know that dwarf genes are recessive but if the phenotype is tall then we have to find its genotype whether it is Tt or TT. I have come across a MCQ : the genotype of hybrid plant obtained from a cross can be determined by crossing the plant with - . To me the ans should be Pure recessive parent at F1 generation. But ans given is Pure recessive parent at F2 generation

Real genetics is complicated

Biology is more complicated that you seem to expect. The answer very much depends upon the underlying genetics of the trait (and the underlying non-genetic factor affecting the trait; see here) as well as the genotype you are crossing it with.

Simplified model

But let's assume an extremely simple model of pure dominance / recessivity at a single bi-allelic locus. Let a be the recessive allele and A be the dominant allele. Let's assume the pure line you are using for the crossing is homozygote for the a allele (and let assume that we know it).

If the parent is AA, then all offspring will be Aa and all will have the dominant phenotype.
If the parent is Aa, then 50% of the offspring will be Aa and have the dominant phenotype and 50% of offspring will be aa and have the recessive phenotype.
If the parent is aa, then all offspring will be aa and have the recessive phenotype.

So, under this simple model, if you can produce a high enough number of offsprings to make good statistics, then yes, looking at the F1 generation is enough to determine the genotype of the parent.

Under a more complex model, it is not necessarily possible to only look at the F1 generation.


Is plasma membrane permeable to sucrose I searched a lot in the net but don't found a clear answer.
I just want to know if plasma membrane is permeable to sucrose.

No, but yes.

Sucrose is a large polar solute.
Because it is polar, it cannot easily pass the hydrophobic core of the membrane.
So, if the lipids of the plasma membrane are mostly impermeable to sucrose, how do cells take in sucrose?

Plants

In biology, membrane-bound proteins are used for efficient transport across the membrane (Brian, 2011 from a review of Suc transport in plant cells).
The specific group of membrane proteins used for sucrose transport are unimaginatively called Suc transporters (SUT).

So in a plant cell, sucrose can be moved across the membrane.

Humans

In mammals, there are no SUTs. Instead, sucrose is broken down into fructose and glucose by the enzyme sucrase.

From there, glucose transporters GLUT proteins carry glucose and fructose across the plasma membrane.


What is the fate of NADH produced in the liver during oxidation of lactic acid? NADH (‘reduced NAD’) is produced during the oxidation of blood lactate in the liver. Glycolysis requires NAD+ (‘oxidised NAD’), whereas gluconeogensis requires NADH. However the NADH is apparently not always used for gluconeogenesis (How is NAD+ used in lactic acid fermentation after it is oxidized from NADH?), i.e. the Cori Cycle does not always operate — so what becomes of the NADH in this case?

My best guess is that, along with the pyruvate, it may be transferred in the blood somehow to do to the site where it is needed, and it will then be taken into the electron transport chain, while the pyruvate will be taken into the Krebs cycle.

The “best guess” in this question is incorrect and the question itself indicates a lack of understanding of the roles of NAD+ and NADH in energy metabolism. (To rectifiy this, Chapters 17 and 18 of Berg et al. are suggested.)

The production of NADH in the oxidation of carbohydrates and fats is the energetic rationale for these processes. Under aerobic conditions the re-oxidation of NADH to NAD+ via the electron transport chain in the mitochondria* generates ATP for the energetic processes of the cell.

The fate of NADH produced by the oxidation of lactate reaching the liver from the blood would be similar under conditions where it is not needed for gluconeogenesis (in the reversal of the GAPDH reaction).  In these circumstances it would be reoxidized to NAD+, generating ATP in the mitochondria*.

[Note also that pyruvate is most likely to be oxidized by the liver mitochondria to produce metabolic intermediates and ATP, rather than transferred to the blood. NADH is certainly not transferred to the blood.]

*Advanced Point: Cytoplasmic and Mitochondrial NAD

The statement above, that NADH is “reoxidized to NAD+, generating ATP in the mitochondria”, is correct, but may be taken to imply that the NADH enters the mitochondria. This is not the case becase the NADH and NAD+ cannot pass through the mitochondrial membrane (as @tomd has commented). However the electrons that represent the reduced state of NADH do pass through the membrane. They do this in the guise of other molecules which are reduced in the cytoplasm by NADH in what are known as electron shuttles. The electrons enter the electron transport chain and are finally accepted by molecular oxygen. More detail of shuttles can be found in section 18.5 of Berg et al.


How do you call "pocoya" bird in English? I am translating a Spanish book and I have here a bird named in Spanish "pocoya", about which I know the following:

1) it flies at night

2) it makes sounds that allow to confuse it with an injured animal

3) it lives in Nicaragua or at least lived several centuries ago.

My own research brought me here: https://en.wikipedia.org/wiki/Pauraque and here: https://en.wikipedia.org/wiki/Ocellated_poorwill.

I don't know which one of them it could be, nor how it could be in English (the first article doesn't have an English version) when spoken (my indigenous people can't use Latin names, for sure...)

Thank you in advance for your  quick response!

I have done some reading based on your descriptors of the bird and your examples, the bird in question is a nightjar and I think they are referring to the Common Paruaque. All nightjars fit your first 2 points, the 3rd point is the only clue we can use to determine what species of nightjar you are describing. There are 11 species of nightjar is Nicaragua.

It seems the Common Pauraque (Nyctidromus albicollis) is commonly known as the "Pocoyo" in spanish, but the spelling may not been certain. Here's a quote from page 9 of an article on the birds of Nicaragua from 1957:

"The species is known in Nicaragua as “Pocoyo” (exact spelling uncertain)".
Reference.

The other bird you describe, the Ocellated Poorwill (Nyctiphrynus ocellatus) is referred to as the "Pocoyo ocelado".

The only other nightjar that might be called Pocoya is the Common Nighthawk (Chordeiles minor), but it is referred to as "Anapero".

I believe when referring to "Pocoya" it is most likely the Common Pauraque as the Ocellated Poorwill would have another descriptive word in it's name in spanish.


Why does ear wax taste sour? Why does ear wax taste sour?

I am interested in both the physiochemical mechanisms and the evolutionary reasons behind the sour taste of earwax.

Earwax, also called cerumen, is slightly acidic (1), with a pH of about 6,  and acidic foods or substances taste sour. The composition of earwax, upon which its taste depends, is related to its functions. Earwax aids in cleaning and lubrication of the ear canal and has an antimicrobial effect. The antimicrobial effect is in part attributed to its acidity, which might give an evolutionary reason for the sour taste.

From Wikipedia:

  Cerumen is produced in the outer third of the cartilaginous portion of
  the ear canal. It is a mixture of viscous secretions from sebaceous
  glands and less-viscous ones from modified apocrine sweat glands.[4]
  The primary components of earwax are shed layers of skin, with 60% of
  the earwax consisting of keratin, 12–20% saturated and unsaturated
  long-chain fatty acids, alcohols, squalene and 6–9% cholesterol.[5]

  (...)

  While studies conducted up until the 1960s found little evidence
  supporting antibacterial activity for cerumen,[15] more recent studies
  have found that cerumen has a bactericidal effect on some strains of
  bacteria. These antimicrobial properties are due principally to the
  presence of saturated fatty acids, lysozyme and, especially, to the
  slight acidity of cerumen.


What nocturnal animal sound am I hearing in the trees in Maine? Every year, during late summer nights (usually around 9:00 pm) in Maine, I hear a noise coming from high up in the trees. The trees I hear it from are mostly maple or conifer, but where I live there are few trees that are not. It sounds like a cardinal's chirp (fourth sound down in link), but longer, scratchier, and lower pitch. The sound starts and ends abruptly. There are three to six chirps in a row from the same tree, and then silence for a few minutes. Sometimes I will hear it again after a few minutes from the same tree and sometimes from a different tree. The skies are usually clear when I hear it. No one else in my family can hear it. I live in a suburban area, but when I go to a more densely forested area I hear it more frequently. Does anyone know what this is?

My initial guess (knowing almost no information) is that it's a Northern saw-whet owl (Aegolius acadicus). These owls live year round in Maine but also increase in number as some migrate from Canada through Maine for winter. You can hear their advertising song here.

Northern Saw-whet Owls have a distinctive too-too-too call -- an insistent series of whistled notes on roughly the same pitch, given at a rate of about 2 notes per second. Males calling to advertise their territory can be heard up to half a mile away. Other males respond with a softer, faster, lower version of the call.


About how many covid-19 virus particles is required in the human body before infection and sickness follows? Our immune systems are often able to destroy germs and virus particles.
About how many of them does it take to make a 70 year old healthy male sick ? Any ideas ?

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


Northern Europe tree identification I've seen it in Nordic countries (Sweden, Latvia). It's a tree that reaches maybe 5 or more meters high and its flowers have a beautiful scent.

It's the common Prunus padus, which flowers with its strong scent now in many parts of Sweden (including my yard). At least if you are referring to the common species found in the wild (there are planted domesticated varieties as well). It is common across many parts of Europe though, and not only the Nordic countries, and can be found in Asia as well.


Which process is right to describe V(D)J recombination? RAG-1 and RSS recurring process I'm studying V(D)J recombination. I think I have two incompatible books about explantaion of the process. Which is right?

In Molecular Biology of the Cell 5th Ed., firstly RAG (-1?) combines to RSSs of V and J genes independently. After that, a hairpin loop is formated by paring random(?) RAGs.
In Janeway's Immunobiology 8th Ed., RAG complex (RAG-1 and RAG-2) has two sites for RSSs from the beginning. And in the figure, V gene is firstly recruited for a site. J gene combines to the RAG complex after V gene.

Excerpt from Cellular and Molecular Immunology, 8th ED, p.181-182. Don't up-vote me, i just thought this text offers a good, up-to-date explanation.

  The Mechanism of V(D)J Recombination

  Rearrangement of Ig and TCR genes represents a special kind of non-homologous DNA recombination
  event, mediated by the coordinated activities of several
  enzymes, some of which are found only in developing
  lymphocytes, whereas others are ubiquitous DNA double-stranded break repair (DSBR) enzymes.Although
  the mechanism of V(D)J recombination is fairly well
  understood and will be described here, how exactly
  specific loci are made accessible to the machinery
  involved in recombination remains to be determined.
  It is likely that the accessibility of the Ig and TCR loci to
  the enzymes that mediate recombination is regulated
  in developing B and T cells by several mechanisms,
  including epigenetic alterations in chromatin structure
  and DNA as discussed earlier, and basal transcriptional
  activity in the gene loci.
  The process of V(D)J recombination can be divided
  into four distinct events that flow sequentially from one
  to the next (Fig. 8-10):

  1. Synapsis: Portions of the chromosome on which the
  antigen receptor gene is located are made accessible
  to the recombination machinery. Two selected coding segments and their adjacent RSSs are brought
  together by a chromosomal looping event and held
  in position for subsequent cleavage, processing, and
  joining.

  2. Cleavage: Double-stranded breaks are enzymatically generated at RSS-coding sequence junctions
  by machinery that is lymphoid specific. Two proteins encoded by lymphoid-specific genes, called
  recombination-activating gene 1and recombination-activating gene 2(RAG1and RAG2), form
  a  complex, containing two molecules of each protein,
  that plays an essential role in V(D)J recombination.
  The Rag-1/Rag-2complex is also known as the V(D)J
  recombinase.The Rag-1 protein, in a manner similar to a restriction endonuclease, recognizes the DNA
  sequence at the junction between a heptamer and a
  coding segment and cleaves it, but it is enzymatically
  active only when complexed with the Rag-2 protein.
  The Rag-2 protein may help link the Rag-1/Rag-2 tetramer to other proteins, including accessibility factors that bring these proteins to specific open receptor
  gene loci at specific times and at defined stages of lymphocyte development. Rag-1 and Rag-2 contribute to
  holding together gene segments during the process of
  chromosomal folding or synapsis. Rag-1 then makes
  a nick (on one DNA strand) between the coding end
  and the heptamer. The released 3′OH of the coding
  end then attacks a phosphodiester bond on the other
  DNA strand, forming a covalent hairpin. The signal
  end (including the heptamer and the rest of the RSS)
  does not form a hairpin and is generated as a blunt
  double-stranded DNA terminus that undergoes no
  further processing. This double-stranded break results
  in a closed hairpin of one coding segment being held
  in apposition to the closed hairpin of the other coding end and two blunt recombination signal ends being placed next to each other. Rag-1 and Rag-2, apart
  from generating the double-stranded breaks, also hold
  the hairpin ends and the blunt ends together before
  the modification of the coding ends and the process of
  ligation.

  RAGgenes are lymphoid specific and are expressed
  only in developing B and T cells. Rag proteins are
  expressed mainly in the G0and G1
  stages of the cell
  cycle and are inactivated in proliferating cells. It is
  thought that limiting DNA cleavage and recombination
  to the G
  0 and G1
  stages minimizes the risk of generating inappropriate DNA breaks during DNA replication or during mitosis. Mice without functional Rag1
  or Rag2genes (Ragknockout mice) fail to develop B or
  T lymphocytes, and Rag-1 or Rag-2 deficiency is also
  a rare cause of SCID, in which patients also lack all
  lymphocytes.

  3. Hairpin opening and end-processing: The broken
  coding ends are modified by the addition or removal
  of bases, and thus greater diversity is generated. After the formation of double-stranded breaks, hairpins must be resolved (opened up) at the coding
  junctions, and bases may be added to or removed
  from the coding ends to ensure even greater diversification. Artemisis an endonuclease that opens
  up the hairpins at the coding ends. In the absence
  of Artemis, hairpins cannot be opened, and mature
  T and B cells cannot be generated. Mutations in
  ARTEMIS are a rare cause of SCID, similar to patients with RAG1or RAG2mutations. (see Chapter
  21). A lymphoid-specific enzyme, called terminal
  deoxynucleotidyl transferase (TdT), adds bases to
  broken DNA ends and will be discussed later in the
  chapter in the context of junctional diversity.

  4. Joining: The broken coding ends as well as the signal ends are brought together and ligated by a double-stranded break repair process found in all cells
  that is called nonhomologous end joining. A number
  of ubiquitous factors participate in nonhomologous
  end joining. Ku70 and Ku80 are DNA end-binding
  proteins that bind to the breaks and recruit the catalytic subunit of DNA-dependent protein kinase
  (DNA-PK), a double-stranded DNA repair enzyme.
  This enzyme is defective in mice carrying the severe
  combined immunodeficiency (scid)mutation, and mutations in the gene encoding this enzyme have also
  been discovered in human SCID patients (see Chapter
  21). Like Rag-deficient mice, scidmice fail to produce
  mature lymphocytes. DNA-PK also phosphorylates
  and activates Artemis, which, as mentioned before, is
  involved in end processing. Ligation of the processed
  broken ends is mediated by DNA ligase IV and XRCC4,
  the latter being a non-catalytic but essential subunit of
  the ligase.

Figure 8-10, Cellular and Molecular Immunology, 8e, p182.


Comparative Genomics Are orthologs and paralogs examples of conserved genes? Orthologs are the genes or DNA that is present in 2 different species, having once been present in a common ancestor. It comes about by a speciation event. Paralogs come about by gene duplication events.

So, would we characterize these genes as conserved genes?

Could not fit in a comment...

To my understanding, paralogs and orthologs refers, as you said, to the relative isolation of gene copy to the isolation of populations (and eventually species).

Gene conservation on the other hand refers to the variability of a given gene along many species. If a gene does not show any variance along many species, than we say that it is a conserved gene.

Eventually, gene duplication may allow for neo-functionalisation, sub-functionalisation or loss yielding to variance among this gene copy. Aside the philosophical problem of what is the identity of the gene, there is no relationships between the concepts of orthologs versus paralogs and gene duplication.


How Much Longer For The Gene For Blue Eyes? In the year 1900 roughly 50% of the people in the United States were homozygous for the gene for blue eyes. By 1950 the number had dropped down to 30%. Just now, (2013) barely 12% of the people living in America are homozygous for the blue eye gene.

Given the current rates of third world immigration into the United States. When will the last blue eyed man and the last blue eyed woman conceive a child with blue eyes? Should people with blue eyes bring reverse discrimination suits?

Reference:http://www.boston.com/news/globe/living/articles/2006/10/17/dont_it_make_my_blue_eyes_brown/ By Douglas Belkin

Never.

Even if the country arrives at the unlikely day when there is no one alive in the United States with the blue eye phenotype, there are still plenty of people with the unexpressed recessive gene, and if two of them get together, those genes can combine to produce another blue-eyed child. If this happens twice, with one boy and one girl, and they happen to meet when they are in college and say "Hey cool, you have the same inexplicably rare kind of eyes as me. I think I want to marry you." then any children they have will also be blue eyed.

So even if the day came when you couldn't find a soul in the world with blue eyes, you will still never know if you've seen the end of them.


What is an auditory upward sweep? I was reading an article in nature communications, when I came across this sentence: "The ‘match’ rule was indicated by either a blue circle or a auditory upward sweep".So I tried googling what was an upward sweep, and came across this: "natural and complex vocalizations consist of basic elements such as upward sweeps, downward sweeps, constant frequency components, amplitude modulations..." I don't understand this. Can someone explain what is an upward sweep?

Here is the link to the article: http://www.nature.com/ncomms/2013/131128/ncomms3878/abs/ncomms3878.html,

But I think you have to pay to view the whole article, so here is another link that discusses the findings of the article:

http://www.uni-tuebingen.de/en/landingpage/newsfullview-landingpage/article/von-wegen-spatzenhirn-wie-nervenzellen-schlaues-verhalten-bei-rabenvoegeln-ermoeglichen.html

Copied from my comment:

It just means a sound that starts at a low frequency and goes up to a higher frequency like a whistle sound. Perhaps someone can give you an example sound file and/or a spectrogram representation of it.


Activity of glucokinase From Solomon et al, 2013 ACC Synthetic biology and from this video :

Here, there are 2 competing reactions for glucose - one with glk as enzyme and other with gdh as enzyme.
In the graph, y axis is gluconate yield and x axis is glk activity. Logically, as glk activity increases, gluconate yield should decrease.
This is the case for most of the graph. But why is there an increase in gluconate production initially(when glk activity is somewhere between 0.2 and 0.27 )?

First of all lets have a look, what these guys want to accomplish: They want to use bacteria to make certain products. To do so, they want to exploit the bacterial metabolism at steps where no alternative pathways are available. One of these steps is the first step of glycolysis, when Glucose gets phosphorylated to glucose-6-phosphate (G6P). In bacteria the phosphorylation is done during the import of glucose into the cell by the "phosphoenolpyruvate (PEP):carbohydrate phosphotransferase system", which uses Phosphorenolpyruvate as a phosphate source. This has the disadvantage, that there is almost no free glucose inside the cell, but mostly G6P.

To overcome this problem, the group expressed alternative transporters (which transport glucose into the cell) and Glucokinase (Glk) to allow the cells to survive. This steps decoupled import and phosphorylation of the glucose and resulted in free glucose inside the cell. This free glucose can now be used by different proceses. It also allows glycolysis, since the Glk phosphorylates the glucose which then enters the glycolysis pathway. The Glk was put under different promoters to make different mutants in order to test how the different expression of Glk affects the cells viability.

To bring in another enzyme which also metabolizes glucose, they used glucose dehydrogenase (Gdh) which was expressed from a plasmid with a strong, IPTG inducible promoter. They then used different concentrations of IPTG to test the effect on the production of gluconate and cell viability (I am not going into this).

The figure above is figure 5 from the paper and shows the effect of the three different IPTG concentrations used to induce the expression of the Gdh. For 10 and 25uM IPTG the yield of gluconate is getting smaller, the higher the Glk activity gets. Only the smalled activity shows a lower yield. This is complete different for the highest concentration, but here the cells get probably messed up by the high expression of the Gdh (which also consumes a lot of energy).

In the paper they give no explanation or at least discuss the behaviour of the gluconate yield at the smallest Glk activity (I would like to read the reviewers comments on that). From the data I would expect a higher production. It is possible that the lower energy production (low amounts of G6P means little glycolysis) has negative side effects on the cells. It is also possible, that the Gdh is inhibited at lower Glk activities by some other substances in the cell. Gdh activity is for example inhibited by higher concentrations of nucleotidtriphosphates (ATP and so on), see here. Since Glk needs ATP as a cofactor it would be possible that the ATP concentration at lower Glk activities has a negative effect on the Gdh activity (my own speculation).

Or it is simply some artefact from the experiment. This has some points which can be critisized (I would like to see the reviewers comments here as well). First the error bars are pretty big, so this can also be somewhat different. In the text they mention that the data was acquired by

  at least 2 parallel cultures in a representative experiment

I would expect some more repetitions (at least three independent experiments), which would make the data more reliable. Then (and this point is much more important) they can not measure the activity of Glk and Gdh in the same culture due to restrictions in the detection system. Glk activity measurements use a coupled system which in the end measure the concentration change in NADH, while Gdh uses NADPH as a co-factor. Both versions can not be differentiated by measuring a spectrum, so activity measurements of Glk can only take place in untransfected cells. Since the expression changes conditions in the cell (and we don't know how), I would expect at least some discussion about it, but it is missing.


Does mung bean nuclease cleave a phosphate group when it's chewing off 5' or 3' ssDNA ends? I'm looking to create blunt ends from sticky ends with mung bean nuclease for subsequent ligation.  Does anyone know full mechanism by which mung bean nuclease will do this?

In particular after the reaction, will the ends of resulting dsDNA have phosphate groups or will I need to phosphorylate the ends with an extra step for successful ligation?

According to Kroeker WD, Kowalski W, Laskowski M. 1976. Mung Bean Nuclease I. Terminally Directed Hydrolysis of Native DNA. Biochemistry 15(20):4463-4467

  It was concluded that the products of the terminally directed hydrolysis of native DNA possess 5’-phosphoryl groups because: (1) greater than 99% of acid-soluble activity applied to the column was recovered in products which coeluted with 5’-terminated standards and (2) the w-monophosphatase activity of mung bean nuclease would have dephosphorylated 3’-phosphoryl-terminated products. The endonucleolytic activity of mung bean nuclease on denatured DNA also results in the production of 5’-phosphoryl-terminated products.

Also, from Promega:

  Mung Bean Nuclease catalyzes the degradation of single-stranded DNA and RNA endonucleolytically to yield 5´-phosphoryl-terminated products


Why does the cold make us sick? From the moment we learn to communicate, we always get told, whether by our parents, or our teachers, or by anyone else, to avoid the cold, or to put a jacket on to avoid catching a cold, to dry our hair before we go outside, because we'll get sick otherwise, so on and so forth. I also was diagnosed with a pneumonia last year, while in Switzerland under chilly conditions ($-20^◦\text{C}$). This made me wonder, why does the cold make us sick? It doesn't seem logical to me that a viral infection like the common cold, or a viral/bacterial infection such as a pneumonia is more prevalent when it's colder outside. I always figured it was because our bodies are less 'effective' under cold temperatures, but this seems lacking to me. Can anyone explain?

it does not, really. unless we're talking about things like frostbite or severe hypothermia.
it's a myth that it does.
the virus is more stable in colder air, however.
see more here:
Study Shows Why the Flu Likes Winter
Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature

Innate responses proved to be comparable between animals housed at 5 °C and 20 °C, suggesting that cold temperature (5 °C) does not impair the innate immune response in this system.


Why are some genomic regions sequenced more than the others? We have to normalise read count data from RNA-Seq experiments in order to account for the fact that some genomic regions are mapped more than others. i.e. we get the tags per million reads (TPM). In other words, they have a higher sequencing depth/vertical coverage.

Why are some genomic regions mapped more than others; what is the reason for this non-uniform distribution of sequencing depth?

For RNAseq, the differences in the read depth can simply arise because of expression (that's trivial). Highly expressed regions will have higher number of reads.

However the read depth non-uniformity also arises because of the nucleotide composition of the regions. This is true for all kinds of nucleic acid sequencing such as RNAseq, whole genome sequencing and ChIP seq. This is called sequence bias. This also depends on the sequencing methodology. A variety of factors play a role such as how well can the region be sheared, how well can it be amplified etc.

For details have a look at this article by Ross et al (2013).

  Sequencing technologies are vulnerable to multiple sources of bias.
  Methods based on bacterial cloning and Sanger-chemistry sequencing [8]
  were subject to many coverage-reducing biases, notably at GC extremes,
  palindromes, inverted repeats, and sequences toxic to the bacterial
  host [9–17]. Illumina sequencing [18] has been shown to lose coverage
  in regions of high or low GC [19–22], a phenomenon also seen in other
  'next-generation' technologies [3, 6]. PCR amplification during
  library construction is a known source of undercoverage of GC-extreme
  regions [20, 21] and similar biases may also be introduced during
  bridge PCR for cluster amplification on the Illumina flowcell [23].
  Illumina strand-specific errors can lead to coverage biases by
  impairing aligner performance [24]. Ion Torrent [25], like 454 [26],
  utilizes a terminator-free chemistry that may limit its ability to
  accurately sequence long homopolymers [4, 27, 28], and may also be
  sensitive to coverage biases introduced by emulsion PCR in library
  construction. Complete Genomics [29] also uses amplification along
  with a complex library construction process. The Pacific Biosciences
  [30] process is amplification-free; therefore, one might expect it to
  exhibit lower levels of coverage bias than the other technologies.

  In addition to sources in the wet lab, bias can be introduced by any
  of the computational steps in the sequencing pipeline.
  Signal-processing and base calling limitations could result in
  under-representation or increased error rates in some locations, as
  can inaccurate alignment. An inaccurate reference or sample-reference
  differences can cause coverage or accuracy variations that may be
  misdiagnosed as sequencing bias. Therefore, detecting bias is only the
  first step and must be followed by more detailed experiments to assign
  responsibility to the library preparation, sequencing, or
  computational stages.

Some analysis software try to correct for these biases while estimating the read abundance.

Ross, Michael G., et al. "Characterizing and measuring bias in sequence data." Genome Biol 14.5 (2013): R51.


What is the difference between the basal membrane and the basal lamina? I'm researching about the basal lamina in lung tissue and I'm not sure if the basal membrane is the same.

What is the difference between them?

The basal lamina is a specialised type of extracellular matrix. It is found on the basal side of all epithelial tissue but can also surround other cell types like myocytes and adipocytes. It is also called the basement membrane, although it is not the traditional plasma membrane that we have come to know and love. Rather, it is composed of proteins (often glycosylated) and polysaccharides.

The basal membrane is the actual plasma membrane on the basal side of an epithelial cell (adjacent to the basal lamina/basement membrane).


enhancers in cell-type-specific signatures I was reading an article in nature : Epigenomics: Roadmap for regulation and was confused by the definition or/and interpretation of enhancers.

  Enhancers are activated through interactions with transcription
  factors, which recognize and bind to specific DNA sequences within the
  enhancer region. Bound transcription factors recruit co-regulators,
  many of which deposit or remove modifications on histones. […]
  Enhancers that are active in cell-type-specific epigenomic signatures
  are typically highly enriched in DNA sequences to which
  lineage-determining and signal-dependent transcription factors bind.

As far as I know enhancers are the DNA sequences to which TFs bind, and then everything including co-activators complexes bind to basal TFs on the promoter.

I am confused by the last line:

  Enhancers that are active in cell-type-specific epigenomic signatures
  are typically highly enriched in DNA sequences to which
  lineage-determining and signal-dependent transcription factors bind.

They state, that in DNA sequences to which TFs bind the active enhancers are highly enriched. For me it sounds strange because the definition of enhancers says that these are the DNA sequences to which TFs bind. And of course enhancers are enriched there because otherwise they would not be called enhancers. As for me they are trying to say that active enhancers (by definition TFs bind to them) are highly enriched in enhancers region to which TFs bind.

Does it make sense or not?

Enhancer is a just a term for a regulatory region distant from a gene that contains specific sites where transcription factors bind. As it happens, a single enhancer can contain DNA binding sites for multiple transcription factors.

For example, an enhancer called TESCO, which regulates a gene called SOX9 (involved in sex determination) has binding sites for many different proteins (confirmed or putative): SRY, SF1, SOX9, ESR1, FOXL2 and likely many more that I haven't heard of. This allows complex regulation of SOX9 through protein-protein interactions.


Does it make sense to classify all humans in a single species? For what biological reasons do we consider that all human beings belong to the same species?

A Thai and a Nigerian share a common ancestor that is 140,000 years old (see Gravel et al. 2010 and this post). Would, for example, a mixed Thai - Nigerian baby suffer from any outbreeding depression?

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

Concept of species

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

Concept of species in sexually reproducing lineages

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

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

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

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

Do we have documented cases of outbreeding depression?

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

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

Udry et al. 2003:

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

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

Potential publication bias and taboo

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

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

Other definitions of species and taboo

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

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

Why same subspecies and not only species?

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

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

Related posts

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


Multistability in the lactose ultization network Reading the paper here, I'm confused about the production of figure 4d. The method of production is detailed in the supplementary information under the heading "Theoretical phase diagram".

Specifically, I'm confused about the use of theta and what it means. I have tried reproducing the figure using MATLAB and the parameters in the paper to see whether I can understand it better, but nothing quite works out.

To be clear, the paper obtains a steady state result for a series of ODEs:
$$
    y = \frac{\alpha  (1+(βy)^2)}{ρ+(βy)^2}
$$
Then rearranges as a cubic:
$$
    y^3 −αy^2 + \frac{ρ}{ β^2} y − \frac{α }{ β^2 } = 0
$$
Apparently, a general cubic with two identical roots has the
form:
$$
    (y-a)(y-a)(y-aθ) = y^3 - (2 + θ)ay^2 + (1+2θ)a^2 y - θa^3
$$
The paper then equates coefficients:
\begin{align}
    ρ &= (1 + 2θ)(1 + 2/θ)\\
    aβ &= \frac{(2 + θ)^{3/2}}{θ^{1/2}}\tag{did you mean?}
\end{align}
And claims that these are the parametric equations that describe the graph in question. When plotting these equations, I get nothing like the graph. I can't really see where it comes from.

The graph in question and some equations are reproduced here on the last page:
http:// web.mit.edu/biophysics/sbio/PDFs/L7_notes.pdf

The equation in the OP has been updated to $(y-a)^2(y-a\theta)$ which yields the correct expansion. Therefore, by equating the coefficients, we obtain
\begin{align}
\alpha &= (2+\theta)a\tag{1}\\
\rho/\beta^2 &= a^2(1+2\theta)\tag{2}\\
\alpha/\beta^2 &= a^3\theta\tag{3}
\end{align}
Using equations (1) to (3), we get the desired $\rho$ and $\alpha\beta$. Now the authors plotted $\frac{\alpha\beta}{\rho}$ and $\frac{1}{\rho}$.

By plotting $\frac{\alpha\beta}{\rho}$ and $\frac{1}{\rho}$, we can re-create the plot in Mathematica with

ParametricPlot[{1/((1 + 2 x) (1 + 2/x)), (2 + x)^(3/2)/(
  Sqrt[x] (1 + 2 x) (1 + 2/x))}, {x, 0.01, 50 \[Pi]},
 PlotRange -> {{0, .15}, {0, 0.6}}, AspectRatio -> 3/4]

If you dont have Mathematica, here is some Python code that will plot it as well.

import numpy as np
import matplotlib.pyplot as plt

fig = plt.figure()
t = np.linspace(0.01, 25*np.pi, 5000)
x = 1/((1+2*t)*(1+2/t))
y = (2+t)**1.5/(np.sqrt(t)*(1+2*t)*(1+2/t))
plt.plot(x,y)

plt.show()

Here is the Python plot which has smoother lines compared to Mathematica's plot.


Speed of passive transport of ions in the dendrite I tried hard to get them, but I didn't get any numbers. My (subjectively) best Google search was for "speed propagation post-synaptic potential".

My question is:

  How fast are ions transported passively inside the dendritic tree (and soma),
  probably depending on their atomic mass, charge, and of the local geometry?

Especially I want to know when a post-synaptic potential generated x μm away from the axon hillock "arrives" there, i.e. can be detected/summed up with other PSPs. Disregarding all of the eventualities (see above):

  What is the order of magnitude of the speed of passively transported
  ions in the dendritic tree?

Your edits do improve the question, but you are still asking two very different questions.
We don't really need to answer these questions:

How fast are ions transported passively inside the dendritic tree (and soma), probably depending on their atomic mass, charge, and of the local geometry?
What is the order of magnitude of the speed of passively transported ions in the dendritic tree?

to answer this part:

Especially I want to know when a post-synaptic potential generated x μm away from the axon hillock "arrives" there, i.e. can be detected/summed up with other PSPs

The speed of propagation of electrical signals in neurons don't depend on particular masses of particular ions or diffusion per se. Instead, passive electrical conduction is best understood using the cable equations which treats conductance within neurons as electrical RC circuit. The electric field propagates at the speed of light.
Therefore, EPSPs actually propagate almost instantaneously (given how short the distances involved are relative to speed of light) in that they produce an electric field. However, the peak decays with distance, and the rise time of an EPSP depends on the compartment because of capacitive filtering along the length of the dendrite. The decay peak is described by the length constant:
$$\lambda = \sqrt{\frac{r_m}{r_i+r_o}}$$
In this equation, rm is the resistance of the membrane, ri is the resistance of the intracellular space, and ro is the resistance of the extracellular space and is effectively negligible.
The length constant is the distance at which the peak amplitude will have decayed 63% from the peak at the signal origin.
The temporal filtering comes from the capacitive properties of the membrane along the length of the dendrite. The authoritative works describing these properties are several papers in the 1960s from Rall, Rall, W. (1962). Theory of physiological properties of dendrites. Annals of the New York Academy of Sciences, 96(1), 1071-1092. and Rall, W. (1969). Time constants and electrotonic length of membrane cylinders and neurons. Biophysical Journal, 9(12), 1483-1508. are good references.
The effective time constant for signals originating closer to the soma is much faster because there is less membrane to charge along the way. Exactly "how far" you have to travel to make a certain amount of difference depends on the properties of the membrane, which vary across neurons, vary in different parts of the dendritic tree, and vary dynamically within a neuron due to synaptic transmission.
Magee, J. C. (2000). Dendritic integration of excitatory synaptic input. Nature reviews. Neuroscience, 1(3), 181. is a fairly accessible review that covers a lot of these issues and more. It's important to recognize that although passive propagation of signals is important in dendrites, it's never purely passive and active conductances have important roles as well; in many cells, these active conductances plus differences in the initial shape of EPSPs throughout the dendritic tree act to mitigate the effects of distance.
See also Koch, C., Rapp, M., & Segev, I. (1996). A brief history of time (constants). Cerebral cortex, 6(2), 93-101. for more on the time constant and some evolution of the ideas about neuronal time constants since Rall.


Explanation of universal model of energy flow I am trying to understand the Universal model of energy flow by Odum.

In this linked diagram I is the input energy(the amount of energy present in the food consumed by this tropic level, say its, the 2nd tropic level, the herbivores), part of this food is excreted as undigested food (the NU) , the rest is digested, absorbed and assimilated reaching the cells and then the energy accumulated at cellular level is called the assimilated energy (A). Now part of A is utilised to make ATPs that are being used to fuel the metabolisms occurring in the organisms which is represented by R and the rest is available to the next tropic level(?) as P ?

Then what makes the standing biomass? The organisms the are not eaten up?

Besides I don't understand the Energy Storage part. What physiological process corresponds to this?

If you were to take a snapshot of the biomass present for a species at an instant of time, that would be its standing biomass. So, in a way you are correct with "the organisms not eaten up". But this can be quite misleading when used to attempt to explain pyramids of production up trophic levels. For example, in some aquatic ecosystems the standing biomass of primary consumers is greater than that of primary producers. On study in the English Channel showed 21 g/m3 of zooplankton but only 4 g/m3 of phytoplankton. This is due to the rapid proliferation of the phytoplankton and the rapid consumption by the zooplankton.

Typically it is preferable to describe the energy flow through ecosystems in terms of energy units, Joules for example. However, you could do this with biomass if you summed the biomass produced over time. When done like this, the English Channel example would look like a proper pyramid with the producers out-massing the consumers over a meaningful period of time.

Energy storage is simply the energy stored in the chemical bonds of the molecules created during growth that add to biomass.

My example, and context, is from Biology, Campbell & Reece, 7th edition.