How can bats achieve good resolution with wide beams?

I have been contemplating about this question for months and although I cannot provide you with a concise short answer, I do wish to share what I have so far.

First off, the acoustic beam that is sent is not really part of the echolocation resolution (the bat's echo-locating acuity). Consider the human field of view, which is nearly 180o wide in the horizontal plane. Covering your eyes and obscuring, say, half of the field will not substantially improve visual acuity, because it simply blocks half of the retinal surface from receiving light - it does not double the retinal surface devoted to the field of view.

Hence, I think it is not so much the bat's projected beam that matters, it is the incoming echo that matters. Note that objects such as a tree may scatter the sound that is reflected back, so the projected beam of 40o may be a dramatic underestimation of the chaotic signals bouncing back to the bat. What can they do to improve spatial detail in the received acoustic field of view?

Bats may increase the pulse repetition rate when they are approaching a target. Hence, they basically build a map by sampling the environment multiple times. Sampling frequencies may exceed 50 Hz (Grinnell and Griffin, 1985). For example, imagine you are blindfolded and allowed to scan an object with your fingers. Scanning it multiple times will definitely help you to mentally reconstruct the image. Indeed, bats can assemble information about echo delay changes over time, enabling them to temporally integrate information of the auditory scene. Moreover, they can change the spectral content of their calls that may help in echolocation (Moss & Surlykke, 2001).

Furthermore, to conclude with a personal thought - I think that bats must learn to decode complex echo profiles. For example, a chaotic huge blob of echo with low-echo efficiency (lots of sound is absorbed) that only changes when the bat moves is probably a tree. A big blob with a large echo-efficiency (a lot of sound comes back) with well-defined edges that only changes when the bat moves is likely a human structure or a rock. A pinpoint-echo that moves with respect to the bat is likely something tasty.

References
- Grinnell & Griffin, Biol Bull (1958): 10-22
- Moss & Surlykke, JASA; 110(4): 2207-26


What are the requirements for a stable carbon cycle in sealed "bottle gardens"`?

The problem lies in soil bacteria.
There has been a project on a larger scale: Biosphere 2. After their initial trial they realised $O_2$ levels are getting much lower from what was predicted. The scientists team investigated the problem deeper and came to the conclusion that there was a lot of dead organic matter in the soil, which got consumed by aerobic bacteria. There were also other hypotheses: not enough sunlight and $O_2$ sequestration by concrete.

A solution for you would be to make sure there is little organic matter in your soil. Perhaps use inorganic "soil" like sand + some nutrients. And also make sure there is enough sunlight.
Start also with small plants - too large plants in the beginning might change $O_2/CO_2$ ratio to abruptly during day and night cycle. (remember that plants are also consuming oxygen at night).


Recent and good quality articles on systems biology

This question is extremely vague, and can't have any real answer without you specifying a question or at least focus. Keep in mind, there is no high-road to research, you will have to dig in and start reading papers to gain understanding of your field. If you want help from others, you should at least take time to list the papers that you have already read and why you liked them to give readers a flavor of your interests.

To start you off, consider this Google Scholar query for systems biology since 2009. If you've read specific older papers that you've liked, for example this popular 2002 minu-survey:

Kitano, H. (2002). Systems biology: a brief overview. Science, 295(5560), 1662-1664.

Then you can learn how the field has advanced since by doing a forward search in Scholar (and restricted to 2009+). Hopefully this will provide you will some ideas so that you can ask a more precise question!


Flies use any object they can find as a landmark.

  The flies patrol well-defined airspaces underneath landmarks like lampshades. ... Male flies approach a landmark from below and, in the absence of other flies, settle to patrol an airspace close to the landmark. A second male approaching the same landmark chases, or is chased away by, the patrolling fly when it comes too close and may eventually settle to patrol 10–30 cm below the airspace occupied by the first fly. ... The position of male patrolling stations relative to the landmark suggests that females might arrive at landmarks from the side (and not from below, as males do), thus crossing the dorsal visual field of patrolling males.

Source: Jochen Zeil. The territorial flight of male houseflies (Fannia canicularis L.) Behavioral Ecology and Sociobiology. August 1986, Volume 19, Issue 3, pp 213-219


Between the eyes and nose, which offers better immune protection

Neither. Both are mucous membranes lined by epithelial cells. Each is their own niche (and the nose has a number of sub-niches), with particular receptors, environmental factors, and immune factors that interact with pathogen factors. The interaction between the two produces the tissue tropism of a particular pathogen. Each is colonized with many commensal microbes, with some overlap (see Murray Medical Microbiology Ch 7 and this study of the eye). As far as "airborne" transmission, vs. inoculation by physical contact, the nose and nasopharynx are important structures in respiration. The eye is not.


The insect in the Photo is a beetle (order Coleoptera), in the scarab family (family Scarabaeidae). It is most likely in the Genus Phyllophaga (June or May bugs) or Phyllopertha (garden chafers).  Beetles such as this are commonly referred to as "Chafers" feeding on plant leaves and flowers during the day. One of the defining characteristics in the photo is the apparent "Hairiness" (setae) visible at the sides of the insect body. I am inclined to agree with the good observations expressed in the comments.  It likely to be a garden chafer Phyllopertha horticola. Some helpful links are below.

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

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

https://www.flickr.com/photos/72271115@N02/galleries/72157651475342046/?rb=1#photo_14184003066

https://www.flickr.com/photos/odonataman/14184003066/in/gallery-72271115@N02-72157651475342046/

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


Short answer
There are no functional nociceptors present in the umbilical cord.

Background
Having had the opportunity to cut the umbilical cord of one of my kids, I can anecdotally confirm neither newborn nor mother gave any sign of pain during the procedure. That is, when cutting the umbilical after the birth of a full-term baby. The only person clenching his teeth was dad :)

In fetuses at gestational age of 18-36 weeks no stress response was noted after puncturing the umbilical (Teixeira et al., 1996), indicative of the absence of pain receptors connected to the baby's brain.

I couldn't find information about pain in the mother, but I cannot imagine that the maternal central pain centers are being connected to the umbilical, which would be pretty extraordinary. This, because long-distance neural connections are rarely, if ever, established in adult humans. Also, I haven't heard any reference to the mother feeling pain because of injury to the umbilical cord. For example, knots in the umbilical cord, or cords wrapped around the fetus' neck due to excessive movements of the fetus are never noticed by the mother, and are only revealed during ultrasounds.

Note, however, that the umbilical cord is innervated by cholinergic neurons that are thought to be involved in the control of blood transfusion to the fetus, but presumably do not carry sensory information to either fetus or mother (Ellison, 1971).

References
- Ellison, Am J Anat (1971); 132: 53-60
- Teixeira et al., The Lancet (1996), 347: 624


The fastest I know of is the heat shock locus in Drosophila.  The transcription factor (HSF) accumulates within about 30 seconds, and RNA Polymerase can be seen to start accumulating within 3 minutes.

Katie L. Zobeck, Martin S. Buckley, Warren R. Zipfel, John T. Lis.  2010. Recruitment Timing and Dynamics of Transcription Factors at the Hsp70 Loci in Living Cells.  Molecular Cell 40(6): 965-975


What are minerals (other than zinc) that the human body cannot store

Essential "minerals", i.e., metal cations are magnesium, zinc, iron, potassium, sodium, manganese, molybdenum, selenium, cobalt, copper and even calcium, as we lose a tiny amount of it through urine and sweat. They are all "stored" in some way, but only temporally, so some amount has to be taken up daily. It would show only weeks later, however, if you have a deficiency.

Wikipedia adds phosphorus and iodine but they are not metals.


Why is an A-U bond less stable than an A-T bond?

I was not previously aware of this assertion, but on doing a little searching found it discussed in the following paper (I'm not sure whether it is open access or not).

  Kamya PR and Muchall HM  (2011) "Revisiting the effects of sequence and structure on the hydrogen bonding and π-stacking interactions in nucleic acids" J Phys Chem A. vol 115 pp. 12800-8

From this it emerges that the claim relates to the effect of substituting U for T in DNA, and the paper references previous claims for a stronger AT hydrogen bond. It also references other studies which did not find any difference, so the question was/is contentious. All studies were made on particular stretches of DNA duplex, and the authors' own studies were on a wider range of duplex structures from the protein data bank and (apparently) used more sophisticated analysis. To quote, they concluded:

  "H-bonding in AT can be stronger or weaker than that in AU base pairs, depending on the particular choice of nucleic acids used for comparison"

They explain this in terms of the influence of neighbouring bases in the duplex on base stacking, which, depending on the bases (i.e. the sequence), can be enhanced by interactions with the methyl group of T. (There may also be other effects caused by distortion of the base-pairs from planarity in particular cases.) So it would appear that AT base-pairs are not intrinsically stronger than AU base-pairs, but can be stronger in certain three-dimensional contexts.

As a generalization, the premise of the question would therefore appear to be false.


About The Selfish Gene Book - How Replicators Molecules forms duplicates?

This is how I think about it.  Here is the original large molecule, with each of its 'parts' represented by a letter.  There are a few different kinds of part:

C-A-A-C-T-A-T-A-C-G-A-C

As it drifts around in a 'soup' of parts, new parts stick to it one by one, like for like.  Here it is after two parts stick to it:

C-A-A-C-T-A-T-A-C-G-A-C
  A         T

Here it is after a few more:

C-A-A-C-T-A-T-A-C-G-A-C
C-A   C   A-T   C   A

Eventually, all the parts have got a similar part stuck to them:

C-A-A-C-T-A-T-A-C-G-A-C
C-A-A-C-T-A-T-A-C-G-A-C

Now, if the two halves split, the molecule has replicated itself.


Can the kidneys utilize ketone bodies for energy?

Alexandria's answer:

This article's abstract says that 3-ketoacid-CoA transferase was found in the kidney: nature.com/pr/journal/v42/n4/abs/pr19972518a.html


What is difference between several mRNA RefSeq for one gene?

I'll walk you through the process of determining this:

Note that there are two gene names presented: HLA-F and HLA-F-AS1. The "AS" part means, "anti-sense", so it's on the opposite strand...so ignore all of the HLA-F-AS1s.
Note the associated chromosomes. chr6 is a normal chromosome, but things like chr6_cox_hap2 aren't. Instead, these are haplotype patches/chromosomes. The HLA regions are highly variable, so having only a single reference sequence ends up being problematic in many analyses, such as finding sequence variants. For your purposes you may or may not want to ignore these, it depends on what your goal is.
If you ignore the haplotype patches then you're left with 3 listings on chr6. These are the 3 isoforms of HLA-F. You end up needing to use the refseq IDs for each of these.

BTW, Gencode/Ensembl list 4 isoforms for HLA-F, rather than 3. Whenever UCSC disagrees with Gencode or Ensembl, go with Gencode or Ensembl.


Is this basic gene diagram correctly labeled?

My professor got back to me and said my diagram is correct -- and that allows me to answer my second question: an ORF does not have to begin in the first exon.

(The UCSC Genome Browser uses a similar format to display genes.)


It looks moderately muddled, but perhaps.  This paper1 is a good place to start; it's free and the intro lists a number of more recent studies.  That study found a connection to lifetime reproductive success in sticklebacks (a fish) with intermediate MHC diversity.  This 2007 study in mice2 is a particularly nice one, dealing with a inbred line outbred to wild mice, finding again, no advantage to heterozygotes.  There are others, but most deal with the concept descriptively (self-delighting in their continued refutation of a commonly-held belief) or predictively (such as this from PNAS in 19923 or a 2009 review4) but specific and proven reasons are sparse.

The general feeling is that it may remain unclear what sort of genetic interactions are involved in MHC (additive effects, overdominance, etc.) but it is probably also complicated due to the nature of immunology.  For example, a paper from 20035 points out that in an immunological response, only a few peptides dominate the response; there may be no real advantage to having extra ones if they are unused, and having those others around might dilute the useful response (That paper also takes an interesting view of serial infections, and shows that heterozygotes are indeed advantaged during coinfection).  The above PNAS publication3 gives the idea, which the stickleback paper1 recapitulated, that if more alleles are present, more T-cells will be self-reactive and will therefore be purged, resulting in an overall decreased T-cell availability.

Other hypotheses are present in the review4 I mentioned, such as perhaps positive selection efficiency is not MHC-diversity dependent whereas negative selection is, or indeed increased autoimmune reactions as you guessed.  My guess would be some combination of the above, with selection for heterozygotes being favored in the real world for multiple and repeated infections but certain specifics resulting in a homozygote preference, of which autoimmunity is likely playing a role.


You have two possibilities: When you only need a quick check if your RNA is ok and you indeed only get one band, you can try a "quick and dirty" method. Heat the sample for 5 minutes at 65°C and then immediately cool it down in an icebath and keep it there until loading. By doing so, you melt up the secondary structure of the RNA and keep it in this state. You will most likely then see only one band.

If this doesn't work or if you want to use a RNA size marker, there is no way around denaturating gel electrophoresis. Here you denature your sample in the loading buffer and then run a denaturating gel in which prevents the secondary structures. There is a good paper about this:

Denaturing RNA electrophoresis in TAE agarose gels

The classical method using formaldehyde (which is more dangerous in handling) is described in the following paper and also in the "Molecular Cloning: A Laboratory Manual" book by Maniatis and colleagues:

RNA molecular weight determinations by gel electrophoresis under
denaturing conditions, a critical reexamination


Is there a word for the assumption that a sufficiently complex and refined organ must be the result of natural selection on a large time scale?

The 'term' you are looking for is actually gradual change or gradual evolution. If you want to make clear that this is an assumption or a theoretical consideration, you could say assumption of gradual change or theory of gradual change, replacing change with evolution if you like.

The idea comes from Darwin directly and was challenged in the 1970's by biologists like Stephen Jay Gould that suggested that evolution is not driven by gradual accumulation of changes but rather by morphological equilibria disturbed by many rapid adaptations forming new species, a concept called punctuated equilibrium.

It speaks for itself that these concepts are opposing but not mutually exclusive. They are rather two extreme states in a continuum.

Edit: As pointed out in a comment by Daniel Weissmann gradual changes also occur in neutral evolution; this is what we call accumulation of mutations - in fact, it also applies to (at least slightly) deleterious variants, especially in populations with small effective population sizes. This means, that the concept of gradual evolution can be generalised to neutral evolutionary processes. However, it does not mean, that the process involving natural selection cannot also be described by gradual evolution. You just have to specify what you are actually talking about. When talking about obviously complex adaptations, you would assume that they have not evolved neutrally.


As for the digestion of fats there are two digestive enzymes active in the stomach:

Lingual lipase (produced with saliva)
Gastric lipase (produced in the stomach chief cells)

Both have activity optima in the acidic pH range.

On the other hand, the salivary amylase that breaks down starch seems to be inactivated by the acidic environment.

Sources:

https://www.ncbi.nlm.nih.gov/pubmed/2134569
https://en.wikipedia.org/wiki/Gastric_lipase
https://en.wikipedia.org/wiki/Lingual_lipase
https://en.wikipedia.org/wiki/Alpha-amylase


How does a tiny spider interpret/cope with gravity?

Your question's title ("Sense of gravity felt by other organisms" - edited since it was originally posted) is quite broad, since "other animals" is all Animalia except Homo sapiens, which gives us at least 1 million species...

Therefore, I'm going to answer only your "The Question", regarding spiders:

  How does a tiny spider senses gravity?

First, it's worth noticing that while the gravitational acceleration is a constant (at sea level), the weight of the organism depends on its mass. Thus, for tiny animals, the effects of the gravitational force can be extremely small, and because of that those animals require very precise sensitive structures in order to measure the gravity.

Aquatic invertebrates have statocysts and statoliths, which are well known. However, spiders use another method to perceive gravity: they use their sensorial "hairs". According to Bender and Frye (2009):

  In the absence of wind, an animal standing at rest is acted upon only by the force of gravity. An animal might not explicitly calculate the global gravitational vector per se, but rather may actively modulate local joint angles and torques to implicitly compensate for gravity's pull. In many instances, insects and crustaceans measure the angles of their appendages' joints using clusters of mechanosensitive hairs, called hair plates.

According to Seyfarth, Gnatzy and Hammer (1990), one of these organs is the coxal hair plate:

  Natural stimulus situation and the spike response to maintained deflection suggest that these hairs are used in proprioception and graviception.

Here is an image:

However, the same authors say:

  Yet behavioral changes following selective hair-plate ablations are not very pronounced. Unilateral removal of hair-plates produced significant increases in average body height in 7 of 10 animals, while the angular orientation of the long body axis with respect to gravity remained unchanged after hair-plate removal.

That means that another sensors may play a role in graviception, such as proprioceptors. Still according to Bender and Frye (2009):

  In addition to measuring joint position, invertebrates also have specializations for measuring joint load. Whereas our bones have no active sensory capacity and instead our sensors are imbedded in surrounding, soft tissues, many invertebrates are equipped with sensory arrays embedded in the exoskeleton at strategic points and with specific orientations. Called campaniform sensilla in insects, lyriform organs in arachnids and centipedes. (emphasis mine)

Sources:

Bender, J. and Frye, M. (2009). Invertebrate solutions for sensing gravity. Current Biology, 19(5), pp.R186-R190.
Seyfarth, E., Gnatzy, W. and Hammer, K. (1990). Coxal hair plates in spiders: physiology, fine structure, and specific central projections. Journal of Comparative Physiology A, 166(5).


Does breathing air containing 3% carbon dioxide gives you a headache?

http://en.wikipedia.org/wiki/Carbon_dioxide#Toxicity

"In concentrations up to 1% (10,000 ppm), it will make some people feel drowsy.[83] Concentrations of 7% to 10% may cause suffocation, even in the presence of sufficient oxygen, manifesting as dizziness, headache, visual and hearing dysfunction, and unconsciousness within a few minutes to an hour.
...
Occupational CO2 exposure limits have been set in the United States at 0.5% (5000 ppm) for an 8-hour period.[90] At this level of CO2, International Space Station crew experienced headaches, lethargy, mental slowness, emotional irritation, and sleep disruption."
So according to this, yes you could breathe it, and yes, you would get a headache."


Is it common to have multiple recessive traits in humans?

It depends on how long a population in your dominant heritage was genetically isolated, how common certain recessive traits are.

However, you might reconsider about the "green eyes".  Iridologists claim that there are only blue eyes, and light brown eyes.  All other colours are indicative of bioaccumulation of various substances (evidenced by a return to blue or light brown when the body is supported in excreting these substances), and health issues in certain tissues.

While there is argument about how scientific a technique iridology is, all medicine begins as observation of patterns, and development of models based on those patterns.  Models in medicine are constantly undergoing upgrading and replacement, as old models no longer explain new and well-observed patterns.


It's a behavioral thing.
The abstract of the paper says: "...mixtures of two drugs from vehicle in two-lever procedures with food reinforcers..."

In operant behavior, rats (in this case) are trained to associate a stimulus (a tone, an odor, a light, etc.) with an action that leads to a reward, the association is trained by delivering a reward only when the 'correct' action is performed, e.g.:

stim A -> press left lever -> get a reward

stim A -> press right lever -> get nothing (or a punishment, but that is a whole different question)

One can quantify the performance of the animal by looking at the probability of responding left (in this case) when stim A is presented.

Now, we think of the association between stim A and left pressing as being reinforced whenever a reward is present, we call it extinction whenever the reward is not present, basically because the reinforced behavior will eventually extinguish, and we say its extinguished when the probability of response to the left and right is 50%.

"...generali[z]ation to ethanol was examined in extinction tests..."
basically means that they substituted stim A for ethanol (I imagine its all olfactory, just read the abstract sorry) and characterize the response to ethanol without ever reinforcing it, hence the extinction.


Selection Pressure on Orca Whale Coloration

You can find a discussion of this topic in the literature:

Mitchell, Edward. 1970. Pigmentation pattern evolution in delphinid cetaceans: an essay in adaptive coloration. Canadian journal of Zoology 48(4): 717-740.

Perrin, W.F., 1972. Color patterns of spinner porpoises (Stenella cf. S. longirostris) of the eastern Pacific and Hawaii, with comments on delphinid pigmentation. Fish. Bull, 70(3), 983-1003

Caro, T., Beeman, K., Stankowich, T. and Whitehead, H., 2011. The functional significance of colouration in cetaceans. Evolutionary Ecology, 25(6), pp.1231-1245. http://web.csulb.edu/~tstankow/Caroetal2011.pdf

And related helpful article:

Evans, W.E., Yablokov, A.V. and Bowles, A.E., 1982. Geographic variation in the color pattern of killer whales (Orcinus orca). Report of the International Whaling Commission, 32, pp.687-694. http://www.kasatka.com/kirsten/ColorVariation.pdf

I'll let you explore these and their citations.

Remember, Google Scholar is your friend.


First you need two, hopefully homozygous, strains that differ in some measurable quantitative trait. In worms it has been done with lifespan; in mice injected with ethanol it has been done with long-sleep and short-sleep periods. The two strains need to differ in their RFLPs. For flies there are probably lots of behavioural traits one could use.

You set up a cross, and then mate individual brothers to sisters, and keep repeating this breeding pattern for multiple generations to establish recombinant inbred lines. After 10 generations they are basically homozygous, and you take the individual lines and assay them first for the trait you are scoring, and second for the molecular markers. The results of the molecular mapping let your draw the haplotype along each chromosome, so you know which parental strain contributed which portion or each chromosome.

The results of each quantitative trait scoring let you classify each recombinant inbred line into one of the two parental phenotype classes (or if it is a multi-locus trait then you may get some intermediate lines).

With those two results you will be able to correlate the absence, or presence, of molecular markers along the chromosomes, with the quantitative trait you are studying.

If it works you will be able to narrow in on a genomic region that co-segregates with the trait. If there are multiple genes involved you may be able to assign a probability or LOD score to different regions.


Differential gene expression analysis between species

It depends on what type of data you have, really. There are methods developed solely for quantifying relative expression based on count data, such as using edgeR or limma-voom.

You don't need to correct for gene length to estimate fold-changes of relative expression, what you need to do is normalise by library size first (and in the process obtain log2 ((counts + 0.5)/1e+06) and then, following quantile normalisation, you can just calculate mouse - human or human - mouse to give you an estimate of fold change.

I still would recommend using something a bit more sophisticated like limma-voom for this task, though, because that also will enable you to get stuff like false-discovery rates for your fold changes.


Essential fatty acids consist of two main EFAs - Omega 3 (Linoleic acid) and Omega 6 (Linolenic acid).

These two play vital roles in the following:

Growth and development
Brain functioning
Skin health
Hair growth
Metabolism
Reproductive system health
Cell membrane integrity.

The fact that are bodies can't make them makes them very important in our diet. They are most important in our cell membranes.

Omega 3 is an amazing anti-flammatory. It does this by blocking the inflammation pathways in the cell.

We need more Omega 3 than 6 - about a ratio of 2:1.

This is a pretty good page if you want more information.


How does TYRP1 affect the synthesis of black and brown eumelanin (on a biochemical level)?

The actual coat color is determined by the ratio of the products of two genes: Tyr and TyrP1. The first oxidizes DHI to Indole-5,6-quinone and forms brown pigment, TyrP1 on the other hand oxidizes DHICA to Indole-5,6-quinone carbolic acid, which forms black pigment. See this pathway diagram (from here):

So loss of TyrP1 activity is not harmful to general pigmentation but prevents the formation of black color, while the inhibition (or loss of function) for Tyr will lead to albinism, since no pigment precursors (from Tyrosine to DOPA can be formed.

You may also be interested in this paper: "TYRP1 and MC1R genotypes and their effects on coat color in dogs."


I'm taking this question at face value. Yes, fish have gills, but we also have a respiratory surface in our lungs so why couldn't we 'breathe' water and extract the oxygen (since extraction is a simple matter of diffusion from the content of the lungs into the blood).

Apparently we use 550 L of pure O2 per day. This works out as approximately 400 g.

The solubility of O2 in fresh water is around 10 mg L-1. Assuming a hypothetical situation where we could breathe water and extract all of the O2 from each lungful this means that we would need to breathe 28 L of water per minute, compared to the 8 L of air that we breathe.

Now of course water has a much higher density than air so that a lot of energy would be expended in moving this much water in and out of the lungs (which in turn would require us to consume more oxygen). Couple this with the fact that realistically we would only be able to use a fraction of the O2 dissolved in each lungful and you can begin to see why this is a non-starter.

Gills allow this problem to be largely circumvented by having a one way flow of water over the respiratory surface, which in the case of fish is often achieved at least in part by moving through the water.


How long the homologous arms of the "repair" sequence must be to do homologous recombination?

As little as 14bp of homology can work. See this reference.

I would recommend at least a length of 90bp but 1kb is probably overkilled. Yes both arms can have different length (staying in the same order of magnitude).


How many human cells are there in our body, on average?

Bianconi et al. 2013 give an estimated lower bound of 3.72 × 10^13 (which, by the way, is approximately the geometric mean of 10^13 and 10^14).

However, from the table in their Supplemental Information (where estimates for about fifty different types of cells are added up), it is clear that the vast majority of these are the erythrocytes, also known as red blood cells: estimated at 2.63 × 10^13. While the second largest class are the glial cells (from the nervous system), estimated at 0.30 × 10^13. Three other classes (endothelial cells {vessels}, dermal fibroblasts {skin}, and platelets {blood}) add up to another 0.58 × 10^13. These, in total, is about 3.5 × 10^13, and we can stop there, because the uncertainty in all these estimates swamps all the other cell type populations, which are much smaller.

This means that if we only consider the 5 most abundant cell types in the body, we already get a very good estimate. Is it likely that we have missed a cell type of which there are a trillion cells in the body? It's not impossible, but unlikely, because it would be hard to miss all these cells.

Maybe there is a long tail (i.e. a large number of minor cell types, each with a small, but significant population) that wasn't considered? Together, these could add up to a significant adjustment to the above figure. I don't know.

This estimate is for a typical human person: 30 year old young adult, 70 kg, 1.72 m tall and with a surface area of 1.85 m^2. For this person, the figure is given with roughly a +-20% uncertainty.

Given all the above, it's probably safe to say "30 to 50 trillion".

(This obviously doesn't take into account any of the bacteria mentioned above.)


"Forma asexualis" as explained in another paper

  The authors favor the use of the expression forma asexualis (f.a.) in the
  description of anamorphic species of the genus
  Cystobasidium and this decision follows the current
  practice of reclassification of asexual yeast taxa (see
  e.g. Lachance 2012; Groenewald and Smith 2013;
  Daniel et al. 2013; Selbmann et al. 2014)

  Lachance MA (2012) In defense of yeast sexual life cycles: the
  forma asexualis: an informal proposal. Yeast Newslett
  61:24–25


Cardiac Excitation Threshold - in C++ modelling

You wouldn't normally apply the stimuli simultaneously. The idea is to apply stimulus1, which has a given amplitude and duration, and follow that with stimulus2, which also has a given amplitude and duration, after a variable lag. You'll then see that the effective refractory period is dependent on the amplitude of stimulus2 (at least until you hit the absolute refractory period).


Immune response to IgA positive bacteria

Depending on the precise details of the experiment, I don't see a particular reason to suppose that being coated with IgA should mean that they'll elicit an IgA response.
I'm assuming that the "coating with IgA" means that the IgA is binding like an antibody, through the variable region binding site on the antibody to some epitope(s) on the bacteria. The way antibody class switching works is that the epitope binding region of the antibody remains the same while the constant regions switch from IgM to IgG or IgA, etc. That means that the ability to bind to the bacteria appeared in a non-IgA antibody, so the ability to bind, per se, is more or less separate from the isotype of the antibody.
The factors that drive a response toward IgA are heavily influenced by location - a response on a mucosal surface is much more likely to drive IgA than one that's systemic (simplistically, because the cytokines and cell types involved are different in the different locations).
An alternate possibility is that the IgA is binding the bacteria through its constant (Fc) region, analogous to Protein A.  If the bacteria have evolved an IgA-binding capability in this way, one might guess that they did so because they need it as a defense, and if it's specific to IgA one might guess that it's because they tend to have an IgA-dominant response. But that's an inference, not a strong argument. As a counterargument to that, Protein A does (sometimes) bind to IgA and that's likely more of a side effect than a primary thing.
So I think the answer is "probably not, but you'd need more information to have a good answer."


By what method do ants dissect and hold soil

Short answer

Ants use specialized facial structures called mandibles to cut, shape and carry soil and other matter.

Background

you say "I know ants break off soil in small quantities, so that a single ant carries very little soil...". On the contrary I would say - Ants can carry relatively a lot of soil, as they can lift up to about 100 times their own body weight. In absolute terms, however, the weight carried is about 500 mg (Spectrum).

Source: The World's Best Photos

The structure that ants use to break off and carry soil are their mandibles:

Source: Tree of Life Web Project

Mandibles are specialized bodily structures typical for insects, and I quote from the University of Sydney website:

  The mandibles are the first pair of jaws in insects, moving laterally (i.e. from side to side) when in use. Mandible shape is strongly influenced by function and is therefore highly variable. For example a chewing insect will have strong tooth-shaped mandibles while in a sucking insect they will be thin and needle-shaped. Mandibles are used to cut, chew and tear food as well as to carry objects, fight and mould materials such as wax or soil.


How much time does it take a human body to replace all of its atoms?

Not all the atoms in the human body are replaced.

Carbon atoms in tooth enamel are not replaced after the enamel is laid down during tooth development. This was demonstrated in the 2005 Nature article "Forensics: Age written in teeth by nuclear tests", where the researchers showed that the amount of carbon-14 in tooth enamel can be used to accurately determine date of birth.


Is there a blood panel lab test that measures all the hormone-producing glands?

There are no composite tests that measure all the clinically important hormone producing glands. There are too many hormones produced by too many hormone producing cells/tissues in the body to test for all of them all at once (i.e. in a panel).

For illustrative purposes only... if you go to wikipedia they have a list of all hormones in the human body which is definitely far from complete! But it gives you an indication of just "how many" hormones there are and why testing for all of them is impossible in a panel.

Even with regard only to pancreatic hormones, there are several hormones produced (e.g. insulin, glucagon, somatostatin) that aren't necessarily a marker of the glands overall function (because they are not necessarily involved in the same function). Each of these hormones has different functions even though they are produced by the same gland.

Regardless, from a medical perspective you would never have a reason to test for all of them anyway. If you tested enough of them you'd find at least one of them that would - by chance - be abnormal.

Additionally, if you asked a handful of scientists to name fifty hormones there would be a lot of different hormones on each of their lists. The definition of hormone is vague, and we are learning more about new hormones every day. In the last decade we have learned that bile acids - chemicals predominately produced by the liver that are involved in dietary fat absorption - also act as hormones. There aren't clinical reasons to study all of these molecules just yet, but this demonstrates that it would be impossible to measure all of them all at the same time in one particular "panel".


Gene configuration : Divergent vs convergent

RNA polymerase produces transcripts by scanning along DNA, linearly. Simplifying things, genes can thus be thought of as having a start (or 5' end) which is the main site where the polymerase begins to transcribe, and and end, where it stops. Divergent promoters are promoters oriented so that the polymerase transcribes in opposite directions, away from the two promoters (like so: <- -> ). Convergent promoters instead transcribe towards each other (like so -> <- ) . This means, for instance, that the polymerases coming from two convergent promoters could collide with one another.


Can someone link me to resources on the efficiency of sticky end ligation?

The best resource for troubleshooting ligations I found (and use frequently) is this NEB page.  That is assuming you've already referred to the instructions provided with the enzyme you're using.   In my case it's T4 Ligase, again from NEB.   It's helpful to check the FAQs and the references listed on that page.    Also, you can make use of their Molar Calculator tool on Ligation setting (see more from first link).

Good luck with high efficiency!


How quickly can the human heart rate rise and fall?

According to the Wikipedia page on Supraventricular tachycardia the heart can go to a new faster rate in the space of a single beat, and then come down again just as quickly, as shown in this image taken from the Wikipedia page.


Hybrid, Japanese or European larch please?

To tell these larches apart from each other the shape of the scales on the cones is a good place to start.

European larch have cones with scales that are straight, rather than curving outwards.

Japanese larch have cones with scales that curve markedly outwards as in this photo below.

From Wikipedia - Larix kaempferi

Hybrid larches, being a cross between the European and the Japanese, have cones that are in between. But as this Forestry Commissions publication,
 "Know your conifers", mentions there is some variation so it is useful to look at cones from more than one tree across a stand.

Summary: Your photo shows a cone with slightly curved scales or bracts, so I don't think that it is European larch. But it could be, it is slightly misleading as the seeds (the thinner bits are protruding).

Japanese larch cones are really curved, which when I was being taught tree ID were described as 'like roses'. So a definite, not Japanese.

So in my opinion it is most likely to be a Hybrid larch, but as the cone is not fully mature and open, and there is only one to look at it could be a European larch.

When looking at cones, I find it best to find old cones on the woodland floor that way you can see them at there most fully developed, and the differences between the species are more marked.

There is another ID feature between European and Japanese, and that is the colour of the stems. The former are straw-coloured and the latter are darker, brown/purplish colour. This becomes more obvious as the season progresses.

There are quite a lot of photos of cones on the web that have been given the wrong names, which makes it quite confusing. Best stick to Forestry Commission literature, or educational institutions.

When looking for photos I came across this YouTube video by Harper Adams University which is good and actually features the Japanese Larch photo that I found on Wikipedia.


Yes, it is a skipper (family Hesperiidae) and very similar to European species in Ochlodes, and my guess is that it belongs to one of the North American species in this genus. For instance, it is very similar to Ochlodes sylvanoides (also called Woodland Skipper), which is common in the western parts of the US. However, I'm not familiar with North American butterflies, and there might be closely related similar species that I'm ignoring.

Images of Ochlodes sylvanoides from http://butterfliesofamerica.com/t/Ochlodes_sylvanoides_a.htm:

More pictures can also be seen at Bugguide.net


Medium preparation, using calcium hydroxide instead of potassium hydroxide

As @Chris said, $\ce{K+}$ salts are soluble in water whereas plenty of $\ce{Ca^{+2}}$ salts such as $\ce{CaSO4}$ and $\ce{Ca3(PO4)2}$ are insoluble in the aqueous medium. Therefore it leads to the precipitation of phosphate-containing proteins and sulfate-containing metabolites. In addition, $\ce{Ca^{+2}}$ forms coordination complexes with calcium-binding proteins which participate in discrete signaling pathways. Interfering with this system could lead to subtle and irreproducible results. $\ce{K+}$ ion mostly participates in creating a voltage gradient across the membrane, nothing more.
Moreover, ionic strengths should be considered. $\ce{Ca^{+2}}$ is a divalent cation. A solution of $\ce{KOH}$ and a solution of $\ce{Ca(OH)2}$ with the same pH would definitely have different ionic strengths. Therefore despite achieving the same pH of the medium, ionic strengths vary depending on the salt used. Abnormal ionic strengths affect the structure of proteins in many ways. In general, it has been proven that changes in $\ce{K+}$ concentration lead to less severe outcomes compared to $\ce{Ca^{+2}}$.
EDIT: $\ce{Ca(OH)2}$ forms precipitates in an aqueous solution because it is barely soluble in water ($K_{sp}$ $\pu{=5.5 \times 10^{-6}}$). The pH of a saturated solution of $\ce{Ca(OH)2}$ is 12.347. To achieve other pHs one must add strong acid or base (a standard $\ce{KOH}$ solution perhaps) or use dilution; so as you can see, introducing $\ce{Ca(OH)2}$ just leads to unnecessary complexity, best to be avoided. Also, $\ce{Ca(OH)2}$ leads to the formation of $\ce{CaCO3}$ in the presence of atmospheric $\ce{CO2}$, making it even a less appropriate material for the preparation of the medium. Calculations using $K_{sp}$ shows a saturated $\ce{Ca(OH)2}$ solution has pH = 12.347 and [$\ce{Ca^{+2}}$] =  0.01111


Example of species that went extinct because of excessive hunting by non-humanoid predators?

The Brown Tree snake (Boiga irregularis) is responsible for five extinctions on the island of Guam. Some of these species existed only on Guam, while others exist elsewhere and so it is the Guam subspecies that has been lost.

Guam flycatcher (Myiagra freycineti). Last sighted in 1983.

Guam rail (Gallirallus owstoni) is extinct in the wild, but is now bred in captivity and has been introduced to the island of Rota.

Guam kingfisher (Todiramphus cinnamominus) is also extinct in the wild and exists only in a captive breeding program.

Guam flying fox (Pteropus tokudae). Went extinct in the late 1960's possibly as a result of the Brown Tree snake.

I had a suprisingly difficult time obtaining accurate lists of the Guam extinctions.

For an example of overgrazing leading to a local extinction, see St. Matthew island in the Bering Sea. The US Coast Guard introduced reindeer in 1944. By 1963 there were ~6,000. Without any natural predation to control the population, they are considered to have overgrazed, causing a population collapse to 42 by 1965 and no reindeer population by the 1980's.


Background:

Iron exists in a wide range of oxidation states, −2 to +6, although +2 and +3 are the most common.

How is Iron Handled by the Body:

According to Wikipedia:

  After uptake in human cells, iron storage is carefully regulated; iron ions are never "free". This is because free iron ions have a high potential for biological toxicity.

Performed by the protein Transferrin that traps the Fe$^{3+}$ ions.

has such a high stability constant that it is very effective at taking up Fe3+ ions even from the most stable complexes.
At the bone marrow, transferrin is reduced from Fe$^{3+}$ and Fe$^{2+}$ and stored as ferritin to be incorporated into hemoglobin.

Dangers of Iron:

A number of sources reference toxicity and dangers of iron:

The Food and Nutrition Board of the U.S. Institute of Medicine indicates that Tolerable Upper Intake Levels (known as ULs) for iron is 45 mg/day. [Source].

Note: Tolerable upper intake level (UL) is the highest level of daily nutrient consumption that is considered to be safe for, and cause no side effects in, 97.5% of healthy individuals in each life-stage and sex group.

The World Health Organization (2003) suggests:

  The average lethal dose of iron is 200–250 mg/kg of body weight, but death has occurred following the ingestion of doses as low as 40 mg/kg of body weight

Of course, one can get iron poisoning due to an acute overload of Fe.

Toxic effects begin to occur at doses above 10–20 mg/kg of elemental iron.
Ingestions of more than 50 mg/kg of elemental iron are associated with severe toxicity
See Abhilash et al. (2013) for an example study examining fatail Fe overdoe in adults.

Note: inhalation of Iron Oxide dusts is complicated but potentially dangerous, but should be of no concern to you.

However, outside of trying to OD on iron supplements, it's not easy to consume that much iron. So even given all tose nasty numbers, I wouldn't be too concerned

According to 2 citations (Greentree & Hall 1995 and Goyer 1996) in The toxicity of iron, an essential element:

  Because iron must be ionized to be absorbed, metallic iron  and iron oxide (rust) are not generally of concern when they are ingested.

Even when iron is heated (and supposedly ionized) very little becomes available for ingestion:

This source cites a 1986 study that found that cooking in a cast iron skillet added typically 1-4 mg (though as high as 7 mg) of iron into the food (well below dangerous levels)
Besides, iron oxide is already present in most drinking water.

Concentrations of iron in drinking-water are normally less than 0.3 mg/L [source] and is seldom found at concentrations greater than 10 mg/L or 10 ppm [source].

Bacteria connection:

There are bacteria associated with rust:

Iron-oxidizing bacteria are chemotrophic bacteria that derive the energy by oxidizing dissolved ferrous iron

However, these species are aquatic, and are more likely to be found in ground water or well-water. (not living in your kettle).

What about Tetanus? From Wikipedia:

  Tetanus is often associated with rust, especially rusty nails. Although rust itself does not cause tetanus, objects that accumulate rust are often found outdoors or in places that harbour anaerobic bacteria. Additionally, the rough surface of rusty metal provides a prime habitat for C. tetani endospores to reside in (due to its high surface area), while a nail affords a means to puncture skin and deliver endospores deep within the body at the site of the wound.[21]

In other words, rust really has nothing directly to do with tetanus, a soil-dwelling species. One might just inconveniently find a sharp, rough rusty item in the soil to introduce the soil-living species into their bodies.(again, it shouldn't be a concern in your case).

Conclusion Would it be safe to drink water boiled in this kettle?

Almost certainly. But if you're concerned about it, just sand off the rust and  boil it to kill off anything that might be living there (more likely from old food/drink residues). Otherwise, get yourself a new kettle :p.

Citations

Goyer RA. (1996). Toxic effects of metals. In: Klaassen CD, ed. Casarett & Doull’s Toxicology: the basic science of poisons. 5th ed. New York City, NY: McGraw-Hill;715-716.
Greentree WF, Hall JO. (1995). Iron toxicosis. In:Bonagura JD, ed. Kirk’s Current therapy XII  small animal practice. Philadelphia, Pa: WB Saunders Co;240-242.
WHO. (2003).  ORIGINALLY PUBLISHED IN: Guidelines for drinking-water quality, 2nd ed. Vol. 2. Health criteria and other supporting information. World Health Organization, Geneva, 1996.


E. coli values for [enzymes], [metabolites] and kinetic rates

I would advise you to use the SMBL for iAF1260 E. Coli with a COBRA toolbox on MATLAB. It has all the constants you are looking for optimized for the steady state and have been extensively tested for simulation of single and multiple genes deletion / mutation. Even if you want to stick with your model you will be able to copy the constants from there.

However depending on what you are doing you might not be satisfied by the whole models, since the they are computationally too complicated to simulate and optimize and lead to computationally unstable results, especially when you try to simulate colony collaborative mechanisms.


Mesophytic Climax community in succession?

The concept of a "climax community" has not been accepted as reality for more than 40-50 years. Frederic Clements was an early botanist examining succession in the first 20 years of the 20th century. It was Clements who developed the concept of the climax: he posited that the habitat and the populations acted upon one another in a reciprocal way until finally a stable state (the climax) was reached.

However, the work of Gleason (e.g, 1926), Tansley, Watt (1957), Whittaker (e.g., 1972), Davis (1969),  etc. have changed the field's understanding of succession and its acceptance of the existence of a stable "climax". Whittaker was first to propose the use of the term "stable state," as it carried less assumptions about the community' inability to be replaced.

It's now clear from work of countless studies and authors (along with my own research), that disturbances play a significant role in plant dynamics and that previously accepted 'stable states' are perhaps only remnants of historical characteristics of the system (see below). As a result, some accepted stable-state communities no longer appear to be the norm in some areas (likely due to both present and past disturbances and fluxes in the system). See Abram's papers for a discussion on hypotheses of this phenomenon in the Eastern deciduous forest of the U.S.

Regardless, even in a system without disturbance (which none exist), the stable-state community would be fully dependent on climate, substrate, community assembly limitations and geographic/environmental/biological filters.


One notorious pest of potato plants are cutworms. Unfortunately due to the the discoloration of the species I am not able to identify for sure which species of cutworm it is.
Cutworms attack a wide host of plants (more info here). According to that same website, the main ways to avoid the damage these larvae can cause are to:

Remove all plant residue from soil after harvest or at least two weeks before planting...

... plastic or foil collars fitted around plant stems to cover the bottom 3 inches above the soil line and extending a couple of inches into the soil can prevent larvae severing plants; hand-pick larvae after dark; spread diatomaceous earth around the base of the plants (this creates a sharp barrier that will cut the insects if they try and crawl over it); apply appropriate insecticides to infested areas of garden or field if not growing organically

These larvae come from a large variety of insects so don't associate them too quickly with one insect or another (many websites associate them with moths but that is not always necessarily accurate).
Here's a source that elaborates a bit more on how to treat them plus another source for how to use pesticides in a garden safely (if no other option is convenient).


Can two proteins sharing a few domains be considered homologous?

Homology means shared evolutionary ancestry. Sequence similarity is often used as a proxy for homology but inferences should be made with care.

The similarity between two genes/proteins should not just be good but has to be statistically significant (metrics like E-value) for the two genes/proteins to be considered homologous.

  INFERRING HOMOLOGY FROM SIMILARITY

  The concept of homology – common evolutionary ancestry – is central to
  computational analyses of protein and DNA sequences, but the link
  between similarity and homology is often misunderstood. We infer
  homology when two sequences or structures share more similarity than
  would be expected by chance; when excess similarity is observed, the
  simplest explanation for that excess is that the two sequences did not
  arise independently, they arose from a common ancestor. Common
  ancestry explains excess similarity (other explanations require
  similar structures to arise independently); thus excess similarity
  implies common ancestry.

  However, homologous sequences do not always share significant sequence
  similarity; there are thousands of homologous protein alignments that
  are not significant, but are clearly homologous based on statistically
  significant structural similarity or strong sequence similarity to an
  intermediate sequence. Thus, when a similarity search finds a
  statistically significant match, we can confidently infer that the two
  sequences are homologous; but if no statistically significant match is
  found in a database, we cannot be certain that no homologs are
  present.

  Pearson, 2013

Members of a protein family are descendants of a common ancestor and are hence homologous. However, in the course of evolution they would have acquired new domains or reshuffled their domains such that their sequences are no longer similar. Proteins that have full length sequence similarity are called homeomorphic (Wu et al., 2004). Therefore, members of a protein family may be homologous but not homeomorphic. However, homeomorphic proteins can evolve independently and therefore may not be considered homologous.

Identifying homologous proteins is, therefore, not a simple task. Machine learning algorithms are used for better identification of homologous proteins. Some of these algorithms are mentioned in the linked papers.

In general, global similarity, rather than local similarity should be considered for identifying homeomorphs. See What is the difference between local and global sequence alignments?


What do you call a virus when it's cured?

Lets start with the definition of a virus (from the Wikipedia page on viruses):

  A virus is a small infectious agent that replicates only inside the
  living cells of other organisms. Viruses can infect all types of life
  forms, from animals and plants to bacteria and archaea.

So basically speaking you have a piece of genetic information (DNA or RNA) which encodes proteins which are important for the function of the virus and a hull (not always, but mostly). These invade a cell type, take over the cell (litarally, after an infection the cell will mostly only make viral proteins and DNA/RNA). Finally new viruses are built inside the cell and released to infect more cells. In principle this works like in the figure below (from here):

There are two possibilities for cures: The first one are vaccinations. Here you either use dead or attenuated viruses (or parts of viruses) to train the immune system. When this has happened, the immune system "knows" this specific agent and can rise a fast and highly specific immune answer against it, before the virus can replicate in high numbers and infect a lot of cells. This happened for example for the small pox virus which could be eradicated from the human population.

The other would be drugs which either target a virus (or some of it functions) specifically or prevent them from spreading. The immune system usually does the final cleanup here.

Both methods only work for people which either take the drug or are vaccinated, so they have no influence on the virus in people which are not protected. For further information have a look on the Wikipedia page on Viruses.


It is an pink flannelmoth because there is no other insect which ressembles it

Usually pinkflannelmoths have orange coloured centers


There will be few rapidly-dividing cells in a fresh wound (which is the wound to which H2O2 is applied). In general, it is a good idea to avoid applying irritants to rapidly dividing tissue.

Hydrogen peroxide is a weak mutagen. It is produced in many body tissues, ingested in drinks, produced by mouth bacteria, etc. It may well cause some cancers. Some OSHA-mandated literature does warn that it is a mutagen and must be handled with care, but these are warnings to people who work with concentrated solutions.

However, a relatively weak hydrogen peroxide solution, even if it is mutagenic, would need to be left in place and active (or renewed) for a long period of time to produce skin cancer. As it has been a staple of first aid kits for decades, and this association has never been made clinically, my best guess is that the benefit (as a bacterocidal agent) far outweighs the risk in the treatment of minor wounds. As in all things, however, prudence is advised. (I myself don't use it because soap and a lot of water is quite effective. Nor is it used in the care of wounds in Emergency Rooms where it is considered to be detrimental to wound healing. If I were in a country where clean water and soap were in short supply, I might well use it if necessary.)

Because it is an irritant (and many irritants can be considered mutagenic), it is actually used to treat precancerous skin lesions, the finding being that it affects the more rapidly dividing pre-cancerous cells than the rest of the epithelium.

Far more potent peroxides have been used topically, which may increase the risk of skin cancer.

Interestingly, one of the responses of skin cells to H2O2 is the generation of an oxygenase to fight the effects.

Topical sulindac combined with hydrogen peroxide in the treatment of actinic keratoses
Effects of Peroxides on Rodent Skin: Epidermal Hyperplasia and Tumor Promotion
Heme oxygenase is the major 32-kDa stress protein induced in human skin fibroblasts by UVA radiation, hydrogen peroxide, and sodium arsenite
Recent Advances in Wound Care, Michael K. Abraham, MD, MS, and Jason S. Oh, MD


Is it correct to regard archeaic humans (i.e.n Neanderthals and Denisovans) as distinct species to Homo sapiens?

This question highlights the different species concepts.

If you go by the reproductive species concept (a population of actually or potentially interbreeding organisms), then yes. Apparently, the populations were interbreeding.

If you go by the typological species concept (morphologically distinct), then no. Homo neandertalensis and the "Denosovian" are morphologically distinct enough to be recognized as such.


I only found this two references, but these are only secondary sources at the moment.
Look here "Clown Fish Anemone" and here "Choosing Clownfish and Anemones for Your Aquarium". It seems that there are only around two handful of anemones capable of supporting clownfish.
Here are some primary sources which confirm the 10 anemone species: "The anemonefish symbiosis: What is known and what is not." and "Field guide to anemonefishes and their host sea anemones". The last two links point to PDFs which contain a lot more references.


In which direction plants' root grow in weightlessness?

Astronomers on the International space station have done exactly that and grown Arabidopsis Thaliana in space. You can read the whole article here.
Plant roots apparently grow away from the seed exactly like on earth seeking out nutrients.


What is the size (diameter) of the SARS-CoV-2 virus?

Electron micrographs of negative-stained 2019-nCoV particles were generally spherical with some pleomorphism (Figure 3). Diameter varied from about 60 to 140 nm. Virus particles had quite distinctive spikes, about 9 to 12 nm, and gave virions the appearance of a solar corona.

--A Novel Coronavirus from Patients with Pneumonia in China, 2019

Figure 3 from that article:


To note: I have no personal experience with this protocol. I am forwarding this paper, passed on to me by a colleague

There are many kits and methods available that don't rely on Qiagen. Or alternatively, if you ask them nicely, they do heavily discount their first kit you buy off them as a sort of trial (as they dont do samples).

However, to answer your primary question, are you adding a detergent and heat denaturing your samples first before phenol-chloroform (Triton/Heat/
Phenol)?

  Blood samples for CFDNA
  analysis are collected into EDTA tubes and held at/or below RT
  (18 °C–22 °C) for no more than 2 h before separation of plasma.
  Plasma should be separated from whole blood samples by double
  centrifugation (800 g and 1600 g for 10 min, separately), avoiding
  leukocyte lysis. We prefer to isolate CFDNA immediately after plasma
  separation to minimize the effect of prolonged storage. Otherwise,
  samples should be aliquoted into small portions and stored at −70 °C
  before extraction because fragmentation of CFDNA might be caused by
  repeated freeze–thaw cycles

  For the THP method, 500 μl of plasma/serum was mixed with 5 μl Triton X-100
  (Sigma-Aldrich, UK) and heat denatured at 98 °C for 5 min. Samples were placed on ice
  for 5 min, then extracted with an equal volume of phenol–chloroform–isoamyl alcohol
  (25:24:1, v:v:v) (Sigma-Aldrich, UK) and centrifuged for 10 min at 14,000 g. The
  aqueous phase was precipitated overnight with 1/10 volume of 3 M NaOAc and 2.5
  volume of 100% ethanol at −20 °C. The DNA pellet was washed with ethanol, air-dried
  and resuspended in 50 μl of ddH2O.

  In the THP protocol, 98 °C incubation was used to inactivate
  PCR inhibitors and denature proteins in plasma/serum samples.
  Different times and temperatures were tested before choosing this.
  Since we had noticed substantial DNA contamination in SDS, Triton
  X-100 was used in the protein solubilization step. Direct conventional
  PCR was performed successfully on heat-denatured samples
  and able to detect 25 ng/ml DNA, indicating that this simple
  procedure offered sufficient protein digestion and inhibitor elimination
  for PCR analysis. The THP protocol gave a significantly
  higher yield of pure DNA solution for qPCR analysis than the
  QIAamp kit. The THP protocol showed high efficiency even with
  small DNA fragments as low as 100 bp.

You might want to read this:
Xue, Xiaoyan, et al. "Optimizing the yield and utility of circulating cell-free DNA from plasma and serum." Clinica Chimica Acta 404.2 (2009): 100-104.

A quick search of google scholar also revealed a few other papers you might be interested in:

Fleischhacker, Michael, et al. "Methods for isolation of cell-free plasma DNA strongly affect DNA yield." Clinica Chimica Acta 412.23 (2011): 2085-2088.

UPDATE:

After reading this (Fong, Siew Lee, et al. "Comparison of 7 methods for extracting cell-free DNA from serum samples of colorectal cancer patients." Clinical chemistry 55.3 (2009): 587-589.) which gives about 7 protocols (sadly without any references for some reason) I went hunting for  came up with this:

  DNA was extracted from 1.0 ml plasma by phenol-chloroform method with slight modifications.
  One ml of plasma was treated with 1x SDS/Proteinase K solution (0.5 mg/ml) (1:1), incubated
  overnight at 56 °C followed by phenol-chloroform (4:1) treatment and centrifuged at 7 000 rpm.
  The upper layer was transferred into fresh 15 ml centrifuge tubes and the same step was repeated
  again; DNA was precipitated by adding glycogen (0.1 µg/µl), ammonium acetate (7.5 M) and
  absolute alcohol. DNA pellet was obtained by centrifuging at 7 000 rpm; was washed with 70%
  alcohol at 10 000 rpm, dried and finally dissolved in TE buffer at 56 °C and stored at -20 °C until
  further use.

You can read about the above method here: Singh, Deepika Misra1 Renu, and Monisha Banerjee. "A simple and reliable method of obtaining fetal DNA from maternal circulation; its accuracy and sensitivity."

Also, if its available to you, it might be worth it:

Gahan, Peter B., ed. Circulating Nucleic Acids in Early Diagnosis, Prognosis and Treatment Monitoring: An Introduction. Vol. 5. Springer, 2014.


Why my base-quality in alignment is not perfect?

When fasta reads are aligned they are by default assigned the phred score of 40, which in phred+33 encoding is represented by I. Phred+33 uses ASCII characters from ! to I:

!"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHI

Phred+33 was originally used by sanger machines but it is now used by all popular platforms such as Illumina, Ion-torrent (also Ion-proton) and Roche 454. Since most platforms now use phred+33, most aligners also assume it by default. You can specify other quality encoding formats if you want (such as phred+64 or Solexa).

Have a look at wikipedia page on FASTQ format for the different quality encoding formats.


Is it possible to extract tissue-culture material from a seed?

Yes. It's quite common, to the degree that it's done by some hobbyist plant breeders. See en.wikipedia.org/wiki/Embryo_rescue  However, AFAIK (I'm not an expert), it wouldn't be done for raising multitudes of plants, like tissue culture.

Rather, it's used in hybridization, where you hope to produce hybrids from plants that don't readily hybridize.  You would typically rescue a number of embryos, grow them on until mature, then perhaps use tissue culture to mass-propagate the ones that have interesting characteristics.


How is duration of efficacy estimated for vaccines?

Duration of efficacy is typically determined by tracking the antibody titers of a cohort of subjects who have gotten the vaccine, and estimating based on the trajectory of those titers where they will eventually cross the threshold to the point where the vaccine no longer confers immune resistance.

These estimates do get revised and estimated as time goes on - you will occasionally see new recommendations for a second or third "booster" dose of a vaccine, which is meant to extend the duration of immunity beyond the duration of the original vaccine.

Two major types of studies track this over time. Phase IV clinical trials, which are clinical trials required post-licensure, and observational epidemiology trials, which tend to be performed when disease transmission starts to occur in supposedly vaccinated populations.

Mechanical snail has raised the issue of viral evolution, so I'll touch on it briefly. The duration of efficacy discussed above is based on how long a patient's body can mount an immune response to a particular challenge. That's a concern for all vaccines.

For some vaccines, there's a secondary process that's of concern - that of the virus evolving in such a way that the antigens targeted by the vaccine are no longer those on the virus itself. This is only a concern for some viruses, notably those that are particularly fast-evolving, like influenza or HIV, and less of an issue for say, measles and HPV.

But that's typically not what people are talking about when they say "duration of efficacy" because it's inherently unpredictable, and less a function of the vaccine and more a function of the virus.


What is the genetic basis of blood type (ABO) system?

I can answer only half your question.

It is not necessary that the child has to have the blood group of parents.
The inheritance is like this :
1.There are 3 alleles Ia , Ib and Io.

2.Ia and Ib are codominant i.e. they will both be expressed if present together.

3.Ia and Ib are dominant over Io. So, blood group O can only be expressed if the genotype is IoIo. IaIa or IaIo is blood group A and IbIb or IbIo is blood group B.

5.IaIb is blood group AB

So in the case of both the parents being AB blood group,the child can not have O group.S/he can have any other blood group.

The inheritance of negative and positive blood group follows simple mendelian inheritance.

Please feel free to correct me!


Is it true that some organs "sleep" at certain times of the day and does this affect dieting or when to take medicine?

No, this is not true. The only "organ" (if you will) that needs to "sleep" is the brain, and even then it is still quite active. The body needs to rest.

When blood is needed in a prioritized manner in certain areas of the body - for example, during a marathon the muscles and the heart need more oxygen - mechanisms are in place to shunt some of the blood away from organs that need it less (the stomach and intestines, for example) to those that need it more. But that doesn't mean the GI tract is sleeping, or even resting.

There is no organ that "sleeps". The brain as a whole is highly active during sleep, even secreting certain hormones predominantly during that time.


Downstream analysis after in vivo pathogen RNAseq

Okay, first, I would say to everyone planning a high-throughput experiment: Hypothesis first, then experiment. Otherwise you're setting up an expensive and time-consuming test that's not going to answer the questions you want answered.

In this case, the question your experiment is designed to answer is "What genes are crucial to growth in vivo that are not crucial to growth on a plate?", which is probably not the clearest model for vaccine/antibiotic design.

I guess you could say that a difference between the plate sample and the in vivo sample is the presence of a host, and therefore it's possible that upregulated pathways represent the bacteria's host adaptation, and maybe you can attack the bacteria by attacking its ability to colonize the host. A gene involved in immune evasion could make a good target.

(That's a very messy model, as there are tons of other differences going on, but since you've already run the experiment it's probably the best you've got.)

So then, use your data for a new round of hypothesis generation. Take your pathways and come up with a way that they might be allowing the bacteria to adapt to the host-- maybe a secretory pathway that could be interfering with the target immune system, or some membrane signalling molecules that get upregulated, or whatever.

Now you have a hypothesis, so design an experiment. For instance, take a key upregulated member of a pathway. The hypothesis is that it's crucial to growth in a host but not to growth in general. So, knock it down, either with chemical inhibitors or with genomic editing, and see if it's less effective at host colonization.

(Although host colonization effectiveness is pretty difficult to measure ethically if your target organism is humans. But you have some sort of proxy or model system to measure that, right?)


Can I find out what resistance bacteria has based on strain? where do I look for that info?

If database and literature searches fail, you can plug the GenBank accession numbers for your genomes into the CARD Resistance Gene Identifier. It takes either protein or nucleotide sequences, though nucleotide seqs. undergo ORF calling first. For example, plugging in NZ_CP009072.1 for E. coli ATCC 25922 gives 7 perfect hits to known antibiotic resistance genes. Granted, carrying the genetic determinants of resistance is different from phenotypic resistance, but it's a place to start.


Why we have to damage our muscles to build them?

Muscles are developed as required by the surrounding environment. This means your body is constantly physically stimulated to grow muscles according to the external forces it experiences (e.g. gravity).

When you train your body, e.g. with weights, you are applying an unusual amount of pressure to your muscle cells, damaging them in the process. In the process of healing your muscle cells, your body will strengthen them in order to adapt to the new physical stimuli, but only when a vast amount of required elements through nutrition is available (proteins).

Quite an impressive feature, right. :-)

I know this from researching personal training/weight training.


What is the last heavy atom of an amino acid?

As mentioned in the comments by Roland, this term is not common and is first used by the authors of the mentioned paper (also the package mentioned by Roland in comments - STING).

From this link you can find the definition of the Last Heavy Atom which is possibly the most distal non-hydrogen (N, C, O, S) atom in the amino-acid side chain.

$$\begin{array}{|c|c|c|c|}
\hline
Ala\ :\ C_\beta & Asp\ :\ O_{\delta^2}  &Trp\ :\ C_{\eta^2}  &Asn\ :\ N_{\delta^2} \\
\hline
Lys\ :\ N_\zeta & Glu\ :\ O_{\epsilon^2}  & Ser\ :\ O_\gamma  & Gln\ :\ N_{\epsilon^2} \\
\hline
Cys\ :\ S_\gamma  & His\ :\ N_{\epsilon^2}  & Tyr\ :\ O_\eta  & Val\ :\ C_{\gamma^2} \\
\hline
Gly\ :\ C_\alpha  & Leu\ :\ C_{\delta^2}  & Met\ :\ C_\epsilon  & Ile\ :\ C_{\delta^1} \\
\hline
Arg\ :\ N_{\eta^2} & Phe\ :\ C_\zeta  & Pro\ :\ C_\delta  & Thr\ :\ C_{\gamma^2} \\
\hline
\end{array}$$

They have mentioned in the same link that:

  If in any of the PDB files (to be analyzed by the BLUE STAR STING components) that specific atom (LHA) is missing in the record, then our algorithms will search for the next closer atom in the side chain that would be considered as the LHA.

The exact location of some of the abovementioned atoms.

Some of the locations might be confusing. So I am just indicating what these are, for a few the amino acids (especially for the branched and cyclic side chains). [Images reproduced from here.]

Arginine

The terminal nitrogens $\eta^1$ and $\eta^2$ are symmetric and the atom that is actually (stereochemically) the most distal is considered the LHA, as inferred from the protein structure. The second choice, obviously is the $\eta^1$-Nitrogen.

Aspartic acid

The two terminal oxygens ($\delta^1$ and $\delta^2$) in the ionized form are equivalent (also otherwise because of resonance). The actual distal atom would be labelled as $\delta^2$

you can extrapolate the same for Glutamic acid

Histidine

$\epsilon^2$ refers to the pyrollic nitogen. .

Leucine

The last carbons ($\delta^1$ and $\delta^2$) are equivalent and the choice is based on the actual distance. Extrapolate for valine

Phenylalanine

$\zeta$ refers to the carbon in the para-position of the benzene ring. For tyrosine the LHA is the oxygen of the para-OH in the benzene ring.

Tryptophan

Proline

For Aspargine and Glutamine the LHA is the amide nitrogen of the side chain.


Septic Shock: I'll kill myself before you kill me

The important thing to recognize about the host response to sepsis is that it is actually a generalization of mechanisms used in local infection response by the innate immune system. When an animal has a local infection, such as at a wound site, innate immune cells such as monocytes and macrophages recognize 'generic' bacterial features, such as lipopolysaccharide (LPS). When they recognize these features, they respond by engulfing the pathogen and releasing cytokines that result in local vasodilation and inflammation. In this context, these responses are close to ideal. Vasodilation helps to isolate the area and promotes the recruitment of more immune cells.

These sorts of small infections are very common for all animals (just about every creature cuts itself at least once), including humans, and the absence of this response would result in sepsis (not the immune response, but just sepsis itself) because the infection would not be contained. Control of such local infections is thus 'life-or-death' for all creatures—which is an extremely powerful selective pressure.

The other thing to consider here is when in nature are these local defences overwhelmed such that sepsis, and then septic shock, which is what you are asking about, occurs. The answer is that it does not happen very often. Transient bacteremia is relatively common (it even happens when you brush your teeth, see this paper for example), but overwhelming bacteremia, sepsis, is not very common in healthy individuals. It is generally a condition that affects weakened individuals and those who have already reproduced. We notice it far more now because it is a major cause of death for humans hospitalized for other conditions, as well as older people with pneumonia. Most of the primary causes of sepsis though—major wounds, pneumonia, weakened immune systems—would be death sentences in themselves in the absence of medicine, irrespective of the organism's response to the sepsis.

That is not to say it is completely invisible to selection, for example this paper, and others like it, demonstrate that the immune cells responsible for septic shock are regulated by hypoxia (a major feature of shock). However, it is reasonable to say that any fitness advantage conveyed by a reduction in the intensity of septic shock would be dwarfed by the fitness penalty paid if that reduction also reduced the efficiency of the response to local infections. For this reason, it is likely that septic shock is an evolutionary accident, a trait that exists in part because it is irrevocably linked to a set of highly advantageous traits (those involved in local infection response), rather than a trait that has been extensively selected on by evolution.

Note that this answer is my opinion only. To the best of my knowledge, there is no definitive answer to this question yet, and future research may prove me wrong.


Are there differences in DNA between humans of today and humans from 2000 years ago?

The larger differences are most likely in epigenetic marks on the DNA. The environment is a lot different today than it was 2000 years ago and those differences are stronger determinants of epigenetic change than sequence change.

2000 years is only about 40 generations and that is not very much to see great differences in DNA sequence or allele frequencies - once founder populations are removed from the analysis.

Height is highly influenced by genetics, but can be masked by environment - notably diet. Diets higher in protein content are more likely to elicit the expression of the "height alleles" but only to a point as too much protein is also unhealthy.

Added in Edit 4 Apr 2012: I should add that my response is written from the perspective of frequency of alleles or epigenetic marks across a population.


While no perfect example exists, there are various different 'ring species' in nature where you have which species are able to interbreed with closely related populations, but there are least two "end" populations in the series. Examples include:

Alauda arvensis, A. japonica and A. gulgula: Species of Skylark birds that coexist around Central Asia

In central Asia, a northern form,, arvensis, a southern form,gulgula, and Oriental,japonica , coexist without interbreeding.These forms are separated
by a gap in distribution in northern China, but a morphologically intermediate
form, japonica, occurs in Japan. Northern japonica are similar to arvensis and
southern japonica resemble gulgula. -Ring species as bridges between microevolution and speciation

Lalage leucopygialis, L. nigra, and L. sueurii: Species of triller birds that coexist on Sulawesi Island.

The existence of ring species like this can, as biologist Ernst Mayr puts it, illustrate "how new species can arise through 'circular overlap', without interruption of gene flow through intervening populations…" and offers proof of speciation through a method other than allopatric speciation: speciation that happens when two populations of the same species become isolated from each other due to geographic changes.


Can one use dialysis tubing several times?

This is more of a long comment than an answer, since I don't know. It could be okay, but if you are unsure whether it will work, is it really worth the risk? Here are some thoughts:

With high AS concentration, there is an initial large influx of water which can stretch the tubing. If this is repeated several times you may stretch the pores to where they no longer retain your protein. You can determine yield after each dialysis to see if loss increases with use.
Clogging up the pores seems like it could plausibly happen. You could add some low molecular weight dye to monitor whether the membrane remains permeable with use.
Dialysis tubing costs like 5 ¢/cm. Unless you're using 10 meters at a time, it's really very cheap.


Is there a stem cell dye for education purposes?

There is no specific dye for stem cells. You would have to do an immuno-histochemical staining for stem cell markers such as Sox2/Oct4 etc.

Usually stem cells have a distinct morphology (round and clustered). You can use Leishman's (or Romanowsky-Giemsa) stain.


Derivation of Michaelis-Menten kinetics for discrete stochastic simulations

I think I figured it out myself. Since $a(S)$ is in $\frac{mol}{s}$ and $v$ is in $\frac{\frac{mol}{l}}{s}$, we have that $a(S)= v * \Omega$.
Therefore
$$
a(S) = \frac{V_{max}\cdot [S]}{K_M + [S]} \cdot \Omega = \frac{V_{max}\cdot S / \Omega \cdot \Omega}{K_M + S / \Omega} = \frac{V_{max}\cdot S}{K_M + S/\Omega}.
$$


The GHK voltage equation also known as just "Goldman equation" is always valid for determining the voltage at which the net current is zero, given internal/external ion concentrations and their permeabilities. This includes times during the action potential, though the result you get from GHK will be changing faster than the actual membrane potential itself, since the change in membrane potential brings about changes in permeabilities.
It's still useful to think about this equation to determine in which direction the membrane potential is changing instantaneously: it will always be changing towards the equilibrium potential. You can also qualitatively estimate the relative rate of change: if the current voltage is very far away from the equilibrium potential, the voltage will change more rapidly than if it is close to equilibrium.
However, this equation is just a steady-state equation. It doesn't tell you how quickly you will get to the new voltage or exactly which ions will move. For this, you need some other equations and other parameters, namely the actual permeabilities (rather than relative permeabilities) of the ions and the membrane capacitance.
The GHK flux equation can help: this will give you the flux of each ion at a given membrane potential (Wikipedia shows how this equation is related algebraically to the Nernst equation, which in turn is equivalent to the Goldman/GHK voltage equation for a single ion). You can also think in terms of the Hodgkin-Huxley model and the simple differential equation for current.

In summary, with respect to your question:

Can GHK equation be used to predict the membrane potential even if the cell is not at resting state?

It can predict where the membrane potential is headed, but not what it actually is or how fast it's changing, and the voltage you get from GHK will itself change as membrane potential changes affect the parameters that go into the GHK equation itself.


It appears to me to be a Night Blooming Cereus:

We had one in our greenhouse in Botany. It rarely bloomed, and the bloom was wilted by mid-morning.

  Night-blooming cereus is the common name referring to a large number of flowering ceroid cacti that bloom at night. The flowers are short lived, and some of these species, such as Selenicereus grandiflorus, bloom only once a year, for a single night. Wikipedia

Dave's garden lists it as "Dutchman's Pipe Cactus, Night blooming Cereus"
Epiphyllum oxypetalum.


Is it possible to calculate the energy required to speak a word?

For animals to check the amount of energy used for a certain behavior you can use a RESPIROMETER. It basically calculates the oxygen consumption.

In your case you could calculate for writing a sentence vs speaking the same sentence.

Regarding your second question:
At least in birds more than the type of sound (the frequency modulation) what matters for energy consumption is the amplitude --> how loud is your sound.


Which fish will have more developed gills?

200m is still pretty deep...

However, I'd give my money for the surfacers. Oxygen concentration decreases with the depth, and so abyssal fishes have very low metabolism, mainly focused on anaerobic muscles. This is also true for fishes that live in the bottom (benthic), which probably also applies for those living in a few hundred meters. If not, they will probably be active swimmers and then they will probably need bigger gills in order to maintain aerobic movement. Even if we're talking about abyssal and non-abyssal benthic species, I think the abyssal ones would probably be even more anaerobic.


How plasma cells switches secreting different Ig classes?

In T-dependent antigen recognition, the B cell can switch the isotype by first altering the heavy chain gene. This is driven by Tfh cells. The specific cytokine stimulating the class switch determines the isotype of the heavy chain to be synthesized. For your example, interleukin 4 (IL-4) drives the class switch to IgE. You also need a costimulatory signal from the CD40/CD40L interaction between the B cell and the Tfh cell. This induces activation-induced deaminase (AID), see bottom paragraph on this.

There are switch regions (denoted S) in the introns between J and C segments at the 5' end of each CH locus, and upstream of that is an I exon (region denoted I) w/ it's own promoter. Induction by CD40 and whatever cytokine is present starts transcription of the I exon, switch region and CH chain of the H-chain the B cell is meant to switch to. This germline transcript facilitates dsDNA breaks at the switch regions Sµ for the IgM (switch region mu) and the switch region for the class to be switched to, Sε in our case for IgE. The intervening DNA is deleted and the coding region Cµ is replaced by Cε coding for the IgE heavy chain BUT, it ends up with the same V domain as the B cell originally had!

Some enzymes involved are AID, which deaminates cytosines and allows the germline transcript to hybridize in the switch region, Uracil N glycoylase UNG which removes uracils from the DNA, and APE I endonuclease that generates a nick at the abasic sites generated. These nicks lead to dsDNA breakages in the switch regions. Text shows that the switch region DNA is G-C rich and can form stable RNA:DNA hybrids with the coding strand of the switch region and the germline transcript. This is what frees up the noncoding strand for alteration by UNG and cutting by APE. The result is that the V region becomes associated w/ a new constant region.

I'd also be careful with the terminology plasma cell as used in the title because we aren't yet at the high-affinity secreting stage when we're talking about class switching. This is mediated at the activation of the actual B cell by Tfh cells.

All information above is summarized from Cellular and Molecular Immunology, 8th ED


This is a hoverfly! Specifically in the genus Helophilus.  A lot of species of hoverflies exhibit Batesian mimicry of wasps/bees, as we see here, while they mainly feed on pollen and nectar.  So please, don't worry about it trying to bite you.

As far as species go, I think it is probably a Helophilus trivittatus.  I am basing that on location and a lot on the banding patterns on the thorax as well as the markings on the prominent terga.  Here is a picture below for you to compare.


Intuitively, symmetry is useful for balance. A weight-nonsymmetric animal would have to expend additional energy to keep itself balanced (and this would also increase neural complexity for maintaining balance).

Mirror-image pieces only have to be coded once in the genome as a rule-of-thumb, allowing reuse of (mostly) the same genetic pieces with a few orientation and growth-origin markers thrown in. If you put vastly different parts on each side, you have to encode them (making the genome larger with more opportunity for mistakes and harmful mutation)


Which blood vessel carries the most impure blood?

It's the renal artery because it will contain everything from the liver as you describe plus all waste accumulated on the way from the liver to the kidney. Here it gets filtered, so there cannot be a place after the kidney that is less "pure".


What can cause a lump in the middle of the neck? (homework case study)

You ask for the fungus causing An erythematous , fluctuant, nontender mass (8cm x 6cm) was present in the midline of the neck.

On the brink of question closure I decided to do a quick search. Based on your descriptions, I found a possible culprit.

In the referenced paper they talk about a fungal Cryptococcosis infection causing, and I quote:

  [A] fluctuant, non-tender mass, five by five cm. in the right costal vertebral angle which was not red or warm.

So this mass was found on the costal vertebral angle, but the remaining symptoms seem reminiscent of your case study. Fungi generally appear white when plated, as far as I know.
However, more information is likely necessary to confirm this genus and identify the species.

costal vertebral angle (CVA). Source: Pinterest

Reference
- Moore, J Invest Dermatol (1957); 28: 159–82


Short answer

Great question! I have done some research on the topic and found so much interesting information. It still seems like a topic that i being researched on, but so far, the research shows that malate is created by a CAM and C4 like pathway while citrate is created from TCA cycle.  Their functions are that they are important biomolecules in metabolism, in particular respiration.

Background

Malic acid and citric acid are the two main organic acids that are accumulated in the fruits and cause the sour taste. Citrus fruits contain more citric acid and other fruits like apples and pears contain malic acid. I will provide a detailed analysis for both cases.

In an article by Deshpande & Ramakrishnan they mention two hypotheses about the accumulation of the citric acid in fruits. One was that the organic acids are not formed in the fruit, but transported to the fruit, in which the fruit acts like a storage organ. The other hypothesis is that the carbohydrates in the fruit is converted to the organic acid. In their research. they tried to isolate some enzymes from the Garcinia fruit to support the second hypothesis. They say:

This [reciprocal relation between acid and sugar content] would indicate the transformation of sugar to citric acid in the fruit tissue itself due to the presence of the requisite enzyme systems.
They suggest that the TCA cycle is how the citric acid is being accumulated and stored.

The article in the comments by Lobit et al. also supports a similar hypothesis of the accumulation of malic acid. The authors tell us that the malic acid is most likely produced in the fruit itself because the pH of the xylem and phloem (the transporting organs of plants) have a pH of close to 7 or higher. It seems that the malic acid is stored in the vacuoles of the mesocarp cells and that the amount of malic acid in the fruit depends on the transport of the malic acid to the vacuoles in the mesocarp cells.

Pathways

The actual pathways for the creation of citric acid and malic acid are very complex. Here is a picture of the different pathways in the cytosol of the mesocarp cells thst create these organic acids (picture taken from Etienne et al.)

The first pathway described is the PEP pathway, which is really a modified CAM or C4 pathway (which are teo ways to deal with photorespiratin, and are adaptations to hot, dry environments). The PEP is converted to oxaloacetate by PEPC, which also takes in CO2, then that oxaloacetate is converted to malate by NAD-MDH. PEPC is regulated by malate concentration and cystolic pH, showing that the activity of PEPC is to indirectly increase the malate concentrations, not just to create more oxaloacetate.Let me note that I still don't fully understand why C4 and CAM-like pathways are present in Fruits from C3 plants.

The major pathway for citrate synthesis is the TCA cycle. Both are also involved in metabolism. TCA cycle (the citric acid cycle) is an important cycle and the second pathway in aerobic respiration. This pathway occurs in the mitochondria. Malate reacts with acetyl-CoA to make citrate and the CoA is released. The citrate then goes on to be repeatedly oxidized and ends up back to oxaloacetate. Now, for metabolic reasons, for example, if the amount of ATP created is top much at the end of aerobic respiration, the citrate could be transported out of the mitochondria, leading to citrate accumulation.

Control of acid accumulation

The control of the organic acid accumulation is different for both malic acid and citric acid. Malic acid accumulation in the vacuoles is controlled by vacuolar storage and vacuolar transport (Etienne et al). This hypothesis was really the subject of the article in the comments. Their article was about modeling the malic acid based on this hypothesis and compare it to actual biochemical analysis of fruits. Their results supported the hypothesis.

The accumulation of citric acid is more dependent on metabolism, therefore respiration. This is since the vacuolar transport is slower for citrate than malate, and so whatever limits thr speed of malate vauolar transport affects citrate. But citrate concentration in thr cytosol would be the only other main factor affecting the vacuolar transport. A model by Wu et al. was created based on this hypothesis and compared to the actual citrate concentrations, and once again, this hypothesis also supported.

Functions of these organic acids

Suprisingly, the only functions of malate and citric acid cycle is mainly for respiration(mainly TCA cycle), and other metabolic processes. Malate does affect the texture, ripening, and starch metabolism and more of fruits, as described in this article. But, malate and citrate are important for all respiring organisms, including us.


Why do animal cells lack a contractile vacuole?

Lodish et al. (2000) explain that animal cells rely on the Na+,K+-ATPase to pump Na+ out of the cell. Exporting electrolytes decreases the hypertonicity of the cell, thereby preventing too much water from entering.

Plant, algal, fungal, and bacterial cells are surrounded by a rigid cell wall. Any osmotic influx of water in a hypotonic solution leads to an increase in intracellular pressure, but not in cell volume. hence, the cell wall effectively prevents the cells from lysis.

Protozoans do not have a rigid cell wall and these organisms sometimes contain a contractile vacuole that permits them to avoid osmotic lysis. A contractile vacuole takes up water from the cytosol and periodically discharges its contents through fusion with the plasma membrane. Thus, even though water continuously enters the protozoan cell by osmotic flow, the contractile vacuole prevents too much water from accumulating in the cell and swelling it to the bursting point.

Reference
- Lodish et al. Molecular Cell Biology. 4th ed. New York: W. H. Freeman (2000)