How does hyperthyroidism cause diarrhea? According to Robbin's Pathology, hyperthyroidism leads to an overactivity of the sympathetic system.

It also goes on to mention that this sympathetic hyperstimulation in the gut leads to increased motility leading to diarrhea and malabsorption.

How would sympathetic stimulation cause hypermotility? Isn't the parasympathetic system responsible for it?

Also, how does hyperthyroidism increase the sympathetic tone?

Hyperthyroidism leads to an overactive sympathetic nervous system, hypermotility and diarrhea (Culp and Piziak 1986) (Geffner and Hershman 1992) (Maitra 2015, p. 1084) (Thomas et al. 1973). A demonstration of this is the patient presenting with the sole symptom of intractable diarrhea. It was found to be secondary to hyperthyroidism, and was treated successfully with β-adrenergic antagonists (Bricker et al. 2001).

Was the hypermotility due to excessive β-adrenergic activity, or insufficient α-adrenergic activity?

An article by Silva and Bianco (2008) states that β-receptor expression is under transcriptional control of a thyroid response element, and is upregulated by increased thyroid signalling. There is much less research on α-receptor expression, I would be much obliged if anyone can provide me with access to the following article:

  *Bilezikian, JP, Loeb JN 1983, ‘The Influence of Hyperthyroidism and Hypothyroidism on α and β-Adrenergic Receptor Systems and Adrenergic
  Responsiveness’, Endocrine Reviews, vol. 4, no. 4, pp. 378-388.*

In any case, they add that increased β-receptor expression is rather modest, often overestimated, and cannot account for the magnitude of amplification in responsiveness induced by thyroid hormone (TH). Rather, thyroid signalling increases cAMP levels associated with a2 and β-receptors to a degree which could account for these changes.

Increased cAMP occurs during normal β-receptor function but is significantly potentiated by TH in several ways: increases in adenylyl cyclase; downregulation of β-receptor G-protein subunits, Gai and Gβ; and downregulation of phosphodiesterases which degrade cAMP. This explains the effectiveness of the β-adrenergic antagonist noted above, as propranolol decreases cAMP levels, thus decreasing hypersensitivity of the hyperproliferated β-receptor (Silva and Bianco 2008).

  “The reduction of the sympathetic activity associated with
  hyperthyroidism outflow (via increased rate of norepinephrine
  metabolism to decrease overall levels) is likely overridden by the
  increased sensitivity, as suggested by the clinically significant
  amelioration of the adrenergic symptoms with β-adrenergic blockage and
  the consistent observation of elevated cAMP production.” (Silva and
  Bianco 2008).

What are the effects of preferential/hyperactive β-receptor function on gastrointestinal motility?

The β1-receptor increases ghrelin secretion from the stomach – a peptide secreted when the stomach is empty to increase hunger, increase gastric acid secretion and gastrointestinal motility. The β2-receptor promotes smooth muscle relaxation (decreased GI motility) but contracts sphincters of the GI tract (Adrenergic receptor 2018).

β-adrenergics also promote the secretion of gastrin – a peptide which increases antral muscle mobility and promotes stomach contractions; relaxes the pyloric sphincter, which increases the rate of gastric emptying; is involved in the relaxation of the ileocecal valve; induces pancreatic secretions and gallbladder emptying; and contributes to the gastrocolic reflex (Gastrin 2018) (Katzung and Trevor 2014, p. 143-144).

What are the effects of relative α-receptor deficiency on gastrointestinal motility?

Considering that β-receptor antagonism causes a relative increase in α-receptor activation we should consider them also. The α1-receptor causes smooth muscle contraction. The α2-receptor causes negative feedback on norepinephrine signalling, relaxes the gastrointestinal tract when activated on presynaptic terminals and contracts of sphincters in the GI tract. It does this by decreasing levels of cAMP (whereas β-receptors work by increasing cAMP) and so it will become less active as TH becomes more active (Adrenergic receptor 2018) (Silva and Bianco 2008).

  What are the adrenergic-mediated effects of hyperthyroidism on gastrointestinal motility?

  Under prolonged conditions of excess TH overall peristalsis will
  increase due to mixed effects on smooth muscle contraction primarily
  via α1, and β2. There will be an increase in hunger and gastric acid
  secretion via ghrelin (Adrenergic receptor 2018). Hyperphagia and
  hypermotility are both suggested to play a part in steatorrhea
  (Culp and Piziak 1986).

How does hypermotility cause diarrhoea?

In addition to the mechanisms above, it has also been suggested that excessive fatty food intake contributes to the steatorrhea seen in patients with hyperthyroidism. This is compounded by a reduction in time that digestive secretions can act on chyme, ultimately leading to a reduction in absorption and an increased liquidity of the stool (R Santra, Calcutta School of Tropical Medicine, 2016).

Finally, it is important to note at this point that not everyone with hyperthyroidism will show hypermotility - some hyperthyroid patients show delayed gastric emptying (Pustorino et al. 2004). Indeed, constipation has been reported in patients with hyperthyroidism (Culp and Piziak 1986). Nonetheless, it is held that dysthyroidisms alter the motility of the gastrointestinal tract, and we do not completely understand how this works (Pustorino et al. 2004).


Parse PDB using DSR-PDB Library I'm trying to parse ATOM section of a PDB file. I'm using the dsr-pdb library for this purpose.

I've encountered a problem. This library interprets CD1 atom of ILE residue in the PDB file as AL_CD instead of AL_CD1*. Does it have a particular reason?

It's maybe helpful that within the source code, in Residue_data.cc, there is a mapping between atom lebels:

Atom_fallback_data atom_fallback_data_[]=
      {{Residue::AL_CD1, Residue::AL_CD},
       {Residue::AL_1HA, Residue::AL_HA},
       {Residue::AL_1HB, Residue::AL_HB},
       {Residue::AL_1HD, Residue::AL_HD},
       {Residue::AL_1HE, Residue::AL_HE},
       {Residue::AL_1HZ, Residue::AL_HZ},
       //{Residue::AL_1HH, Residue::AL_HH},
       {Residue::AL_1HD1, Residue::AL_1HD},
       {Residue::AL_2HD1, Residue::AL_2HD},
       {Residue::AL_3HD1, Residue::AL_3HD},
       {Residue::AL_INVALID, Residue::AL_INVALID}};

It means that AL_CD1 is deliberately converted to AL_CD or for example AL_1HA to AL_HA.

Thanks.

In general, in dsr-pdb library, AL_X is the atom label of atom X.

Isoleucine only has one delta carbon, which we can just call CD. But it seems like some PDB files still name it CD1, and hence programs map CD1 to CD in this case. (E.g. see this tutorial where this practice is shown.)


Is the golden ratio of anatomic measurements universally beneficial for sexual reproduction? It is often claimed, in popular media, that the golden ratio (Fibonacci series) in for example some face measurements is aesthetically (and hence reproductively) attractive with respect to the humans. I wonder if this is particular for today's (maybe since 10,000's of years or so) human anatomy and aesthetics. As in an after-the-fact acquired taste which was culturally psychologically emerged from the actual human ratios of anatomy as it has happened to evolve for whatever practical reasons, way out of intuitive comprehension for human consciousness. Or if it is deeply biological and evolutionary across all lifeforms.

Is the golden ratio as verifiable (if at all) also for the primates who came before us? Some examples are easy to find, but how statistically significant is the golden ratio as an advantage for sexual evolution for non-humans?

I have some insight into this from an engineering perspective. Years ago, I worked on some computational and search algorithms which used a growth factor to determine how far to widen a search space, or how much more memory to allocate. For some of these algorithms, I ran a series of random trials to search for an optimal growth factor and found that for some, that optimal factor approached 1.618. Completely outside the realm of biology, this golden mean popped up as the most efficient growth factor for some of my algorithms.

Over the years since then, I have recognized that this is an optimal factor for various engineering problems (although in practice I often find it more trouble than it's worth to explain to colleagues why they want to use it). So, I have gradually come to believe that this is why we see this ratio all over nature, in the way seashells grow, the proportions of various body parts, the arrangement of seed structures, etc. It appears that natural processes have ultimately led various lifeforms all over our world to tend toward this ratio to optimize their own functions.

The fact that we find this ratio "beautiful" is a far more fascinating study of what appears to be a meta-adaptation. Consider all of the various ways that the recognition of this ratio is important beyond just sexual reproduction. When we select our food, choosing vegetable or meat specimens which exhibit this ratio most perfectly is more likely to lead us to the healthiest food. Choosing to take shelter under the more "beautiful" tree may also be a good bet that it is the more stable, healthy tree. Making tools, clothing, or structures with this ratio may serendipitously lead us to better formed products. We don't have to find this ratio more beautiful to look at, but because we do, it leads us to better choices in a variety of odd ways. So, those of us whose brains appreciate these things thrive a little more.

Your question was not about underlying causes, but about statistical prevalence. I don't know the answer to that. And I think it would be very difficult to obtain those numbers accurately for another loosely related reason. The human brain is very attuned to finding patterns, and the human brain likes to find this ratio. Taken together, this presents a huge bias for any researcher trying to objectively measure the frequency of this ratio in nature.

However, once we understand that this ratio is the solution to a variety of engineering problems, it becomes clear that it is an indicator of optimization, or proximity to perfection. And even if we cannot say how many species are able to recognize, appreciate, and seek after this ratio, we can say that those who do will most likely find it a beneficial adaptation.


Do sulfate reducing bacteria ingest their sulfate as solid, or as dissolved in water? Do sulfate reducing bacteria ingest their sulfate as solid, or liquid or gas?

I understand that almost all forms of sulfate are solid.. and sulfate can be dissolved in water(thus no longer solid, but liquid).

So, do sulfate reducing bacteria ingest sulfate in its solid form, or do they require it to be dissolved in water?

A similar question in fact, for nitrifying bacteria, though if that's complex I might make it a separate question.

Also, even though it's respiration(which tends to be associated either with the breathing process - in the case of physiological respiration, or with having breathed prior - in the case of cellular respiration), here it's not using a gas. So i'm curious if biologists ever use the word "breathing" for such a process.  wikipedia for example, says https://en.wikipedia.org/wiki/Sulfate-reducing_bacteria  " In a sense, these organisms "breathe" sulfate.." I wonder if biologists use the term 'breath' in such a general sense(to include consuming a substance dissolved in water), or only in a specific sense of gas or air, or if they don't use the term 'breath' at all. So, how strictly is the term breath defined in biology.

Sulfates in water would not be liquid. Their melting points are far to high. When a sulfate dissolves into sulfate ions and some cation such as potassium, we say it is solvated, not liquid. Sulfates would also not be present as gasses due to their ionic nature as well as high molecular weights. So that leaves solvated sulfate ions and solid sulfates that have not completely dissolved.

To be ingested in bulk as a solid would require endocytosis which is not performed by prokaryotes: http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit1/proeu/proeu.html

Further research indicates sulfate, as ions, enters the cell through permeases: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.532.943&rep=rep1&type=pdf

Edit: Here's some files to help with the idea of how ions and other molecules enter cells. Again, bacteria do not engulf substances whole, in the process of endocytosis, such as eukaryotes are capable of. Here is an image of a nitrate ion within a transport protein. Only a few amino acids of the protein are shown here, the actual protein is much larger and spans across the entire membrane creating a channel for the ion to enter. http://www.rcsb.org/pdb/ngl/ngl.do?pdbid=4U4W&preset=ligandInteraction&sele=[NO3]

Here's another channel, aquaporin, which allows transport of water across the membrane. http://pdb101.rcsb.org/motm/173 The top left image shows the channel in the protein leading to the interior. The third image down shows the interaction between the water and the amino acids (backbones only are shown) which facilitate the water's passage.


Is it possible to completely puncture a human hand and have no blood come out? Illusionist David Blaine sometimes performs a trick where he takes a very long and thin ice pick, insterts it in his hand, and comes out the other side (the palm). However, there is no blood present. Is this possible at all? (Warning: Graphic Content) Here is the video (already timestamped)

Yes, it is possible.
The needle should be passed through Fistula, which is an abnormal or surgically made entry between an empty or tubular organ and the body surface, or between two empty or tubular organs.
According to Magic Secrets Explained >>

This provides us with a reasonable explanation for Blaine's needle
trick. He has a fistula through his arm. He created this fistula to
himself, by repeatedly causing small damage to his arm in the same
direction, probably by actually stabbing a needle into it.
He basically drilled a tube of scar tissue through his arm just so he could perform this one trick.

In order to further cement their logic, they attached another video of a man who had a fistula through his body which empowered him to have swords cut through his body without hurting him.
Fistulas are also incorporated in dialysis, and infact referred to as dialyses’ lifeline. An article by Big D and Me expands more on this plus explains how it also threatens lives.


How long does it take for a genetic trait to dissipate if its no longer selected for? Have their been any studies or experiments done that provide insight into the persistence of genetic traits if an environmental shift suddenly causes that trait to be neutrally selected for? Does it take 100s of generations to reach equilibrium or only a few?

For example, how long can we expect the effects of birth control to take in decoupling human behavior related to sex from human behavior related to having children?

There is no way to answer this question as there are way too many factors influencing this time.

It depends on too many factors

It depends on:

whether it is neutrally or negatively selected (and how strongly so)
the population size
mutation rate
mutational variance
level of genetic variance for this trait to start with.

This variance can be calculated at equilibrium (assuming no important demographic change "recently") from the above parameters though.

It may take between 1 generation and a billion generations.

For example

Consider for example that your trait is neutral. Assume that the trait can only take two binary state A and B and that only a single locus affect this trait, which two states are also named A and B for simplicity. Let's say A is the ancestral state and we want to know how much time it takes to have a population of B. Imagine the haploid population size is $N=10^5$. The mutation rate for the locus of interest is $\mu=10^{-9}$.

Slow Case

If at the start there are no alleles B, then you have to wait for a mutation to occur. The time for such a mutation to occur follows an exponential distribution with parameter $\mu=10^{-9}$. Because we assumed neutrality, the probability of fixation (fixation is the state when the whole population carry the same allele) is $\frac{1}{N}=10^{-5}$. Conditioning on fixation, the expected time for fixation to occur is $-4N \left(\frac{1-p_0}{p_0}\right)\ln(1-p_0)=399998$ generations. In consequence, the expected time to fixation in this case is $10^{5}*10^{9}+399998 ≈ 10^{14}$ generations, that is about 77 times the age of the earth assuming there is one generation per day! So Obviously, the environment has time to change again. Note that variance is about $10^{28}$ generations! Of course this example is just an extreme slow case, but I have been using realistic parameter values.

Fast Case

If you have a population size of $N=50$ and the B allele is already present at frequency 0.1 and that the B allele is beneficial with a selection coefficient of 1.5, then it might take about 100 generations.


What does T and the numbers mean in T coliphages? I have searched a number of websites and articles relating to nomenclatures or phages but never found anything explaining what T in T-4,5,6.. Phages mean in the Coliphages. Also, what does the number mean? I have seen that many times, the T - even are grouped as one, why is it so?
Thank you.

The "T" stands for "Type" as in type 1, type 2 etc. To quote Wikipedia on Escherichia virus T4 (emphasis mine):

Bacteriophages were first discovered by the English scientist Frederick Twort in 1915 and Félix d'Hérelle in 1917. In the late 1930s, T. L. Rakieten proposed either a mixture of raw sewerage or a lysate from E. coli infected with raw sewerage to the two researchers Milislav Demerec and Ugo Fano. These two researchers isolated T3, T4, T5, and T6 from E.coli. Also, in 1932, the researcher J. Bronfenbrenner had studied and worked on the T2 phage, at which the T2 phage was isolated from the virus.[39] This isolation was made from a fecal material rather than from sewerage. At any rate, Max Delbrück was involved in the discovery of the T even phages. His part was naming the bacteriophages into Type 1(T1), Type 2 (T2), Type 3 (T3), etc.

It turns out Wikipedia is incorrect: The original use of Type as a designation for these viruses comes from a paper published in 1945 (PDF) by M Demeric and U Fano: BACTERIOPHAGE-RESISTANT MUTANTS IN ESCHERICHIA COLI Genetics 30:119. In this paper they collected phages from Luria (of LB/Luria Broth (actually properly known as lysogeny broth)) and Delbruck amongst others and collated them all for comparison. Delbruck references them in his review article (PDF, possible paywall, summary here), also from 1945.
I could find no evidence for why the phages were numbered as they were, though strains from Luria (actually previously from his supervisor as P28 and PC) were labeled T1 (Luria alpha) and T2 (Luria gamma), so it is possible that it was simply in order that they were received or possibly in order of discovery amongst the several groups working on these viruses.
The T-even phages were grouped because of structural similarities, and are now strains of the species escherichia virus T4 in the genus Tequatrovirus (see link for taxonomy).


Can anyone identify this creature that looks like a stick? This thing was on me. I thought was a stick until it moved. It had a black worm like thing come out one end and stood up and thats how it moved. It would stick to fabric also. In Louisiana

It may be a Caddisfly (Trichoptera). Though my guess is a moth (Lepidoptera). Specifically one of the Psychidae family, also known as "bagworm moths." They are common pests in most parts of the world and while they're typically seen fixed in place they spend much of their life mobile. Both of these groups spin a case from silk and attach detritus to the outside so without a better look at the resident insect it is basically impossible to distinguish them from a photograph. However, as a general rule (with some exceptions), Caddisfly larva tend to be aquatic.
Here are a couple of links to descriptions of the groups (with pictures!) as they appear on BugGuide:
Psychidae

Trichoptera


What allows the hypothalamus to detect a lack of thyroid hormones? On the website www.yourhormones.com it is written:

  "If there is insufficient thyroid hormone available for the brain, this will be detected by the hypothalamus and thyrotropin-releasing hormone will be released into the blood supplying the pituitary gland."

What allows the hypothalamus to detect a lack of thyroid hormones? Are there chemoreceptors in the bloodstream that send afferent signals to hypothalamus when the concentration of thyroid hormones is low (similarly to how chemoreceptors inform the cardiovascular center of the medulla oblongata in the brain stem when there is a lack of oxygen and/or excess of carbon dioxide)?

The thyroid hormone, thyroxin has a multitude of effects in various cells of the body. It is a lipophilic hormone and acts via nuclear receptors, i.e. the receptors for the hormone are not on the cell surface but inside it. This hormone-receptor complex then travels into the nucleus to attend to transcriptional changes.

The picture above is for steroid hormones but is almost similar for thyroxin too.

Inside the cell, the effect of the hormone depends on which cell it is in. For thyroxin - in heart muscles, it increases cardiac contractility, in fat cells, increases fat catabolism, and in the very same way, in the hypothalamus, its function is to reduce the production of TRH. And the control of this production is at the level of gene transcription.

Hence there is a lovely feedback loop that is formed. Increased thyroxin would lead to reduced TRH production and vice versa. So the hypothalamus responds to the thyroxin hormone by regulating the production of TRH. There is nothing special that the thyroxin is doing here. It just has different effects in different cells and in this particular cell (the neurons of the hypothalamus), the effect happens to be its own feedback loop regulation (via TRH).

The effect of thyroxin is through its receptor that is an intracellular protein and is more or less the same in all cells.

Chemoreceptors are a different ballgame. They sense changes in pH, pO2, and other biochemical parameters through their direct effect on neurons and their firing. Although their functioning is not particularly clear, they interfere with channel conductivities in particular neurons. There is no receptor and transcriptional changes as in thyroxin.


can auditory/ocular reflexes exist? In the same way the knee-jerk reflex is a thing (I think the nerve signal doesn't go through the brain?), can stimuli received by the eyes or ears trigger "instantaneous" (faster than the brain can process it) responses?

Short answer would be yes. There are very simple examples such as responses to sudden bright lights controlled in the Trigeminal nerve bundle to constrict pupils. Visual reflexes are interesting because it can frequently involve a neuron crossover in the nerve bundle. This would be an inappropriate reflex due to a stimuli. The most common being suddenly being exposed to a bright light causing you to sneeze like pepper was thrown in your face. Also interestingly this is an autosomal dominant trait so one of your parents will have to have the same response for you to inherite it.
Photic sneeze response


Can threat to survival increase mutation rates in germline cells? Can stress that is related to a threat of survival of a population of animals or plants in some environment, like due to hunger, thirst, fear from predators, etc..; results in an increase in average mutation rate in germline cells of individuals of that population, thereby increasing the likelihood of producing heritable trait(s) that might be beneficial to that population in combating those adverse survival conditions in that environment?

In bacteria this is known as "Stress Induced Mutagensis"

Is there something comparable to that in animals and plants?

Well... since I can't delete this accepted answer... it's going to be a reverse ferret, to some extent. One 2014 review by Ram and Hadany lists a fair number of SIM occurrences outside of bacteria:

Stress-induced mutagenesis (SIM)—the increase of mutation rates in stressed or maladapted individuals—has been demonstrated in several species, including both prokaryotes and eukaryotes. [...] SIM has also been observed in yeast, algae, nematodes, flies and human cancer cells.

The one for algae (Goho and Bell, 2000) appears/claims to have been the fist:

Cultures of Chlamydomonas were exposed to a range of relatively mild stresses for a period of 24 h. These stresses comprised high and low temperatures, osmotic stress, low pH, starvation and toxic stress. Fitness was then assayed as the rate of division of isolated cells on agar. We found that there was a strong tendency for stressed cultures to have lower mean fitness and greater standardized variance in fitness than the negative controls which had been cultured throughout in unmodified minimal medium. The same tendency was shown, as expected, by positive controls which received mutagenic doses of ultraviolet irradiation. We concluded that the most reasonable interpretation of these observations is that mild stress increases the genomic rate of mutation.  This appears to be the first time that this phenomenon has been noticed in eukaryotes.

The paper cited for Drosophila, Sharp and Agrawal (2012)

Our results show that mutation rates are sensitive to genetic stress, such that individuals with low-quality genotypes will produce offspring of even lower genetic quality, in a mutational positive feedback loop. This type of variation in mutation rate is expected to alter a variety of predictions based on mutation load theory and accelerate adaptation to new environments. Positive mutational feedback could affect human health by increasing the rate of germline mutation, and possibly somatic mutation, in individuals of poor health because of genetic or environmental stress.

Clearly this one is quite bold in extrapolating its findings.
And long story short, the paper on nematodes (Matsuba et al., 2012) finds a temperature dependant mutation rate.
What seems to be the weak point in these paper, and perhaps why a more critical review of Lynch et al., 2016 of SIM doesn't mention them, is that no explicit mediating mechanism appear to have been identified in these studies on eukaryotes. In bacteria (e.g. the paper linked by the OP) how SIM works inside the cell is pretty well understood, there are in fact several mechanisms that all respond (convergently) to various forms of stress.
There's an acknowledgement (in the Drosophila) paper, that such mechanisms in eukaryotes might differ from bacteria

The sources and mechanisms underlying this variation have been best studied in microbes, but the sources of variation in microbes may differ from those in multicellular eukaryotes for several reasons. [...]
In animals, mutation rate varies among genotypes, although the functional sources of this variation are unknown. [...]

It does go on into some theories how it might work.
As for yeast, Rodriguez et al. (2012)

Mismatch repair (MMR) is a major DNA repair pathway in cells from all branches of life that removes replication errors in a strand-specific manner, such that mismatched nucleotides are preferentially removed from the newly replicated strand of DNA. Here we demonstrate a role for MMR in helping create new phenotypes in nondividing cells. We show that mispairs in yeast that escape MMR during replication can later be subject to MMR activity in a replication strand-independent manner in nondividing cells, resulting in either fully wild-type or mutant DNA sequence. In one case, this activity is responsible for what appears to be adaptive mutation. This replication strand-independent MMR activity could contribute to the formation of tumors arising in nondividing cells and could also contribute to mutagenesis observed during somatic hypermutation of Ig genes.

I guess a weak point of this paper vis-a-vis of SIM (which they only mention in passing) is that it's not obvious in their setup what the stress was. Basically they saw (adaptive) mutation-rate change (in response to the environment), but they don't pinpoint what exactly they think the stressor was. So this paper is a way the reverse of the other three I, i.e. the mechanism is clear, but stress is not.


What's the name of this beetle? I found him in a kitchen located in Toronto, Ontario, Canada.

This looks very similar to a click beetle. Some of them are pretty popular in south Canada.


Why do provitamins-A do not cause Vitamin-A toxicity? Why do beta-carotene and other provitamins like alpha-carotene not cause vitamin-A toxicity but rather carotenosis (Orange skin) whereas retinal, retinol, and retinoic acid cause vitamin A toxicity with dosage as low as 4000 IU?

Since, you didn't state whether you were referring to a concentrate or not, i'm assuming the following forms of Vitamin A were obtained via pill or topical suspension - except for the Carotenoid.

α-carotene and β-carotene are (primary) precursors to Vitamin A. Likewise with, Retinal, Retinol but not with Retinoic Acid (irreversibly metabolized/end point) however, i'm assuming that these first generation Retinoids are produced via ex situ (a facility) metabolism and hence, they do not contain the carotenoid component that cause yellowing of the skin due to the absence of lipid soluble orange/yellow pigments (Xanthaemia). Albeit, the color of the aforementioned FG retinoids when in a concentrated solid state are all yellow still due to molecular structure - explained in midsection.

For example:
Retinal:  Otherwise known as Retinaldehyde, is ingested via meat (as a single/complete molecule) or produced by ingestion of carotenoid containing food-stuff (e.g. carots). The pigment causing the color are, Carotenes. Carotene is a component of the Carotenoid molecule; α-carotene and β-carotene.
Alternatively, Retinal can be produced from the metabolism of β-cryptoxanthin, a Xanthophyll containing compound. Xanthophyll and Carotene are similar in terms of molecular structure, however, a Xanthophyll molecule contains Hydroxyl groups and hence, Oxygen atoms - Carotenes are hydrocarbons.

On that note, hypervitaminosis A can be caused by an over ingestion of α-carotene and β-carotene sources e.g. Carrots, due to the process of metabolism; over an extended period of time.

Generally;
Retinyl ester <=> Retinol <=>  Retinal => Retinoic acid

What causes Xanthemia in this context?

α-carotene and β-carotene, are absorbed via (passive) diffusion within the gastrointestinal tract. From there, they are metabolized (not fully/partially) at the the mucousal layer of the intestine for the substance to be transported into the liver. Next, the metabolite is diffused into the peripheral tissues by the blood plasma. This is were the "issue" is: Excretion. Carotenoids are excreted via bowel movements (gastrointestinal secretions), Urination, through the secretion of sebum and by sweating.

If very high levels of Carotenoids are being ingested, the pigment tends to show itself when a "build up" occurs, in the sweet glands of our dermis and more noticeably, in areas of which there are a large amount of sweat glands e.g. nasolabial folds.

The orange color is defined is due to the classification of what Carotenoids are. All carotenoids are tetraterpenoids: essentially being tetraterpenes that have been modified by chemical transformations such as oxidation or cyclization. Furtherly, tetraterpenoids are made up 40 carbon atoms and contain 8 isoprene molecules. α-carotene and β-carotene, are bicylcic tetraterpenoids. This molecular classification may have an affect on the amount of energy that the molecule can absorb, and more formally, the colour. Albeit, the greatest majority of reasoning in regards to the orange color, is in favor of the long conjugated chain'ed structure of the molecule.

Carotenoids absorb light in the blue-green and violet region and reflect the longer yellow, red, and orange wavelengths; these pigments also dispose excess energy out of the cell.

Conclusion

Retinal and Retinal are preformed retinoids and are not obtained by means of carotenoid metabolism so, they won't contain the the yellow/orange dark pigment that is found within some plant-based food (Carotene).

Retinoic Acid, is a retinoid although it's function is as a cell signalling molecule. The difference between it and the other retinoids is the functional group present of the tail of the carbon-carbon backbone

Theoretically, speaking, and due to retinoids having a shorter/less extended  conjugated system with less unsaturated (multiple) bonds in the molecules it will have shifted the absorption to shorter wavelengths (The two carotene precursors have 11 conjugated bonds and the latter retinoids contain 5).

Furtherly, I don't think that the carboxyl group attached to the Retinoic acid molecule could be classed as an Auxochrome although the remainder of the retinoic acids carbon-carbon chain is still the molecules Chromophore - likewise with the other retinoids.  For example, this would mean that there is possibility that the retinoic acid molecule will be more inclined to absorb shorter wavelengths and hence, less orange/yellow. This is relevant as, you will often find retinoic acid in topical preparations that are used to treat certain dermatological conditions.

I don't think that there is a 100% correct answer for this question as there is no evidence to prove that it would be true in this particular case.

So, you are susceptible to toxicity at lower levels in regards to retinol, retinal and retinoic acid because, of the fact that they are metabolites/concentrates and you need ingest less in order to get to the same point of toxicity. Carotenoids are "raw" in contrast to the preformed retinoids   and require breakdown. Look at the image below to get an idea of how much the molecular mass will have reduced when the carotenoid is metabolized into a useful form of Vitamin A.

Another example would be, you needing to eat more daffodil bulbs to get the required dose of Galantamine hydrobromide (used in Alzheimer's disease treatment) - that's a bit different though, to be fair.


What are the olfactory chemicals in whiteboard/permanent markers and what do they bind to in the nose, lungs, and brain? What are the olfactory chemicals in whiteboard/permanent markers and what do they bind to in the nose, lungs, and brain?

The smell of dry erase markers come from the chemicals ethanol, butanol and isopropyl alcohol. Like all chemicals inhaled through the nose, they bind to the Receptor neurons in the located in the back of the nose. The neurons interpret the chemicals using a 'lock-and-key' model but the specific way its coded and perceived in humans is still being researched and the process is not completely understood.


Can GFP reporting be used to track localization of peptides in the ER, Golgi, and plasma membrane? Suppose I want to study the trafficking of a peptide throughout the ER, Golgi, and plasma membrane. An idea I had was labeling a secreted or plasma membrane integral protein with GFP and using time-series live cell microscopy to track it through the secretory pathway.
However, I am concerned that by the time everything is set up, the cell will be at steady state, which means GFP signal would be present throughout the secretory pathway, preventing me from doing this tracking.
How might I overcome this, without changing the fundamental technology (GFP reporting)?

Historically speaking, the use of VSVG (Vesicular Stomatitis Virus G protein) labeled with GFP was indeed a practical method to define the secretory pathway. (@tyersome comment)

However, I am concerned that by the time everything is set up, the cell will be at steady state, which means GFP signal would be present throughout the secretory pathway, preventing me from doing this tracking.

Sec mutations in S.cerevisiae: Many biochemical pathways are initially identified owing to a particular mutation in the synthesis process. Recall Beadle and Tatum experiment and the logic they used to clarify the existence of 3 enzymes used in arginine metabolism.

(Image taken From https://www.chegg.com/homework-help/questions-and-answers/following-experiments-beadle-tatum-searching-mutations-disrupt-arginine-biosynthesis-pathw-q41797559)
A similar approach was taken back then to identify the distinct parts of the secretory pathway. Five different mutations in S.cerevisiae were identified named from A to E. Culturing all A to E mutated strains plus VSVG-GFP assay would clearly demonstrate the entire route.

(Image taken from https://slideplayer.com/slide/4382105/)
For example, even if the mutated class B, reaches the steady/equilibrated state, transport vesicles, Golgi, and the rest will not show the fluorescence activity (characteristic of VSVG-GFP) because all of the proteins have accumulated in the previous step(i.e budding from Rough ER)
Further Readings :
https://pubmed.ncbi.nlm.nih.gov/2188733/
https://www.sciencedirect.com/science/article/abs/pii/0092867481900647
MCB Lodish et al 8th edition chapter 14 section 14.1
https://www.nature.com/articles/35073068


Do some genes follow Rock-Paper-Scissors model of dominance? Assuming there are at least 3 alleles of the gene $G$ in total - $G_R$, $G_S$ and $G_P$ - is there any gene for which the following is true?

$G_R$ is more dominant than $G_S$.
$G_S$ is more dominant than $G_P$.
$G_P$ is more dominant than $G_R$.

A quick search gives this same question in this Reddit post.

Apparently, there is not yet an existing example of such dominance of three alleles on one another.

That said, if you're interested in rock-paper-scissor patterns in nature, then you will be interested in the side-blotched lizard. It has three genetically encoded male "sexes", that also determines their behaviour. At a population level, the three sexes follow a rock-paper-scissor pattern of successful sexual competition, in that orange-throated individuals can outcompete yellow-throated ones, which can outcompete blue-throated ones, which can outcome orange-throated ones. A simulation has been carried out to model the underlying genetics, but that model doesn't involve a rock-paper-scissors pattern of genetic dominance.


How a particular composition of molecules result into life in form of cell? I had read biology in childhood only, but as far as I can remember every living thing/being is made up of cells in the lowest level. Cells again are made up of some particular composition of molecules. But my question is how a particular composition of molecules become alive? Or What's that which turn compositions of molecules sentient?  I'm trying to understand when or how insentient compositions of molecules become sentient.

Science does not have an answer to how the first reproducing cell came about.  The actual event has left no traces except life as we see it today. There are theories about parts of how it might have happened, but evidence about it essentially doesn't exist.  If you want to get a flavor of recent ideas of scientists in this area, here is a video of a lecture on "The Origin of Cellular Life on Earth".


How can I determine the sex of a tree seedling? I would like to plant some home grown female mulberry trees in a circle, with a male plant in the center for pollination. How do I determine the gender of a tree seedling? I know it's possible, because I've seen mulberry trees labeled as 'male or 'female' at nurseries. Do I need special equipment?

I've seen the related question: Can you tell the sex of a white willow when it's not flowering?

There is absolutely no way to tell to be honest because mulberry trees have the capability of changing sex (reference). From a paper titled "Diversification of mulberry (Morus indica var. S36), a vegetatively propagated tree species", I quote

  The sex expression of plants appears to be a function of hormonal
  control; there seems to be evidence that dioeciously plants (male and
  female reproductive organs on separate plants) are potentially
  bisexual and that a delicate internal hormonal balance results in one
  sex "over-riding" the other. A traumatic incident might, therefore,
  act by temporarily upsetting this balance, which is later restored in
  a way that leads to the opposite sexual character being manifested.
  Another pointer in this direction is the fact that a variety of
  artificially applied chemical substances has been shown to affect the
  sexual expression of a significant number of different plants. It is
  also reported that some chemicals known as the steroid hormones might
  be a major key to the sex expression lock. Thus, it is
  possible that to "create" a new sex in a plant by either a physical
  shock or a controlled chemical process

They could also have male and female flowers (monoecious) on one plant with most of them being self pollinating (references).

So, in effect, nurseries that are advertising these trees by sex are ignorant or quite plainly taking people for a ride. I would suggest that you plant your seeds and don't worry about it too much since they have the ability to self pollinate. If by bad luck, you find them all male/female or are not pollinating to your liking, go for a tree sex change after consulting an expert on the topic. Here is a basic guide to identifying between male and female trees/branches (reference)

White mulberry male flowers (reference)

red mulberry female flowers (reference)


What is the purpose of ethanol in a DNA extraction experiment? We were doing a lab experiment in biology class in which we extracted DNA from a banana-detergent solution mixture.(The detergent solution was made of 100ml of detergent, 90ml of water, and 5g of salt.) We then added ethanol to the mixture.

I know detergent breaks down the lipids in cells and salt takes away the moisture from cells but how does ethanol affect cells?

In the case you describe the ethanol is not there to do anything with the cells but to make the DNA precipitate out of solution. DNA is very poorly soluble in 50-70% ethanol and it will precipitate out as a white sticky pellet. It works even better if the alcohol is kept very cold.

Ethanol does kill cells by denaturing proteins and disturbing the lipid bilayers but after you have added the soap, most cells will already have been disrupted.


Help identify the insects I keep finding at my house (Auburn, WA) Could anyone tell me what is this living being is called? I keep finding his relatives flying/crawling in my house once in a while since late Summer this year. We live in Auburn, WA, in case it helps narrowing down the list of who it can be...

Knowing the name will help me figuring out:

whether it's dangerous for my wife, or our infant;
how to get rid of it (I start suspecting they either breed inside the house, or somewhere very close because I only find these insects when it's getting warmer outside).

Sorry for the low quality of the photo. By the way, this animal is about 15mm or 5/8" long (not measuring the legs).

It is a Halyomorpha halys, commonly known as a stink bug.  Your photo shows a brown marmorated stink bug.  More information can be found on this Wikipedia page.

As far as your two questions:

Stink bugs do not normally bite people and are not poisonous.
A good way of controlling them in your home is by sealing any
openings that they are entering through.

Source: http://stinkbugsguide.net/facts.htm


Has an ectopic pregnancy's blastocyst ever been made to implant? Has an ectopic pregnancy's blastocyst ever been successfully extracted from the Fallopian tube and made to implant in the uterus?

Not in an independently confirmed case.

A paper was once published claiming this was performed successfully:

Pearce JM, Manyonda IT, Chamberlain GV. Term delivery after intrauterine relocation of an ectopic pregancy. Br J Obs Gynaecol. 1994; 101:716–7.

This article and several others by the same author Malcolm Pearce were found to be fraudulent and were retracted:

Lock S. Lessons from the Pearce affair: handling scientific fraud. BMJ. 1995; 310(6994):1547-8.


Understanding of the saturation function in the Monod-Wyman-Changeux Model I am reading Mathematical Physiology, Sneyd. I am a undergraduate mathematician interested in pursuing the field, so forgive me if my terminology is off. In this example, the writer considers a protein with two binding sites. The subscript $i$ indicates the number of bound ligands.
This expression, called the saturation function, appears on page 18:

$$Y = \frac{r_1 + 2r_2 + t_1 + 2t_2}{2(r_0+r_1 + r_2 + t_0 + t_1 + t_2)}$$

Where, $r_i, t_i$ denote the concentrations of chemical species $R_i, T_i$ respectively.
It looks like the weighted average of the ezymes that have occupied binding sites.

The fact that $t_0, r_0$ do not appear in the numerator suggest that it is the saturation of enzyme binding sites,  the $2$ in front of the $r_2,t_2$ indicates that the enzyme with both binding sites occupied is "double concentrated". The two on the denominator indicates the number of available binding sites in the enzyme. Perhaps, if we were considering an enzyme with three binding sites:

$$Y = \frac{r_1 + 2r_2 + 3r_3 + t_1 + 2t_2 + 3t_3}{3(r_0+r_1 + r_2+ r_3 + t_0 + t_1 + t_2 + t_3)}$$

  Would this description be correct?

I don't have access to Sneyd's Mathematical Physiology, but in Wikipedia's description of the Monod-Wyman-Changeux model, they call Y the "fractional occupancy of the ligand binding site". Other references refer to it as the "fractional saturation".

In other words, it's simply the fraction of the binding sites which currently have ligands bound to them. The denominator, then, is the total number of binding sites, which is equivalent (for a unit volume) to the total concentration of the protein (i.e. the sum of every protein form) times the number of binding sites per protein.

The numerator is the number of ligand-bound binding sites. Which is equivalent (for a unit volume) to the concentration of each form, multiplied by the number of ligands bound to it. So the zero-ligand forms are multiplied by zero, the one-ligand forms are multiplied by one, the two-ligand forms are multiplied by two, etc. (This doesn't reflect "doubly concentrated", rather it reflects the stoichiometry: for each protein molecule in the 2-bound state, there are two ligand molecules bound to it.)

So the answer to your boxed question is yes: that would be the appropriate form for a cooperative protein with three binding sites.


From which end of mRNA does transcription start? The book "Understanding bioinformatics", says that "RNA polymerase transcribes the anticoding strand in the direction from 3' to 5', so that the mRNA strand is produced from the 5' to the 3' end".

But from Khan Academy's article, I got "RNA polymerase builds an RNA strand in the 5' to 3' direction, adding each new nucleotide to the 3' end of the strand". Also "the codons of an mRNA are read in order (from the 5' end to the 3' end)". Which one is correct?

They're both correct. The confusion stems from the book talking about the anticoding strand as well as the newly-formed coding RNA strand, whereas Khan Academy talks only about the coding strand.

From the book:

  The anticoding strand is transcribed from 3' to 5'.
  Therefore the coding strand is produced from 5' to 3', meaning the very first nucleotide added by the RNA polymerase is the 5' end, and you add to it in the 3' direction.

From Khan Academy:

  The RNA polymerase produces a strand of RNA from 5' to 3'.


AMPK, PAN-AMPK, western blot What does it mean by adding PAN before the AMPK. I am trying to do a western blot assay on AMPK and I am confused by PAN-AMPK, AMPK. does it mean pancreases? Is pan-ampk the total ampk?

Adenosine monophosphate activated protein kinase or AMPK is not a single protein, but is a trimeric enzyme composed of $\alpha$, $\beta$, and $\gamma$ subunits. There are 2 alpha genes, 2 beta genes, and 3 gamma genes, each coding for closely-related but not identical isoforms. In addition, like most protein kinases (and many other proteins), it is regulated by the phosphorylation and dephosphorylation of some of its residues, most notably Thr172, but at numerous other locations as well.
A "pan-AMPK" antibody will bind all of the AMPK isoforms independently of phosphorylation or other post-translational modification (PTM) state. There are also isoform-specific total AMPK antibodies that just bind the $\alpha2$ subunit, or all 3 $\gamma$ subunits, for example. Finally, there are phospho-specific antibodies to various residues that only bind when the protein is phosphorylated at that site.
Both the pan and isoform-specific antibodies are known as "total" antibodies, as they bind independently of PTMs and will show the total amounts of their target(s) on a Western blot, for example.

Source:
I used to be a Product Scientist for a company that makes antibodies, PTM-specific and total, to AMPK and many other targets.


Are there any proteins not found in the brain that are affected by prions? A prion is an abnormally folded protein that is capable of causing otherwise normal proteins to also misfold and become prions. They are responsible for causing diseases such as Kuru and Creutzfeldt–Jakob disease. These are both diseases of the brain. Are there any non-brain proteins that also have corresponding prions that can cause disease, or do prion diseases only affect the brain?

Yes, malformed prion proteins can affect tissues outside of the brain.

Via: https://www.merckmanuals.com/home/brain,-spinal-cord,-and-nerve-disorders/prion-diseases/overview-of-prion-diseases

  Another familial prion disease has been recently discovered. It differs from other prion diseases because it causes diarrhea and affects nerves throughout the body years before symptoms of brain malfunction develop. It is described as prion disease associated with diarrhea and autonomic neuropathy.

Via: https://www.merckmanuals.com/home/brain,-spinal-cord,-and-nerve-disorders/prion-diseases/prion-disease-associated-with-diarrhea-and-autonomic-neuropathy

  Symptoms begin when people are in their 30s. People have persistent watery diarrhea and bloating. They may lose weight. Because the nerves that control body processes are affected, people may not be able to pass urine (called urinary retention) or may lose control of their bladder (urinary incontinence). Their blood pressure may drop when they stand up, causing them to feel dizzy or light-headed (called orthostatic hypotension). People may lose sensation in their feet. Later, when people are in their 40s or 50s, mental function deteriorates, and seizures may occur.


Short videos on evolutionary biology What I am looking for
I'm considering to eventually start my teaching sessions with short emotional, awe-inspiring or exciting videos that are somehow related to evolutionary biology incl. diversity of life, history of evolution on earth, specific evolutionary processes (sexual conflict, evolution of ageing, evolution of mutation rate, speciation rate, ...), diversity in mating systems, major transitions, etc...
3-minute long movies would be perfect. 15 minutes would be too long. The videos should be easily accessible for Bachelor students having little background in evolutionary biology.
Examples
Asap Science video about the evolutionary history of life would be a good fit.
The beginning of We are all related by vsauce would be a good fit.
This video from SciShow is typically too long
This video on the evolution of human face would do but I am not quite sure how exact it is and it feels a little weird that the end product is a white male!
It'd be great if not all suggestions were about recent human history or about dinosaurs :)
Do you have any suggestions?

I saw this HHMI video today. It is called The Animated Life of A.R. Wallace, and it discusses the contributions that Alfred R. Wallace made to evolutionary theory. It is a little long for your stated time of 3-minutes. but it talks about how in fits of malaria he came up with his ideas on evolution.

HHMI also has a whole series of videos and modules on Evolution, though Wallace's came to mind as it showed his ambition and desire to solve the problem, even though he had not received formal training in the sciences.


Characters do not make the genus, but the genus gives the characters? In his Origin of species, in the chapter entitled 'Mutual Affinities of Organic Beings: Morphology: Embryology: Rudimentary Organs', Darwin, speaking of the nature of classification systems of living organisms, writes:

  Such expressions as that famous one of Linnaeus, and which we often meet with in a more or less concealed form, that the characters do not make the genus, but that the genus gives the characters, seem to imply that something more is included in our classification, than mere resemblance. I believe that something more is included; and that propinquity of descent, the only known cause of the similarity of organic beings, is the bond, hidden as it is by various degrees of modification, which is partially revealed to us by our classifications.

What does he mean by  "that the characters do not make the genus, but that the genus gives the characters"?

It has been a long time since, I've read The Origin of Species, but it sounds like the intent of the phrase is to suggest that the presence of similar characteristics in two species do not imply that they are related, but that related species would be expected to share characteristics. I.e. that similar characteristics do not imply relatedness, but relatedness implies similar characteristics. Genus -> Characteristics, rather than Characteristics -> Genus. These two possibilities are logically distinct.

The assumption that Genus -> Characteristics segues into the key concept of his theory of evolution, that related species (a genus) arise from the descent with modification of an shared ancestral population. Remember that Darwin wrote long before we understand the role of DNA as the carrier of genetic information. He knew nothing about the physical substance or the mechanism of transmission that passed characteristics to offspring, but through his observations built a strong case that such a substance exists and that gradual changes in this substance occur over time in a population. He later posits that natural selection leads to the accumulation subsets of descendants with modifications that are advantageous in their environment. Thus the species within a genus could arise, their similarities the result of their shared ancestry, their differences that result of descent with modification and selection.


Why cooked food considered nutritious if proteins decompose at much lower temperatures? Food is cooked/baked at temperatures that are significantly higher than what's considered normal for proteins/amino acids (40°C). Why is it, then, that such food is still considered nutritious after cooking? (meat, cheesecake, lentils, quinoa, mushrooms, etc.)

Cooking is just a form of digestion.

  What is digestion?

Digestion is the process of breaking down big molecules into smaller molecules. When you cook food you break down big molecules into its small components.

  Why do we digest food?

Think about a long sequence of DNA for example. You eat corn and you have in your body a long sequence of corn DNA. What can you do with that long molecule....well, nothing. You need to break this long molecule down in order to be able to assimilate the constitutive nutrients. With those nutrients, you can now make up your own DNA. In other words, we need to break the big Lego castle that is food to get the building blocks in order to rebuild a spaceship. Digestion refer to the first process (breaking up the Lego castle). We refer to the part of the metabolism who breaks things down as catabolism and we refer to the part of metabolism that build things up as anabolism. Note that catabolism + anabolism = metabolism.

  Why do we cook then instead of digesting by ourself

Digestion takes much energy and require the organism to have the right organs and to have the right matter (enzymes and stuff). We can save up energy (and the other stuff) by digesting the food outside our body. One could say that humans, (just like spiders for example) are performing external digestion.

  Why cooked food considered nutritious

Cooked food don't have more nutrients than raw food. It is actually likely that in the process of cooking you would lose some nutrients going in the water that you throw away typically.

The big difference is that nutrients in cooked food are easy to assimilate which might end up being more healthy depending on the specific food source. Cooking may also destroy potentially toxic products.

Note that in response to the cooking behaviour, human gut has evolved to be shorter than it was in our ancestor.


Bug species identification Found this bug in my bed. Don't think it's a bed bug. Pretty small but fat and round and had deep reddish coloring.

That is not a bed bug. The picture is rather poor, which makes an ID difficult, but I think it might be the beetle Ptinus fur (spider beetle), or another species from the same genus. This species is found all over the world, and often indoors (they can e.g. feed on dry foods).

Reasons for this suggestion is the body shape (incl relatively hidden head), color ("reddish"),long legs with thick femurs, long hind legs, and long antenna. The long legs together with the long antenna (the antenna can look similar to a fourth set of legs), as well as the hidden head (so the body look two-segmented) is what makes it look somewhat like a spider .

(picture from bugguide.net)

(from weedimages.com)


What is happening to this tree? I was walking down to my mailbox when I saw this tree:

And by the looks of the branches, the tree seems to be dying because it has no leaves.  What is happening to the tree?

The tree is dying.  From what you say, it has no leaves wduring a time it should, it has saprophitic growth along the trunk; it looks like there's a crack in the bark on the right, and there are shoots coming up from the base of the trunk, the last hurrah from the tree to try to regenerate.

Trees send up suckers as a reaction to stress (like slowly dying). If you cut the trunk in such a way as to discourage rot, it will likely be replaced by this shrubby growth if the roots are sound. Some loggers use this as a way to quick-start new lumber trees.


Mathematics for genetics What types of mathematics are useful for studying genetics? Of course, statistics is, and I'm guessing set theory and group theory, but anything else? What about ordinary and partial differential equations?

Genetics is a very wide field of knowledge and many different areas of mathematics are being applied to genetics. Here is a probably not exhaustive list of the fields of mathematics that I have encountered in genetics (you will note that the elements of the list are not mutually exclusive)

diffusion equations
differential equations
markov processes
birth-death process
probability theory (a lot of it)
Bayesian probabilities
statistics
Math related to MCMC processes as well as HMC processes
Many fields of theoretical computer science are being applied and I guess theoretical computer science is a field of mathematics.
Graph theory
numerical integration
Analysis of dynamic systems

You say

set theory

Yes of course

group theory

Probably not so much or maybe I jsut don't really know what it is

ordinary and partial differential equations

I think pretty much any field of science applying mathematics will use differential equations.

But of course, not all geneticists are good mathematicians. Each geneticist specialize in a particular subfield. Some of them do a lot of mathematical modelling, others don't do any. Statistics and everything related to data science will always be useful though.


What is the name of this thorny plant? Location: South India

Month: June

Tree:

Leaf:

Its Flower:

EDIT:
For avoid confusion about ID this species, I even added its flower now.

Your tree appears to be from the Genus Dichrostachys.

It has several species, quiet a number of them have been reported only in Madagascar.

There are two species found in India, D. santapaui and D. cinerea.

How have I reached this plant?

The leaves of your plant are bipinnately compound. They gave me the impression of Mimosa pudica.

Of course it is not one. Mimosa pudica become creepers with time
and have short and thin prickly thorns.
Resemblance of an unknown organism with a known one can indicate shared derived character(s) (Synapomorphy), meaning they can be related.

Google's algorithm is often able to trace this relation. Look at the keywords I had used. If it doesn't one needs to experiment with the keyworks, note the word Fabaceae, it is the family to which Mimosa belongs.
Wikipedia  often is just the right place to start one's research.

The description of Dichrostachys cinerea is what I checked next, after having ascertained that is found in India.

  Dichrostachys cinerea is a tree characterized by bark on young branches, dark grey-brown fissures on older branches and stems and smooth on the spines.

  They typically grow up to 7 metres (23 ft) in height and have strong alternate thorns, generally up to 8 cm (3.1 in) long.
  Flowers of the Dichrostachys cinerea are characteristically in bicoloured cylindrical spikes that resemble Chinese lanterns and are 6–8 cm long and fragrant.

  The species tends to grow in rainforest zones.In India, it can occur in dry deciduous forest.

Every thing fits well upto Genus Dichrostachys.

  Dichrostachys is an Old World genus of legumes in the Fabaceae family.

  Their Acacia-like leaves are bi-pinnately compound.

  Unlike Acacia their thorns are hardened branchlets rather than modified stipules. They are native from Africa to Australasia...

The next thing I exhaustively checked were the species under this
    genus. I checked their
    locations,
    out of all two species have only been reported in India; D.
    santapaui and D. cinerea.

The reason behind this unusual format is to show you  how to fish. I will leave the rest of the hard work of digging up the species to you .

Few interesting facts about this genus:

Its name is derived from the Greek words dis (two), chroos (colour) and stachys (grain ear or spike), which in combination suggests their bi-colored inflorescences.

Dichrostachys cinerea, known as Sicklebush, Bell mimosa, Chinese lantern tree or Kalahari Christmas tree (South Africa).
D. cinerea is used in Ayurveda.


What produces the strong odor of decaying dead animals? Are there specific chemicals responsible for producing the strong, putrid odor that is present after an animal deceases? Also, how long does this odor last?

Two compounds are specifically associated with the smell of decaying cadavers (Hoffman et al., 2009), namely:

1,5-pentanediamine (cadaverine), and
1,4-butanediamine (putrescine)

Cadaverine is produced by breakdown of lysin and putrescine by the breakdown of ornithine (Science ME). Both are nitrogen-rich compounds and particularly pungent-smelling.

Source: Science ME

Both compounds are also responsible, in part, for the smell of bodily fluids such as urine and semen, smell of rancid butter, bad breath and stinky cheeses (Science ME).

Forensic Science Central UK mentions that after death, the body begins to decay after about 5-11 days (after an initial phase of bloating). The putrid smells subside mostly after 10-24 days, although a rancid cheesy smell might persist due to butyric acid. Note that many factors will affect decomposition rates and will affect this time course. Moreover, trained police dogs may be able to sniff out minute amounts of putrescine and cadaverine long after humans cannot detect it anymore.

Note that, given the complex composition of animals and the complexity of the decomposition process, a host of volatile organic components are released during decomposition besides putrescine and cadaverine.

Reference
- Hoffman et al. Forensic Science International 2009; 186: 6-13


In marine DNA viral diversity studies, what would "paradigm of rampant mosaicism" refer to? The recent paper in Cell Marine DNA Viral Macro- and Microdiversity from Pole to Pole describes the (huge) new Global Ocean Viromes 2.0 (GOV 2.0) dataset.

In the Results and Discussion section, the subsection Validating Viral “Population” Boundaries begins with the paragraph:

  Defining species is controversial for eukaryotes and prokaryotes (Kunz, 2013, Cohan, 2002, Fraser et al., 2009) and even more so for viruses (Bobay and Ochman, 2018), largely because of the paradigm of rampant mosaicism stemming from rapidly evolving ssDNA and RNA viruses, whose evolutionary rates are much higher than dsDNA viruses (for review, see Duffy et al., 2008). The biological species concept, often referred to as the gold standard for defining species, defines species as interbreeding individuals that remain reproductively isolated from other such groups. To adapt this to prokaryotes and viruses, studies have explored patterns of gene flow to determine whether they might maintain discrete lineages as reproductive isolation does in eukaryotes. Indeed, gene flow and selection define clear boundaries between groups of bacteria, archaea, and viruses, although the required scale of data are only available for cyanophages and mycophages among viruses (Shapiro et al., 2012, Cadillo-Quiroz et al., 2012, Gregory et al., 2016, Bobay and Ochman, 2018).

I know what "rampant" means in the colloquial sense, and the colloquial form of "paradigm" is familliar as well. Mosaicism usually relates to genetic differences between groups of cells within an individual multicellular organism. I am not sure how it applies to virus populations.

Is it possible to explain the meaning of "paradigm of rampant mosaicism" in this particular context, and give it some background?

As I understand it from skimming the Cell paper and that by Bobay and Ochman, 2018, which it cites, the concern is the validity of the established method of defining viral species. Quoting from this latter paper:

  Members of a biological species are defined by their ability to exchange genetic material…

The problem would appear to be that ssDNA and RNA viruses evolve rapidly (rampant is probably meant to convey this idea), but most importantly, not just by acquiring point mutations or deletions, but by horizontal gene transfer from other viruses (and from bacteria).

The net result of this is that such viruses are made up of segments from different sources, some evolved by conventional mutation and others ‘hijacked wholesale’ (my own hyperbole) from other organisms. Another way of putting this is that their genome is a mosaic of genes from different organisms. An example of this is in the diagram below, taken from a paper by Juhala et al. entitled “Genomic Sequences of Bacteriophages HK97 and HK022: Pervasive Genetic Mosaicism in the Lambdoid Bacteriophages”.

For anyone unfamiliar with the word ‘mosaic’ (or its applicability in relation to genomes) I reproduce below a Roman mosaic from Pompeii. The idea is that what appears as an integrated organism is composed of disparate pieces with distinct boundaries.

(The protagonists in the mosaic are about to exchange blows, rather than genes. There are also mosaics at Pompeii depicting the latter type of exchange, but these are a little too ‘rampant’ to present here.)

The implications of ‘mosaicism’ for defining viral species is — I imagine — that viruses which could be regarded as distinct species from examining the sequences of the majority of their genes might still be able to exchange genetic material by crossing-over at genes they have acquired by horizontal transfer.

Oh, and what about paradigm? It would clearly be unfair of me to suggest that this is a fancy word that the authors have used to sound important. The Oxford Dictionary online defines it as:

  A typical example or pattern of something; a pattern or model.

I think that the authors mean that the viruses provide a good example of horizontal gene transfer.


What is the transcriptome in layman's term? I am new to the bioinformatics field and am trying to understand a research paper that includes some terminology without definitions. The term transcriptome in particular is banded around in the literature, but is not clearly defined.

Can someone provide a reference or source to guide me to some learning material where I can get the basics.

There are three "omic" definitions that might help you.

The DNA is the long term storage of the information. You're probably familiar with this concept, and the study of this type of information is genomics.

One of the major functions of DNA is it's use as the blueprint for the production of proteins. Proteins carry out all sorts of structural and functional roles in the cell. Which proteins are present at a certain times and locations is known as the proteome. This is studied in proteomics.

Inbetween the DNA and the protein is an intermediate step. The DNA is transcribed to RNA, and then the RNA is translated to the protein. During the transcription of DNA to RNA, certain sequences of the DNA are not transcribed to RNA for a variety of reasons. The study of what exactly is transcribed at what time in which locations is transcriptomics.


Which organisms have their cell wall made of polysaccharides and amino acids? I came across a question which somewhat goes like

  In which of the following kingdom, most of the members have a cell wall made of polysaccharide and amino acids ? - Monera or Fungi.

To me it looks like both are correct answers because both are having hetero polymers of glucose and amine. Please enlighten me if I am wrong.

The correct answer is Monera.

It is so because their cell wall is made up of peptidoglycan.

  Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of most bacteria, forming the cell wall. The sugar component consists of alternating residues of β-(1,4) linked N-acetylglucosamine and N-acetylmuramic acid. Attached to the N-acetylmuramic acid is a peptide chain of three to five amino acids. The peptide chain can be cross-linked to the peptide chain of another strand forming the 3D mesh-like layer.

Fungi is wrong because its cell wall is made of chitin which lacks amino acids.

  Chitin $(C_8H_{13}O_5N)_n$ is a long-chain polymer of an N-acetylglucosamine, a derivative of glucose, and is found in many places throughout the natural world. It is a characteristic component of the cell walls of fungi, the exoskeletons of arthropods such as crustaceans (e.g., crabs, lobsters and shrimps) and insects, the radulae of molluscs, and the beaks and internal shells of cephalopods, including squid and octopuses and on the scales and other soft tissues of fish and lissamphibians.


How do biologists estimate that there is 8% of protein coding genes in human genome? In class, the professor said that there is about 8% of protein-coding genes in human. I wonder how biologists estimate this without annotating all of human genes. Thank you!

S/he's off by about 6 - 7%.

As per the national human genome research institute approximately 1% of the human genome encodes proteins. We can tell this by looking at the sequence (which we're now able to do quite quickly) and identifying those portions of the sequence can be translated to protein using the genetic code.

  Scientists have been able to identify approximately 21,000 protein-coding genes, in large part by using the long-ago established genetic code. But these protein-coding regions make up only approximately 1 percent of the human genome...


Can the knowledge about torsion angles alone be sufficient for specifying secondary structures of protein? I have read that Ramachandran plots are used to identify secondary structures of proteins. Also, alpha helices and beta strands cluster around specific regions of the plot which gives us the information about how much of these structures are present in the protein. But, it seems intuitively unreasonable. I can't convince myself "why there can't be other structures with the same torsion angles as alpha helices or beta sheets". Am I missing something?

Its not true that the Ramachandran plot will determine the secondary structure of an amino acid.

Ramachandran plots show the sterically allowed phi/psi angles of an amino acid.  As such nearly all non-glycine amino acids are in alpha/beta spaces.  Random coil segments of structure consist mostly of alpha and beta conformation amino acids in nonsense orders. (alpha/beta/beta/alpha/alpha and etc)

The dihedral angles repeated in a pattern over a several consecutive amino acids create secondary structure (N>4 or 7 for helices - strands need other strands forming sheets).


DNA is charged negative. Where is all the positive charge in my body? DNA is charged negative because of its phosphate backbone. Since charges need to be balanced (so that there are no charges building up somewhere), what is the positive charge which neutralizes this negative charge?

DNA in the body is not available as a free molecule, it is organized around DNA binding proteins, mostly the histone octamers. These proteins carry positive charges (mostly from lysine side chains) which interact with the phosphate backbone of the DNA. It is like in the figure below, the charges play an important role in the tight packaging. See here for more details.

The charge (or the temporary neutralization at some points of the DNA) is also important for the regulation of the DNA. Acetylation neutralizes the histone tail and loosens the DNA-protein structure (see here for more information).

Positively charged ions don't play a role in neutralizing the DNA charge in living cells (this is different for precipitations), as both are solubilized and split into ions. The concentration of positively charged ions like sodium and potassium are tightly controlled by the cells, as they are important for the function of transporters (for example the sodium-glucose transporters and others) or for keeping up membrane potentials. Moving the ions, which have to neutralize the DNA charge around would lead to a polarized nucleus.


Biological meaning/interpretation of clustering coefficience I have been looking for some time to find an answer to the following question. I would be grateful for any help/advice or directions.

I work very frequently with large number of proteins and assess their importance in a biological network. Traditionally there are two methods used to visualise proteins in a network and withdraw conclusions purely on network architecture bases, before one looks at the top hits in details using databases. One is degree and the other is clustering coefficience.

Degree refers to a node being connected to edges. The higher the degree, the more nodes are connected to a given node. Traditionally people interpret nodes with high degree as being biologically important, so called hubs. Since hubs are so highly connected it means that a failure of a biological hub has catastrophic consequences since the functions of many proteins are related/dependent on hubs.

However what confuses me is the biological meaning of clustering coefficient of a node in a given network. I’m aware that clustering coefficience refers to the tendency of a nodes neighbours to connect to each other; however, I was unsure as to what it means biologically and whether that means a node with a high clustering coefficience is more “important” than a node with low clustering coefficience. This just seems unlikely to me because hub proteins, are considered important proteins; however, hubs usually have low clustering coefficience but that doesn’t mean they are less important since they are highly connected (high degree). Therefore to put it in plain english, why do people use clustering coeffience in biological networks and what biological information is it providing them?

So I would appreciate any explanation/advice and references you could provide that would help me understand the biological meaning/interpretation of clustering coefficience.

First of all, I find this an interesting question.

In short:

Clustering coefficience is widely used
It is widely accepted that hub genes are more essential than poorly connected genes
but research is not always interested in the hub genes / proteins / molecules (for example most metabolic pathways involve water)

Answering your question, why people would want to use this kind of method:
If you would take a random model (pathway) most of the lines will be equally distributed between the nodes. This is not the case for most biological networks. Because of this, the global clustering coeffiecence can be used to see if a network could be biological. Clustering coeffiecence can also be used to find out about more specific nodes. For example if a protein has a relationship with two other proteins (binding, regulation, etc.), the two other proteins are also more likely to have a relationship with each other (similar to a social network).

References:

http://en.wikipedia.org/wiki/Clustering_coefficient

http://www.biomedcentral.com/1752-0509/6/34

http://www.pnas.org/content/99/12/7821.full.pdf+html


Do hornets return to the same nest after winter each year? I have what I think is a hornet nest on the soffit of my house.

The nest has been removed, however, the hornets keep rebuilding. Also, they have started to swarm the sewer vent pipe (not shown in photo).

If fail to get rid of the hornets this fall, will they return to the same nest next year (or overwinter and continue to live there)?

I'm not sure if this is relevant or not:

To give you an idea of what kind of winters I am dealing with, I am near Toronto, Ontario; the temperature goes down to -25 degrees Celsius.

If fail to get rid of the hornets this fall, will they return to the same nest next year (or overwinter and continue to live there)?

No. The nest, likely made of wood pulp (and maybe mud), will/should degenerate to unusable over the winter, though the bulk could remain for a couple of years. All wasps die, except for the new queens (fertile, mated females) who overwinter in sheltered crevices somewhere.

In spring, it is a single wasp that starts a hive: the new queen. She builds a new, small hive in which to lay eggs, which is added to initially by the queen and then by workers who have hatched.

While she will not return to an old hive, the conditions which appeared advantageous to one queen (shelter from rain, intense sunlight, winds, etc.) will also seem advantageous to other queens, which is why nests appear in the same places year after year.

Edited to add: It appears most likely that the queens that overwinter are "new queens", that is, mated female offspring of the queen. H/T @Brian Krause.


Do male marsupials have a pouch? Do male marsupials have a pouch, or is it a female organ only (like the womb)?

In most marsupials, only the females have a pouch. However, males of the water opossum and the extinct tasmanian tiger (or thylacine) also have a pouch.  The males of both the thylacine and water opposum used/use their pouch to keep their genitalia from getting entangled in vegetation.


What are the constraints on an operon? From what I understand, the term operon is loosely defined to be a collection of genes that are found to be in the same proximity in a genome.

Some definitions enforce that an operon is only regulated by a single promoter and all of the genes are transcribed together.

If the above definition is strict, that would imply a couple of things

Genes are opposite strands cannot be in the same operon (since they cannot be transcribed together)
Overlapping genes cannot be in the same operon for the same reason.

I realize that part of the issue with these definitions stems from an ongoing investigation behind this phenomenon.  But are there strict standards surrounding the definition an operon? What is the minimal definition of an operon?

Relevant links

What is an operon?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161906/pdf/12864_2013_Article_6422.pdf
https://en.wikipedia.org/wiki/Operon

From Henderson's Dictionary of Biology 14 ed. An operon is: a type of gene organization in bacteria, in which the genes coding for the enzymes of a metabolic pathway are clustered together in the DNA and transcribed together into a single mRNA. This mRNA is then translated to give the individual proteins. The expression of all the genes in an operon is controlled by a single promoter.

I'm not sure what an overlapping gene is, but according to this definition, yes genes on opposite directions of a promoter or different loci cannot be a part of an operon because they wouldn't be on the same mRNA.


Effect of mutation on phenotype Is there a type of mutation that changes the phenotype of an organism, but not the protein sequence?

Yes. It is actually the case of most mutations that affect the phenotype!

Only 1.5% of the human genome codes for proteins. About 5-10% of the human genome are regulatory sequences which do not produce any protein but greatly impact the phenotype by regulating the expression of coding sequences. A mutation in a regulatory sequence does not directly impact the protein sequence but can have drastic impact on the phenotype (and fitness).

There are a lot of such mutations that have been identified. Here are a few quick examples

Variation in Vertebrate Cis-Regulatory Elements in Evolution and Disease
A cis-Regulatory Mutation of PDSS2 Causes Silky-Feather in Chickens
A regulatory mutation in IGF2 causes a major QTL effect on muscle growth in the pig
Blue eye color in humans may be caused by a perfectly associated founder mutation in a regulatory element [..]


Why is amyloplast produced by some plant cells but not other cells? For example I know it is produced in Potato's and fruits and its purpose is to synthesize glucose in to starch through polymerization. But why is it only present in some cells? Is it only present in cells with higher glucose content?

Amyloplasts are non pigmented organelles responsible for plant sugar storage, release and gravity perception (or tropism). This being the case they are commonly found in root caps (for gravity) and storage sites like tubers, fruits and grains.

So due to cell differentiation, it is not possible for these plastid organelles to be present in all cells the same way chloroplasts (another type of plastid) is not present in the stem (with the exception of small plants and succulents) and most of the root cells (Reece Urry et al, 2011).

Reference

Reece J.B., Urry L.A., Cain M.L., Wasserman S.A. et al (2011). “Campbell Biology 9th ed” Pearson Education, Inc., publishing as Pearson Benjamin Cummings, 1301 Sansome St., San Francisco, CA 94111.


Why does cut grass cause allergies? I know that cut grass from a lawn or field can cause allergies in some people.
I also know that most plant allergies are due to plant pollen.

However, most people do not allow their lawn grass to flower, and therefore, any allergy from cut grass is likely not due to pollen.

So, what exactly in the grass is causing the allergy?

I did a google search but only found evidence and info for grass-pollen allergies.

Does anyone know what's going on here?

www.allergicliving.com claims that the cause to such an allergy is not the grass but is actually mold:

  Often patients will have allergy symptoms with fresh cut grass...That's not grass pollen allergy, that may be mold allergy from the molds being stirred up.

The site also mentions that simply having the physical presence of lawn mower "dust" in one's nose may cause symptoms.

Source: www.allergicliving.com/2010/07/02/outdoor-allergy-grass-allergy-attack


Identifying three species of Datura I have found a large, wild patch, some 200m long, of mainly Datura Stramonium, in our street. I have always been keenly interested and well read on the shamanic, and - very rare - medicinal uses of this species, but scattered amongst them, like family, are two other plants I don't know, but am convinced are also some kind of Datura. I would please like some help on identifying the other two based on the two photos I have of all three.

This is the well known - to me - Stramonium flower, the plant characterized by jagged leaves and the well known spiked seed pod of Jimson Weed seeds.

It looks like user29734's answer is correct, and the above is Morning Glory, but of course subject to confirmation. I now do recognize at least the purple flower as Morning Glory, but from some 30 odd years ago. And it now looks like what I confused with Datura Alba is really just another colour flower of the Morning Glory.

If anyone could please confirm my ID of the Stramonium, and confirm the identification of the second image as morning glory, and suggest what species.

These plants are all around my neighbourhood, with is the northern part of Randburg, South Africa. This city borders on the Northern side of Johannesburg. 1 It's a temperate climate, with very hot and rainy summers, and bitterly cold and dry winters. The soil is reddish and lacks much humus.

It is a semi-rural area, having been rapidly urbanised over the last ten or so years, when it was still just farms and small holdings. Farming is mainly vegetables or lucerne; and lots of maize further out from the city. We are a few km south of the Cradle of Humankind.

1 Strangely enough, there are two cities in the US with the same names, both in California, I believe. I know Johannesburg is.

The second flower is, I'm guessing by the valentine shaped leaf and violet tubular flowers, a morning glory vine (ipomoea violacea or ipomea tricolor). These plants both are closely related cultivars of ololioqui and tlitlitzen which had a history of shamanic use in southern Mexico.


Shine-Dalgarno sequence and expressing proteins Shine-Dalgarno sequence present in the prokaryotic mRNA plays a role in initiation of translation. In eukaryotes a Shine-Dalgarno like sequence is present but does not play an important role in initiation of translation.
We often try to express a eukaryotic gene in a prokaryote. For example : expressing insulin gene in E.Coli.

My question : If eukaryotes do not have the shine dalgarno sequence , then how can a eukaryotic protein be expressed in a prokaryote ? (I am especially interested in knowing about this in case of cDNA expression)

Eukaryotes have an analogous sequence called the Kozak sequence. cDNA is easily expressed in prokaryotes by substitution of the Kozak sequence for the Shine-Dalgarno sequence, using standard molecular biology techniques. A caveat is that not all eukaryotic protein will be properly expressed in bacteria because of they lack the ability to carry out post-translational modifications that would occur in a eukaryotic Golgi apparatus (e.g., glycosylation). Insulin is a special case because it is a small, unmodified peptides.


Protein Isolation from mammalian cells What non-SDS buffer can I use to isolate protein from mammalian cells? The protein is intended for testing electron transport chain complexes.

Short answer - you will need to use a nonionic detergent. These will dissolve lipid membranes but leave most protein complexes intact, and many proteins in active form.

However there are many of these available and finding the right one for a particular job is a black art.

The usual approach is to start off with something widely-used and not too expensive like Triton X-100. Detergents with glycoside head groups are also widely-used but tend towards the expensive.


What was the biological mechanism that allowed Tarrare to eat so much? Are there any conjectured mechanisms that cause Tarrare's extremely oversized stomach and abdominal cavity? Along with his superhuman appetite of course.  Whether from a medical perspective or a genetic one (I.e a potential diagnosis that is perhaps quite similar or the genes that would be at play).

Even correlated genes and their subsequent mechanisms that are being affected could be an interesting addendum.

*I would like to make sure that any answer is also trying to explain the enlarged esophagus and abdominal cavity(seen during autopsy) along with the appetite, sweating, and other observed manifestations of an underlying condition(see Death section of Wiki for info and associated source material in book "Two-headed Boy and other Medical Marvels").

Tarrare

Tarrare was a showman who was renowned for his insatiable appetite including eating cats, dogs, and snakes sometimes raw.
He is also said to have eaten many inedible items.
At the time, he was alleged to have committed cannibalism of a 14-month-old baby and was caught in the act of cannibalising cadavers by hospital staff.

He was given away as a child by his parents and served in the French Revolutionary Army.

Tarrare died at the age of around 26.
From the book "Anomalies and Curiosities of Medicine" originally published in 1896 by Gould and Pyle:

  He was of middle height and was always heated and sweating. He died of a purulent diarrhea, all his intestines and peritoneum being in a suppurating condition.

This record is 100 years after Tarreres death and is largely based on the 1819  London Medical and Physical Journal.
The earlier record claims:

  At seventeen years of age, Tarrare weighed only one hundred pounds,
  and was already able to eat, in twenty-four hours, a quarter of a
  bullock of that weight.

From these accounts, I form the opinion that Tarrare ate an incredibly poor diet of raw meat and offal and countless inedible objects.
There are references to throwing up after consuming raw animals and chronic diarrhoea. There are references to sleeping for large periods of time after eating large quantities of food.

Autopsy

A passage from the 1819 London Medical and Physical Journal:

This is the closest article we have to a contemporary record.
From this account we gather that his stomach was enlarged and ulcerated, his gall bladder was enlarged, and his liver was diseased and enlarged.
Also, it might be a factor that his appetite was lost during these final days, common among patients with diarrhoea.
The record at the time, as quoted above, attributes the cause of death to diarrhoea.

Although the picture is painted that the autopsy occurred soon after death, we have no idea if this was hours, days, weeks, and conditions were much less sterile than modern morgues. I am not sure if the  "corruption" mentioned is significant.
One source claims Tarrare died of TB, however, I cannot find any corroborating evidence.
Another source recounts Tarrare blaming his demise on eating a golden fork.

These post mortem observations could have developed from 20 years of eating an exceptionally poor, unhygienic, and often inedible diet and may or may not have been the cause of his underlying condition.

Summary

So we have a few things to consider.

Polyphagia including inedible object consumption
Died young
Gastrointestinal abnormalities identified post mortum
Chronic fever and sweating
Chronic diarrhoea and vomiting
Periods of prolonged sleep

Polyphagia

The London Medical and Physical Journal describes Tarrare as having polyphagia which in his case could not be cured by acids, opium, or tobacco.

Colloquially, polyphagia means ingesting a wide variety of items.
However, if they meant "polyphagia" medically, it could be a symptom.

Polyphagia is a medical symptom defined as excessive hunger.
In modern times, this can indicate a disorder such as diabetes (improper production or reception of insulin) or Kleine–Levin syndrome (a disorder of the hypothalamus).
It could also indicate a genetic condition Prader–Willi syndrome and Bardet–Biedl syndrome.

The full list of causes from Wikipedia is:

Anxiety
Stress
Depression
Orexigenic drugs
Diabetes mellitus
Hyperthyroidism
Hypoglycemia
Fatigue
Premenstrual syndrome
Prader–Willi syndrome

From the
NHS:
Prader-Willi syndrome is a rare genetic condition that causes a wide range of physical symptoms, learning difficulties and behavioural
problems.

Bulimia
Graves' disease

Autoimmune thyroid disorder that can lead to an intolerance of heat

Kleine–Levin syndrome

A sleep disorder

We cannot know if Tarrare's polyphagia was brought on by his stressful exhausting life, his poor diet, or some genetic condition.
We cannot even be sure if his condition was responsible directly or indirectly for his death.
We cannot know if his sweating was related to; his underlying condition, or a chronic state of infection.
The only cause for his eating we can rule out from the above list of underlying causes is premenstrual syndrome (PMS) and orexigenic drugs (which are not documented).
There could be a case made for most of the other causes.

Concluding remarks

Given the scarceness of good quality medical records, the anecdotal nature of what was recorded, and the relatively poor diagnostic power of medical practitioners of the time, it would be, in my non-medical opinion, impossible to conclusively form a diagnosis.


Why is the threshold between human embryo and human fetus defined as 8 weeks after fertilization? Why is the threshold between human embryo and human fetus defined as 8 weeks after fertilization? What's happening on the 8th week?

Note: definition of embryo based on Wikipedia's current definition.

An embryo is called a fetus at a more advanced stage of development
  and up until birth or hatching. In humans, this is from the eighth
  week of gestation. However, animals which develop in eggs outside the
  mother's body are usually referred to as embryos throughout
  development; e.g. one would refer to a chick embryo, not a "chick
  fetus" even at late stages.

wikipedia - embryo

I can answer what "more advanced" means with the following 2 pictures. I think you can see the difference. (Real photos were too disgusting for me.)

Figure 1 - 7th week embryo - source

Figure 2 - 8th week fetus - source

For the sake of blind people and google, the 8th week fetus has a face and a human form, while the 7th week embryo doesn't.

  From the 10th week of gestation (8th week of development), the
  developing organism is called a fetus.

  All major structures are already formed in the fetus, but they
  continue to grow and develop.

  Since the precursors of all the major organs are created by this time,
  the fetal period is described both by organ and by a list of changes
  by weeks of gestational age.

  Because the precursors of the organs are now formed, the fetus is not
  as sensitive to damage from environmental exposure as the embryo was.
  Instead, toxic exposure often causes physiological abnormalities or
  minor congenital malformation.

wikipedia - prenatal development

So the scientific explanation of the threshold is that the precursors of all the major organs are created by that time.


What is intercalary mitosis in bacteria? According to Wikipedia, in vegetative reproduction fragmentation takes place, and Spirogyra simply undergoes intercalary mitosis to form new filaments.

How is 'intercalary' defined in a bacterial context, does have to do anything blank or dead cells of Spirogyra?

To define, intercalary differentiation or mitosis applies to any cytogenesis through mitosis which arises between different specialised tissues or cells. Spirogyra may undertake either sexual reproduction, should conditions prove to be adverse, or asexual. The latter involves an 'intercalary mitosis'. This entails a fragmentation in the original filament in order to produce additional filaments.

Within bacteria, a good analogy may be the 'Blue-Green algae', a deceptive misnomer for phototrophic cyanobacteria. Thus, in the context of filamentous bacterial colonies, you may consider intercalary binary fission, cell division within the filament.

More information available from: http://bioweb.uwlax.edu/bio203/2010/fenske_megh/reproduction.htm


When are population dynamics models useful? When are population dynamics models useful? There seems to have been a lot of research about it, but how does it help? If I need data about how a population will evolve under what conditions, I need it because I need data for a decision (such as "can we kill 50% of population X without doing too much damage?"), right? But for that, the model needs to be aware of what causes what. And for that, I have to do experiments, right? Like "let's kill a significant amount of population X and see what happens in the next ten years". I really don't get it.

Population dynamics occupies a whole subset of mathematical biology. Perhaps the most pragmatic uses for modelling population dynamics come from the fields of epidemiology for modelling disease infection and transmission through a population (one such article), or ecology modelling things like forestation, fishing dynamics, predator-prey relationships (an example). Then there are more abstract uses, when you cannot measure a population to test a hypothesis because the labour is too intensive, or it's too costly, or no such surveillance mechanism exists. Theoretical models of population dynamics are built to gain an understanding of what the system as a whole may do under certain conditions. In this sense, population models are more of a theoretical exercise or a thought experiment.


Understanding the picture of a synapse I need help to see exactly what is going on here. According to the textbook here is shown a synapse, but I cannot quite see the things the textbook says are there.

From what I understand: (1) At1 and At2 are axons?, (2), The black thing on the bottom left is a dendrite?, (3) s1 and s2 are post-synaptic densities?

Is there more to see here that I am missing?

You can tell that the structures labelled At are axons, or rather axon terminals, due to the presence of the synaptic vesicles.

I think this is a fine photo that's a bit more a clear representation:

Source

PSDs are really just protein aggregates that are thought to facilitate neurotransmitter trafficking. So the structures here make sense. At least, they make sense if you know the tissue you're running in TEM, and you understand that how you cut the samples for microscopy affect the way they end up looking. My only assumption that Den is a dendrite is knowing that axon terminals synapse with other dendrites: they're receiving structures. I'm also somewhat sure the cell body from which the dendrites extend have that characteristically large nucleus.

The other understanding is that these pictures are just snippets of a larger image and you only get used to identifying structures through practice and experience. Rather, the author wants you to see this section and for lack of context has identified the structures for you.