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Does heterogeneous resistance have an impact on the zone diameter observed in disk diffusion susceptibility testing?
Question
Does the presence of small, discrete colonies within the zone of inhibition, suggesting heterogeneous resistance, impact the zone diameter in disk diffusion susceptibility testing?
"Help us so we can help you"
ASM recommends that such occurrences should be ultimately interpreted as resistance to the antimicrobial:

Distinct, discrete colonies within an obvious zone of inhibition
should not be considered swarming. These colonies are either mutant
organisms that are more resistant to the drug being tested, or the
culture was not pure and they are a different organism. If it is
determined by repeat testing that the phenomenon repeats itself, the
organism must be considered resistant to that drug.
https://asm.org/getattachment/2594ce26-bd44-47f6-8287-0657aa9185ad/Kirby-Bauer-Disk-Diffusion-Susceptibility-Test-Protocol-pdf.pdf

I can't see how this is a sound judgment as there is no way to tell that the persisting variants weren't initially among the inoculum population and didn't appear due to the antimicrobial exposure stress.
Then there is another question: does the presence of this occurrence in vitro also mean that it would ultimately appear in the different in vivo conditions?
Whatever the case, I want to know whether the emergence of such persisters would affect the zone of diameter or not.
It seems to me that it would depend on the mechanism of resistance to the antimicrobial in question: antimicrobials that are resisted by the organism in question through inactivating enzymes are the ones that can be affected. This is obviously because less antimicrobial concentration would be available for the whole population. Then, this is disk diffusion after all not the broth dilution method; organisms have access to the diffusing antibiotic gradient that passes through the part of the plate where they are located.
But if bacteria can't diffuse around (assuming non-swarming bacteria), what about their inactivating enzymes, could they diffuse away from the cells that released them in a significant manner? Then there is another question: shouldn't the appearance of persister colonies alert us to the possibility of additional, unseen microcolonies and could their produced inactivating enzymes affect the outcome of the zone diameter?
Edit:

Still other significant resistances may be subtly evident and appear
as individual colonies in an obvious zone of inhibition (Figure 12-9).
When such colonies are seen, purity of the test isolate must be
confirmed. If purity is confirmed, the individual colonies are
variants or resistant mutants of the same species, and the test
isolate should be considered resistant. Bailey & Scott's Diagnostic Microbiology

Does a purity plate with monogenetic phenotypic variants considered pure in this context?


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Is the presence of a specific gene in one bacterial species enough to conclude it has the same function in another species within the same genus?
I was wondering if the answer should be more or less conclusive given the following givens and some of their implications that I feel by gut feeling could play a role in the answer:

The species belong to bacteria:
Bacteria have higher genetic diversity than most plants and animals, yet some bacterial species belonging to the same genus can't be easily differentiated phenotypically.
The two species belong to the same genus
The genes I'm interested in are those encoding virulence factors, for example:

A. baumannii possesses a chaperone-usher pilus system, known as Csu pili, which facilitates the adherence of Acinetobacter baumannii to some surfaces.

In addition, all strains possessed the two genes that code for BfmRS
(except ATCC_19194, where only the bfmR gene was detected), a
two-component system that regulates Csu (Chaperone-usher) pili, which
are important for biofilm formation, adherence to abiotic surfaces,
and capsule production (Weber et al., 2016; Lee et al., 2017).
However, most of the Csu pilus components were annotated as
hypothetical proteins (CsuA/B, CsuC, and CsuE).
Chromosome Architecture and Gene Content of the Emergent Pathogen Acinetobacter haemolyticus https://doi.org/10.3389/fmicb.2020.00926

Is this enough to say that the Csu pili is one of the virulence factors of Acinetobacter haemolyticus as in Acinetobacter baumannii?
Edit:
If Acinetobacter baumanii is known to have a certain virulence factor, why is it assumed that all A. baumanii strains, as implied from text referring to such strains by A. baumanii period, have it?
What i want to say is that there could be, at some level, the capability of a working interpolation.

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In the diffraction pattern of a protein crystal what exactly determines the intensities of the spots?
What I have read is that the contents of the unit cell affect the intensities, but how? I am also unclear on why you need to know the symmetry of the unit cell, what is that used for?
I understand segments of this topic (x-ray crystallography) but I am having trouble piecing all the segments together to make a complete picture. I've been spending hours every day on this on this, any help would be really appreciated!

Two questions here:
1) What does the symmetry of the crystal mean?
The symmetry of the unit cell is the symmetry of the crystal.  Its really useful thing to know about the crystal in practice.  You can always pretend that any crystal is space group P1 - with no internal symmetry.  This implies half of the diffraction data is needed to get a complete set.  Why half? The Laue symmetry of typical X-ray diffraction shows that the diffraction should be centrosymmetric  I(hkl) = I(-h,-k,-l).
If you do this and the crystal has more symmetry than that you are collecting too many data.  Here I take the example of a 2-fold axis.  Along that axis the space group shows that the symmetry of the crystal should be 4 fold along the x axis (x axis is chosen by convention):
I(hkl) = I(-h,-k,-l) (as above) and I(hkl) = I(h,-k,-l)
This fact means we actually can collect less data and know the crystal diffraction pattern easily.  In practice we collect from more than just the unique data, but the more diffraction data we take it also means that we can assume equivalence and have taken more  measurements, giving us better experimental accuracy for the same effort. It also means that when we build a molecular model for structure in the crystal we have a simpler model - one only creates a model for the unique assymmetric unit of the crystal unit cell. Fewer atoms in the structure, fewer degrees of freedom and less error in our resulting model.
There's more... screw axes 2(1), 3(1) and non primitive lattices create systematic absences which helps us collect more accurate data and do refinement more easily in the same vein...  but maybe this gives you an idea...
2) how does the unit cell contents reflect the diffraction intensities
X-ray scattering from crystals is the result of the photon causing an elastic scatter from atomic, inner shell electrons - Bragg scattering.  By considering the crystal as a series of slits in 3 dimensions, it can be shown that the average positions of atoms in the crystal reinforce each other to give the reciprocal lattice that is diffraction data in 3D.

In the picture above from Wikipedia you can see a beautiful protein crystal diffraction pattern.  The rings of spots are a spherical section from a 3D orthorhombic lattice of spots.
Rather than digress into the reason the diffraction appears this way, back to your question: what causes the intensities to vary from spot to spot and crystal to crystal.  The crystal lattice contains atoms which are in the same position in every unit cell which are creating the diffraction by Bragg scattering.  As such, it is the positions, relative electrons in orbit that dictate the diffraction intensities measured.
The models built to model diffraction typically translate a set of atomic positions to the structure factors (square roots of the diffraction intensities), but this is an approximation that works pretty well - the full model is not atomic positions, but an electron density function in space.
There are other sorts of scattering methods, more that could be said about all these subjects, but I hope that gives you some help with your specific questions. If you want clarifications in this, I can edit the answer from comments...

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Do women have greater reproductive success than men?
What proportion of men who go through their whole lives and never find a mate at all, and what proportion of women do? And is the proportion of men greater than the proportion of women?

Related

I think the answer runs along the same logic as this question: Which sex has higher variance of reproductive rate in modern societies - male or females?
Because its easier for a male to have offspring with multiple partners, more women would typically produce offspring than men.  In polygamous cultures, it can lead to significant differences of reproductive success between the genders.

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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?

Yes, this has been done by

Wallace, C. J. (1917) Transplantation of ectopic pregnancy from fallopian tube in cavity of uterus. Surg Gynecol Obstet 24, 578-579
Shettles, L. B. (1990) Tubal embryo successfully transferred in utero. Am J Obstet Gynecol 163, 2026-2027

Shettles has a questionable reputation at best, and I don't know what to say about the 1917 report. I would also note Shettles 1990 case report was of a case 10 years prior.

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.

What do you mean by "independently confirmed case"? Reproducible?

@Geremia The one I referred to was an obvious case of fraud once investigated. The ones you refer to in your answer were 1) a case report 10 years after the fact by an also troubled researcher, and 2) a case report from 1917. Both from single authors claiming to have done something thought to be quite difficult, and neither with any follow-up. Though it's possible they are real, they each have little more support than a Bigfoot sighting.

I'd also add that none of these articles are cited afterwards by anything but papers discussing ethics, suggesting that they have had no impact on clinical practice.

What is that? IVF successfully implants embryos (albeit at a low rate, <37.1%, depending on female age). Are in vitro conditions better than those in the Fallopian tube?

@Geremia There's a huge difference between implanting an IVF embryo de novo into the uterus, where it belongs, versus taking one that's been growing in a fallopian tube, where it does not belong, extracting it, and then reimplanting it in the uterus long after the time it would have normally implanted. There are good reasons this is not the typical course for dealing with ectopic pregnancy.

Extracting it intact is the hardest part?

Let us continue this discussion in chat.

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Corpus luteum during the luteal phase and gonadotropins
Does the corpus luteum operate independently of the hypothalamic-hypophyseal-ovarian axis? I know that hCG sustains the corpus luteum in the absence of FSH and LH, but in an ovarian cycle where there is no pregnancy, do FSH and LH affect the corpus luteum? It seems to produce a lot of estrogens and progesterone even when FSH and LH levels are low.
(Online I saw that the corpus luteum degenerates because of low FSH and LH levels. Is this true? Why doesn’t the corpus luteum degenerate immediately after the LH surge, then, whereafter FSH and LH levels are so low? If not, then why does the corpus luteum degenerate?)

http://biology.stackexchange.com/questions/43937/how-only-one-follicle-develops-into-graffian-follicle

Lots of questions, so I'll break them down one at a time:

Does the corpus luteum operate independently of the hypothalamic-hypophyseal-ovarian axis?

The corpus luteum does depend on intact pituitary signalling.  Hypophysectomy at the beginning of lutenization will result in cessation of corpus luteal growth and subsequent drop in progesterone; in essence, the corpus luteum won't grow and function properly in the absence of pituitary hormones.  In some species, estradiol is needed, so intact gonadal steroidogenesis is also required.

In an ovarian cycle where there is no pregnancy, do FSH and LH affect the corpus luteum?

Elaborating on the above, yes pulsatile secretion of LH is required to fully develop and maintain the corpus luteum (not so much for FSH).  Other pituitary hormones, such as growth hormone are also involved.  In pregnancy (or pharmacologically), a large dose of hCG can sustain the corpus luteum.  hCG and LH are homologous.  Depending on the species, prolactin and estradiol are also required.

Is it true that the corpus luteum degenerates because of low FSH and LH levels?

The corpus luteum degenerates (luteolysis) because of prostaglandin produced by the uterus.  In the absence of a uterus (and therefore prostaglandin), luteolysis is delayed.  It is reported that estradiol from the next batch of follicles triggers oxytocin release by the posterior pituitary and subsequent release of prostaglandin and thus is the penultimate cause of luteolysis.

Why doesn’t the corpus luteum degenerate immediately after the LH surge, then, whereafter FSH and LH levels are so low?

As described above, it is not low FSH and LH that cause luteolysis.

If not, then why does the corpus luteum degenerate?

Described above.

Source: http://physrev.physiology.org/content/80/1/1.long


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Where exactly is 'Colloid' with regards to synthesis of thyroid hormones?
I've researched colloid and it seems to be a substance of microfibres and thin films in which thyroid hormones may be synthesised, but I was wondering where this exactly is... I think it could be in the inter membrane space but I have no evidence of that, or is it just surrounding all cells?

Colloid is found in thyroid follicles and is composed of the protein from which thyroid hormones are made.
This link below states: "Follicles are filled with colloid, a proteinaceous depot of thyroid hormone precursor."
That precursor is called thyroglobulin.
The image below shows micrographs of the thyroid.
In the image, the colloid is surrounded by thyroid epithelial cells, which collectively form a follicle. The lower mag on the left shows many follicles filled with colloid.  The image on the right shows one follicle. The white areas inside the follicle near the epithelial cells show uptake of colloid by the epithelial cells, which are activity synthesizing thyroid hormone.

http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/thyroid/anatomy.html


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Does Mn always exist in Photosystem II?
I had the impression that PSII (photosystem II) always has four Manganese atoms
(4 Mn). Is there any reason that these atoms are needed?
Is Mn or Fe also present in bacteria LH1 or LH2?

I'm having some difficulty understanding your question... can you write everything out and not use abbreviations? This will help. Thanks!

I have wrote EVERYTHING out i.e. PSII is photosystem II, and Manganese is Mn.....what else? LH is light harvesting

Mn Fe are standard chemical symbols while PS2 is also standard abbreviation. Please stop these politics. Thanks.

I made some edits to your title because the previous isn't in the correct english syntax

I guess you are referring to Magnesium and not Manganese. Are you sure you are talking about manganese?

Thanks. I am not a native speaker. Therefore, my English surely have some problem. But manganese....I guess was copied from a paper....But what is really there?

Is Fe also part of Water splitting complex or OEC ?

Could this Mn be replaced by other atoms like Zn or Fe

Manganese is part of the oxygen-evolving complex and is essentiell for the oxidation of the water to generate electrons, protons and oxygen. This is done by changing the oxidation state of the mangane from +2 to +4, as shown in the figure (from here):

These manganese atoms are the center of the reaction - important here are the different oxidation states they can take, other examples are copper (in tyrosinase for example) or iron (hemoglobin) which are also present in the active center of enzymes.
For more information see references 1 and 2.
Anoxygenic bacterial photosynthesis also needs metal ions in the bacteriochlorophyll, this is magnesium (as in the chlorophyll of green plants), the light harvesting complexes contain iron-sulphur complexes.
For a general overview see reference 3, for more detail on the reaction centers and their evolution, see reference 4.
References:

Where water is oxidized to dioxygen: structure of the photosynthetic
Mn4Ca cluster.
Reduction-induced inhibition and Mn(II) release from the photosystem
II oxygen-evolving complex by hydroquinone or NH2OH are consistent
with a Mn(III)/Mn(III)/Mn(IV)/Mn(IV) oxidation state for the
dark-adapted enzyme.
Bacterial Photosynthesis
Reaction centres: the structure and evolution of biological solar
power.

There seems to have some LH1 or LH2 do not need such atoms. I am not sure whether PS I or PS II...

any physical reason why these atoms must be there? (for instance they need a spin or entropy...)

@latra Besides having the function as electron acceptors/donors? Not that I know of.

So, it is biochemistry instead of biophysics. The picture above came from a biophysics course note.

@latra If you want to see the real flow of the electrons on the molecular level, this is mixed biochemistry-biophysics.

Yes, I indeed want to see the real flow of ....photon...perhaps also electron...But is it possible?

what is wrong with the fourth paper ?  http://www.sciencedirect.com/science/article/pii/S0968000401020345   i got only junk codes

@latra I don't know, it worked. I have updated this to a different source, which should be ok.

no...the same...the title, the abstract, the figure caption and the section heading...are all in Greek letters........

You said in the above that Mn is the center of reaction. I think you are talking about type I RC. Only type I RC contains Mn.


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Why do many people seem to prefer unhealthy compared to healthy foods?
I don't have any concrete statistics on this but many of us seem to love the taste of food that is unhealthy for us.
Over the centuries, wouldn't it have been a non negligible advantage to those who preferred (and hence ate) healthier food?
So, why don't most of us inherently find healthier food to also be tastier?
Apologies if this is a silly question or something that is frequently asked. I know very little about biology in general.

I blame cavemen and biochemists....

It's a very simple answer. "Unhealthy" foods, for example potato chips, sugary drinks, and other fatty, cheesy or sugary edible items, have only been around a few hundred (at most) years. In prehistoric times (before agriculture, when the primary source of food was hunting and gathering), when food was scarce, fatty and sugary foods would be of great importance. They would supply the body with large quantities of energy (a gramme of fat gives about 9 calories, a gramme of carbs gives around 4 calories). Since we survived mostly on fruits, vegetables, meat, and whatever roots we could find, something as energy rich as, say, a serving of deep fried cheese covered bacon would have sustained us for days. So eating anything with high calorific value, like a fat rich tuber would release 'feel-good' chemicals, like dopamine and serotonin, among others, which make us feel happy (dopamine is also released in response to hugs and accomplishing goals, serotonin is released, in very large quantities, during nicotine consumption).
Our body these days just isn't used to our relatively sedentary lifestyle with  guaranteed food. Our body still hoards fat like it did during our time as hunter-gatherers, and our body still secretes dopamine everytime we dig into a sumptuous serving of cake.
A couple of good sources:
http://www.ncbi.nlm.nih.gov/pubmed/8697046

Serotonin-releasing brain neurons are unique in that the amount of neurotransmitter they release is normally controlled by food intake: Carbohydrate consumption--acting via insulin secretion and the "plasma tryptophan ratio"--increases serotonin release; protein intake lacks this effect. This ability of neurons to couple neuronal signaling properties to food consumption is a link in the feedback mechanism that normally keeps carbohydrate and protein intakes more or less constant. However, serotonin release is also involved in such functions as sleep onset, pain sensitivity, blood pressure regulation, and control of the mood. Hence many patients learn to overeat carbohydrates (particularly snack foods, like potato chips or pastries, which are rich in carbohydrates and fats) to make themselves feel better. This tendency to use certain foods as though they were drugs is a frequent cause of weight gain, and can also be seen in patients who become fat when exposed to stress, or in women with premenstrual syndrome, or in patients with "winter depression," or in people who are attempting to give up smoking. (Nicotine, like dietary carbohydrates, increases brain serotonin secretion; nicotine withdrawal has the opposite effect.)

http://www.scientificamerican.com/article/addicted-to-fat-eating/

Like many pleasurable behaviors—including sex and drug use—eating can trigger the release of dopamine, a feel-good neurotransmitter in the brain. This internal chemical reward, in turn, increases the likelihood that the associated action will eventually become habitual through positive reinforcement conditioning.

http://www.ncbi.nlm.nih.gov/pubmed/8697045

There is an intimate relationship between nutritional intake (eating) and serotonin activity. ...
Traditionally, serotonin has been linked to the macronutrient carbohydrate via the intermediary step of plasma amino acid ratios.

TL;DR:
You would have starved if you didn't eat fatty foods back before we had food so readily available, so your body automatically stocks up in case you ever run out.
Watch this video for more information:
Why our brains love junk food

You had me at "deep fried cheese covered bacon"

@MattDMo deep fried cheese covered bacon is a health food, though - right?

http://theawkwardyeti.com/comic/salad/

The primary source of animal fat was probably the marrow inside animal long bones, which was inaccessible without tools.  So, it's an evolutionary advantage to like animal fat.

@MalharKhushu It would be great if you can add a citation. Youtube videos are fine as a learning/teaching tool but are not, by themselves, strong references. The video does cite a PNAS paper and some other references. Can you please add those references (and others, like cross references from the paper, if necessary) along with the video link?

Great reply, Malhar Khushu!
One additional point... In reference to the cal/g energy densities of fats and carbohydrates, Alcoholism may be positively influenced by the 7cal/g density of ethanol!!! Yay science

sorry for a not scientific answer, this is general knowledge.
you can try to search for proofs you need.
there are several different types of unhealthy food and the resulting addiction/desire to eat them. the unhealthy food tricks the brain.
cholesterol/carbohydrates:
the brain is built from cholesterol partially.
the brain can make cholesterol from carbohydrates.
so so-called "unhealthy" food it is good for you kind of. unless you are sick.
so some times a moderate amount of cholesterol is good for you in general, the brain can make its own cholesterol. cholesterol supports memory.
cholesterol is bad if you have an internal wound like an inflammation, maybe of blood vessels or heart arteries. cholesterol made by the liver usually patches the would holes. later to be fixed using protein(if there is also vitamin c). however, if there is an inflammation going and there is a wound filled with cholesterol, new cholesterol will stick to already existing cholesterol. and clog arteries worse.
depriving the brain of cholesterol deprives memory. because neurons make vesicles - like small soap bubbles filled with dopamine that marginally pre-excite neurons. those vesicles are made of cholesterol. if you ingest something that dissolves cholesterol for a long time like a statin or antioxidant you will lose memory and lose the ability to form memory.
also, the brain is energy hungry, so it brain gets activated on high energy foods. however, if fructose or sugar is ingested with food. a large percent of it is stored into fat. using insulin that is made from sugar.
chemical foods:
like things that make the brain make neurotransmitters like acids, ions, and sweet poisons are bad for you.
they trick the brain and stress the brain. things like coffee and sugar and sodium glutamate. coffee makes adrenaline and ticks you to release saved energy.
sugar acts on dopamine center and tricks you think you do something good even if it is bad. sugar also gives you some glucose. however, all dopamine from sugar is consumed immediately.
some other things dopamine-making:
the brain seeks dopamine, and while on dopamine the brain does not think rather acts as before in an automatic manner. like, do the same thing again. also if the situation not as before the brain will mistake. sometimes brain confuses one thing to another. because they both make the same level of result. one real one fake. the fake quicker and you need to do it again and again. so people fall for a quicker and easier way. the solution is to delay time, to prevent instant action and try to solve basic body needs like rest and food


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Assuming if height was fully determined genetically, what would be the concordance between monozygotic pairs?
I fully understand the differences between monozygotic and dyzogtic twin pairings, but I wondered how I could put into words the reasons why the concordance would be very high.

Derived from same zygote, so precisely the same genetic material from mother and father.

Would this suffice as a scientific answer?

This is a homework (or homework-like) question. Can you please show your thoughts and your efforts at answering the question.

I feel as though monozygotic twins would have low concordance at birth because of the clear disparity in terms of nutrition etc during pregnancy and the fact they're not yet fully developed (development obviously follows genetics mainly, with nutrition being an influence but not to the same level)

Low birth weight can be an environmentally associated phenotype for example

If height was fully determined genetically (and no trait is), then concordance between monozygotic pairs would be almost perfect, modulo some variation due to somatic mutation in early development (e.g. a mutation happens in in cell directly after the embryo splits).

Thanks for explaining this for me so well Dermot.
I was just wondering, if I had two sets of data for concordance between sets of twins at 8 years of age, with concordance values being 0.94 for monozygotic and 0.49 for dizygotic twins, would this suggest that height is largely controlled by genetic factors?
I personally think it clearly implies an important influence, but the data set might not be large enough and also we have factors such as nutrition to consider.

Yes, it would imply that the trait is almost completely determined by additive genetics. If you assume identical twins are as similiar in their environment as dizygotic twins (which twin studies do), then environmental factors like nutrition should be controlled for, and there are simple models you can use to account for sample size. There are a LOT of caveats to all this though, it's a complex field. There are good recommendations for books on population genetics on this forum that i recommend you pick up, if you want to do this kind of analysis.

Fantastic thank you for helping me out!
Just out of my own personal interest, how come the concordance at birth in my data set is so low for monozygotic twins? Is it linked to the idea of shared nutrition in the womb etc?

Does anybody out there know why the concordance at birth might be so low for monozygotic twins?

@DermotHarnett If I may... Even in absence of environmental variances, there is also developmental noise (such as cellular noise during development) that may account for little variation too. But... obviously it is a detail does not necessarily need to be raised on this post :)

Remi.b - yes, that's one reason why 'no trait is'. The full genetic determination would imply the absence of developmental noise. The 'environment' term in the breeders equation includes everything that isn't genetic.


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Are there available fluids that can be used in place of blood to facilitate oxygen and carbon dioxide exchange during major surgery/trauma?
Are there any available fluid alternatives that can be used instead of blood replacement that adequately exchange oxygen and carbon dioxide?

I'm not sure I follow your question - - - are you asking if another fluid can be used in the airways to help exchange oxygen and carbon dioxide?

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

No sir. I meant are there alternative IV fluid that can help to transport oxygen in the cardiovasular system in cases like major sugery where parallel blood infusion can't  meet up with the rate of blood loss. Thanks


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Can dead scorpions still sting?
I found a dead scorpion on the sidewalk today, and brought it home, being careful not to touch its stinger. Bees can sting even after they are dead, if you step on them in such a way that it pushes their stinger out.
Does the same apply to scorpions?  Do I need to be careful not to touch its stinger?

Yes, the bark scorpion can still sting after death. I learned this myself after stepping on one. As I make a nightly habit of patrolling inside my home for their presence, I can conclude the offender had died within 12 hours of my stepping on it. When they die their tails stretch straight behind their bodies, this was the position I found it in.


text:
Do goosebumps always appear in the same spots on the skin?
Often one gets goosebumps when one is cold. I am curious whether the precise location of the goosebumps on, say, one's leg changes from occurrence to occurrence or not? In case if their precise locations are always identical is there anything particular about those locations that differentiate them from other parts of one's skin?
Thus the question: do goosebumps appear at the same spots on one's body every time or their exact location changes?

Goosebumps are caused by the contraction of the arrector pili muscles, which are attached to hair follicles. Accordingly, they appear at the same spots on one's body every time.


text:
Growing Mouth Bacteria in a bowl of sugar water
I want to teach my nephew why brushing in necessary and how sugar in mouth reduced by bacteria to acid.
I plan to put sugar mixed water in bowl and take swab from his mouth and dip in bowl, and test ph using Litmus paper to show him that sugar is converted to acid.
Is it possible to grow mouth acid making bacteria in this solution and will it change pH enough to show in litmus paper?

It's really going to depend on the concentration and type of microbiome... and it'll probably be more complicated than just "put bacteria in sugar water"; the concentration of sugar has to be low enough not to dehydrate the bacteria, you'll also need some salts and nitrogen source, again in low enough concentrations.  The simple answer is probably "try and see," because we don't know the exact paramaters.

I like the concept of this demonstration for teaching science!
As rotaredom's comment pointed out, bacteria does not grow in plain water with sugar. Bacteria require a nitrogen source, trace minerals and vitamins to grow in significant numbers.
I have a few recommendations that you can try, but I attached an extensive guide to kitchen microbiology below.

Growing the microbes in diluted milk (~ 1:10 dilution) + salt (a pinch for half glass) with and without added sugar (1 teaspoon for half a glass) might be a good starting point. Add yeast extract if you have some (not bakers yeast, but this is the killed version of that).

Make sure to boil and cool the milk, the container and other ingredients to keep conditions sterile.

Avoid a cotton swab if you can (as the cotton might not be sterile), I would take some milk solution, swirl it in my mouth and spit it back into the same container.

Also have a sterile culture in the experiment, without the oral microbes for comparison and a great teaching point.

Grow the microbes for 2-4 days with an air permeable cap (the air allows faster growing aerobic organisms, the cap ensures dust does not fall in)
Extensive source: Microbiology at Home: A short non-laboratory manual for enthusiasts and bioartists
PS: I'm studying PhD to be a microbiologist


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How is omega 3 deficiency determined?
I read quite a bit online about omega 3 deficiency. How is this actually determined - that is, what happens in the lab to determine this ?
n-3 fatty acids have roles in many different human tissues, so does the definition of sufficiency vary depending upon which tissue is being studied ?


text:
When can helices form coiled-coils?
The other day, my teacher suggested we find out whether a chain of the following amino acid sequence would be able to form a coiled-coil:
N-KIAEVRAQYEDVANKVRLIVE-C

Now, I can see that the chain is not amphiphilic as it does not alternate between polar and non polar amino acids. But when I come across an exercise of this type, how do I determine if it can actually form coiled coils? I can feel this will be a question on the final test.
All help is deeply appreciated.

http://onlinelibrary.wiley.com/doi/10.1002/cbic.200300781/full

Thank you so much!! I still have the same question. In every article I read, it says: A and G positions are typically hydrophobic. Why typically? Can positions that are not A and G be hydrophobic and still make up a coiled coil?

I don't know, but I expect that exceptions to the rule can be tolerated. You should ask your instructor what they are expecting from you.

Okay, thank you anyway for trying to help me. I, too, think that exceptions can be tolerated just by looking at alpha-keratin sequences that have so many exceptions and yet they form coiled coils! But it is hard to translate to simple cases as the one I proposed above. Thanks again!


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How well do ants and other insects smell odors other than pheromones, or are they highly tuned to pheromones only?
I have a vague understanding that ants and moths use pheromones in a variety of ways, but recently after a heavy rain my office is being explored by a some small ants looking for food. They decided it was a potentially interesting area to explore after finding a drink lid that had left on my desk. That the ants left a pheromone trail for other ant's to follow I understand, and after removing the lid, the number of ants has gone down as expected.
However this morning I came in put my Starbuck's  (Mocha with an extra pump of chocolate) on my desk and after a couple of minutes saw what appears to be the last remaining little ant climbing up the side of the cup. So my question is:
a) Was the ant just very lucky? Wandering around anyway and encountered the cup?
b) Did the ant smell the Mocha/coffee and decided to investigate because it smelled like there was something good in the area?
This led me to wonder how much insects use their sense of smell to find food. I was generally aware that flowers are brightly colored and some patterned in the ultraviolet, and I guess it might be obvious that flowers also might smell good and flies are attracted to rotting flesh etc. I think I also read some time ago Luna Moth's find each other by airborne pheromones and the antenna are very sensitive and they can follow the gradient to find the moth to mate with.
So do ant's find food by smell? How much do non flying insects depend on smell to find food?
Thinking about it, it must be yes, but are there specific 'food' molecules ants are especially responsive to?

Insects are highly developed to respond to smell. The fruit fly, Drosophila melanogaster, has genes for over 50 odorant-binding proteins which can be found here and genes for over 120 chemoreceptors, which include both odorant receptors and gustatory receptors.
There is a link to the FlyBase entry for each gene where further information can be found.
There is less information about other insects, but indications are that each has a large repertoire, honed to its particular sources of food.

Interesting, I am guessing that flying insects would tend to develop more sophisticated smelling mechanisms, but have no evidence to support that.


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Identification of protozoa under microscope
I observed maybe Protozoa from standing FRESH water and from slowly flowing FRESH water. I am complete dilettante. Can you tell what these creatures are?
https://www.youtube.com/watch?v=6D5ck3zNJzA&t=474s
Thank you.
Added picture for to be more specific

What level of magnification was employed within the video?

something around 200 I guess

Please put a snapshot of the organism that you want to identify, instead of linking to youtube.

I cut it from the video, it is not very good, but at least it is specific.

At first glance, the organisms may hold the appearance of protozoans like ciliates. However, I am of the belief that these 'totally tubular' micro organisms are in fact diatoms.
The diatoms are a diverse range of eucaryotic microalgae which comprise a large percentage of the phytoplankton group. (Diatomaceous earth is the residual remains of their calcareous walls)
They are likely diatoms because of their apparent hard membrane, and slight brown-green pigment, typical of heterokont diatoms.
I would be unable to specify the organism to family level. However, you may wish to complete your investigation by looking under the order 'Pennales'.
For general information regarding the Diatoms, you may visit https://en.wikipedia.org/wiki/Diatom
Morphology and description available from: https://books.google.co.uk/books?id=xhLJvNa3hw0C&printsec=frontcover&source=gbs_ge_summary_r&cad=0#v=onepage&q&f=false
Good luck

Ok, as noob I need explanation. You mean they are not Protozoan rather algae? And by "they" you mean those which are smaller, but there is plenty of them with "balls" at the end and at beginning and also in the middle of the cell?
(i hope someday make better video with known magnification).

I also asked my former biology teacher and she guessed "Diatomeae". Though I have to google it and translate it.

@weatherman It is likely that your teacher were indeed referring to the Diatom class. 'Diatomea' is deemed a synonym for the Diatom class Bacillariophyceae: https://en.wikipedia.org/wiki/Diatom


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How do we sweat immediately after drinking water on a hot day?
On hot summer days, when I drink water to quench my thirst, my body immediately responds by sweating in 5 to 10 seconds or maybe less. How does our body detect the presence of water in the stomach so fast. Does our body detect the sudden decrease in temperature of the stomach or is it by some other mechanism. Why do we sweat after drinking water in the first place. Is it to remove the excess water or to cool the body down on a hot day?

interesting biology experiment: lemon balm is one of the most comment garden herbs, that looks a bit like mint, and that grows in most gardens and wild. If you drink it in a tea, it causes immediate sweating. check wiki if you want. I tried some on a hot day and i was immediately cooled by profusive sweating. cool. https://www.anniesremedy.com/diaphoreticsudorific-property-39.php

Me too, same situation.  Happy to see i am not alone

Not everyone sweats in seconds after drinking water in summer.
Also, sweating in seconds after drinking water is not likely due to water being absorbed (Nutrition Reviews, 2015):

Ingested fluids are not immediately available for assimilation into
  the body. They are initially stored in the stomach, and there is
  little net absorption of water or solute across the gastric mucosa.

There are a lot of receptors, including stretch receptors and various chemoreceptors, in the stomach, so your stomach will likely recognize water as water and signal the brain via the nervous system, probably via the visceral afferent fibers.
One of two things may then happen:

Your brain can perceive a sudden appearance of water in your stomach as stress and react with sweating, like when you are embarrassed or excited.
When dehydrated, you sweat less to prevent further dehydration; when your brain recognizes there is new water in your stomach, it can now allow the signals coming from warm skin to trigger sympathetic nerves to release some sweat to cool you down.

Thanks for the answer. Do you have any idea why this is more likely in summer? And not everyone? Why me? It's cool to know that we have chemoreceptors in the stomach. Is there any other   normal day-to-day situation when we can be aware of the chemoreceptors in the stomach?

If it's only in summer, it's more likely related to thermoregulation, as I suggested in my second hypothesis (in winter it may not be warm enough to sweat). Why not everyone? Because there can be great personal differences in how someone reacts to "stress" (water suddenly appearing in your stomach). It may be partially psychological. It's like when people are embarrassed or scared, but not everyone responds by sweating. Other examples or receptors: The stomach can detect the amount of calories in the food and releases only a certain amount of calories in a certain time into the intestine...

...Stomach can detect toxins from spoiled food and signals the vomiting center in the brain, which induces vomiting. Most gastrointestinal receptors are associated with nutrients and satiety, though.


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Identification of a young tree in the alpine region of southeastern France
I have a young tree growing in my backyard (in Grenoble, France), and I was not able to identify it, despite searching with many identifier tools.
It's 2 years old now and must be 2 meters high. It has a grey trunk, its leaves grow on brown/red stems that protrude irregularly from the trunk.

The leaves are pointed, gently serrated, covered with a light fuzz, with a distinct lattice of veins.

Could you help me identify it?

This reminds me of "lilas" (Syringa): http://www2.csdm.qc.ca/st-fabien/projets/arborophile/Lilas/lilas.htm I'm not at all confident about the identification, though.

I have a lilas nearby, unfortunately they do not look alike. The lilas leaves are smooth and go two by two. Sorry for taking so much time to reply. The tree is still growing really fast, some of its leaves are huge, but there is still nothing more to help identification, no fruit or flower.

Could you add a photo with a zoom on the connection between a leaf and a branch?

The tree grew its first fruits this spring, so that I could definitely identify it: it is a goat willow! This is consistent with its spontaneous sprouting in my yard, as it is a common tree in my region.


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How can I estimate the total number of yeast cell in a medium?
So I want to run an experiment with yeast. I want to monitor the population as close as possible in regard to its size. I am aware I could use a colorimeter or such, but I can only get a microscope. Is there a way I can estimate the population with a microscope?

Determination of cell concentration using a microscope is usually done by using a hemocytometer, also called counting chamber or Neubauer-counting chamber.
Basically, you count the cells in a defined volume within a specific area. This way you can calculate the concentration in your medium and also the total cell count.
I found a good explanation especially for counting yeast cells here.

Is there a way to find the concentration without using a hemocytometer?

@BrianBlumberg You can plate the cells after serial dilution and count the colonies. Since you mentioned that you want to use a microscope, you need to use a haemocytometer; you cannot estimate true concentration on a normal slide. Also, haemocytometer is more accurate than OD, if the cells have different sizes.


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How can I measure the population growth of yeast?
I will soon have to carry out an experiment. I want to estimate the rate of growth of a population of yeast, although I don't know if it is possible to at least estimate the number of yeast bacteria in a set yeast population. Does someone know of a way this can be carried out? Thanks.

Otherwise, is there any other fast growing organisim that someone can recommend me to use in my experiment? I am looking for an organsim whose population increases rapidly (such as yeast) and that the population growth can be effectively measured.

The standard way to measure growth in a liquid culture is to measure the optical density (OD) of the solution – basically, how cloudy it is. Bacteria or yeast in a solution will absorb light that passes through it, making it more cloudy (or turbid). Within a certain range of turbidity, the OD of the solution is directly proportional to the concentration of organisms in the solution, and you can use it to accurately estimate the population in your sample. Outside of this range, you'll need to accurately dilute your sample to get it into this linear range.
Generally, we use a spectrophotometer to measure absorbance of red-orange light (this is called OD 600, for optical density for light with a wavelength of 600nm). A google search turns up a number of plans to make cheap, homemade spectrophotometers that could let you take these measurements without having access to a lab, though I can't speak to how accurate they may be. You might also look at home-brewing supplies, as brewers are also interested in measuring yeast growth and tend to have lower budgets than molecular biologists.
You only need a spectrophotometer that uses visible light to measure bacterial/yeast growth. Many specs also work in the UV spectrum which allows them to measure DNA concentration, but you won't need that.


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Can a gene transfer from a plasmid to a bacterial chromosome?
Plasmids are involved in providing resistance to antibiotics. So, can that gene or any other gene transfer from the plasmid to the bacterial chromosome?
Is there any chance where antibiotic resistance is conferred by chromosomal DNA (not plasmid DNA)?

Briefly: yes.
It has been known for some decades that plasmids (including those that encode antibiotic resistance) can recombine with the host genome.
Indeed, the selective pressure to perform such transfers makes it possibly more interesting to infer why it doesn't happen (in appropriate contexts), for example in this paper.


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How does changing the shape of ATP synthase specifically prevent the enzyme from working any longer?
I am currently stuck on working out how to answer this question:
"A random mutation causes the enzyme ATP synthase to change shape so that it can no longer function. Describe the impact this would have upon respiration and the overall production of ATP."
My question is: How does changing the shape of ATP synthase specifically prevent the enzyme from working any longer?

That shouldn't get you stuck - just delete the word "shape" from the question (since it doesn't affect the answer).

If you look at an enzyme and its substrate you can also see this as a lock (the enzyme) and the key (the substrate). The key fits the lock and opens it, the substrate fits into the active pocket of the enzyme and a reaction takes place. See this figure for illustration (from here):

If the enzyme (or the substrate) changes its outer shape (this is what happens when amino acids of a protein are changed), this fit will not happen anymore and the reaction which is catalysed by the enzyme will not take place (the lock will not open).


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Why do cells in meristematic tissues lack vacuoles?
Cells located in meristematic cells in plants lack vacuoles. However, this contradicts with the fact that plant cells have large vacuoles to store water and keep the plant in an upright position. I would also like to add that meristematic tissues are generally found in roots and stems of plants. Finally, I would like to ask why do meristems lack vacuoles?
Sources

Turgor pressure exerted by the vacuole is also essential in supporting plants in an upright position: Wikipedia

Apical mertisem is present at the growing tips of stems and roots and increases the length of the stem and the root. The girth of the stem or root increases due to lateral mertisem (cambium): Science for Class 9 by National Council of Educational Research & Training, page number 69

Cells of meristematic tissue are very active, they have dense cytoplasm, thin cellulose walls and prominent nuclei. They lack vacuoles: Science for Class 9 by National Council of Educational Research & Training, page number 70

Please do not edit the title to "answered", please accept the answer.

@Chris Well, I need to wait sixteen more hours to do that. Thank you!

I haven't looked at the times :-) It would be good if you could do it, then it is marked as answered and accepted on the starting page.

Meristematic tissues or meristems contain cells which can rapidly divide or reproduce and is responsible for the overall growth of the plant. Apical meristems and lateral meristems are found in the roots and stems of the plants. Please note that the whole stem or root is not laded with these tissues. Plant cells usually have a large central vacuole which applies turgor pressure to keep the plant upright, as mentioned in one of your sources.
The tips do not require to be very stiff and straight. So, a central vacuole is just not required. Also, meristematic cells grow various organelles as they mature.


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Cell division - meiosis
Really confused. How many chromosomes pairs do humans have in their sex cells? How many single chromosomes do humans have in their sex cells?

Human sex cells, or gametes, have 23 chromosomes - they are haploid. Somatic cells are diploid - they have 23 pairs of chromosomes, for a total of 46.

To add on @MattDMo's comment, each chromosome can be made of a single or two chromatids depending on the phase of the cell cycle you are in.

Terminology is what is holding you back.
What chromosome implies depends on context, i.e. is it replicated or not.
In Meiosis. Gametes arise from Germline cells that have 23 PAIRS of chromosomes. That means, that while there are 23 different chromosomes they come in doubles/pairs. This is the typical X like shape we think about when we hear chromosomes.
Another way, chromosome can means either 1X or 2 single chromatid
MEIOSIS I -- 23X chromosome pairs are duplicate and end up as 46X chromosome pairs (46 pairs of X OR, 92 separate chromatid)
These 46X are divided equally among two daughter cells just like in mitosis. Where now each daughter cell receives 23X = 23 pairs.
MEIOSIS II. The daughter cells in end of Meiosis I divide without DNA replication and the 23 pairs are split among 2 new cells. So now each new daughter cell (in total 4) has 23 individual chromatid (individual chromosomes)
and these are the gametes.
When the gametes fertilize to form a zygote, the zugote product ends up 24X each.
Each X contains, 1 chromatid (|) from the father and 1 chromatid {|} from the mother.
Haploid means once copy of each chromosome.
23
Diploid means two copies chromosomes or 23X
Ref
- Allison Q.N,.(2015), Freeman Biological Science.

Gametes have 23 PAIRS of chromosomes. No. Gametes have 23 chromosomes - they are haploid. Somatic cells are diploid - they have 23 pairs.

Cheers MattDMo cleared it up.


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Can lactate be created in ketosis?
After looking at Cori Cycle (from wikipedia)

I have a question about how the lactate can be produced in ketosis. According to this article:

in a low-glucose state, where the body senses that dietary glucose might not be coming anytime soon, peripheral insulin resistance is triggered. This prevents the muscles from taking up “precious” glucose that the brain requires. The brain’s sensitivity to insulin is preserved, allowing it to grab what glucose it needs from the paltry – but sufficient – levels available to it.

it seems that the glucose is not even transfered into muscle cells. In spite of this fact, the lactate is still somehow created during hard exercise even in full ketosis when ketones are present in the bloodstream. How is it possible?

First, there are inaccuracies and misconceptions in the article you quote, which also relates to obese people with insulin-resistance (pre type II diabetics) rather than normal people. These are:

I’m not sure what a “low glucose state” is supposed to mean, but the tissues of the organism co-operate to ensure that the blood glucose concentration normally never falls below about 4 mM, with a range of approx. 4–8 mM. Thus, glucose is available in the blood for tissues that can take it up in a particular circumstance. These are not “paltry levels”, as quoted.
The body’s metabolism cannot predict the future. The scientific credentials of anyone who writes “the body senses that dietary glucose might not be coming anytime soon” are hardly to be trusted. (I don't think much of his literary style either.)
In short-term starvation, when the blood glucose concentration falls towards the lower end of its range, insulin resistance is not triggered. Insulin secretion from the pancreas stops (and glucagon secretion starts).
The brain is not sensitive to insulin (i.e. its glucose
transporter(s) is not), whereas the muscle is. This is what allows the brain continued access to glucose.

Some of this is elaborated in my answers to: “What is the purpose of gluconeogenesis?”,  “How do muscle cells synthesize glycogen?” and “During starvation, does the human body do anything to prioritize which organs receive nutrients?”. A section from Berg et al. may also be of interest.
Answer
Lactate can (and must) be generated by non-aerobic muscle metabolism (i.e. in muscle lacking mitochondria) during exercise because anaerobic glycolysis, with conversion of pyruvate to lactate, is the only way the muscle can obtain ATP to power its contraction. The source of this is the glycogen stores laid down in the muscle after a meal, and glucose taken up from the blood.
I don’t know anything about low-carb diets, but I assume they include protein, so that some of the amino acids from this can be converted to glucose by the liver (glucogenic amino acids) as well as those that cannot (the ketogenic ones that can give rise to ketone bodies). Even if the blood glucose is at the lower end of its range, in the non-starved state the muscle can take it up from the blood. (The blood glucose will be restored by the so-called Cori Cycle.) Even in starvation, if the muscle is working there will be a concentration difference between blood and muscle glucose that will allow uptake.
I think that this question is provoked by the feeling that the existence of ketosis means that glucose is not available to cells. This, as I hope I have explained, is a misconception, perhaps arising from confusion with the different situation of ketosis in long-term starvation.
Finally, there are other sources of lactate besides muscle, regardless of diet. One is the erythrocytes which lack mitochondria and therefore can only use anaerobic glycolysis to produce the ATP they need for active cation transport etc.

Thanks for clarification and links. It's the case for long-term ketosis - how is  the situation different?

Can you clarify a couple of things so that I know 'where you are coming from'. When you say 'long-term ketosis', do you mean as a result of following this low-carb diet for a long time? And what is this balance of carb/protein/fat in the diet that is producing this ketosis? Also, why are you so concerned about lactate — do you have figures for it or is it just a general concern?

80% fat, 20% protein and trying to avoid carbs for 3 months. I have no figures about lactate, it is just curiosity - I was not sure which articles should I trust.

In the circumstances I wouldn't expect any difference from what I have in my answer (although I'm not a nutritionist). If you are feeling well then you obviously don't have low blood sugar. I presume that the ketone bodies produced from fat and ketogenic amino acids are helping offset the brain's need for glucose and the glucogenic amino acids and any carb is keeping the blood glucose normal and allowing the muscle (and brain etc.) to replenish glycogen stores when needed. Assuming that you are an athlete, your usage will depend on which muscles you use for sport.

Answer
Even in ketosis, your body still needs some glucose for certain functions, like brain activity and high-intensity exercise. When you’re in ketosis for prolonged periods, your body gets glucose from several sources:
Gluconeogenesis: This is the process of creating glucose from non-carbohydrate sources. Your body can convert amino acids (from protein) and glycerol (from fat) into glucose to ensure there's enough available for necessary functions.
Glycogen Stores: Although limited, your liver and muscles store some glycogen. When needed, these stores can be broken down into glucose. During prolonged ketosis, these stores are typically quite low.
Dietary Intake: Even on a ketogenic diet, there are small amounts of carbohydrates consumed that can contribute to glucose levels.
These mechanisms ensure your body maintains a baseline level of glucose, even while primarily burning fats and ketones for energy.
Also, when you're in ketosis, your body relies more on fat for energy instead of carbohydrates. This can reduce the amount of lactic acid produced during exercise because less glucose is metabolised anaerobically.


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eye myopia power changes with brightness
Is there a condition where myopic power changes with ambient brightness. When I drive in the morning in bright sunlight my power is -4.0; however when I wear the same -4.0 glass in the evening (dusk time and night) I cant see properly. The images are blurred. I have to change to -5.0 glass. However the same situation does not happen in my right eye which has a constant -5.0 power in both daylight and night. I have observed this for many years (15+).

NIGHT MYOPIA -  is a tendency for eyes to become near-sighted in dim illumination.  There are multiple theories explaining the phenomenon, most of them are related to accommodation or chromatic shift in scotopic light conditions when to light is focused before the fovea thus worsening the existing myopia.
Citation:

In dark adaptation the eye becomes more sensitive to shorter wave
  lengths (Purkinje shift- In the light-adapted eye the region of
  maximal brightness is in the yellow; in the dark adapted eye, the
  region of maximal brightness is in the green),and visual acuity
  depends on parafoveal blue cones. Shorter wavelengths come into focus
  in front of the retina, and this chromatic aberration accounts for
  some of the relative myopia that a normal eye experiences at night;
  much of the remainder is due to an increase in accommodative tone in
  the dark.  It is also called dark focus of accommodation, or tonic
  accommodation, or resting state of accommodation. Consequently, a
  measurement of the refraction (i.e. the determination of appropriate
  optical glasses to obtain good vision on these distant objects) gives
  the result that the eye is myopic. Night myopia can reach values of up
  to about - 4.0 D. Night myopia decreases with age31 and therefore it
  can be of special importance for young drivers at night. In one
  experiment with people aged 16 to 25 years, 38% had night myopia of -
  0.75 D or more, and 4% had – 2.50 D or more. Cause of Night Myopia:
Spherical aberration (The optical effect of the larger pupil decreases
  the depth of focus) Chromatic aberration. Parkinje shift Ciliary spasm
  At low light levels there is a change of the biochemistry of imaging
  on the retina: in bright light the receptors in the retina are cones
  with higher image acuity, and imaging of colors, whereas in low light
  the receptors in the retina are rods with reduced image acuity, and
  imaging of black and white only. The transition between both states,
  i.e. to get maximum sensitivity when moving from the bright to the
  dark, doesn't happen immediately, but takes some minutes33. This is a
  problem e.g. when driving a car in sunlight and entering a tunnel. The
  low light imaging by rods in the retina can be further reduced by a
  lack of vitamin A and zinc Symptoms:
  1. Blur vision only in low luminance.
  2. Feeling discomfort while maintaining fixation in low illumination level.
  3. Difficulty in night driving.
  4. Hallows around light.

While this link may answer the question, it is better to include the essential parts of the answer here and provide the link for reference.  Link-only answers can become invalid if the linked page changes.

@SatwikPasani thanks for your constructive comment. The  answer changed appropriately.


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Pippin prep kits - expiration date
Do you use Pippin prep? We would like to buy it, but we need more info. What is the expiration date of kits for Pippin prep? Thanks!

Have you contacted the manufacturer to ask?

@Atl LED of course yes, but they dont answer yet. I need this info right now :)

You tried calling 800-284-8474 and they didn't know off hand?  Ask to speak to tech support if you don't get anywhere else.  Best not to make lab purchases when you have to make a decision in less than half a day...

According to this document (page 11) the shelf life for the cassettes is 1 year. The other ingredients (running buffer, DNA size markers, loading dye) appear to be standard reagents. Of those, the DNA size marker will probably have the shortest shelf life, but it stands to reason that the reagents should have a shelf life at least as long as the cassettes, seeing as only their shelf life is mentioned. It is possible to buy reagent replacement kits.


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Do you have experience with PacBio?
I prepare a experiment and I found $PacBio SMRT$ as the great way to sequence my PCR products. I find the cost: library preparation 655 dollars + sequencing 435 dollars. It seems very low. Do you have some experience how much of sample can I sequence in one run (by coverage around 30) and if it is really for this price?

If it is a good idea to use PacBio depends a lot on what you want to sequence and what you want to do with the data you get. In short: you get longer reads but about 15% error per base. This means, you will have to cope with those errors, there are possibilities to do that. How much coverage you will get of you sample I cannot tell you, as I do not know what kind of sample you want to sequence.
How much data you get out of one SMRTcell depends also on the chemistry, I think it currently is between 275 Mb and 375 Mb, depending on chemistry. They have a nice brochure you could look at.
Anyway, you probably will have to get some advice by a bioinformatician of you choice on how to design and analyse your sequencing experiment.

I am planning to sequence mouse genes of MHC a TLRs (about 2000 bp). Can you get me a fictitious example about how much sample can I involved by certain covarage?? Thanks a lot! ;)

I have never done this calculation for a sample this small with PacBio. To keep it short, from one SMRTcell you would get 30x coverage of the E. coli genome (no fiction, they have done 3 cells and got 100x coverage). I guess this is a bit oversized for your short samples. Still, I would rather not do any more "virtual" calculations about this, you need to have someone you can talk to who understands your experiment and probably has seen more PacBio sequencing than I have.


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How to measure quality and quantity of DNA?
I would like to mesure DNA. I quantify the concentration with Qubit fluorometer, but I would like to know also quality of DNA. I try BioAnalyzer (Agilent),but without success. Bioanalyzer measure DNA samples from 100 to 7 000 bp (12 000 bp). Problem is that my DNA is not sheared, I would like to quantify whole mouse DNA. Have you any idea? Thanks!

You can run your DNA sample on agarose gel to see, whether you have significant degradation.
If you are interested in contamination, you can make a standard photometric analysis to assess the 260/280 and 260/230 ratios and absorbance at 320 nm on NanoDrop or even something similar to Eppendorf's BioPhotometer.
In case RNA may be an obstacle for some down-stream procedures, with Qubit you can also measure separately DNA and RNA concentrations and then decide if you have too much RNA and it's worth treating your sample with RNase.

I run DNA on gel...but I need some number for comparison...NanoDrop is probably the best option in my case :) Thanks!


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MTT assay normalization
Since the precise amount of cells in each well of an MTT assay varies, how can I normalize the results by cell number/concentration?
How can I take into account the number of cells that have already disappeared due to the action of a toxin applied previously as part of this assay?


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Is urine dirty as soon as it leaves the human body?
Human urine is sterile as long as it is in the human body. But is it dirty after leaving the human body? Could you get sick from it, if you drink it or don't wash your hands, for example?

It was believed for a long time that urine stored in the urinary bladder is sterile. However, Wolfe et al(1). recently found evidence of bacterial presence in the urine extracted from bladders of healthy women. In an article just published, Hilt et al. found that at least some bacteria found in the bladder of healthy women are viable and can be grown in a laboratory after extraction from the bladder).2 (Paywall). They expect that the same is the case for men.
From the Hilt et al. paper:

Thirty-five different genera and 85 different species were identified
  by EQUC. The most prevalent genera isolated were Lactobacillus (15%),
  followed by Corynebacterium (14.2%), Streptococcus (11.9%),
  Actinomyces (6.9%), and Staphylococcus (6.9%). Other genera commonly
  isolated include Aerococcus, Gardnerella, Bifidobacterium, and
  Actinobaculum.

Note that these species for the most part (Actinobaculum being one exception, as a possible uropathogen) appear to be part of the normal microbiome (collection of microorganisms) in healthy people in the same way as bacteria inhabit other parts of healthy persons. Additionally, the recovered organisms required special care to achieve growth:

Most of the bacteria isolated required either increased CO2 or
  anaerobic conditions for growth, along with prolonged incubation, and
  they often were present in numbers below the threshold of detection
  used in routine diagnostic urine culture protocols.

Thus, fresh urine is non-sterile but probably unlikely to cause infection in healthy persons.
In the process of leaving the body, there is a chance of contamination from organisms living in the urinary tract or on the surface of the body. However, if organisms picked up from the urinary tract made you sick, I except that you would already be having symptoms of an urinary tract infection, as the stomach is hardly a more forgiving environment. The risk of contamination from the surface of the body would depend on personal hygiene.
See also this question on https://outdoors.stackexchange.com/questions/264/is-drinking-urine-safe
Edit: This might go without saying, but apart from possible pathogens, there are of course other aspects of urine which makes it unfit for general consumption.


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Propagation of tool use in primates?
There are several famous cases of great apes demonstrating a surprising degree of wherewithal in communication and tool use - even monkeys can learn some tool use from each other observationally, even if "teaching" would be an exaggeration.
The ready availability of this information will preclude me from bothering to cite a palate of examples.
Has anyone ever considered, as an experiment, taking such primates which display exemplary tool use in the lab and (at least partially) reintroducing them into the wild and seeing if (perhaps specially crafted) tool lessons learned form us humans propagates among their fellows?
If not, why not?

Those that exhibit those behaviors are far too valuable to release. Also, biologists never interfere with natural processes if they can help it. E.g. they don't help a severely wounded animal in the wild because that would meddle with the natural order of things.


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From a purely biological perspective, how does an optimal human diet look?
There is hardly any subject as contested in the media as what humans should eat. Usually, such discussions are devoid of actual scientific reasoning, though they all claim to be backed by scientific studies (typically without naming those studies). The colorful spectrum of suggestions ranges from eating only bananas, to avoiding "refined" sugars and red meats, to avoiding meat altogether, to eating as much meat as possible etc. Clearly, many of them are completely contradictory.
From a purely biological, evidence-based perspective, how does an optimal human diet look? In particular, I'm interested in the following questions:

Is there a single diet that can be recommended to all humans, regardless of lifestyle, which only needs to be scaled in quantity (i.e. more physically active people should eat more of it) but not content?
Excluding diseases, does the optimal diet for an individual depend not only on their lifestyle but also on their genetic makeup?
Knowing nothing about their genetic makeup and living an average industrialized-society lifestyle, what is the best guess for what a human should eat?

Answers should be backed by solid reasoning and (ideally) references to verified (meta-)studies published in actual scientific journals supporting the claim. It seems strange to have to ask such a question, as one might expect it to have been answered thousands of times already, and of course it has, but the answers vary so wildly that I suspect I'm being fed hogwash mostly.

Is this question just a coincidence? See new topic at BioSE Meta: http://meta.biology.stackexchange.com/questions/556/policy-on-health-questions

I think you should refine your question, and split it into subquestions. This is really broad, and there are lots of diets out there. You should also define what you mean with optimal (what is the "target"?), since this could refer to e.g. keeping a healthy weight, nutritional balance, life span etc. Different diets may be optimal for different targets. Without a clear definition of a target, this question borders on primarily opinion-based ("what is the best...?").

No, there isn't a single diet that can be recommended from a biological perspective.
The most popular diet from a pseudo-scientific perspective is the Paleo diet, saying we should eat what our ancestors in the Paleolithic were eating, but it makes a mistake of forgetting that our metabolism has evolved since then. There are also numerous other flaws in the Paleo diet but I won't go through them all.
The most notable example to use here would be dairy products, as we're among the few species that can drink milk at adult age. Drinking milk as an adult isn't normal, and yet we evolved the ability to do so. Some individuals can't drink milk, same goes for consuming gluten, nuts, and several other things, but the species as a whole can consume all of the above. Some people must avoid certain foods because of their individual genetic makeup though. Most evolved to process gluten and this ability is greatly responsible for the fact that there are 7 billion of us now. If you read an article "gluten is bad", remember that gluten grew the human race and without it at least a third of the world's population would die through starvation. If you read an article about the Paleo diet, remember we wouldn't be here if the agricultural revolution didn't happen.
The correct answer would be - humans can consume everything that isn't toxic and provides them with energy. We're very capable omnivores, which is probably one of the reasons why we've done so well as a species. In other words, you won't die from eating processed sugar. There are healthier and less healthy foods, but none will kill you.
You are correct, there are numerous answers (or attempts to answer) to this question, and the way the research is concluded definitely doesn't help. Research is mostly conducted through polls designed to prove the scientist's original unverified claim, and virtually no research is conducted on the biological level, e.g. what happens to the body when you consume a certain carbohydrate. The whole field became pseudoscientific. The "food pyramid" is...pretty much wrong.
Body needs proteins, body needs carbohydrates, body needs fat. You could come up with a vague answer if you eliminate the foods that body doesn't need, such as processed sugars, but it's still energy and you won't die from consuming it.
There is no scientific research that consumation of any food, or elimination of any food, affects life span. Meaning, there's no differential survival rate depending on what you eat.
To put things in perspective, imagine a lion preoccupied with attempting to answer whether it would be better for his body to eat an antilope or a gazelle. 10.000 calories is 10.000 calories and if he eats either he'll live another day.

If by "the body needs carbohydrates" you mean carbohydrates in the diet, then I disagree. We can make all of the carbohydrates that we need from other nutrients (unless you class ascorbate as a carbohydrate). This is in contrast to both fatty acids and amino acids, for which there are dietary essential species.

I agree with you, I was just making a different point so this error slipped through. Thanks for pointing it out.


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Is bacterial "colonization" restricted to human body surfaces not the deep tissues?
This seems to be the point where the perspective of human beings from a medical viewpoint intersects with that from an ecological perspective.

Colonization is the presence of bacteria on a body surface (like on
the skin, mouth, intestines or airway) without causing disease in the
person. Gale Encyclopedia of Medicine

These bacteria [Enterococcus, Proteus, Pseudomonas, Micrococcus,
Klebsiella, Enterobacter, Serratia, Acinetobacter, and Citrobacter]
colonize deep tissues and may cause an immediate inflammatory reaction
but also may remain dormant in deep tissues. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4487244/

I'm confused now whether dormant microorganisms in deep tissues are "invading" the human being or merely "colonizing" it.
Is the process of reaching deep tissues almost always result in a disease?

The presence of indwelling medical devices (catheters, stents, etc.) should be considered when evaluating positive cultures from normally
sterile sites such as the blood, cerebral spinal fluid, pleura, etc.
If no such devices exist, then the isolate represents an infection and
should be treated.
https://link.springer.com/article/10.1007/s40121-022-00597-w

Maybe the mean (or the process) itself, not the end, what matters, in other words, bacteria getting into the blood vs. bacteria in the blood, but how and why? Maybe invasive factors, the factors how the organism reached the blood, are usually sufficiently immunogenic?

I think you should go and look up the terms invasion and colonization in a dictionary. Invasion just means entry into, colonization means setting up residence.

how do bacterial infections kill people?

Awfully big question you've put in the comments. Can you narrow it down and show your research, then post it as a separate question in its own thread.


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What is a reference strain in DNA-DNA hybridization DNA groups?

Results
DNA groups identified:
All intra-group relatedness values are shown in
Table I.
By means of reference strains, most of the DNA groups could be identified as groups described by Bouvet & Grimont (1986) and we
found it most convenient to number them in the same way.
**Tjernberg, I., & Ursing, J. (1989). Clinical strains of Acinetobacter classified by DNA-DNA hybridization. APMIS : acta pathologica, microbiologica, et immunologica Scandinavica, 97(7), 595–605. https://doi.org/10.1111/j.1699-0463.1989.tb00449.x**B

Table 1:

Is it decided with the "least square" method, so that the so-called reference strain is well representative of the DNA group despite the possible intraspecies variations among group members?
Does this mean that instead of comparing each member in each DNA group with those of Bouvet & Grimont, they compared only the reference strain of each group?

Have you read the paper any further? It looks like that's just a quote from the abstract. I can't access the paper, but given your reference to least squares as the way of picking them, I'm assuming that you have access. can you provide any further information where they describe how they choose or define reference strains?

The same statement is used elsewhere in the results of the paper. There is no mention of least squares, but I'm guessing.  I'm editing to mention more details.

"Instead, two other reference strains (ATCC 17925 and ATCC 9957) were investigated as representatives of DNA groups 8 and 9 described by Bouvet and Grimont (1). "
https://www.microbiologyresearch.org/content/journal/ijsem/10.1099/00207713-47-3-837#R1
another study calls these reference strains "representative strains" which makes more sense.

This is a question and answer site about general problems in biology. It is not a journal club, where one has to read a paper to discuss the validity of its results of methods.

What's wrong with you, i was asking what is generally meant by "reference strain" in the context of grouping strains by their DNA relatedness.

Do i have to refer every single study that includes this context so that I'm understandable that I'm not after a single article per se.


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Can Gravity convection incubators negatively affect the growth of strict aerobic bacteria?
Background
Gravity incubators rely on natural convection for heat distribution. There is no fan or blower system, and the heat rises from the heating element at the bottom of the incubator.

https://www.thermoline.com.au/blog/fan-forced-vs-gravity-incubators#:~:text=Gravity%20incubators%20rely%20on%20natural,as%20in%20fan-forced%20incubators.

Problem
I'm working on a strict aerobic bacteria. I have a problem with the growth rate of broth cultures; the growth seems too light in comparison to the inoculum size (4-5 colonies), low broth volume (4-5ml), and incubation conditions (24 hrs). The incubator available to me is of the type gravity convection incubator with no mean of shaking. I use screw cap test tubes for the broth cultures,  the degree of tightness of the caps greatly affects the produced turbidity. However, even after learning about this and making sure the caps are loosened, the growth rate is increased but still inadequate.
I have a colleague that has access to a fan-forced incubator and they seem to have a higher growth rate.
Question
Can Gravity convection incubators negatively affect the growth of strict aerobic bacteria?
Prior work
I have not found any text on the internet that discusses this matter. I have great experience in searching.

Can you update the question to include details about shaking?

Done (mentioned that no shaking incubator was used, as it is not available)

Hard to make a definitive answer without more information. I would confirm the temperature where your cultures are growing in the incubator with a thermometer. Flasks are generally better than tubes for gas exchange, but not sure if that applies to static cultures. Pre-warming the media can help. And best practice is to inoculate from a single colony whenever possible. Even minor genetic variations between colonies can result in competition between two or more clonal lineages, slowing outgrowth during the lag phase.

I used to do single colonies before afriend suggested doing more. I don't intend by using definite values in some of the givens I mentioned to build a complete scientific picture, all I need is the effect of using gravity convection incubators on the growth of broth cultures of aerobes, from practical experience.


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What is the carbohydrate found in almonds, cashews, pecans, hazlenuts and pistachios?
What is the carbohydrate found in almonds, cashews, pecans, hazelnuts, and pistachios? I first thought they probably have starch but I am not sure. Can someone verify this for me, and/or send a link where I could find this information?

Firstly you must realize that all the above mentioned nuts are actually the seeds of plants.
So the question now is which carbohydrate is mainly found in seeds of plants.
During the double fertilization of angiosperms, one sperm fertilizes the egg to form the embryo while the other fertilizes the endosperm nucleus to form the endosperm which acts as the nutrient storage for seeds.
The major carbohydrate for seed endosperm is Starch, often stored as granules for their property as being insoluble and compact.
However there are other carbohydrates such as free sugars, glucofructans and hemicelluoses present.
Hope this helped.
References
https://link.springer.com/chapter/10.1007/978-1-4615-2672-8_8

For the plants listed in the question (almonds, cashews, pecans, hazelnuts, pistachios) the primary storage is not the endosperm but the cotyledons. These seeds have two distinct halves, each a cotyledon, with an embryo sandwiched between. Starch is likely the most abundant carbohydrate, but there are other "nonstructural carbohydrates" as well as cellulose. Since these are intact cells that may go on to photosynthesize, these carbohydrates can be very diverse, and will differ between the species. Note, too, that these seeds will store many other nutrients, like proteins and fats.


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Why are there no endoparasitic mammals or reptiles or birds?
I am curious why there aren’t any endoparasitic mammals, reptiles or birds
Endoparasite being a parasite that live In the host whereas ectoparasite lives On the host
I hope this clears up confusion

Can you please define "parasite"? Aren't humans parasites of wolves and elephants? Aren't cuckoo parasites? How about vampire bats, vampire finch, cookie cutter shark, hood mockingbird, cowbird, oxpeckers or hyena? We can largely qualify them all as parasite. Note that you might want to define reptile too (see here)

I'm voting to close this question as off-topic because it is based on a false claim that there are no mammal / bird / reptile parasites.

I mean endoparasites that are mammals birds or reptiles. I know there are endoparasites worms, protozoan sect. But I don’t think there are any mammals birds or reptiles that are endoparasites. Sorry for the confusing wording of the question

If there are any, can you give examples? I don’t know of any

Oh... you should definitely edit your post to say "endoparasite" then (and make sure to define the term). For the moment the post still says "parasite". No, I can't think of any example of endoparasitic mammal / bird / reptile except if you would consider a woodpecker a tree endoparasite, would you? Humans could be considered parasite of earth if you consider earth as a living organism (see Gaia by Lovelock) but that's a bit of a stretch. Intuitively I would think a big part of the answer is going to be "because they're big!"

I edited the question now to make it clearer. Thank you Remi.b

@Remi.b I'm not really aware of any commonly-used definitions of parasite that would classify humans as parasites of wolves or elephants (endo- or ecto-).

I would honestly suggest "parasite" is fine here, but that the question is revised to "are there any X parasites - and if not, why?"

In the most clearly defined concept of parasite, a parasite and a predator are confounded. If species A have a beneficial impact on species B and species B have a negative impact on species A, then A is a prey/host and A is a predator/parasite. In such terms, yes, humans are parasite of elephants. My point was to highlight that whether or not there are mammals parasite depends upon the definition once want to use. IMO, the question now makes much more sense with the prefix endo. It still bothers me a little that the woodpecker examples is not resolved.

@remi since woodpeckers are digging into the trees to pull out and eat insects that burrow into the tree the net impact on the tree is arguable.

If I had to guess, I would say that it's a matter of basal metabolic rate.  Birds and mammals are warm-blooded, and so have to breathe regularly (and eat a lot of food) to maintain body temperature.  It's pretty hard to do this if you're an endoparasite, and there doesn't seem to be an obvious evolutionary route to get to a lower rate.

These sorts of "why didn't this evolve" questions are not answerable without profound speculation.

Short answer size.
endo/ectoparasites need to be small to go unnoticed, and be hard to eliminate. The smallest mammals and birds are still much larger than a flea, fluke or other endoparasite. That's why larger parasites leave after feeding, if a vampire bat hung on the cow indefinitely the cow would eventually notice and do something, something as simple as rolling over could kill them quite effectively. While an animals infested with fleas can not do much to get rid of the fleas. The few large endoparasites either evolved from much smaller parasites (tapeworms) or exploit some strange insensitivity in the host(cymothoa) This means there is no path to ectoparasite which could lead to endoparasite.
Why there are endoparasites evolved by other means in vertebrates what exactly would they evolve from, there are no birds or mammals that would survive being cut off from outside oxygen or passing through a digestive system. It is like asking why no flying trees have evolved there just is no path to get there or from where they are now, or if there is a path it is so unlikely that it has not occured.


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How having sickle cell trait would provide resistance to malarial parasites?
It's mentioned in my textbook that subjects with sickle cell trait develop resistance to malaria. I've read a few research papers predisposing involvement of macrophages and papers asserting involvement of the heme oxygenase system rendering me confused; so what actually causes this resistance. And is this resistance also present in the subjects with sickle cell anemia? Also some African tribes are generally mutated to provide malaria resistance. See this https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499995/

Possible duplicate of Why do heterozygous individuals have increased resistance to malaria?

@DeNovo I was having a hard time understanding it; another approach to answer the question would be appreciated.

In someone with sickle cell trait (a heterozygote), red cells are typically normal. When those red cells are infected with P. falciparum, though, they sickle and are easy for phagocytes to capture and kill. This makes it hard for the parasite to reproduce and cause significant disease.

I would not consider it a duplicate the linked question does not address the mechanism of resistance.

@John the answer goes through it in good, simple detail.

@DeNovo No it doesn't, it completely glosses over what it is about sickle cells that actually makes them detrimental to plasmodium infection. "the chances are bigger they will be phagocytized" is the sum total of the explanation, without even a mention of why the chances are higher.

I would say that there are at least 2 explanations:

Higher levels of free heme in the blood of individuals with sickle cell anaemia/sickle cell anaemia trait. Free heme is toxic to Plasmodium.sp Science. 1981 Nov 6;214(4521):667-9., detailed mechanism is described here: J Mol Med (Berl). 2008 Oct;86(10):1097-111. This effect is also observed in people with other diseases affecting stability of erythrocyte's membrane, such as thalasemia or spherocytosis.
It is also possible that, when erythrocyte's membrane is prone to disruption, Plasmodium.sp  antigenes are present in higher concentrations and may be faster presented to the immune cells.

Sickle cell anaemia is where the red blood cells become sickle shaped hence since Plasmodium infests itself in the red blood cell for oxygen, it doesn't survive because sickle celled RBCs carry less volumes of oxygen.

do you have a source for this?


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Why there is no vaccine against Human Immunodeficiency Virus (HIV)?
I was informed by my teacher that this retrovirus changes its RNA, so there is not a drug which can recognize the RNA and somehow inactivates it. Are there any other reasons explaining why there isn't a vaccine for the HIV?

That's a good answer, and I'd say it's a duplicate.

On review, I see this question is asking for other reasons, as well as the antigenic variability. I'll undelete my answer.

One of the reasons we don't have an HIV vaccine yet is we've only been trying to make one for a little over 30 years. It can take a long time to develop a vaccine. Beyond that, there are a number of specific challenges.
One of them is that, yes as your teacher said, the virus is highly variable. Specifically, the parts of the viral proteins involved in binding and infecting a host cell are highly variable. There are a number of other challenges. One important and related challenge is that, unlike with many vaccine preventable diseases (e.g., measles), an successful HIV vaccine will have to entirely prevent infection  rather than just control and clear infection without developing disease. Once a reservoir of infected cells is established, the opportunity for clearance is gone. This makes the production and maintenance of high titers of neutralizing antibodies that much more important.
There is a very good review of the challenges and current directions of HIV vaccine development here

"Once a reservoir of infected cells is established, the opportunity for clearance is gone." So with current advances crispr to cut out the established DNA is a good idea? (and not just me being spontanous (as I don't remember if I remember, sorry...):):-) Thank you.

Also, it'd be interesting to hear about a general principle of antibody vaccinaton not being fast enough - with aids, it's the establishment in the genome that has advantage, in case of Covid the equivalent would be infectivity, i.e. if antibodies are too late the person might not get sick ut it will spread the virus for a while, before antibodies get to grips and stop the replication. That's correct?


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Why is atropine a CNS stimulant, although it blocks the muscarinic receptors in the brain?
I know that atropine is a muscarinic  antagonist, so why does atropine have excitatory actions on the brain while it is blocking muscarinic receptors?

Short answer
Atropine inhibits an inhibitor and hence its effects are excitatory.
Background
According to the wiki page on muscarine M2 receptor:

M2 muscarinic receptors act via a Gi type receptor, which causes a
  decrease in cAMP in the cell, generally leading to inhibitory-type
  effects.

Atropine is an antimuscarinic (anticholinergic) drug.According to the wiki page on atropine:

[R]eactions to atropine include ventricular fibrillation, supraventricular or ventricular tachycardia, dizziness, nausea, blurred vision, loss of balance, dilated pupils, photophobia, dry mouth and potentially extreme confusion, deliriant hallucinations, and excitation especially among the elderly.

So atropine blocks inhibitory muscarinic receptors, and hence causes excitation.

But the brain has M1 receptors which work with all the three Gq, Gs, Gi proteins! (The question has been corrected, pardon.)


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How does acetylcholine (aCh) cause erection?
I have read this article on physiology of erection :

Activation of cholinergic receptors on the endothelial cell by acetylcholine or stretching of the endothelial cells as a result of increased blood flow may elicit underlying smooth muscle relaxation through the release of NO.

I know erection is caused by parasympathetic outflow; but how come the cholinergic receptors on the endothelial cells are activated by aCh because there are no parasympathetic neuronal endings on endothelium, as from what I've learned and there could not be aCh freely released in penile arteries because butrylcholinesterase in blood would inactivate the aCh?
I understand that the corpora cavernosa are relaxed to help sinusoids accumulate blood and corpora spongiosum are contracted to prevent venous outflow of the blood to maintain the erection.

ACh is released onto blood vessels and affects receptors on smooth muscle and endothelium. Can you cite your assertion that this doesn't occur?

You may be confused because most peripheral blood vessels do not have direct parasympathetic innervation. The pelvic region is unique here (pelvic blood vessels do have direct parasympathetic innervation)

@DeNovo Maybe not quite unique, but "special" perhaps?

@BryanKrause yes, you're right. Lets go with special.

@DeNovo I've got my answer then.


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Does the hepatic portal system form capillary beds?
Does the hepatic portal system form capillary beds?  If so, is the capillary bed coordinated with that of arterial capillaries?
What review paper might I look in?

In anatomy, a "portal circulation" is simply when you have a capillary bed that is interposed between two venous circulations BEFORE blood flows back to the heart. There are a couple of places in the body where this occurs, including the liver (hepatic portal system) and the pituitary (hypophyseal portal system).
To answer your question... yes, the hepatic portal circulation drains into the liver sinusoids, which is one large capillary circulation.
The hepatic arteries and portal vein give off branches that make up the portal triad which delivers blood (both arterial and venous blood) to the functional units of the liver which are the hepatic lobules.
The hepatic portal system drains into the liver and forms a highly fenestrated network of capillary beds within the liver parenchyma. In the case of the hepatic portal circulation, the flow through the liver sinusoids is considered this capillary bed. In humans, the flow of blood that makes up the hepatic portal circulation is mostly venous blood from the gastrointestinal tract.  This allows blood to flow through the liver for clearance of substances like drugs and hormones before those substances reach the peripheral circulation. Specifically, arterial blood flows to the majority of the stomach, small intestine and colon from the celiac, superior and inferior mesenteric arteries. This arterial blood flows through the capillary beds in the mesenteric circulation (i.e. the capillary beds around the intestinal enterocytes) and then into the major veins that drain the intestinal tract. There are two major veins that drain the intestinal tract, the superior and inferior mesenteric veins. The inferior mesenteric vein drains into the splenic vein and then the splenic vein and superior mesenteric veins merge to form the portal vein of the liver. Once blood flows into the portal vein it flows through the hepatic sinusoids (another capillary bed) before flowing out of the hepatic veins into the inferior vena cava, and then back into the heart.

The figure below is a picture of the intestinal veins from Gray's Anatomy  (wikipedia) that form the hepatic portal vein, the superior and inferior mesenteric as well as the splenic vein. In the figure the older term lienal vein is used instead of splenic vein. The latin word for spleen is lineal.

The picture below is a schematic of the hepatic lobule that receives its blood from a portal triad. In the center of the lobule is the "central vein". The blood flows from the portal triad to the central vein, and then the central veins coalesce to form the hepatic veins (which then drain into the inferior vena cava). The picture below is available from this website, along with some other text and picture for more information.

And another nice picture from wikipedia on "hepatic lobules".
.

As for a "freely available review" that you asked for, I can't find any with better pictures from PubMed that what is already in this answer.

This picure is from Junqueira histology book:

as it shows a branch of hepatic portal vain and a branch of hepatic artery form hepatic sinusoid which is some sort of capillaries.
hope it helps :)