What is a good source for info on disease frequency distribution among age groups? I need information on the disease frequency distribution among age groups for an Android app I'm building... Hopefully I've come to the right place. Is there a good data source for this? Like a bioinformatics database?

You may need to study each disease individually or do a literature review.  The Online Mendelian Inheritance in Man website may be a good starting point http://www.omim.org/
The Centers for Disease Control and Prevention lists several diseases with a variety of different statistics here:  http://www.cdc.gov/DiseasesConditions/


Why minimum infective dose of a virus is not just 1 particle? I've stumbled upon a term "minimum infective dose" (for example, of HIV), but don't exactly understand what is it? Why it is not always equal to 1 virus particle? I expect 1 lucky virus to be able to start infection just like 1 lucky spark can start a fire.

The following options comes to mind:

Multiple particles of the same virus need to act in cooperation to trigger their reproduction;
There is some 100% working, but limited use immunity that knocks down first N viruses;
Infection probability lower than some theshold % is not considered by statistics.

In general, how infection probability and severity correlates with the number of particles? Is it linear (double the number of viruses => double probability or infection) or something trickier?

From Merriam Webster:

  the smallest quantity of infective material that regularly produces infection

(emphasis mine)

The word "minimum" here is not meant as a strict minimum it is meant as a statistical bound, the absolute probability for which depends on the types of tests done and their inherent accuracy/inaccuracy.

Reasons that this "minimum" is greater than 1 could include:

Probability that a given particle actually finds a suitable host cell, enters the cell, and replicates; failures can occur at many stages along that chain
Rate of immune system reaction/response. At low exposure levels, the immune system may detect and clear the infection at a rate faster than it can spread, such that the infection stays asymptomatic. Some vaccines use weakened or low doses of pathogens specifically to evoke an immune response. The intent is that the weakened pathogen will not spread fast enough to overcome the immune response and will not produce a full disease.
Clearance of the infectious agent before it reaches symptomatic levels. This probably applies more to bacteria but I don't see why it couldn't also apply to viruses. I think the best example is exposure to bacteria that cause gastrointestinal infections like E.coli or Salmonella. Small numbers may grow and multiply in the gut, but they grow slowly if they aren't present in a high enough concentration and they may pass through the gut before causing any noticeable symptoms.

The minimum infective dose can also vary from individual to individual or due to environmental factors (for example, see this paper).

Some additional references:

Leggett, H. C., Cornwallis, C. K., & West, S. A. (2012). Mechanisms of pathogenesis, infective dose and virulence in human parasites. PLoS pathogens, 8(2), e1002512.

Ward, R. L., Akin, E. W., & D'Alessio, D. J. (1984). Minimum infective dose of animal viruses. Critical Reviews in Environmental Control, 14(4), 297-310.

Yezli, S., & Otter, J. A. (2011). Minimum infective dose of the major human respiratory and enteric viruses transmitted through food and the environment. Food and Environmental Virology, 3(1), 1-30.


What is the etymology for Pinus halepensis? I have a problem of figuring out the etymology of Pinus halepnesis.

An etymonline search with halepensis brought no result.

It is unclear to me from the English wikipedia article and from the English WikiSpecies article what is the source of the name.

It is often called "Aleppo pine" --- maybe this is the source.

In Israeli Hebrew (as in Hebrew Wikipedia) it is called "Jerusalem pine" (אורן ירושלים) which is clearly different than standard.

What is the etymology for Pinus halepnesis?

If you search for this plant (properly spelled Pinus Halepensis) in the International Plant Names Index (IPNI), you'll find this page providing publication reference for this species of pine:

Gardeners Dictionary, Edition 8. London

According to IPNI, this publication by Phillip Miller in 17681 was the first to officially name this species. You can find the first half of he publication online here and the portion of the publication with info regarding P. halepensis here [p. 477].
Miller 1768 provides the following:

Pinus (Halepenſis) foliis geminis tenuiſſimis, conis obtuſis , ramis patulis. Tab. 208, Pine-tree with two narrow leaves in each ſheath, obtuſe cones, and ſpreading branches. Pinus Halepenſis, foliis tenuibus lætè viridibus. Rand. Hort. Chelf. Cat. 158. aleppo Pine with very narrow dark green leaves.

* Note: a longer description about this tree also continues on the subsequent page in Miller's book -- you can find it in the middle of the right column of the following page.
However, this publication does not make clear why Miller chose this specific epithet.

Elwes & Henry (1906)2 likewise describe this species [see online here] and mention that the epithet had been used for more than 100 years. However, they, too, do not provide meaning behind its use.

Further sleuthing suggests the following:
From Antropocene.it:

The specific epithet halepensis derives from Aleppo, the current city of Haleb in northern Syria.

Note, however, that this specific epithet doesn't only apply to this species of Pine. Linnaeus assigned this epithet to a grass (Sorghum halepense) he called Holcus halepensis (Linnaeus Sp. Pl. (1753) 1047)3 more than a decade before Miller named the pine in question.
Using this connection, SEINet suggests the following etymologies for halepense:

Halepense means "from Aleppo, Syria."

This is the best I could do for you in a short amount of time. I, like you, could not find much explicit explanation for this word, and I admit I find its use a little strange given the relatively widespread range of the species mentioned (at least that both exist much wider than Aleppo).

 1. Miller, P. 1768. The Gardener's Dictionary, ed. 8. London. Pinus no. 8
 2. Elwes, H.J. and Henry, A., 1906-1913. The Trees of Great Britain and Ireland. Edinburgh: R & R Clark, 7.
 3. Linnaeus, C. 1753. Species plantarum. https://doi.org/10.5962/bhl.title.669. [more info here and on wikipedia]


RNA-Seq library construction challenges: the biases of RNA fragmentation vs cDNA fragmentation I recently watched a presentation on RNA-seq that covered some of the choices one can make along the way, and I didn't fully understand one of the choices in particular.  Near the beginning of the process, you can choose a fragmentation method (e.g. RNA: nebulization, hydrolysis; cDNA: sonication, Dnase I treatment). Each fragmentation method is biased in its own way, and the goals of the study may influence the choice of method.
I didn't fully understand the reasons for the characteristic biases (how do they happen?), and when to choose one method versus the other (which methods work best for which goals?).  Put another way, what are the mechanistic explanations for the characteristic biases that result from each method, and what is the significance as far as downstream processing and associated challenges?
Edit:
The heart of this question is about fully understanding the particular choice of when and how to fragment.  The reason I have not accepted an answer, yet, is that the answers provided so far address the mechanism part of the question, but not the ultimate reasons for choosing one versus the other.

Good question, a lot of this is still being figured out. Here's what's known so far:

Fragmentation methods based on restriction enzymes aren't random.

Reverse-transcription performed with poly dT-oligomers, which bind to the 3' poly-A tails, is strongly biased towards 3’ end of transcripts.

Reverse-transcription with random hexamers results in an under-representation of 3’ ends. This is from the reduced number of priming positions at which the reverse transcriptase enzyme can start cDNA synthesis.


Is eradication of the Common Cold possible? This is a thought experiment, but everywhere I've read seems to say that colds ALWAYS come from someone else. There's no mention of a cold arising in someone without it coming from another infected being.

So my question is, if everyone in the world stayed out of physical contact and air space with everyone else for 2 weeks (or until every cold virus would have completely disappeared), would all variations of the cold virus then be extinct leading to a world without colds?

Or is there somewhere else that colds can arise from?

You'd think there would be numbers of papers on this. I have two references but they're not great.  The answer is not really.  Many people carry cold viruses asymptomatically.  This can be either a natural immunity, or that their body has beaten it down but not entirely eliminated it.  Cold viruses do not survive long outside of the body as you stated.  The only way they've made it this far is some survive inside the body until they are spread to other people.  In essence we are the reservoir.  So you could isolate everyone for two weeks, but that won't cause a problem for the viruses that are just tagging along.  There may be other reservoir animals as well for many of the viruses.  But even those that only affect and are carried by humans would survive.

The group of cold viruses is just too varied and different to eliminate them.  Also the cost of such an effort would not really be justifiable given the typically mild symptoms.

Natural Reservoir


Virus viability on fabrics According to the article How long do viruses live on surfaces: Plastic, stainless steel, fabric, and more:

  With fabrics, it's unclear how long viruses can last. But generally, they tend to last for a shorter amount of time on fabric compared to hard surfaces like stainless steel, according to the Mayo Clinic.

Can someone kindly explain why this is so?

What is it about fabrics that decreases virus viability?

I would like to point out here that in many cultures our ancestors had figured it out empirically.  In North India, where I hail from, many old people will eat bread, snacks etc. from a cloth (especially a woolen fabric) if their hands are dirty.  The simplistic explanation given is that this type of fabric "stays pure".

A VERY interesting question that I had to think a lot about, and frankly I couldn't come up with an answer.

Nevertheless, this article may have.

https://www.statnews.com/2020/03/19/coronavirus-survives-on-surfaces-how-to-protect-yourself/

"Viruses covered in “envelopes” have the most trouble surviving outside a living cell. On surfaces, the surrounding light, heat, and dryness break down the envelope, killing the virus. (Porous surfaces pull moisture away from viruses that land on them, accelerating the destruction of the envelope.) Most rhinoviruses have such envelopes; so do some influenza viruses. Norovirus doesn’t, enabling it to last longer in the environment."

Here are the author's relevant credentials.

Sharon Begley, senior science writer, covers genetics, cancer, neuroscience, and other fields of basic biomedical research. She was previously the senior health and science correspondent at Reuters, the science columnist at the Wall Street Journal, and the science editor at Newsweek. Among her favorite awards are an honorary doctorate from the University of North Carolina and the Public Understanding of Science Award from the Exploratorium in San Francisco.


what are the ethical considerations when preparing a bacterial culture for testing antibiotic resistance? I cannot think of any ethical issues associated with preparing a bacterial culture to test antibiotic resistance. The bacteria I am using is Bacillus Megaterium so its not pathogenic.
Thanks in advance for your help!

While I think the question is off-topic, I could not help but trying to answer it! It is easy to find ethical issues in every activity.

Potential ethical issues

You are killing bacteria
Your research has an environmental cost. You consume loads of plastic thingies for example.
Your research costs money as well. You consume tax payer money (depending on your source of funds)
You are selecting for anti-biotic resistance and might, by mistake, release them in nature (of even they are not pathogens, they might become, they might transfer their resistance to pathogenic bacteria as well or your experience may have all sorts of unexpected consequences)
Are you sure it is not pathogenic? We are never sure of anything, so just don't take risks.
Don't play with nature, you are not God!
Are you helping those nasty big pharmaceutical companies, huh?
You are a clever person. There are so many other things you could do for the world that would be so much more beneficial. Your time could be used for better purposes. You could work on improving sanitation conditions in India, or improve women's right around the world, or help children involved in the current civil war in Somalia for examples.

Basics of philosophy of ethics

For any question of ethics, one has to define his/her own values and from this point this person can formulate an opinion on a particular case. Of course, I personally do not feel bad about killing bacteria and consider antibiotic resistance a very important field of study to improve our everyday well-being but other people may disagree based on their own values.

I am not formally trained as a philosopher. So, please read the wikipedia articles on ethics and values I linked above and if you have any other question of Philosophy, you can ask them on Philosophy.SE


Why don't phospholipid bilayers dissolve? I just started learning about the structure and composition of cell's membrane and there is something that I fail to understand.

The membrane is composed of a phospholipid bilayer. The phospholipid has a polar, hydrophilic head and a nonpolar, hydrophobic tail. My question: Why doesn't the hydrophilic head dissolve in the extracellular fluid outside the cell? I suppose that the extracellular fluid is watery, so how come that the water-loving head doesn't interact with the water from the extracellular fluid?

We should first understand what happens when a substance dissolves. During dissolution water interacts with the solute molecule; if the strength of interaction between the molecule and water is higher than the strength of interaction among the solute molecules then the solute dissolves.
(Also have a look at this post).

Phospholipid is an amphipathic molecule — it has both hydrophobic and hydrophilic parts (this you understand very well). The hydrophobic part is a long chain of hydrocarbon (hence tail) whereas the hydrophilic part is a small but highly polar region (hence head). You should note that these parts are not disjoint but are covalently bonded.

Even though the hydrophilic part interacts with water (which helps the cell survive in an aqueous environment), the strength of covalent bond (between hydrophilic and hydrophobic regions) is very strong and cannot be broken by physical interaction with water.
The lipid bilayer (even a monolayer) stays together because the water cannot interact with hydrophobic parts but they interact with each other via a pseudo-interaction called hydrophobic interaction.

I call it a pseudo-interaction (not a standard usage) because there is not actual molecular interaction that stabilizes the system. Hydrophobic interaction happens via increase in entropy of the system. Read the wikipedia page for details.


Are bryophyte sporangia multicellular? My research on the matter can be summarized in a sentence: "It [sporangium] can be composed of a single cell or can be multicellular" (Source: https://en.wikipedia.org/wiki/Sporangium). Yet there shouldn't be a reply placed between "They are" and "They aren't" test options, speaking of "Are bryophyte sporangia multicellular?". A link to the source where I could ascertain whether the bryophyte sporangia is multicellular (if I could ascertain) is highly appreciated.

In Embryophyta (land plants), including bryophytes, the sporangium is usually a multicellular structure.

Perhaps you meant to ask about the number of spore mother cells (SMCs) in each sporangium? That varies across groups. In bryophytes, each sporangium has many SMCs, and accordingly produces a large number of spores. (Contrast this with angiosperms, where a megasporangium [called an ovule] has only one megaspore mother cell.)

References and further reading:

https://courses.lumenlearning.com/boundless-biology/chapter/bryophytes/

https://www.britannica.com/science/plant-development

Image attribution:
By LadyofHats. (Public domain;
https://commons.wikimedia.org/wiki/File:Hornwort_structures.jpg)


Is it possible to directly uploaded controlled imagery into a person's conscience? I was wondering, is it possible to use electrical charges and/or EM waves to induce imagery directly into a person's mind?

I got this idea because since almost everybody dreams, and dreams are images created by the brain, i wondered if it was possible for an outside source to forcibly make someone see a different image without harming them.

In principle there's no reason why we shouldn't be able to do so. In practice, we do not seem to be anywhere near able to do so.

We are barely able to decode natural images from fMRI information, and before you can hope to induce imagery you should usually first be able to decode it.


What's the mechanism of action of Levomepromazine's analgesic effects? I have absolutely no idea as to how Levomepromazine elicits its analgesic effects so please do direct me to journal articles and other credible sources with you, the answerer, making a summary of Levomepromazine's mechanism of action in your answer.

According to Drugbank and the articles cited below, Levomepromazine is an antagonist of several different receptors: These include dopaminergic 2, dopaminergic 4, alpha-1 adrenoceptor, 5HT-2, histamine type 1 and muscarinic-cholinergic receptors.

References:

Evidence for the use of Levomepromazine for symptom control in the
palliative care setting: a systematic review
Muscarinic cholinergic and histamine H1 receptor binding of
phenothiazine drug metabolites
Levomepromazine receptor binding profile in human brain—implications
for treatment—resistant schizophrenia
Phenothiazine drug metabolites: Dopamine D2 receptor, α1-and
α2-adrenoceptor binding


Help identifying a moth It looks like it might be an emerald moth but its hard to tell from the discoloration in the wings and it is too high up for me to get a better look.

When: July 23rd 2018

Where: Central Illinois

It looks like an Imperial Moth (Eacles imperialis):

Source: https://www.butterfliesandmoths.org/species/Eacles-imperialis

As shown on the distribution map at this link, they can be found in central Illinois.


Why WHO has not eliminated chicken pox like smallpox? Chicken pox is a viral disease, so why then has the World Health Organization (WHO) not eliminated chicken pox like smallpox?

Smallpox still exists in labs.

Eliminating a virus from the world is an immensely costly undertaking. As with most things in real life, cost vs. benefit (and feasibility) need to be taken into account. Unfortunately, there is a limited amount of money available to fight disease.

The overall mortality rate of smallpox is about 30%. That's a very high mortality rate, one that shaped history significantly.

By contrast, of a yearly 4 million people who contracted chicken pox (in the US, before the vaccine), only 100 to 150 died each year.

The death rate of smallpox: 30%. The death rate of chicken pox: .00375%

Maybe someday chicken pox will go the way of small pox. But our limited monies need to be devoted to eliminating viruses that cause greater harm, e.g. polio and others.

Also, not all viruses are equally "eliminatable", e.g. H1N1, HIV, etc.

Smallpox Vaccine: The Good, the Bad, and the Ugly
Monitoring the Impact of Varicella Vaccination


ID of this flower/plant and origin if possible Hello again all you helpers out there!

So this plant or flower is found in Virginia (USA) rural area mainly woodland and grassplains, when it comes up, it rarely last for very long, so with a photo of the plant in its glory, i hope some of you could tell me, what kind of plant/flower it is and where it came from, thank you very much and have a great weekend!

/Beo

Look like a Spider lily (Lycoris radiata):

Source: NC State University


Probably a moth larvae but better to confirm What I know,
It reacts to light
the red seems to be blood but can't say for sure
1 to 10 mm
it has a casing of something soft fabric possibly
it grabs to walls

This is probably a larvae of Tinea pellionella, the case-bearing clothes moth.
T. pellionella is a species of tineoid moth in the family Tineidae (i.e. the fungus moths).


Did vertebrates diverge from other deuterostomes via neoteny? Question: Is there any research corroborating my suspicion that vertebrates diverged from other deuterostomes via neoteny (the attainment of sexual maturity while still in larval stage)?

Context: Most echinoderms have pelagic, bilaterally symmetric larvae, while the adults are not bilaterally symmetric (except for sea cucumbers) and live on the sea floor. The same is true for tunicates, which are supposed to be the sister group to vertebrates.

Adult echinoderms also have very reduced nervous systems, although I am not sure whether the larvae have more advanced nervous systems than the adults. For tunicates, which are more closely related to vertebrates, the nervous system definitely does degenerate when transitioning from pelagic larvae to sessile adults.

Echinoderms are also one of the few clades of bilateria, except for vertebrates, which have endoskeletons. And of course, echinoderms, tunicates, and vertebrates are all deuterostomes.

In contrast to tunicates and echinoderms, the MRCA of vertebrates is thought to have resembled a lancelet, which is pelagic and which has a more advanced nervous system than adult tunicates or echinoderms. In other words, it seems like ancestral vertebrates retained larval features into adulthood, and then just grew bigger in size.

echinoderms are sort of bilaterally symmetrical, imagine if you took a velvet worm and then twisted it around in a big loop with the legs sticking out until the head was stuck to the tail end but still pointed away from each other. That is basically how echinoderms went from bilateral to radial. of course in practice this is done by rearranging hox genes but it is a good way to visualize it.  https://evodevojournal.biomedcentral.com/articles/10.1186/2041-9139-5-22

as for chordates look at hemichordates (which also have endoskeletons) and you can see why the general belief is that tunicates evolved that life stage after branching off(kinda like barnacles) instead of vertebrates losing that life stage.


Does too much Genetical Modification leads to formation of new species? I think Genetical Modification can be termed as 'Artificial Mutation'.
Is it possible that genes can be modified so much that it leads to the introduction of new Species i.e Can integration of large no. of Helpful mutations lead to quick evolution?

yes it possible, in one article show a study for Mycoplasma genitalium which have 525 gene, however only 382 genes are essential for biological functions, they take out the nature gene and place the ' artifical gene' which synthsis in vitro, to test if the M. genitalium will survival when the No. of gene lower than 382. If it survival it will be a new species.


What causes the yellow and brown spots on our sour cherry tree? So at the end of spring (maybe at the beginning of summer) our sour cherry tree started producing these yellowish/brownish spots on its leaves. Can you help me identify the couse of this? What can we do against it? I cannot see any bugs on it, my best guess would be some kind of a fungus, but I am way far from being an expert. Thank you in forward for the answers!
Edit: I am located in Hungary. The brown spots are not bigger than my nails, but the yellow area can cover even the whole leaves. Also, the capillaries visible on the leaves can turn red, as you can see on the pictures. Unfortunately, the exact species of the cherry is unknown to me.

The tree is most likely sick. Plant diseases take years to develop versus diseases in animals caused by either bacteria, viruses, or parasites. This is because the tree has thick cell walls that can be a huge barrier hindering viral infection. Another thing is that trees lack a circulatory system and rely on partial water pressure from the air to draw water from the roots up to the leaves.
Your tree might have a virus that is slowly killing it. Which insects are endemic to your region? We can deduce the virus if we know the main types of bugs living in your area.


Thyroid hormone metabolism and excretion My understanding is that hormones generated by the thyroid gland, including, for example, T4, are excreted and recirculated in the body through the digestive tract. The reason for thinking this is that bile acid sequestrants such as cholestyramine cause a lowering of serum T4. In fact, patients who have hypothyroidism are explicitly warned not to use sequestrants for this exact reason. Here is a statement from a clinical trial discussing the effect:

  The enterohepatic circulation of thyroid hormones is increased in
  thyrotoxicosis.Bile-salt sequestrants (ionic exchange resins) bind
  thyroid hormones in the intestine and thereby increase their fecal
  excretion. Based on these observations, the use of cholestyramine has
  been tried. The present study evaluates the effect of low doses of
  cholestyramine as an adjunctive therapy in the management of
  hyperthyroidism. -- clinical trial NCT00677469

Therefore, there would appear to be a metabolic pathway in which T4 is being excreted into the digestive tract and then is later re-absorbed in the lower intestine somehow.

What is this metabolic pathway? How exactly does this mechanism work? Does it have a name?

For more information on thyroid hormone sequestration see:

https://clinicaltrials.gov/ct2/show/NCT00677469

http://www.ncbi.nlm.nih.gov/pubmed/8435884

I have partially answered this question by discovering that the metabolic pathway is called enterohepatic circulation. In this interaction bile salts are absorbed and transported out of ileal mucosal cells by binding to albumin.

However, it is still unkown to me exactly how it is that thyroxine and other hormones are moderated in this process and how it works. Does the albumin collect thyroxine as well as bile salts? How is the process moderated? In other words, bile salts are allowed to be excreted according to some moderated control mechanism. What is this mechanism?


Is Protein-to-DNA ratio a good estimate of cell size? I need help interpreting the result of an experiment. My class performed an experiment measuring protein concentration between heart, liver, and kidney tissue samples. The results were:

Heart: 4.714 mg/ml
Liver: 10.586 mg/ml
Kidney: 9.140 mg/ml

The DNA concentration was given to us and they were:

Heart: 8.6 ug/ml
Liver: 57.6 ug/ml
Kidney: 28 ug/ml

Computing the Protein:DNA ratio:

Heart: 0.548
Liver: 0.184
Kidney: 0.326

Doesn't this mean that the protein-to-DNA ratio has an inverse relationship with cell size as the results show that the liver tissue has the highest protein concentration and DNA concentration, yet has the lowest protein:DNA ratio. Also, why does DNA concentration differ so significantly between each tissue sample? My understanding is that genome remains the same between different cell types. So why does DNA size change?

So after discussing my concerns with my professor, I have found out that I overlooked the simple fact that the DNA concentration is not measured based on a single cell of tissue type.

Protein-to-DNA ratio is directly proportional to cell size and the reason why liver cells has the highest DNA concentration at 57.6 ug/ml is because they have a smaller cellular size compared to the other two. So a single ml of liver homogenate is going to present with a significantly higher cell count and thus, a higher DNA concentration. This is also why a single ml of heart muscle DNA concentration is only 8.6 ug/ml due to there much larger cellular size.

This finding can be confirmed from calculating the Protein:DNA ratio as the liver homogenate with its smaller cellular size is only 0.184 and the heart homogenate with its larger cellular size is the highest at 0.548.

Thank you everyone for trying to help me with this problem!


Why do small organisms make faster movements than big organisms? I hesitated to ask this question because it seems so obvious and intuitive. However, I am not able to explain this tendency.

Background

It seems to me that small organisms make faster movements than big organisms. I don't mean that they are able to travel at higher speed (the cheetah is a big animal and is the fastest terrestrial species) but I mean that their movement are fast, quick and their members undergo high acceleration.

Examples

I would guess for example that the legs of a tiger beetle (clade of fast sprinter beetles) (see movie) undergo much higher acceleration than the legs of a cheetah (fastest terrestrial organism on earth) (see movie). To avoid taking the extreme, I would think that the legs of a Drosophila (see movie) undergo higher acceleration than the legs of a dog (see movie). The organism that is able to create the fastest acceleration is the mantis shrimp. Wikipedia says:

  Both types (smashers and spearers) strike by rapidly unfolding and swinging their raptorial claws at the prey, and are capable of inflicting serious damage on victims significantly greater in size than themselves. In smashers, these two weapons are employed with blinding quickness, with an acceleration of 10,400 g (102,000 m/s2 or 335,000 ft/s2) and speeds of 23 m/s from a standing start. Because they strike so rapidly, they generate cavitation bubbles between the appendage and the striking surface. The collapse of these cavitation bubbles produces measurable forces on their prey in addition to the instantaneous forces of 1,500 newtons that are caused by the impact of the appendage against the striking surface, which means that the prey is hit twice by a single strike; first by the claw and then by the collapsing cavitation bubbles that immediately follow. Even if the initial strike misses the prey, the resulting shock wave can be enough to stun or kill the prey.

Finally, note that Gabel and Berg (2003) show that the flagella can rotates up to 270 Hz.

Questions

Am I right to think that small organisms tend to make faster movements than big organisms?
If yes: Why do small creatures make faster movements?

Does it has to do with time for chemical diffusion?
Does it has to do with mechanics? ($F=ma$... But muscles are smaller as well).
Does it has to do with the resistence of biological tissues?
...

It's a general phenomenon that the time scale correlates with the size scale of complex systems.
Energy consumption is the main concern dealing with the speed for biological organizations.
In the absolute sense, a turtle has a higher speed than a small bug. But based on their sizes, the bug seems much quicker and faster. So we need to normalize the speed with the size scale which we can temporarily call 'fastness".

Here is the relationship between the fastness and the mass:

Where u is speed of the organism, M is mass, alpha is a constant which we assume that the metabolic energy is related to the body mass of the organism with a power law.

The final equation says that if alpha > 1.67 then the larger would be faster. But our observation tells us that the smaller the faster. Therefore, we know alpha < 1.67.
In fact Kleiber's law tells us that the alpha is about 0.75.

You can check some numbers related to some animals here


Relationship between leaf structure and Photosynthesis rate We can see numerous leaf structures in plant kingdom. As the leaves are designed for photosynthesis, their structure must be a factor for any optimization in photosynthesis or chlorophyll distribution.

This link describes many leaf structures but I cannot find what I am looking for in anywhere.

I think taxonomy of plants deals with the flower structure but is their any relationship among plant species that we can describe with leaf structure ?
Do the leaf structure is optimized for maximum photosynthesis rate if so then why these different structures ?
Any other advantage for these diverse leaf structures ?

1) Your understanding of taxonomy is outdated by a few hundred years. Linneaus' original system was based on flower morphology, but we since realized that the most effective taxonomy takes into account many different traits. In today's times, we mainly use DNA sequencing to determine relationships between organisms.

2) The leaf structure is not necessarily only optimized for maximum photosynthesis rate. For instance, the leaves of cacti are spines: thin and pointy to minimize water loss and defend the plant. In fact in cacti the stem is the photosynthetic part of the plant, not the leaves. More generally, leaves may be thicker or thinner to cope with drought. You can check out the wikipedia page for Specific Leaf Area for more information.

Long story short: different plants grow in different environmental conditions, so the optimal leaf shape for any one plant depends on conditions like drought and shade.

3) There are many advantages that can be conferred by leaf shape. One example is how leaf shape can affect what is known as the boundary layer of the leaf. The boundary layer is thicker in larger, uniformly-shaped leaves and thinner in dissected or compound leaves. The intro on this webpage seems like a good resource

Overall, good question. You have to keep in mind that any trait is going to be the product of many different factors; no one factor can entirely determine a trait's morphology. For leaves, it's many different factors including photosynthetic rate, drought, shade tolerance, defense against predators, etc. that determine the shape of the leaf.


How do axon terminals report to the soma? It is important to bear in mind that the distance between a neuron's axon terminal and its soma can be extensive, up to about 1m in the human body. The fastest transport along the axon is 400mm/day (For this purpose I suppose Source: Wikipedia).

Of course the axon terminals also need to be supplied with a steady stream of proteins to maintain normal turnover, for example the terminal may need enzymes which metabolise the neurotransmitter, membrane proteins for signalling, vesicle coating and membrane fusion proteins etc.

However, sudden changes are possible in the level available of a certain protein. An example could be sudden depletion of SNAREs (required for vesicle fusion in neurotransmitter exocytosis) caused by botulinum toxin.

My question is, does the terminal somehow report back to the soma in any way if a certain protein needs to be made available more or less? And if so, how? Especially considering that retrograde transport, according to Wikipedia, gets up to 200mm/day only. If that was the mechanism for feedback, it would create a large discrepancy between signals received at the soma and the terminal's actual state.

We can consider the classical example of Long Term Potentiation.

CREB is a transcription factor which is activated during LTP by phosphorylation.

Your reasoning about the delay between signal and transcriptional response is correct and thats why neurons have local translation factories near the dendritic spines and gene regulation (fast responses) is mostly post-transcriptional. (there is no article which says exactly so but you can refer so some articles  which report that miRNA-repressed genes are reactivated upon certain signals. They hint that post translational regulation is very important in neurons)

http://www.cell.com/neuron/abstract/S0896-6273%2809%2900939-8

http://nar.oxfordjournals.org/content/40/11/5088


gene duplicated on genome but is different I've been looking at a miRNA cluster on a genome and I found it three times. The first two are right next to each other and look exactly the same, the third sequences is on a different scaffold of the genome and is both shorter and has a number of mismatches with the first two sequences.

Is there a particular name for this? The first two are most likely some sort of gene duplication, but I'm not too sure on what to call the third,

Thanks

That sounds line one of two things. Either a sequencing or assembly error (quite likely since you're talking about scaffolds so, presumably, not a completely assembled genome) or duplication and subsequent pseudogenization.

It is relatively common for genes to be duplicated and then to be rendered inactive by a mutation event. Such genes can still be detected in the genome and are called pseudogenes. The process of their creation is, unsurprisingly, called pseudogenization. You can think of such genes as fossils. They often have significant sequence similarity to the original and can even be transcribed.

A quick search brought up a couple of articles discussing the pseudogenization of specific genes:

Pseudogenization of CCL14 in the Ochotonidae (pika) family.
Pseudogenization of sopA and sopE2 is functionally linked and contributes to virulence of Salmonella enterica serovar Typhi.

That said, is also quite possible that what you describe is a simple duplicate that has diverged without becoming a pseudogene. The details will depend on the particular sequence. Are there in-frame STOP codons? Can the gene still be transcribed? Such duplication events give rise to paralogs (note that all three of the genes you mention would be paralogs of each other, it's just that one has diverged more than the others). You can read more about those here: What is the difference between orthologs, paralogs and homologs?


Alcohol and athletes? I've seen a lot of articles claiming that alcohol has a very bad impact on athletic performance. Examples include, but are by far not limited to:

http://oade.nd.edu/educate-yourself-alcohol/alcohol-and-athletes/
http://www.theguardian.com/lifeandstyle/the-running-blog/2014/apr/23/how-does-alcohol-affect-athletic-performance
https://www.acsm.org/docs/current-comments/alcoholandathleticperformance.pdf
http://www.athletestore.co.uk/wordpress/wp-content/uploads/2013/01/The_Effect_of_Alcohol_on_Athletic_Performance.7.pdf

I'm of course not in position to doubt those articles, as I'm a no expert in biology.

However. There is one thing I find odd.

Namely. These articles themselves claim that alcohol is widely consumed even by the highest ranking athletes. I mean, if alcohol has that bad effects... then it couldn't have been consumed by highest-ranking athletes, as alcohol-consuming athletes could never rich the heights of the tops of proffessional sports?

Also. AFAIK mediaval knights were not abstinents by any means, they were drinking beer and wine and mead to excess; yet they were able to bring their strength, stamina, etc, to an extreme.

This is not something I wish to argue about; rather, this is something I fail to understand.

BTW. This question is not personal; I don't do sports and I very rarely drink. And I regret the former, not the latter.

Whenever you look at any parameter in a population, you will have a spread. Let's take I.Q., for instance (and lets not quibble about how it's measured; it's irrelevant for our purposes):

This is the famous "bell shaped curve". You can see how few people are significantly above normal. Now, that line continues to include people with an I.Q. of 200+. That's not immediately obvious from the graph. It also continues the other way - people with an I.Q. so low that they cannot participate in their own testing. That's because the vast majority of people fall between 70 and 130.

The same principle applies to physical skill, bravery in battle, etc. The curve may be flattened or sharper depending on what parameter is being measured, but rest assured, paid professional athletes fall in the upper 1 percentile.

Lets go back to intelligence for a moment. Take someone like Bobby Fischer (Chess Player), I.Q.: 187

I guarantee you that even falling-down drunk, Bobby Fischer would have beaten me easily in a game of chess (and it's not because my I.Q. is average or below). It's because he was so very much, unimaginably better at chess than I am.

I guarantee you that even falling-down drunk, Albert Einstein could solve mathematical equations I can't even write. It's because he was so very much, unimaginably more intelligent than I am.

It's the same with great athletes. Even if they drink every night, a great athlete will outperform you or me on any given day.

That's why you are just dead wrong when you state "then it couldn't have been consumed by highest-ranking athletes, as alcohol-consuming athletes could never rich the heights of the tops of proffessional sports".

You are just laboring under a completely false premise. These people are so much better than people only 1 percentile below them that drinking doesn't necessitate that they fall in the ranks.


If mantis shrimp have 16 photoreceptors then how many other colors on the spectrum are there? Mantis shrimp have 12 to 16 photoreceptors and humans have 2, and in rare occasions even 3. But if mantis shrimp can see 16, how many other colors are out there? How many photoreceptors is possible? How much of the spectrum is not ever going to be seen by any creature ever?

The first source you posted pretty much answers your question. Here are some others, probably referring to the same study but talking about it differently:
The Mantis Shrimp Sees Like A Satellite (National Geographic; this article is referred to in your first source)
Study Offers Insights into Unique Color Vision of Mantis Shrimp
Mantis shrimp's super colour vision debunked (Nature)
Here is the paper that those three articles are based on:
A Different Form of Color Vision in Mantis Shrimp
And what seems to be the author's (slightly more recent) thesis on the subject:
Colour vision in mantis shrimps: understanding one of the most complex visual systems in the world
The big thing to understand is that there is no such thing as "the color spectrum". There is the electromagnetic spectrum, which is one-dimensional: you can describe an electromagnetic wave's position on the spectrum with one number, its wavelength. But if you look at a picture of the electromagnetic spectrum with the colors associated you can notice something immediately:

You don't see a uniform increasing of a single quantity from one number to the next, you see several distinct colors following each other.
That's because the point of color vision isn't to detect variations along the electromagnetic spectrum per se; the aim is to allow our brains to get more information about the world around, based on the fact that light comes in many different wavelengths. Different objects will reflect different combinations of those wavelengths, meaning being able to tell some of those wavelengths apart improves our ability to tell objects apart based on those differences.
The key here is that there isn't a perfect way of doing this; nobody has a system where you detect the exact wavelength of each photon and tell exactly how many of each wavelength you receive. What human eyes do is have some specific receptors be more receptive to some wavelengths than others, and then the brain compares how excited each receptor is and puts all that information together to generate a sense of "color", which is basically a way of telling some things apart when they reflect certain different wavelengths. It's related to wavelength, but isn't the same thing; for example our brains recognize wavelengths that excite the red and green receptors equally as "yellow". This includes wavelengths that fall between the red and green wavelengths, but also combinations of red and green wavelengths. That's how you get the color wheel, the ability to make some colors out of others, and the fact you can generate all colors that we see from three primary colors. An organism with an extra receptor between the red and green would be able to tell those different combinations of wavelengths apart so that "yellow" to us would look like several different possible colors to them. Conversely, trichromatic humans are able to tell colors apart, like red and green, that are one single color to dichromatic mammals.
So the answer to "how many colors on the spectrum are there" is "there is no universal color spectrum". Every organism with its own system of light receptors can theoretically have its own color spectrum; how many colors they see is a question of how many different combinations of wavelengths they can tell apart, and that's a function of how many receptors they have but there can also be other factors (like the sensitivity of given receptors, how much processing power they're dedicating to color vision, exploiting different aspects of physics that affect wavelength... In humans even language and culture can influence color discrimination to some extent).
And where does the mantis shrimp come in? Well this is interesting, because it's been generally thought as you put it that the mantis shrimp would be able to see many more colors than we do, due to its much more numerous receptors, but the recent studies mentioned in the first source you linked to suggest that the mantis shrimp is worse at discriminating colors than we are, i.e. it sees fewer colors. However it appears its color vision functions very differently, and that's where the 16 different receptors come in. It's possible that the different receptors allow the mantis shrimp not to detect more colors, but to process the colors it does detect much faster. To quote the Nature article:

If the shrimp eye compared adjacent spectra, like the human eye does, it would have allowed the animals to discriminate between wavelengths as close as 1–5 nanometres, the authors say. Instead, each type of photoreceptor seems to pick up a specific colour, identifying it in a way that is less sensitive than the human eye but does not require brain-power-heavy comparisons. That probably gives the predatory shrimp a speed advantage in distinguishing between different-coloured prey, says Roy Caldwell, a behavioural ecologist at the University of California, Berkeley.

And the National Geographic one:

Their working hypothesis is that the mantis shrimps analyse the outputs from all of their 12 receptors at once. Rather than making comparisons between those receptors, they pass the entire pattern of outputs onto the brain, without any processing. “One could imagine that they have a look-up table in their brain,” says Marshall. So rather than discriminating between colours like we do, their eyes are adapted for recognising colours.
“Oddly enough, the closest device to stomatopods would be a satellite,” says Marshall. “Remote sensing algorithms have look-up tables of colour to fill in the image that the satellite forms.”

For your other questions:

How many photoreceptors is possible?

Theoretically the limit would only be how many you can pack in an eye and how many chemical pigments exist, but in practice there is a trade-off between color and spatial discrimination (after all any color receptor is a light receptor that's limiting itself to certain wavelengths only, so you lose in overall light perception). Another article in the Science journal the article on Mantis shrimp color vision appeared in suggests the optimal number is isn't over 4 (in organisms that use our system of color vision of course, not the mantis shrimp's):

In fact, theory predicts that two to four receptor types are optimal for discriminating the spectra of natural materials and maximizing the number of objects that could be distinguished by color.

And:

How much of the spectrum is not ever going to be seen by any creature ever?

Again, considering every set of photoreceptors leads to its own color spectrum (and every brain probably cooks it to its own sauce beyond that), that question applied to the set of all colors isn't really meaningful. The answer would probably be along the lines of "almost all of it" because the set of actual color vision systems in the natural world is an infinitesimal percentage of the set of theoretically possible color vision systems... but it's not like those colors are "out there to be seen" in anything but the most abstract sense; they exist in the same sense that a child that's the combination of a sperm and egg that haven't met exists.
If by "spectrum" we mean "electromagnetic spectrum", then there is likely an upper and lower bound to the wavelengths that can be detected, where wavelengths on the upper bound are too deadly for a cell to survive let alone detect (though bodies can and do sacrifice cells to exploit inhospitable environments, see the cells lining our stomachs, so even that might not be an absolute obstacle), and on the lower bound aren't energetic enough to cause pigment molecules to react to them. I don't know what those bounds are though; it's likely that more important constraints are how useful it is to detect those higher and lower wavelengths, that any organism would bother evolving the ability. (also, for the lower wavelengths, whether their detection is associated with forming an image. For example we can detect infrared radiation as heat but we don't think of that as "seeing". On the other hand "eyespots" that detect visible light without forming an image are often thought of as a primitive form of sight; there is a level of arbitrariness there but it's also true that lower wavelengths have different optical properties).


Correlating beta-lactamase expression to absorbance When penicillin-resistant bacteria are grown in liquid culture media,
  β-lactamase is secreted into the medium. The supernatant of such a medium can be assayed for β-lactamase activity. Culture supernatants
  different organisms , which are suspected to be penicillin-resistant,
  were obtained and were assayed for β-lactamase activity. The corresponding absorbance value were measured at a certain wavelength.

Let us assume that supernatant from organism 1's culture had absorbance value X and 2 had absorbance value Y.

My question : If X>Y, does that mean that more β-lactamase was being produced by organism 1 ?

In the β-lactamase test, an inhibitor of β-lactamase is added to a sample of the culture medium. The inhibitor binds to the enzyme and changes its color, which is in direct correlation to the concentration of the β-lactamase. More β-lactamase means more inhibitor binding and this results in more color development leading to a higher absorption. So higher absorption means more β-lactamase in the supernatant.


Are there comprehensive species descriptions on most species? I was having a browse through Wikipedia and noticed how even the rarest, hardest to find species of bird have comprehensive articles and comprehensive descriptions, but other species like the 1400 Andrena species have next-to-no information.

I tried to do a search for resources on individual species of Andrena bees but found very little - at best a short description and the name of the entomologist who described it. Is there a place I could go to find comprehensive resources on these bees? If not, why are the available resources on these species much less comprehensive than those on other species?

To suggest a new species, someone must necessarily makes a rather thorough effort of description. A good solution to get some info could be to go to the original paper however, these papers can be very old and hard to find. Also, the standards at that time might be very different from today's. After all, K. Linnaeus managed to describe 13,000 species also maybe because the description were more simple than they are today (see this related post). Andrena hattorfiana was described by Fabricius in 1775 but I could not find the original paper.

Note that the english wikpedia article for A. hattorfiana is relatively decent.

The IUCN red list is also a good source (see here)

The page for the Encyclopedia Of Life is unfortunately a little empty.

Here are some amazing pictures on flickr

You can also just search papers that refer to a given species. Here are a number of papers on A. hattorfiana.


How is the activation energy lowered in an enzyme by just orientating the reactants closer to one another? If the activation energy is lowered, bond strength has decreased. How does purely orientating the reactants closer to one another lower the activation energy in a protein? The only thing I can think of is steric strain.

The activation energy is not only lowered by orientating the substrate but by stabilizing the transition state.

According to the induced fit model many enzymes show a higher binding affinity to the transition state of a substrate.


Roughly at least, how many types of cells comprise human blood? A long time ago there were only three kinds - red, white, and rose platelets. Advances in cell sorters and more recently in genetic techniques and differentiation studies have led to the identification of a wide variety and complex lineage of cells that comprise human blood.

Roughly at least, how many types of cells are currently identified?

I understand that "types" is a non-technical term, and I'll try to better define what I mean. For example, I do not mean to enumerate each antigen specificity separately because that would make the number fairly large and probably dependent on the individual's history.

One possible definition of a "type" would be that it has been given a name.

I don't mean to include cells that are present due to injury, clean-up, trash collection, or foreign cells including bacteria, viruses, parasites etc.

Just for an example, here is an overview of types of hematopoietic stem cells. There may be further recognized subdivisions, I don't know how far it goes. There are certainly other cells that comprise human blood. (From here.)

I think any answer to this question will be subjective, depending on what you consider to be distinct cell types --- how detailed the classification should be.

As you mentioned, if you consider all immune cell populations that can be separated by surface antigens, that's already a pretty large number. In 2013, the Immunological Genome (Immgen) project reported characterization of 249 immune cell types, and I think they are still working on expanding their catalogue (see immgen.org). One can argue about which of these are really different enough to be called "cell types", but I think it gives a pretty good ballpark number.

At some level of resolution though, the notion of "cell type" itself becomes slippery. While previously it was thought that many cell types were terminally differentiated (unable to change back to more primitive forms), we now increasingly find that these "cell types" are more like temporary "cell states", or phenotypes, that can change over time. For immune cells, this phenomenon is often called "plasticity"; for more information, see for example this paper. The advent of single-cell genomics has further strengthened this view, demonstrating that individual cells can dynamically change their gene expression pattens. These issues makes it hard to uniquely define and count cell types, and it might be more useful to reason quantitatively in terms of the phenotypes and behavior we can measure --- expression patterns, signalling molecules, metabolism and so on.


Parallel Autonomic regulation of Cough and Runny Nose I describe here the serous inflammation of runny nose.
Cough is mediated by Cough center.

I think Runny nose is also controlled by the autonomic nervous system and probably by some reflex.

Assume you have mild runny nose under Montelukast medication.
You have irritated cough (coughing so much you cannot sleep).
You stop the cough by codeine before sleeping.
You sleep at 30 degree angle.
Sometimes, you also feel that the runny nose stops i.e. complete relieve of runny nose in both nostrils and whole nose for about 30 seconds to a minute - perfectly clear nose and no serous inflammation - no symptoms of imflammation in the nose.

Then, it (serous inflammation) starts again - not like mucose running back - but the feeling of uneasiness in the whole nose starts again - then mucose can also continue to migrate from one nostril to another.
What is causing this kind of behaviour i.e complete relieve of of runny nose for about 30 seconds?
What is causing the stopping of serous inflammation in the nose?

I think the Runny nose can also be controlled by medulla oblongata because Codeine is blocking the cough center there.

I tried to achieve this behaviour by stimulating by lymphatic system in regulating breathing by abdominal muscles - lymphatic drainage massage - breathing inside with abdomen (not with thorax) and deeply exhale with abdomen).
At that time, I did not hear any creaky sounds in my throat.
After trying to stop the serous inflammation again, I heard them without managing to stop serous inflammation in both nostrils at the same time.

How is the control of Cough and Runny nose regulated by the autonomic nervous system?
Probably, some parallelism there.

Processes going on regulating Cough and Runny nose

reflex from medulla oblongata
sympaticus and parasympaticus (not sure about these)
possible parallelism of irritated cough and runny nose control

Skymninge mentioned opioidreceptors and the withdrawal symptom of opiods as a runny nose: codein binds to opioidreceptors.

I think now that the cough can trigger runny nose.
I breathed with empty nose some 15 minutes.
Then, I had a deep dry cough and right after it a stuffy nose.
I really felt this time the negative gradient at the level of kidneys and also posteriorly.
I do not know how this kind of pain was felt, I think, near or on the kidneys.
I do not understand the effects of deep dry coughs.
They seem to be linked to several processes and locations in the body.

After this deep dry cough, I did some abdominal breathes and this way massaging the lymphatic circulation systemically, the stuffy nose disappeared.
My thorax is opposite of astonic person (say if you remember the name in Propedeutics).
This can be a restricting factor in the circulation of the lymph.

My conjecture is that the people with big chests (opposite of astonic) need to concentrate more on abdominal breathing such that to keep out of stuffy noses.
Restricted lymphatic circulation causes less wastes returned to the blood circulation.
Thus, accumulation of bacteria in the larynges which increases the risk of a dry cough.
Good lymphatic circulation ensures that bacteria is not congested in the larynx.
So cough seems to be a mechanism to start a runny nose.

This all is finely regulated.
There are several receptors in the body.
The deep cough however seems to be linked to a reflex which causes a runny nose.

Some studies about opiates and respiratory activity

The effects of opiates on the respiratory activity of thoracic motoneurones in the anaesthetized and decerebrate rabbit.


How do lipid-soluble substances diffuse through the cell membrane? It’s said that water-soluble substances can diffuse through cell membrane with less ease than lipid-soluble substances because the former encounters impedance in the hydrophobic region of the phospholipid bilayer. However, does the same logic not apply for hydrophobic substances, in that they cannot traverse the hydrophilic outer/inner surfaces of the plasma membrane? How would they be able to enter or leave the cell with greater ease?

See this paragraph and image from The Cell: A Molecular Approach. 2nd edition.:

  During passive diffusion, a molecule simply dissolves in the phospholipid bilayer, diffuses across it, and then dissolves in the aqueous solution at the other side of the membrane...Passive diffusion is thus a nonselective process by which any molecule able to dissolve in the phospholipid bilayer is able to cross the plasma membrane and equilibrate between the inside and outside of the cell. Importantly, only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates (Figure 12.15). Thus, gases (such as O2 and CO2), hydrophobic molecules (such as benzene), and small polar but uncharged molecules (such as H2O and ethanol) are able to diffuse across the plasma membrane. Other biological molecules, however, are unable to dissolve in the hydrophobic interior of the phospholipid bilayer. Consequently, larger uncharged polar molecules such as glucose are unable to cross the plasma membrane by passive diffusion, as are charged molecules of any size (including small ions such as H+, Na+, K+, and Cl-). The passage of these molecules across the membrane instead requires the activity of specific transport and channel proteins, which therefore control the traffic of most biological molecules into and out of the cell.

As shown in above paragraph, molecules have to dissolve in phospholipid bilayer to diffuse through it. But since the hydrophilic part is already interacting with water, so dissolving is mainly for the hydrophobic part. Now, since hydrophobic part is non-polar, so it can dissolve only non-polar substances (like dissolves like). Thus, small gases like O2, CO2 and non-polar molecules like benzene easily dissolve in hydrophobic part and diffuse through it. Also, molecules like water and ethanol can also dissolve in it in small amounts due to their small size and very less polarity. That's why only some molecules of water can diffuse passively, large amount of water would require aquaporins. Now, since bigger molecules like glucose have large size and high polarity, they cannot dissolve in the membrane and thus require transmembrane channels even for diffusion. Similar case is with ionic substances too: they require ion channels for their diffusion.

Hope this helps. Comment below if you have any further doubts.


Can Palisade Cells Survive Independently? I have been intrigued by this question. Can palisade cells survive independently from its parent plant in a chemical environment? For example, if we were to separate a palisade cell from a plant and place it in sucrose solution, how long would it survive?

Yes they can. In 1902 Haberlandt reported single palisade cell culture from leaves in knop’s salt solution. Now there are many different methods of plant tissue culture

for PLANT TISSUE CULTURE see


What is this flying insect? This insect was captured in Australia near Canberra. It has a very hard exoskeleton and is over an inch long. It seems to have 6 wings - 2 large pairs and one very small pair. I did not see a stinger - however I have no idea.

I believe this is the Hairy Flower Wasp, Scolia soror. I don't know what you mean when you refer to six wings, however. Like all other wasps, this species has four wings.


Virus that can enter all cell types As I understand, each virus type can enter a particular cell type. For example HIV can enter CD4 & CD8 cells, while HBV can enter liver cells, some other viruses can enter other cell types like brain cells and cause brain diseases.

Is there any kind of virus that can enter all mammalian cell type so it can be used as a general gene transfer method?

I don't know if there is any "universal" virus that really gets into every cell type, but lentiviruses come pretty close. Lentiviral transfection vectors have been developed for a wide range of human (or mammalian) cell types, including immune cells and terminally differentiated cell types such as neurons and skeletal muscle.

But these are of course experimentally modified viruses that have been optimized in various ways for transfection; typically, the naturally occurring virus is much less efficient. I would guess it's unlikely that a natural virus can enter any (human) cell type, because this capability would be expensive for the virus to maintain, and there is probably little pressure to do so --- as long as the virus has a working route of transmission, via the airways for example, there is probably little benefit in being able to transfect other tissues.


Do Yeast Insertion constructs revert? If I insert a new gene with a yeast integrating plasmid and select with a drop out culture once, can I assume that the newly integrated gene will stay in the strain without putting selective pressure on it?  (i.e. can i use normal liquid culture and plates after getting the yeast with the newly integrated strain?

It depends upon exactly what you have done.

The standard way of using a yeast intergrating plasmid (YIp) is for it to integrate into the genome by recombination between a piece of yeast DNA that the YIp carries and the same DNA in the genome. This is often, but not necessarily, the selectable marker. So for example a YIp carrying the URA3 gene as its only yeast DNA will integrate at the URA3 locus (probably mutant to allow selection for Ura+, so more correctly ura3).

If the YIp is linearised by cutting at a site within the URA3 marker this will direct insertion and will increase the transformation efficiency.

Once insertion has taken place, the configuration at the integration site is:

chromosome...URA3...other YIp sequences...ura3...chromosome

This is inherently unstable because a looping-out event can take place via recombination between the URA3/ura3 regions. So removing selection means that you run the risk of losing the insert. Furthermore, it is possible for looping out to occur leaving the URA3 allele behind instead of the ura3 allele. So you can lose the vector even when selection is maintained (but this will depend on the exact nature of the mutation).

More complex configurations are possible where the targetting sequence is separate from the selectable marker, and where digestion removes a whole chunk of the targetting sequence before transformation. So for example if the TRP1 gene was used for targetting a plasmid with the URA3 marker in a TRP1 ura3 strain you would get:

chromosome...TRP1 fragment A...URA3+other YIp sequences...TRP1 fragment B...chromosome

the resulting transformant is now Ura+ because of the integrated URA3 plasmid, but some TRP1 DNA is now missing (the DNA that was excised when the plasmid was digested) so the strain is trp1. The appearance of this Trp- phenotype indicates that the transformation has probably occurred by the pathway described.

In this case the inserted plasmid is much more stable because those two remaining fragments of TRP1 DNA are not identical, so there is no possibility of looping out.

In summary, if your transformant has the insert carrying the "new gene" flanked by a repeating sequence then it is unstable, otherwise it is ok to remove selection. In the first case, if the new gene is at all deleterious then there will be a strong selective pressure in favour of cells which have lost the insert.

Addendum

You can avoid using YIp plasmids altogether by integrating your new gene at any locus using long targetting primers, as shown in the Figure below.

Design primers to amplify your gene as usual, but synthesise them with 40 bp 5' extensions corresponding to two sequences at the extreme ends of the integration site (URA3 used here for illustration purposes). The resulting fragment can then be used in a transformation and will integrate at the URA3 site by homologous recombination, replacing the resident DNA. The advantage of using URA3 for this is that you can select for integrants as Ura- cells by resistance to fluoorotic acid (FOA). Although you can probably select directly for this, I have always co-transformed the fragment together with another selectable plasmid (LEU2, TRP1 etc., but not a CEN plasmid) Then your e.g. Leu+ transformants can be screened for those that have also become FOAR. This co-transformation happens at quite high frequency because the cells that do take up DNA take up a lot of it. Once you remove selection for the co-transforming plasmid it will soon get lost, leaving you with a clean non-reverting integrant.

It's been a while since I did this sort of thing - probably there are even smarter methods around now.


Neurophotonics vs. Optogenetics What is the difference between the two? I see them frequently listed together in conference descriptions but can't seem to find anything that clearly explains the difference.

Neurophotonics refers to the use of light to study the brain, including measurement (i.e. microscopy, including the use of fluorescent molecules that allow measurement of ions or voltages in live tissue, but also including histological techniques) and manipulation (using light to activate, inactivate, modulate, etc neural activity).

Optogenetics refers to the use of genetically encoded (whether delivered via virus or in a transgenic animal) constructs that respond to light and are introduced into cells where they are not normally found, often neurons. Neurophotonics is a broad term that would include optogenetics.

In my personal opinion, optogenetics is a fairly specific term that is useful, though it certainly has some popular buzz around it. Neurophotonics is a new buzzword that encompasses a lot of techniques that have been around a long time, and while these techniques are constantly improved upon, the neurophotonics label isn't really necessary (but sounds fun).


What is the name of the baboons that live in Saudi Arabia In Saudi Arabia there are a lot of baboons in the mountain area. I would like to know what's the name of this specific baboons so I can read about them more:

These look like Hamadryas Baboons (Papio hamadryas). They also fit the geographical location.


How is excess semen removed if ejaculation does not occur? There are some attempts to answer the question that I found via cursory Google search, but none of them were appropriately sourced.

This site claims that they are "recycled like blood cells", but the blood cells are recycled using the spleen, and I don't think spermatozoa normally enter the blood stream at any point in time.

This other site contradicts the first site, and claims that they are removed from the body by "dripping" them, therefore expelling them in the normal urine stream.

What is the actual process through which semen is removed if ejaculation does not occur?

Well as far as my knowledge goes in this aspect..

If sperms are not ejaculated then they are simply reabsorbed by the epididymis and recycled.
I would say the first website you have linked up there is what is a more appropriate explanation.


Why is wombat scat (feces) shaped like cubes? I've heard that wombat scat is cube shaped, but I don't understand how that can happen. Has anyone studied the phenomenon? What would the evolutionary pressure have been to cause this?

I'm almost certain that your question is based on the press that Patricia J Yang's research is receiving (e.g., here and here).
Yang and her co-authors examined the structure and mechanics of some dead wombats to investigate this question further. They found that varying degrees of pressure in the latter portion of the wombat's intestines (in conjunction with a dehydrating of the fecal matter) led to the characteristic cube shape:
From their abstract:

In the final 8 percent of the intestine, feces changed from a liquid-like state into a solid state composed of separated cubes of length 2 cm. This shape change was due to the azimuthally varying elastic properties of the intestinal wall. By emptying the intestine and inflating it with a long balloon, we found that the local strain varies from 20 percent at the cube's corners to 75 percent at its edges. Thus, the intestine stretches preferentially at the walls to facilitate cube formation.

Why do this?
There seems to be two major reasons:

Mark territory
Attract mates

For example, see Wells 19891:

The rubbing of posts, logs and overhanging branches with their backs and rumps and deposition of faeces along trails may be a means of olfactory communication used in the maintenance of territories

One hypothesis is that by being square, the droppings don't roll as easily and therefore stay in the place that the wombat intended to mark.
I've also seen hypotheses about wombats stacking their square feces as some sort of signaling, but I couldn't find any reputable literature sources that make this suggestion.

1: Wells, R.T., 1989. Vombatidae. Fauna of Australia, 1, pp.755-768.


Are there differences between the activation proteins of Eukaryotes and those of Prokaryotes I'm in BIO 203 (for reference to my skill level), and I noticed the textbook makes a whole section out of transcriptional activator proteins, their function and applications in eukaryotes, but in prokaryotes the term "activator protein" is used only once when mentioning the lac operon.

Are they the same type of activator proteins? Do they employ the same mechanisms?

In general transcription activators are transcription factors. These are very different in eukaryotes although some families share similar domains (e.g. two component signalization). I recommend you read through these two chapters to get a more complete overview on the differences.

https://www.ncbi.nlm.nih.gov/books/NBK21683/

https://www.ncbi.nlm.nih.gov/books/NBK21572/


What is a good review article source for Physiology? I am looking review articles for Physiology.
For instance, Physiological explanation of steps of measurement of the metabolism by Douglas-Haldane.

There is no section for Physiology or metabolism in Advanced Search of Nature Review.

What is a good review article source of Physiology?

The Journal of Physiology

Annual Reviews Physiology

Journals from American Physiological Society

Frontiers in Physiology

Experimental Physiology

Often, notable research papers are published in journals with high impact factors, although being published in a journal with high impact factor does not mean the research is better over research in smaller journals. But it can be a rough indication.


Are specific primers or detectors, or both, used in COVID-19 tests? I am trying to learn about the rRT-PCR testing procedure used to test for COVID-19, but I am slightly confused on one point. Are highly specific primers used with a non-specific detector, or are highly specific detectors used, or are both specific primers and detectors used? Some of the sources say that multiplex PCR is used, which indicates a specific detector, but as I am still a beginner on the subject, I am not sure. I would also really appreciate it if somebody could also point to a source that details the some of the testing procedures.

Thank you

When you run a PCR reaction, you are making copies of a DNA sequence of interest (cDNA in case of retrotranscription, since retrovirus have RNA as the genetic material). The sequence of interest is presumed to be in a sample, that you take from the patient, or some organism (I say 'presumed' because the PCR is precisely to confirm this). These copies are made by a group of 'generalist' enzymes, called polymerases, and by generalists I mean that they do not discriminate on which DNA sequence they are copying. But, they cannot copy DNA de novo (from scratch). The copying process needs to be 'primed' by a short sequence of nucleotides that is complementary to the DNA of interest. These are called primers, and they effectively serve as probes to target the copying of the specific sequence you need to amplify. And this is where scientists put a lot of care on: primer design. Bad primers will not be very specific, or will not be very efficient during the amplification process. As for the 'machine' that actually detects the copies, there are many variants. The most typically used in research and diagnostic laboratories, involves staining the amplified DNA with some molecule that binds nucleic acids (which there are many), and visualize it via DNA electrophoresis. What you visualize is a population of DNA copies (via the staining you make), so you need to know beforehand what to expect. For instance, do you expect a small fragment (a couple hundred basepairs) or a big one (a few thousands?). You have a 'ladder' (also called marker) that gives you a reference to compare, like in this image:

People know what to expect because they already know the DNA (or RNA) sequence they are amplifying (otherwise they could not have designed the target primers). They know the sequence because they've done some form of nucleic acid sequencing (labs, health institutes, and so, do this all the time and deposit the sequences in some platform, for instance GeneBank).

A 'positive' amplification will give you a band in the expected size range, and no other bands (because your primers are targeted for a particular DNA sequence). But as you mentioned, there exists also a multiplex PCR reaction. In it, you design multiple primers to target different sequences (using the same DNA sample -e.g. from a patient or organism-), but the verification process is basically the same. Here people are extra careful to avoid cross-interactions among the primers added to the reaction.

PCR is a family of techniques, not a single one. There are variations in the actual process, and also in the 'detection' (for instance, qPCR uses real time detection of copy numbers). But the general principle is the same: primers are specific, while the 'detection device' is not really.


Does turbidometeric method count cell number or cell mass? Here it says that scattering is inversely proportional to cell number but also says that we can observe greater absorbance as cell number increases.

So does turbidometeric method work on cell mass or number ?

Your text says that scattering is proportional to cell number, which is correct. It is not inversely proportional, as you stated.


Why can you not tickle yourself? It's the age old question, why can't we tickle ourselves? If you rub your fingers along your skin, sure there's sensation but you don't break down into a laughing fit (at least I don't :P), if someone else does it to you, you're rolling around on the ground begging them to stop tickling you.

Why is it that other people can tickle us but we can't tickle ourselves by touch? (I'm aware that if you use a feather or foreign object on yourself you can be tickled by it so that doesn't count.)

In short, it's because your brain processes external and self-produced stimuli differently.

If someone tickles you, you feel that ticklish feeling, but when trying to tickle yourself, there is a reduction in the sensation. When you are tickled by someone, a part of your brain activates causing you to laugh, etc., but it seems that when you trying tickling yourself, your brain doesn't react the same way and that section of the brain does not activate as if someone were tickling you.

Blakemore, S.J., D.M. Wolpert, and C.D. Frith. 1998. Central cancellation of self-produced tickle sensation. Nature Neuroscience 1(7): 635–640. doi:10.1038/2870


What is the name if this glittery fly seen in Pittsburgh? I have photographed the following fly which is iridescent green in Pittsburgh, PA.
I guess it was about 0.5-1.5cm long.

Can you help me to identify it?

Looks like a green bottle fly.

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

Might be a Common Green bottle fly.

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


Formula for Oxygen Consumption for Atlantic Salmon (Mathematical) - insecurities regarding variable The oxygen is calculated in mg per kg per something, so what does $h^{-1}$ stand for? hours maybe?

The formula given below is an estimation of oxygen consumption for Atlantic salmon

  \begin{equation}
        V_{O_{2}} (mg \cdot kg^{-1} \cdot h^{-1}) = 61.6(\pm6.6) BW^{-0.33(\pm0.11)} \cdot 1.03(\pm0.10)^{T} \cdot 1.79(\pm(0.10))^{U}
    \label{eq:salmonoxygenconsumption}
\end{equation}

Here is a link containing the scientific article describing the formula - ScienceDirect

Yeah, it's hours.
Further down in the paper, you can read,

The mass exponent was estimated to be −0.33 (b in Eq. (4)) for the specific metabolic rate \begin{equation} V_{O_{2}} (mg\space {O_{2}} \cdot kg^{-1} \cdot h^{-1}) \end{equation}

Rate by very definition implies an extent of time; since mg refers to oxygen and kg refers to water, the only variable left is h, which evidently refers to hours. Hours also jives well with the experimental design.

Source:

Grøttum JA, Sigholt T. 1998. A model for oxygen consumption of atlantic salmon (salmo salar) based on measurements of individual fish in a tunnel respirometer. Aquacultural Engineering 17(4): 241-251.


Insect crawling Identification What kind of insect is this, and is this venomous, or dangerous? Don't need full species name just common name will do, color is red. Grandma always warned me of this, they usually are seen in monsoon season during heavy rains. They coil upwhen disturb .
Location: Country: India, lower himalayas
Google Map :Exact location
A miniature version of this also exist in my area don't have pic though.

Given the shape and the number of legs. That most definitely is not an insect. An insect has exactly 6 legs. No more, no less.
That critter in your picture is some kind of millipede (“a thousand feet”; not literally a thousand, of course; https://en.m.wikipedia.org/wiki/Millipede), not to be confused with a centipede (“a hundred feet”; also not literally a hundred).
Millepedes are mostly harmless to humans. They eat things like dead plant matter or fungi. They sometimes also eat seedlings so they can be considered pests in gardens.
And given the colour, that’s possibly a rusty millipede (https://en.m.wikipedia.org/wiki/Trigoniulus_corallinus). They have a very wide distribution around the Indo-Malayan region. Although there seems to be no recorded observation of it on iNaturalist around your region (https://www.inaturalist.org/observations?place_id=9248&taxon_id=123010).


Thousands of Reporters Integrated in Parallel (TRIP) barcodes Has anyone worked with constructing barcodes for TRIP? How does constructing of barcodes work in general? I don't seem to be able to grasp the basics of constructing these barcodes.

From the paper and user manual it seems that barcodes are random sequences of pre-defined length of 16-20bp ± 1bp. On data analysis step they are combined and all barcodes 2 Hamming distance apart (it means that two words have difference in one letter from each other) will be discarded from the list of genuine barcodes.


Proof of the equivalence between two ways of defining ESS Background

Two common ways of defining what an Evolutionary Stable Strategy (ESS) are:

First definition:
Consider a population composed of populations playing two strategies, $\mathbf{p}$ and $\mathbf{q}$.
Let us denote $W(\mathbf{p})$ the average fitness of the
strategy $\mathbf{p}$. A population consisting of individuals playing $\mathbf{p}$ will be an ESS if, whenever a small amount of deviant individuals playing $\mathbf{q}$, the old type $\mathbf{p}$ fares batter than the newcomers $\mathbf{q}$. This means that for all
$\mathbf{p}\neq \mathbf{q}$,
\begin{equation}
  W(\mathbf{p}) > W (\mathbf{q})
\end{equation}

Second definition: $E(\mathbf{p},\mathbf{q})$ is the payoff for $\mathbf{p}$-strategist against a $\mathbf{q}$-strategist. The strategy $\mathbf{p}$ is an ESS if and only if the following conditions are satisfied:

$E(\mathbf{p},\mathbf{p})\geq E(\mathbf{q},\mathbf{p}) \quad \forall
  \mathbf{q}$
If $\mathbf{q}\neq \mathbf{p}$ and $E(\mathbf{p},\mathbf{p}) = E(\mathbf{q},\mathbf{p})$, then
$E(\mathbf{p},\mathbf{q})> E(\mathbf{q},\mathbf{q})$

Question (shorter version)

The above two ways of defining what an ESS should be equivalent. How can I prove such an equivalence? Alternatively, do you know of a book (or a paper) that has this proof?

Question (longer version)

I understand that the first definition implies the second. According to the first definition:
\begin{align*}
   W(\mathbf{p}) - W (\mathbf{q}) &>0\\
   (1-\epsilon) [E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})]
   + \epsilon [E(\mathbf{p},\mathbf{q}) - E(\mathbf{q},\mathbf{q})] &>0
 \end{align*}
where $\epsilon$ is frequency of individuals playing $\mathbf{q}$. Since $0<\epsilon<1$, if the above inequality is true, the conditions 1 and 2 in the second definition must be true. The part that I find less clear is how the second definition implies the first definition. More specifically, that if $\mathbf{p}$ is a strict Nash equilibrium (i.e., $E(\mathbf{p},\mathbf{p})> E(\mathbf{q},\mathbf{p})$), then $W(\mathbf{p}) > W (\mathbf{q})$.

We need to show that if $\mathbf{p}$ is a strict Nash equilibrium, $E(\mathbf{p},\mathbf{p})> E(\mathbf{q},\mathbf{p})$, then $W(\mathbf{p}) > W (\mathbf{q})$ for some sufficiently small $\epsilon$. When $E(\mathbf{p},\mathbf{q}) \geq E(\mathbf{q},\mathbf{q})$, $\mathbf{p}$ clearly dominates $\mathbf{q}$.The less obvious case is when $E(\mathbf{p},\mathbf{q}) < E(\mathbf{q},\mathbf{q})$.

Since $E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})>0$, there should be a strictly positive number $k$ such that
$$k[E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})]+ E(\mathbf{p},\mathbf{q}) - E(\mathbf{q},\mathbf{q})>0$$
is true. Whatever this number is, we can write $k$ as $(1-\epsilon)/\epsilon$ for $0<\epsilon<1$. Substituting this into the equation above gives us the desired result.


How can computer predictions of protein folding be verified computationally? Currently, there is a lot of research focused on solving the folding patterns of proteins using computers (Folding@Home, https://fold.it/portal/, etc.).

The question that I have is: How do you know when you get it right?  Is there some way of verifying, in silico, that you have found a legitimate/correct structure for a protein?

Overview

Modelling has come on leaps and bounds over the last decade or so and in many cases has acted as a sometimes viable, and inexpensive substitute for experimental structures.

  How do you know when you get it right?

Ultimately, one still needs experimental evidence to know when a model generated in silico is right. But there are ways of scoring a model for how likely it is to be right.

  Is there some way of verifying, in silico, that you have found a legitimate/correct structure for a protein?

There are lots of ways to score and verify your models. Each method tells you something slightly different about the merits, or lack thereof, of your structural model. Some are designed to weed out the obviously awful models and some allow you to detect exactly where your model looks to be accurate or inaccurate.

MODELLER Homology modelling output verification on the fly.

I am most familiar with modeller for homology modelling. Other softwares are available and they are each evaluated by CASP every two years since 1994.

In homology modelling there are 3 common scoring systems that can be used to assess the biochemical viability of a model. This email covers when to use each one. My answer expands and explains a bit more.

molpdf is the Modeller objective function.
GA341, discussed here is derived from  Z-score (calculated with a statistical potential
function), which is a target-template sequence identity, and a
measure of structural compactness.
DOPE is a more up to date method, first published in 2006, and is more true to "biological viability". From the publication:

  DOPE is based on an improved reference
  state that corresponds to noninteracting atoms in a homogeneous sphere with the radius dependent on
  a sample native structure; it thus accounts for the finite and spherical shape of the native structures.

Which to use depends on what you want to do with the model, but of those three scores, DOPE is the most reliable at separating native-like models from "decoys".  DOPE is usually the starting place for figuring out which models might be right and which models are just plain rubbish.

Note:  If you use Rosetta then there will be equivalents to these, or you can run your generated models through these techniques. If you are using SWISS MODEL that comes with it's own somewhat black box verification techniques but you can still export the model for further verification.

General model check against experimental data.

A further validation of homology modelling methods or other structural models is ProSA. ProSA provides a great visual representation of where the z-score lies amongst actual crystal and NMR structures. There are probably others that do similar functions, but this is my personal go-to to get an idea of where my structure lies among experimentally gathered structures.

Sensitive residue by residue verification.

Although the aforementioned methods examine each residue, they usually output an overall score. Residue by residue scores are also available and require a lot of careful interpretation. For example, if you are analysing catalytic activity, a surface looping region that scores poorly might not be an issue, but a core catalytic residue that scores poorly renders the model useless. This means that just because your model has a good (lower) overall DOPE score than another model, doesn't mean it is necessarily a more accurate model for what you are interested in.

There are plenty of sensitive modelling scoring systems. Some of which are XdVal, MTZdump, the famous albeit old-school Ramachandran Plotting method, pdbU, pdbSNAFU, PROCHECK, Verify3D, and ERRAT to name a few. Each has a place when checking how correct your model is.


"Heterozygotic expection" - when heterozygote differs from both homozygotes, but homozygotes are similar For simple 2-alleles genetic model {a,A} and corresponding quantitative trait Q is typically true that

Q(aa)>=Q(aA)>=Q(AA)

or conversely

Q(AA)>=Q(aA)>=Q(aA).

For example, dominance means that Q(aa) < Q(aA)=Q(AA) , recesivity Q(aa)=Q(aA) < Q(AA) ; in additive models Q(aa) < Q(aA) < Q(AA) etc.

The situation when Q(aA)>Q(aa)~Q(AA) is atypical in biology ("heterozygotic expection ?", "uncooperative alleles ?"). Known example is HBB gene (heterozygotic form gives resistence to malaria but homozygotic mutation form is sickle-cell anaemia). But this is weak example only, because f is evolutionary advantage, not a measurable  phenotypical or biochemical trait.

QUESTION 1: Are there any systematic reviews about this atypical phenomena? (about "heterozygotic expection")

QUESTION 2: Is there a standard scientific term for this phenomena?

You question is a bit unclear, and I think there might be a couple of mistakes in your inequalities. However, I think you are looking for the terms Overdominance (also called Heterozygote advantage) and Heterosis (also Hybrid vigor). Both of these concepts imply that heterozygotes and/or hybrids have a phenotype that lies outside of the range described by the homozygotes (or, for heterosis, either parent or parent population).

Here is a section from "Genetic Dominance: Genotype-Phenotype Relationships" from Nature education - Scitable, which has a bit more information and a couple of references:

  In particular, the phenomenon known as overdominance occurs when a heterozygote has a more extreme phenotype than that of either of its parents. Indeed, in a few examples, a trait that shows overdominance sometimes confers a survival advantage in the heterozygote (Parsons & Bodmer, 1961).

You will find more information about overdominance and heterosis in any textbook on evolutionary biology, e.g. Futuyma's Evolution. There are also lots of relevant papers on the subject, and this one might be a nice example and starting point:

Frascaroli et al. 2007. Classical Genetic and Quantitative Trait Loci Analyses of Heterosis in a Maize Hybrid Between Two Elite Inbred Lines. Genetics 176(1): 625-644.


Pathogenesis of chronic venous congestion in skin? I think CVC cannot lead to heart failure primarily.
So let's think its pathogenesis in skin now only.

I think the pathogenesis is like this

dilation of veins and capillaries due to impaired venous drainage
reduced outflow of blood from a tissue
passive process
$\to$ local increase in blood volumes
$\to$ local increase in venous pressure
pathological
$\to$ shortage of oxygen and built-up metabolic waste
$\to$ structural changes in microvasculature
$\to$ increased venous permeability % hallmark of acute inflammation
$\to$ increased size of venous caliber
$\to$ emigration of leucocytes
$\to$ accumulation at site of injury
activation of acute inflammation
$\to$ protein into extravascular space
$\to$ increased viscosity of blood
$\to$ deoxygenated blood blood stasis
$\to$ congested tissue
$\to$ leucocytes move to endothelial wall (selectins)
$\to$ roll
$\to$ adhere (integrin to stop)
$\to$ migrate
$\to$ dysky reddish-bluish skin (cyanotic)
$\to$ healing via fibrosis
$\to$ scar
Causes: venous thrombosis; venous compression; heart failure;

I am not sure about the role of leucocytes exactly in this process.
I am not sure if they play a big role in the formation of cyanotic skin.
I think the outcome is mostly because of increased vascular permeability and its deoxygenated blood in extracellular space.

What is the right pathogenesis of chronic venous congestion in skin?

Probably so simple answer is enough

acrocyanosis (manifestation of heart failure) which lead to distant (acro - distant) cyanosis, bluish skin.


Why do we feel headache after ice cold drink? Whenever we drink ice cold drinks, after a couple of seconds, suddenly we feel intense pain rising from upper nose to forehead. What is reason behind this pain after too cold drink and why it's felt in that particular part of head?

The cold drink causes the blood in blood vessels of gums to freeze. This stimulates nerve endings and causes a sensation in brain.


Did early 20th century researchers state why they used E. coli as a model organism? I am investigating the early uses of E. coli as a model organism. Sadly, many early 20th century papers are not in English. In those that are, I have been unable to find explicit statements as to why a researcher chose to use E. coli as a model organism.

Does anyone know of early literature in which this reasoning is stated? I imagine that prior to the widespread use of E. coli, scientists would have had to argue why they chose to use it to investigate biological phenomena not limited to this bacterium alone.

Historical Fallacies implicit in the Question

  “…why a researcher chose to use E. coli as a model organism.”

Researchers did not work with E. coli because they regarded it as a “model organism”. They worked with it because they were bacteriologists and it was a convenient bacterium to use. As Joshua Lederberg wrote in Microbiology Today (2004):

  From the beginning, although pathogenic strains were also found, E. coli was used as a representative, harmless bacterium that could be safely and easily cultivated even on synthetic media. On rich media, it will grow with a
  doubling time of 20 minutes; hence readily visible colonies can be seen overnight when it is plated on agar. Specialized media, like MacConkey’s agar,were developed for the selective isolation and identification of E. coli, as this was used as a global indicator for the pollution of water supplies. Hence, during the first half of the twentieth century E. coli was well known to bacteriologists. However, it was rarely, if ever, mentioned in general biology texts, as bacteria were generally regarded as pre-cellular in complexity and devoid of the nuclei and other genetic apparatus of ‘real’ organisms.

Indeed the term ‘model organism’ was not used in this sense until about 1970, as this Google ngram shows.

  “I imagine that prior to the widespread use of E. coli, scientists would have had to argue why they chose to use it to investigate biological phenomena not limited to this bacterium alone.”

You imagine wrongly. They were not sitting down and saying “we want to study this biological phenomenon, what bacteria shall we choose?” and certainly not having to justify themselves on publication. In general they published in specialized bacteriological journals where audience and referees would know why they were using E. coli or whatever. Even when Tatum and Lederberg (see below) published a letter on bacterial recombination in the general science journal, Nature, in 1946 they did not waste space on species justification:

No. You are imposing modern attitudes — governed by the contemporary state of science and its funding — upon the science of a completely different era. That is not the way to approach history.

Why did E. coli become the most studied bacterium?

It would seem that the discovery of bacterial recombination in E. coli by Lederberg and Tatum (for which they shared the 1958 Nobel Prize for Physiology or Medicine with George Beadle) was one of the key factors leading to the expansion in the use of E. coli (see Microbiology Today article previously cited). This phenomenon was originally suggested by studies on the transformation pneumococcal bacteria, but its demonstration in the bacterial workhorse, E. coli, opened the doors to the use of a wide range of genetic techniques that could be used for biochemical, as well as molecular biological, studies.