Alcohol effect on heart and vascular system How does alcohol weaken heart muscles and why does it increase blood pressure both temporarily and long term? Is the long term effect due to increase of plaque or is it due to other effects?

The actual mechanism through which alcohol increases blood pressure is poorly understood (1,2). However, there is a mountain of evidence that shows that there is a strong correlation between alcohol intake and hypertension (small, infrequent amounts may have positive effects whereas excessive consumption has very negative effects (3)).

Back to the underlying mechanisms however, there is a good paper by Kazim Husain, Rais A Ansari, and Leon Ferder, which presents all the possible mechanisms that may contribute to alcohol-induced hypertension. The core ideas are as follows:

Mechanisms of alcohol-induced hypertension. CNS: Central nervous system; SNS: Sympathetic nervous system; RASAS: Renin-angiotensin system and aldosterone system.
Image taken from: Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention

Central nervous system in alcohol-induced hypertension

  [..] greater effect [of] alcohol on systolic blood pressure compared with
  diastolic blood pressure may indicate an imbalance between central
  nervous system factors influencing cardiac output and the peripheral
  vascular effects of alcohol

Baroreceptors in alcohol-induced hypertension

  Alcohol diminishes the baro (presso) reflex by interacting with receptors in the brain stem, i.e. nucleus tractus solitarii and rostral ventrolateral medulla.

Sympathetic nervous system in alcohol-induced hypertension

  Several studies reported increased sympathetic nervous system activation and discharge of sympathetic amines after alcohol consumption.

Renin-angiotensin-aldosterone system in alcohol-induced hypertension

  The serum levels of vasoactive substances such as renin-aldosterone have been reported to be affected by alcohol ingestion in vivo or ethanol in vitro.

Cortisol in alcohol-induced hypertension

  Certain studies have implicated the role of cortisol in alcohol-induced rise in blood pressure. Potter et al have reported a significant rise in plasma cortisol levels following alcohol consumption and a drop in plasma cortisol levels when alcohol intake was discontinued.

Increased intracellular calcium and vascular reactivity in alcohol-induced hypertension

  Rats treated with ethanol showed constriction of blood vessels due to greater shifts in the binding of the calcium ion (Ca2+) in arterial and arteriolar smooth muscle cells causes increased sensitivity to endogenous vasoconstrictors.

Endothelium and oxidative stress in alcohol-induced hypertension

  Imbalance of specific endogenous vasoconstrictor such as angiotensin II, endothelin-1 and nor-epinephrine and vasodilator nitric oxide (NO) may also play an important role in alcohol-induced hypertension. Alcohol stimulates the release of endothelin 1 and 2 from vascular endothelium in a dose dependent manner. Alcohol also increases the angiotensin II levels in the blood and vessels. Endothelin 1 and 2 as well as angiotensin II are known to be potent vasoconstrictors of the blood vessels.

References:

Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention
Saunders et al 1981 - Alcohol-induced hypertension
Grønbæk et al - 2009 - The positive and negative health effects of alcohol‐ and the public health implications


Where do Red Blood Cells use energy? I know that RBCs use glycolysis of glucose to lactate to produce most of their energy, but, if they are just carrier cells, where do they use the energy?

Erythrocytes are far more than inert "bags" of oxygen. They are complex, highly specialized cells and, like all cells, they require a number of basic processes to be maintained to work properly.

A good example (out of many) of why red blood cells need energy would be the active transport of ions across the membrane, a mechanism important for any type of human cell.

Quoting an article by Knight & Welt (J General Physio, 1974):

  The human red blood cell maintains a high intracellular potassium (K) and low sodium (Na) apparently by balancing passive movements of the ions with their active transport in the opposite direction. Thus the cell extrudes Na and accumulates K in a linked process (...). The component of Na-K transport (...) is dependent on adenosine triphosphate (ATP) in the cell.

A visual explanation of how export of sodium and import of potassium are linked to the consumption of ATP:

This means that to maintain correct gradients across the membrane (important to maintain osmotic level, and to provide a potential energy exploited in other import-export processes) the cell must continuously spend molecular energy.

Producing ATP in red blood cell is also important to maintain a pool of phosphate-donors for phosphorylation signals, involved in cell signaling for example.

Interestingly, it was also shown that releasing ATP is also a way for erythrocytes to communicate with their environment, possibly to stimulate microvessel dilatation and thereby allowing proper circulation of oxygen near the destination site (see Ellsworth et al, Acta Physiol 2016 for a detailed review).

All these processes require ATP, and therefore a continuous metabolic activity.


In practice, do fishes die from old age? I was watching sea birds eating fishes and wondered if fishes actually died from old age, or if they are all eaten before this can happen?

I reckon some big predator fishes must be able to live long enough to die from their age, but fishes who are lower in the food chain, do any of them actually reach an age old enough to die peacefully or are they all somewhat doomed to feed a bird or another fish?

Yes, at least some fishes have intrinsic lifespans and deaths that are related to their own life-history and not to external forces such as predation or disease.

  Fishes show three types of senescence. Lampreys, eels and pacific
  salmon exhibit rapid senescence and sudden death at first spawning.
  The guppy, red panchax, medaka, platyfish, Indian murrel and many
  other teleosts undergo gradual senescence, as observed in most of the
  vertebrates. A number of fishes (e.g. sturgeons, paddlefish, female
  plaice, flatfish, rockfish) show indeterminate growth, the occurrence
  of senescence in them is supposed to be very slow or negligible.

Patnaik BK, N Mahapatro, and BS Jena. 1994. 'Ageing in fishes' Gerontology 40:113-32


Why do OX5034 GM mosquitos require the presence of tetracycline to survive? What does the drug do in this case? I'm confused. Debug Fresno; why are the released mosquitos said to be sterile? from 2017 addresses male mosquitos released with a bacteria that will affect fertility of females after mating. They are not genetically modified.
CNN's 2021 article First-ever US release of genetically modified mosquitoes begins in Florida Keys describes release of Oxitec's OX5034 GM mosquito Aedes aegypti. Curiously, these can be kept viable for reproduction when maintained in an environment that includes tetracyline, an antibiotic.
Question: Without the bacterial infection, is it just a coincidence that the GM strain needs an antibiotic to survive? What does the tetracycline do in this case? Why was this drug chosen?
Potentially helpful resources:

https://www.oxitec.com/en/our-technology
https://endmalaria.org/sites/default/files/Enca%20Martin-Rendon.pdf

They don't go into any detail on the sites you link to and I don't have time to look into patents, but from the context it sounds like they may be using a tetracycline repressible promoter. This is often referred to as a Tet-Off promoter.
The core elements of these promoters were discovered in the bacterium Escherichia coli1 and several variations have been developed. These types of promoters work in organisms from bacteria to yeast to mammals1-3.
References
1: Gossen, M., & Bujard, H. (1992). Tight control of gene expression in mammalian cells by tetracycline-responsive promoters. Proceedings of the National Academy of Sciences, 89(12), 5547-5551.
2: Baron, U., & Bujard, H. (2000). Tet repressor-based system for regulated gene expression in eukaryotic cells: principles and advances. Methods in enzymology, 327, 401-421.
3: Orth, P., Schnappinger, D., Hillen, W., Saenger, W., & Hinrichs, W. (2000). Structural basis of gene regulation by the tetracycline inducible Tet repressor–operator system. Nature structural biology, 7(3), 215-219.


Does anyone know the explanation for branches with different flower colors (see picture)? As you can see in the below picture, there's a branch with white-colored flowers, while the rest of the tree has pink flowers.

I googled a number of questions but it is a bit complicated to formulate in a search. Plus I have no background in botany or even biology.

Many ornamental cherries are grown on a hardier root stock, that is, they are propagated by grafting onto hardy wild cherry saplings. This is because the ornamental variety will not produce offspring that are true to the parents, if they produce offspring at all.

  All are grafted plants and mainly on wild cherry (gean) rootstock.  Such trees should be planted with the graft union above ground level.  Seed, rarely produced, will give rise to new hybrids.

This is a picture of an ornamental cherry of the pompom variety:

My guess is that the tree in your picture sent a shoot off the main trunk under the graft site, resulting in a branch of native cherry, which is mostly white and a much simpler flower than the ornamental variety that was grafter onto it. Another possibility is that two different specimens were grafted onto the same stock (but since the white blossoms are very simple - like a wild cherry - I would guess the former occurred.)

This is a picture of a wild cherry (gean):

So you have the grafted ornamental cherry blooming alongside of the rootstock cherry it was grafted to.

The rootstock (although usually wild cherry) can vary, so... can't identify with certainty the rootstock, but can explain what you're seeing.

It's not rare, but it's not usually desirable. Some newer growers are grafting several varietues of cherries onto the same rootstock to intentionally produce a tree with different kinds and colors of flowers. See, for example, this artist's work.

The Hamada Cherries


Neural coupling between Pinsky-Rinzel (reduced Traub) neuron with a Wang-Buzsaki neuron? I have read two papers related to modeling neurons. The first one is the paper by Pinsky and Rinzel and the second one by Wang and Buzsaki. The first mentioned neuron model is a excitatory neuron based on NMDA and AMPA neurotransmitters. The second one is inhibitory neuron model based on GABA. So I modeled them individually. Now trying to couple such that pre synaptic PR neuron will connect to post synaptic WB neuron which also connects to PR neuron. That is in effect an excitatory-inhibitory coupling with feedback.

Now how would the action potentials of both neuron look like?
Will both oscillate, or only WB neuron alone oscillate?
Is there any specific conditions for the oscillations to occur?

Any speculations, ideas, references (like books, related papers) would be helpful.

NOTE : By action potentials, I mean the neuronal membrane voltage signal which varies with time.

There is no straightforward answer to this.
It completely depends on the properties of the neurons and the network they are in.

I would recommend you to study Central pattern generators. Those are usually small networks that can create a repetitive pattern of action potentials. However, the exact pattern they generate depends on how they are connected (number and type of synapses, network structure,...) and a presumably large number of neuronal properties (like the conductance, the shape of their dendrites, the expression level of various ion channels and all kinds of intracellular messengers/peptides/proteins/molecules). For example, there are "leaky" ion channels that can cause a neuron to spontaneously depolarize (and fire action potentials) regularly without requiring any synaptic input. This means that you can have a regularly firing neuron even without network feedback mechanisms. example

There are many different rhythms in the brain and they are all generated by smaller and/or larger networks of neurons with different properties. Neurons can even participate in multiple different rhythms, depending on the situation (e.g. theta rhythm vs. SPWs in the hippocampus). Thus, even the same neurons in the same network can generate different rhythms.

So, the rhythms that you can build depend on how you tune the neurons' properties and the way they are connected. With just the information you provided (simulated excitatory and inhibitory neurons, but no info on their excitability, network,...) I can't tell you what the resulting rhythm will look like.

I'm afraid I didn't really answer your question, but I hope this was still helpful.


How do aminoacyl-tRNA synthases distinguish between similar amino acids? How do aminoacyl tRNA synthases recognize the right amino acid for their tRNA? What is the structural reason behind the selective recognition? I have difficulty in seeing how, for example, leucine and isoleucine can be selectively recognized by different binding pockets when they exhibit similar hydrophobicity, molecular volume etc.

Aminoacyl-tRNA sythetases are highly specific to their corresponding amino acid. First, the activation site, where the amino acid binds, constitutes a complex network of intermolecular interactions. For example, threonine, catalyzed by  threonyl-tRNA synthetase, is very similar to valine and serine. Valine has a methyl group instead of the hydroxy group of threonine, and serine, on the other side, has no additional methyl side group. Uniquely to threonyl-tRNA synthetase, it contains a Zn2+ ion that exhibits an interaction structure specific to threonine. Nonetheless, the threonyl-tRNA synthetase could still be mischarged with serine because the zinc ion site is not specific enough, leading to 1% mischarged tRNAs. For this purpose, aminoacyl-tRNA synthetases have a second, editing site that proofreads the charged tRNA.  The editing site can recognize serine and cleave it from the tRNA.

Figure: Interaction network of the activation site of the threonyl-tRNA synthetase in A. pernix. The  threonine-AMP  is shown in green.

Sources:

a Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Section 29.2, Aminoacyl-Transfer RNA Synthetases Read the Genetic Code. Available from: https://www.ncbi.nlm.nih.gov/books/NBK22356/

b Nagaoka, Yoshiyuki, et al. "EVOLUTION AND tRNA RECOGNITION OF THREONYL-tRNA SYNTHETASE FROM AN EXTREME THERMOPHILIC ARCHAEON, Aeropyrum pernix K1." Viva Origino 1.31 (2003), http://www.origin-life.gr.jp/3101/3101062/3101062.html


Why are the other bases not used for RNA capping and tailing? Why does the addition of a 5' cap and that of a 3' tail involve guanine and adenine respectively? Why aren't any of the other two bases added to an mRNA to protect its ends or act as a signal to transport it to the cytoplasm?

I don't think definite answers exist but I can think of theoretical reasons:

First, Poly A tail can efficiently be synthesized because ATP is the
most readily available nTP, being the main energy source.

More to the mechanism, but this is no explanation to the evolution:
The termination sequence 'TTTATT' on the DNA template and 'AAUAAA'on the RNA is the start of poly-adenylation. But this falls in the 'chicken-egg problem' category.

As a bioinformatician, I happen to know, that 3'UTR is highest in A-content of the 3 genomic contexts and the 5'UTR is highest in G-content of the 3 contexts, so possibly these post-transcriptional modifications further strengthen the compositional differences of the contexts.

For the poly-A tail it might also be relevant to mention that G or C sequences have higher propensities towards structure due to amount of hydrogen-bonds.

I hope there were some helpful pieces of information.


Are there seeds intended to feed eaters? Seeds are meant to survive digestive systems of the animals that disperse them. Are there seeds meant for a creature, who will digest most of the seeds for nutrition and disperse only a minority of intact seeds?

There's a very interesting case of mutualism between the species Homo sapiens and Oryza Sativa (also Triticum aestivum...). The humans have bred the plants to produce highly nutritious seeds, much greater then non-adapted species, and in return the humans save a small fraction of the seeds and will cultivate the plant for many generations.

It goes further then that in that humans also will protect their mutualistic plant partners from other invasive species and cultivate them, ensuring their mutual survival.


Are there yearly variations in HIOMT (HydroxyIndole-O-MethylTransferase) availability? I'm reading a booklet on melatonin published in 1996, titled "Melatonin and the Biological Clock". And see the following statement:

  HIOMT (HydroxyIndole-O-MethylTransferase), one of enzymes of melatonin
  synthesis, rises and falls in an annual rhythm, with troughs in March
  and October and peaks in January and July.

Seeing how HIOMT is the last methyltransferase involved in Melatonin synthesis in humans, I'm interested in learning if there's indeed a yearly variation in this MT production in humans, and if it is regulated by genetics or photoperiod duration.

Thank you for your input!

This isn't really a complete answer but I can't fit it into a comment.
I've found that there is a large body of literature on seasonality of melatonin levels in various vertebrates, particularly livestock, because of its interaction with breeding patterns. Similar studies in humans are however, difficult to find, but the review paper cited below looks at a link between seasonal variations in melatonin levels and seasonal variations in immune system functions. It cites a few references that might be worth following up.

Srinivasan, V. et al. (2008) Immunomodulation by melatonin: Its significance for seasonally occurring diseases. Neuroimmunomodulation 15: 93-101 DOI: 10.1159/000148191
Abstract
Melatonin is not only synthesized by the pineal gland but also in many other organs and tissues of the body, particularly by lymphoid organs such as the bone marrow, thymus and lymphocytes. Melatonin participates in various functions of the body, among which its immunomodulatory role has assumed considerable significance in recent years. Melatonin has been shown to be involved in the regulation of both cellular and humoral immunity. Melatonin not only stimulates the production of natural killer cells, monocytes and leukocytes, but also alters the balance of T helper (Th)-1 and Th-2 cells mainly towards Th-1 responses and increas- es the production of relevant cytokines such as interleukin (IL)-2, IL-6, IL-12 and interferon-γ. The regulatory function of melatonin on immune mechanisms is seasonally dependent. This fact may in part account for the cyclic pattern of symptom expression shown by certain infectious diseases, which become more pronounced at particular times of the year. Moreover, melatonin-induced seasonal changes in immune function have also been implicated in the pathogenesis of seasonal affective disorder and rheumatoid arthritis. The clinical significance of the seasonally changing immunomodulatory role of melatonin is discussed in this review.


What is the minimum air pressure the human body can tolerate if oxygen supply is not an issue? Disregarding hypoxia, what is the minimum air pressure that the human body can tolerate?

(i.e. at what air pressure would the blood start to boil, or skin start to burst, or whatever else might happen that would kill you but isn't related to oxygen?)

Disregarding hypoxia, the lowest atmospheric pressure the human body can withstand is around 6 percent sea level pressure, or 61.8 millibars, below that pressure the water and blood in your body starts to boil. Harry George Armstrong, a physician, and an airman, was the first to recognise this limit, which on Earth occurs at an altitude of roughly 63,000 feet, beyond which humans absolutely cannot survive in an unpressurised environment. The limit was named in his honour and so is called the Armstrong Limit. The lowest atmospheric pressure humans can breathe in, with a pure oxygen supply on hand, is roughly around 12.2 percent sea level air pressure or 121.7 millibars, the pressure found at 49,000 feet. Or, as a slightly madder alternative example, in a terraforming Mars situation, which might arise one day; a fit person could in theory walk around outside without a spacesuit on, but breathing from an oxygen tank, only when the atmospheric pressure got above about 120 millibars, and hope to survive for long.


Resources for finding all drugs of a certain class I may be embarking on a project involving a fairly extensive healthcare records data set, looking for the use of a particular type of drug (for example, "Proton Pump Inhibitors"). But these drugs are usually listed by their trade or generic names - is there a well maintained resource for looking up what drugs are members of a certain class (if class is indeed the right word)?

The WHO has their own methodology, the Anatomical Therapeutic Chemical (ATC, thank you commenter) classification system, for organizing such data (its impetus is comparing results between studies).

Also, if you have $900 sitting around, you can get a subscription for the United States Pharmacopeia.  I'm not sure if that can be spread across multiple subscriptions for an organization like the Red Book David mentions.


Which mushroom is this? I found those mushrooms in my garden in Luxembourg and I was wondering what species they might be.

That mushroom is from the Boletus family with sponge gills. A Red Cracked Bolete.

Only one sponge gill toadstool neighbor of the boletus family mushrooms has ever been know to kill a single person, or require a liver transpant, because, if you get an amanite wrong, you can survive, but only with a liver transplant. It is said that: if you found an Amanite, and put a triangle of it in your mouth and spat it out, it may taste fairly scary, but it will not kill you or even make you vomit or Hospitalizeded, although you may experience some discomfort, as long as you spit it out entirely and not swallow it.

In temperate climantes, The only boletus that are quite noxious are the red and beige ones which sometimes smell ghastly are in the family of the devil's bolete. There are other boletes that can make you vomit or ill, i.e. some blue and yellow ones. some boletes are strange and interesting such as the pepper boletus which can be used to flavor a dish because it produces very hot pepper flavor same as capsiacin.

Your mushroom is clearly a Red-Cracked bolete, which make sludgy, insipid soup, they have no texture, gelatious, flavorless, are extremely common, have yellow gills changing to blueish grey, and small red cracks often appear in the top which has the habit of cracking when ripe, hence the name, red cracked bolete. it is harmless and quite a waste of time to cook. https://www.google.fr/search?q=red+cracked+boletus&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiWn7Ljg9fVAhXDJlAKHe-HADwQ_AUICigB&biw=895&bih=530

The only boletus: sponge-gill toadstool (tail and cap) mushroom ever implicated for someone's death (by artery malfunction in the gut) was a woody tough red one related to boletus satanicus: https://en.wikipedia.org/wiki/Rubroboletus_pulcherrimus

Anyone trained biologist who can identify species from books, has a good chance of never falling ill from Boletus species, as long as he makes very positive identifications of mushrooms that don't have potential deadly or noxious look alikes. many mushrooms like the death cap are particularly deadly because they can be mistaken for small farm agaricus in field edges. especially angel of death and Panther-Cap, which smell of humus, earth, and apples.

The main identifier on a red cracked bolete is the squishy texture, not fibrous, and the velvet. dryish, textured large sporing body which starts as pine colored and matures to olive or bark colored.


What kind of spider is this? And is it dangerous? (photo) I found this spider hanging from a web off the side of my house (in Buffalo, NY). It's probably 3-4in total length. Any thoughts on what kind of spider this is? And if it's dangerous?

I would think this is a European garden spider (or cross spider). See here and here.
It can bite humans but it is not dangerous for them.


What is the molecular mechanism of cystine bond formation? My bioinorganic and redox chemistry isn't up to par and I'm having a very difficult time understanding the chemical mechanism behind cystine bond formation. Most reactive environments are actually reductive whereas an oxidative environment is important for cystine bond formation. How does the oxidative environment oxidize the thiols, rearrange the orbitals and form a disulfide bond?

If your question is with respect to a eukaryotic cell, the di-sulfide bridge/bond is formed in the rough endoplasmic reticulum which is an oxidative environment (unlike most other organelles which are reductive). This paper may be of relevance to you:

Pathways for protein disulphide bond formation - Frand et al, Trends Cell Biol. 2000 May;10(5):203-10.


Which part of a female mantises's DNA causes her to be a few times larger than a male mantis? Which part of a female mantises's DNA causes her to be a few times larger than a male mantis?

Do other species have that part of DNA?

Insects and spiders have tremendous sexual dimorphism, with males often being much smaller than females.  They are pretty much just sperm carriers and sometimes do not eat.  Insects may have two or one sex chromosome, where males my have only one chromosome.   As is pointed out in the comments, not all mantis' species display this dimorphism.

Since such dimorphism is probably due to small changes in the genome due to environmental selection pressures and the genetic mechanisms of control are probably not simple.

Its difficult to say which genes are responsible for size per-se.  Recent studies of human height indicate that scores of genes may be involved in human size and insects have at least as many genes as humans do; it is pretty hard to look at a human genome sequence and say what height that person is without some other help.  I imagine for specific insect species this too would be difficult.


How to search for a protein sequence of an specific taxa in NCBI? My example: Sequence of HBB (Hemoglobin Beta) in Fishes.

How can I do a good search to obtain above sequences in NCBI? (I know hot to download them into a FASTA file)

Try going to http://www.ncbi.nlm.nih.gov/protein and searching for ' (hemoglobin beta[Protein Name] OR (hemoglobin[All Fields] AND beta[All Fields])) AND "Fish"[ORGN] '.

Search filters can be changed with the panel to the left of the search results.


Why aren't we ambidextrous? It seems so simple that if my brain can tell my right hand to do something, then it should be able to tell equally well to the left ? This seems like a pretty major evolutionary advantage. Why haven't we evolved so during millions of years ?

Having a dominant side is advantageous. Instead of seeing it as the brain influences our fine motor skill, think of it the other way round. The way we use our hands or any other part of our body sends feedback to the brain to increase the portion of the brain devoted to that region of the body and of course with disuse the reverse occurs. The more you do a certain task the more that portion of the brain gets better and coordinating the movement. The portion I talk about is the primary and supplementary motor cortices. So basically we are specialising. In the same way a heart doctor is better with treating conditions of the heart than a foot doctor. So we can either devote our experience to the one hand, or both or the other hand. If we use both hands equally our brain adapts so that we are ambidextrous, if instead we use just the one hand our brain develops just that side. But if you do focus on both you are using your dominant hand less so overall same amount of development just over both sides of the brain rather than just one side. You can probably see the benefit of having this plasticity of improving only what is used because why improve what we don't use and waste resources? And you may also see the benefits of higher specialising of one hand rather than having two slightly specialised hands. There are few tasks that require both hands to be very specialised, but if that were the case then the body would go ahead and do that but in spending time training your hands you are probably training your legs or something else less.

///

Why not have a switch between the two hemispheres to give the hand currently being used the fine motor skill located in the other hemisphere? (from comment)

I see. In my answer I only talked about one aspect. The brain doesn't have to learn skills for each hand completely independently. For example imagine if you learn to play a musical piece with your right hand only. If you try it with your left you won't be amazing but you'll definitely be better than a complete novice. Our brain can learn how to do by seeing which is vital for development. But there's a limit to that, your hands aren't completely identical so there's still a portion that needs fine tuning. Your muscles have different stregth, fatigue, resistance, recruitment patterns, places they innervate. Your hands are mirror images. The weight of your hand is different. And not only that but these variables aren't fixed, there's lots of them and they are different for different tasks. So to use your analogy, the more expensive remote can be used but it wasn't bought for use with the black plane. It'll give more control to the black plane but it still won't be the best ever until it learns what the muscle strength is etc. then it will be just as great.


Geographical distribution of malaria and tuberculosis Unlike malaria, tuberculosis (TB) is found across the whole world. Why and explain? I mean why are people affected with TB more than malaria and some say that in cold and developed countries malaria is less but TB cases are more.

The statement in the question about the current distribution of these diseases is not strictly accurate, as shown by the graphic below.

[Malaria graphic: Wikipedia user, Percherie (2006); TB graphic: Corbett et al. (2003)]

However there is no disputing that the contemporary and historical geographical distribution of these diseases differ. Why?

The crux of the answer is that this is because of the different agents that cause these diseases. Malaria is transmitted by certain mosquitoes and is therefore restricted to places in which these mosquitoes are found. TB is a bacterial disease, the geographical range of which is determined by human contact under conditions which favour its transmission.

To expand:

Malaria is transmitted by Anopheles mosquitoes, especially in Africa by Anopheles gambia together with the Plasmodium falciparum parasite. One of the factors determining the mosquito habitat is standing water and the elimination of malaria from Southern Europe followed drainage of the marches and swamps in which it breeds.

That is not to say that this is the only factor in the elimination of the malarial mosquitos from certain parts of the world in recent historic times. For example malaria has not been eliminated from Africa partly because of the cost and logistic problems of implementing programmes of eradication using drugs etc.

Tuberculosis (TB) in humans is caused by the bacterium, Mycobacterium tuberculosis. Its airborne spread was favoured by the crowded conditions in cities following the industrial revolution, and its elimination fostered by improved living conditions and the development of antibiotics in the twentieth century.

Footnote: Some Factors affecting Malarial Outbreaks in Africa

A section from an article by Tarekegn A. Abeku, entitled Response to Malaria Epidemics in Africa, is relevant:

  In highlands, transmission is unstable due to fluctuations in temperatures that are normally low. Temperature affects duration of the sporogonic cycle of the Plasmodium parasite within the Anopheles vector, survival and feeding frequency of the adult female, and duration of the aquatic stages.

and

  Semi-arid areas, on the other hand, have mostly warm climates, and epidemics are associated with anomalous rainfall, which causes increases in vector breeding and survival.


Are there viruses that affect cells across different species? I'm not a professional in biology nor a student, but I'm curious about this. To be more specific: why doesn't a plant virus affect animal cells?

I suspect that different kinds of cells have different ways to replicate DNA and that this is the reason for the specialization of viruses.

I wonder if someone in the field can explain this to me. Thanks.

Firstly, it's important to recognize that "plant viruses" do not exist. There are only "viruses that affect particular plant cells", or "viruses that affect a particular cell type". You'll see why in a moment.

One of the structural components of many virus is its protein coat. Different types of biological molecules protrude from the surface of this protein coat, deemed signalling molecules. The structure of these molecules are specific to a certain type of virus.

Analogously, specific cell types have specific biological molecules that protrude from their plasma membrane, deemed receptor molecules. For a virus to affect a particular type of cell, their signalling and receptor molecules must "fit within each other", like lock and key. Once they do so, a virus may interact with this molecule, in whichever way it does.

Although your hypothesis wasn't entirely correct, as viral contact with a cell must first be established, viruses do interact with DNA replication in different ways, as in the lytic or lysogenic cycle.


Do "Giraffe Weevil" males build Nests I had came across an insect  near my backyard in India(Kerala). I haven't seen this one before and I searched web to find out what insect is this and found its image which saying its a "Giraffe Weevil" (Trachelophorus giraffa). The link below says that this insect is endemic to Madagascar.

http://en.wikipedia.org/wiki/Giraffe_weevil and

They are herbivore insects, with adults feeding on a tree that is commonly known as the "giraffe beetle tree"
(Dichaetanthera arborea)

This states that these insects need the "giraffe beetle tree"(Dichaetanthera arborea) which is also native to Madagascar.

So how come this insect could be found in India(Kerala), and further more all the above links state that the long neck of these dimorphic insects are evolved for fighting and nest making but they do tell that after mating the females will make the nest and lay one egg inside, So did the male insect make any nest in reality, if so then why the male have to perform both nest making and fighting.[Sorry for the errors,also there are more links to this]

As the comment by @terdon says, the most likely explanation is that your species identification is mistaken. The superfamily Curculionoidea, which contains the weevils (Curculionidae are the true weevils) is also extremely species rich. Without seeing a picture of what you found, there are many other similar species with long necks in the family Attelabidae, which is the family of Trachelophorus giraffa. For instance, the wikipedia page includes a picture Apoderus longicollis which is very similar to the Giraffe weevil from Madagaskar, and it is supposed to be found in India (see GBIF info):

Paracycnotrachelus is another genus found in Asia where some species have long necks. Another giraffe-necked species is also found in New-Zealand - see Lasiorynchus barbicornis - so the overall body shape is not that unique (note that much of the elongation in this species is of the snout though):

Even if we should never rule out the possibility of range changes/introductions, this must be based on close examinations of the specimen, and it is even more unlikely in this case since Trachelophorus giraffa seems to be a very specialized species.


How C. Elegans is used for siliencing genes The experiment that is using C. Elegans to silence the Genes. I have a question about Why and how C. Elegans can use the DNA plasmid that is generated with the gene of interest in the bacteria by being fed the bacteria?

From the way that you have described your experiment, feeding C.elegans bacteria that are expressing a plasmid that will induce gene silencing, then both @Kendall and I think that you are likely performing an RNAi (interference) experiment.
As @Kendall writes:

If it's what I'm thinking of, you probably have GFP+ worms that end up getting fed some
DH5-α E. coli that were transformed using CaCl2. The outcome is your control worms should nicely fluoresce, and the experimental worms will be a noticeably weaker color. The RNAi process is explained nicely in that link provided by AMR. –  Kendall

The bacteria will transcribe RNA molecules encoded by the DNA plasmid. These RNAs will have complimentary sequences to sequences from your gene of interest.
When the nematode eats the bacteria, they RNA molecules that the bacteria has produced will be taken up by the cells of the worm.
The Dicer enzyme then cleaves the dsRNA into small fragments. These fragments are then able to hybridize with the mRNAs transcribed from the gene of interest. This will either cause the ribosomes not to bind properly or will start translation out of frame or without key amino acids or will terminate translation early.
The net effect is that the cells will either not produce the protein encoded by the gene of interest or will produce a non-functional protein. If, as @Kendall said, the gene of interest is a reporter gene such as GFP, then the result of the interference experiment will be C.elegans that do not fluoresce. If the gene of interest is a structural protein such as actin, then you will see the effects of knocking out the actin gene on the cells of the worm.
This online video protocol from JoVE.com gives a detailed overview of the RNAi in C.elegans experiment and also demonstrates how the protocol is carried out.


Irradiation instead of pasteurization? Can we just replace pasteurization with simple irradiation for most (if not all) foods? (For example, such as milk, to sterilize and preserve flavors)

Both pasteurisation and irradiation work by killing micro- (and macro-) organisms in food. The two processes are broadly similar and in both cases the objective is to reduce the number of bacteria or other microorganisms in the food rather than completely sterilise it. Due to this and other similarities food irradiation is sometimes called cold pasteurisation (for example in this paper).

Food sterilisation has some advantages over pasteurisation: for instance, it can be used on (most) solid foodstuffs, including fruits, vegetables, grain foods, spices and meats (such as chicken), while pasteurisation can only be used on liquids. However, irradiation cannot be used on dairy products or eggs as it results in changes in flavour and texture (source).

There are other reasons why irradiation is not used as widely as it might be. One is that some markets were already saturated with pasteurisation, which is an older technology. Another is that public acceptance of irradiation is lower, with (for example) concerns about safety of the products, although these are not rational concerns and Crawford and Ruff note that similar concerns affected acceptance of pasteurisation when it was introduced. This may also partially explain why irradiation is sometimes called cold pasteurisation, although by international agreement irradiated unprocessed food sold in stores (not in restaurants, or processed foods) is labelled with the Radura symbol anyway.

I also have a suspicion that the startup costs associated with food irradiation plants are relatively high, but couldn't find a reference for this yet.

Some further reading

Lester M.Crawford, Eric H.Ruff (1996) "A review of the safety of cold pasteurization through irradiation" Food Control Volume 7, Issue 2, April 1996, Pages 87-97

"Advantages and disadvantages of the use of irradiation for food preservation" Journal of Agricultural and Environmental Ethics March 1991, Volume 4, Issue 1, pp 14–30

"Food irradiation", Better Health programme, Victoria State Government website (accessed 2017-10-24)


Is water vapour a product of fossil fuel oxidation? In textbooks, while water vapour and carbon dioxide are said to be the greenhouses gases which are most abundant in the atmosphere, when a table is given showing the top greenhouse gases emitted by humans, water vapour is omitted (carbon dioxide and methane are the top two).

However, when methane is oxidised to release energy from fossil fuels, the products are carbon dioxide and water (i.e. water vapour), therefore, aren't humans responsible for the concentration of water vapour present in the atmosphere?
Why is water vapour generally omitted from the tables?

Althugh water vapor contributes to greenhouse warming of the atmosphere, changes in atmospheric water vapor tend to follow rather than drive changes in temperature. Also, in the form of clouds, atmospheric water can have a cooling effect on earth temperature.

Clouds illustrate why water vapor, unlike carbon dioxide and methane, is not thought of as a driver of recent changes in earth temperature but rather is more of a follower. Unlike those other two gases, if you keep trying to put water vapor gas into the atmosphere it will convert to liquid water at some point, leaving only a constant level of water in the form of gas. That's what happens when a cloud forms; what you see and what can shield you from the sun is a collection of water droplets or ice crystals. Large amounts of water vapor are also regularly put into the atmosphere by evaporation of water from the earth's surface, dwarfing the contribution from human respiration. Eventually the atmosphere gets locally saturated with water vapor and it falls back to earth as rain or snow in the hydrologic cycle.

In principle methane and carbon dioxide could similarly condense out of the gas phase, but not at temperatures that occur in our atmosphere. You need to go far out into cold reaches of the Solar System to find naturally occurring methane lakes or solid carbon dioxide. There is no equivalent of rain to remove excess of those gases from our atmosphere. Carbon dioxide can dissolve in water to leave the atmosphere, but at the cost of acidifying the water. Ocean acidification is another serious result of adding carbon dioxide to the atmosphere.

The amount of vapor you can add before conversion to liquid water increases with the temperature. So as land temperature increases the rate of evaporation of water into the atmosphere can increase, and as atmospheric temperatures increases the amount of water vapor that the atmosphere can hold also increases. So in principle water vapor might thus serve to amplify the greenhouse warming from other gases, although its transition to liquid or ice in the atmosphere might tend to counteract that. This is a major issue being investigated in attempts to understand the interplay of factors that determine earth temperature.

A focus on carbon dioxide has an important practical aspect. If you control the excess release of carbon dioxide due to fuel combustion, you necessarily also control the associated excess release of water vapor.

In summary, human activity ends up having much less direct influence on changes in atmospheric water vapor than it does on changes in carbon dioxide or methane. That's why the latter two gases rightfully receive more attention as controllable greenhouse gases.

The American Chemical Society also discusses this issue.


What is this blue-green bioluminescent jellyfish I saw at Aquarium of the Pacific? I took this picture of an animal in the bioluminescent section of Aquarium of the Pacific in Long Beach, California, but I neglected to write down what it was.  I've searched the Aquarium's web site, but it doesn't appear to have information about the individual species on exhibit.  (Or else I just can't find it.)  I've also looked at Wikipedia and Google Images, but can't seem to find a creature that looks like this one.

I suspected it could be a jellyfish, and the answer below confirms that.  But I'd like to know what species of jellyfish it is.  (Either common name or scientific name.)

That is a Jellyfish! :D

Someone else took a picture of that same Jellyfish:

http://www.yelp.com/biz_photos/aquarium-of-the-pacific-long-beach?select=36BuiiqeN7OIFbowSDkPcw

Here is a picture from an article about the exhibit's jelly fish:

Source: New Jellies Exhibit at Aquarium of the Pacific Explores the Mysterious Lives of These Gelatinous Sea Creatures


What are the pros and cons of eating earth (soil)? I wonder if there are any benefits to eat earth. What I mean by earth is the topsoil that is sometimes on vegetable (I eat organic vegetables and some of them like spinach are full of topsoil).

I found this article (a study about why people, in certain culture, eat earth) but it doesn't clearly answer my question as it's about clay and not topsoil. Topsoil has a highest concentration of organic matter than clay.

I wonder if we can digest the soil nutrient (Phosphorus, Potassium, Calcium, Magnesium, Manganese, Zinc, Copper) just as we would if there were coming from vegetable and fruits.

What are the other pros and cons of eating earth (soil)? (I am aware of the cons about parasite and bacteria but my question is not about these risks. It's about nutritive value of earth.)

The article (a PDF can be found here) suggests that this happens neither for feeding reasons (to get your belly filled, when anything else is available) nor that this is done for supplemental reasons.

They suggest that this happens more for protective reasons. In the abstract they write:

  Our results indicate that human geophagy is best explained as
  providing protection from dietary chemicals, parasites, and pathogens,
  whereas animal geophagy may involve both micronutrient acquisition and
  protection.

In the paper they give a few examples for this. First the earth eaten is usually digged up from deeper layers of the ground and sometimes even cooked. Then they bring in the example of people, which eat soil, when they have gastrointestinal problems as a kind of medicine to calm down the problems.

In my opinion there is not much nutritional value in eating soil. Organic compounds can usually not be metabolized (for example we don't have the possibility to break down cellulose). I am not sure, if we can get minerals from clay into our body, since a lot of them is present in soil as unsoluble minerals.


Did the first cell self-replicate or was it multiple first cells? We're almost sure by now that the first cell was born in a some kind of underwater vents environment which harvested all the necessary conditions for it to exist.

However, did the first cell self-replicate to have other cells or did the same process lead to the birth of others as well? If the latter is true, doesn't this make the evolution of cells more common once the primitive conditions exist?

Good question. Simple answer here: we have absolutely no idea.

I would hazard a guess to say that the first proto-cell probably did not have the ability to replicate, so there must have been many proto-cells prior to the occurrence of the first true cell with the property to replicate itself with some degree of fidelity. Whether or not at some point cells existed that could be traced to two or more independent abiotic generations, that is unknown. The likelihood of this event is all we can talk about. I defer to biochemists working on this (still very open) problem, but I think it is honest to mention that they too have no idea, really. This is because, as we can surely appreciate, likelihood and outcome are two entirely different things. And unlikely events happen all the time. Each life form and individual is astonishingly unlikely, but historical contingency so happens to have brought us all here despite the odds.


Breathing with Clogged Nose during Sleep This just happened to me recently, I was trying to sleep with clogged nose, so I tried breathing through my mouth. As you can imagine it was hard, but I managed to sleep deeply.

So I became curious, how does our body know whether to breathe through the nose or the mouth especially when we have a clogged nose during the time when we are in deep sleep?

NOTE: I tried researching this, but most result just shows how to clear clogged nose before sleeping

Most people with colds/allergies/stuffy noses don't die in the middle of the night. Why?
Prevention of oxygen deprivation is powerfully regulated. If insufficient air intake is possible through the nose, the mouth opens automatically (regulated by the autonomic nervous system. If you exercise, at some point, nasal breathing isn't enough, and you start mouth breathing. It's not conscious.

The autonomic nervous system (ANS)... is a division of the peripheral nervous system that supplies smooth muscle and glands, and thus influences the function of internal organs. The autonomic nervous system is a control system that acts largely unconsciously and regulates bodily functions such as the heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal. This system is the primary mechanism in control of the fight-or-flight response.
Within the brain, the autonomic nervous system is regulated by the hypothalamus. Autonomic functions include control of respiration, cardiac regulation (the cardiac control center), vasomotor activity (the vasomotor center), and certain reflex actions such as coughing, sneezing, swallowing and vomiting. Those are then subdivided into other areas and are also linked to ANS subsystems and nervous systems external to the brain. The hypothalamus, just above the brain stem, acts as an integrator for autonomic functions, receiving ANS regulatory input from the limbic system to do so. (emphasis mine)

The answer is a complex interaction between blood pH and oxygen/CO2 receptors and the autonomic nevous system.


How do cats survive falling from great heights? Among mammals, cats are able to land safely when falling from great heights. For example, when compared to dogs or humans they can survive drops from relative large heights. How do they manage?

A 1987 study from the Journal of the American Veterinary Medical Association. Two vets examined 132 cases of cats that had fallen out of high-rise windows and were brought to the Animal Medical Center, a New York veterinary hospital, for treatment. On average the cats fell 5.5 stories, yet 90 percent survived.

See wiki on cats.

How can cats do this?

The reason why cats are superb jumpers has not received much attention, but one article in Nature was entirely devoted to just this (Diamond, 1988). Here follows a partly quoted and partly adapted text from this article:

First , because mass increases as the cube, but surface area as the square of linear dimensions, falling large animals are in general more injury-prone than small ones, as they suffer greater impact stress, their bones experience greater stress, and they reach higher terminal velocities in free-fall because of a less favorable area/mass ratio. While a small drop breaks an elephant's leg, a falling mouse reaches terminal velocity in the atmosphere much sooner and at a much lower value than do falling elephants.

Second, falling cats have a superb vestibular system and make gyroscopic turns
such that all four feet are soon pointing downwards, regardless of the cat's
orientation at the start of the fall. Hence cats dissipate the impact force over all four limbs. Falling human adults  tend to tumble uncontrollably but land most often
on two feet, next most often on their heads. These facts contribute to the low mortality of falling cats and to their low chance of breaking limbs after the fall.

Third, a cat falling in the atmosphere reaches a terminal  velocity  of  about  60 m.p.h. (compared with 120 m.p.h. for adult humans) after only  about  100 feet. As long as it experiences acceleration, the cat probably extends its limbs reflexively , but on reaching terminal velocity it may relax and extend the limbs more horizontally in flying-squirrel fashion, thus not only reducing the velocity of fall but also absorbing the  impact  over  a greater  area of its body. This may explain the paradoxical decrease of mortality and injury in cats that fall more than 100 feet.

Finally, cats that land with their limbs flexed dissipate much of the impact force through soft tissue. Parachutists are trained to dissipate impact forces by landing with knees and hips flexed, then rolling.

Reference
Diamond. Nature 1988; 332:586-7

Further reading
BBC news


Stem cell research and female egg synthesis In terms of years, how far is stem cell research from being able to produce a female human egg from other female body cells?

I suppose that there is no connection between producing egg from somatic cells and stem cell research. The thing that you have mentioned: "produce a female human egg from other female body cells" was already done in 1996 (!) in sheep. Technically, there is no reason that this procedure will not work in Human as well. So in term of years: this was possible 20 years ago ... :-)


Maintaining purebred pedigrees and how to lessen chance of getting disease? Many breeds of dogs are known for a high incidence of genetic disorders. German shepherd and Saint Bernard dogs are predisposed to developing a crippling condition called hip dysplasia.

Q: What advice would you give to dog breeders who want to maintain their dogs' purebred pedigrees, but also want their dogs to be as healthy as possible?

Many races of dogs are relatively new with most of them appearing (were bred) in the last few hundred years. These variations are caused by small mutations in certain genes and this is also the problem. To keep a race pure, it has to be interbred to maintain the special set of mutations. And this makes the dogs vulnerable to collect more damaging mutations, especially when the number of animals used for breeding are too small. This is the same problem, that animal conservation projects face in zoos.

A good example for that is the Dalmatian dog. Its characteristic spotted pattern is caused by genes, that can also cause sensineural deafness. To avoid this, deaf dogs are excluded from the breeding and a backcross project was started.


Tool use by animals: research history I was under impression that data about quite a lot different species using different tools is a fairly modern phenomenon, i.e., all of the research is fairly recent.

Around 50 years ago it was widely believed, by scientists too, that it was only apes that are able to use tools. I was recently told that it's basically nonsense and scientists have been studying different tool-using animals since the beginning of the 20th century or earlier.

Where could I get more info on research done in this area? I'd be especially thankful for those done in USSR, since it used to be my country and my knowledge on everything was basically limited by the Iron Curtain. However, I am also interested in research done worldwide as well.

Best tip I can give you is buying a textbook or popular science book about ethology. That should give you an overview about research done in the past decades. Konrad Lorenz was a pioneer of ethology, so a book should summarize his work, e.g. this one

For more current stuff look up some journals in this field:

Animal Behaviour
Journal of Comparative Psychology

Animals having a small brain compared to mammals but nevertheless showing very intelligent and reflective behaviour like this rook are currently interesting research objects. This kind of research is not really tricky or expensive as you see, it just has to be done by a student :) But behaviorism as the leading paradigm in the middle of the 20th century has probably made a lot of more fruitful research approaches impossible.


Species identification - What is this "bug" The title says it all. What the heck is it?

Edit:
I found this on my car, in Kansas city.

After conducting a small investigation, it would appear most likely that the spider captured in the attached photograph is an arachnid in the family 'Thomsidae' or 'Crab Spiders'.

Although the proposed genus of Araniella proposed above by user137 shares a superficial similarity to this family, thomsids generally do not construct webs to ensnare prey - I might hazard that the web on your car does not hold the same structure, as shown below, to that of an Orb Weaver Spider (Araniella).

From the available information it is challenging to propose a genus, let alone a species. Based on the location of the car, I may propose the sub-family Misumenoides or genus Thomisus.

The general characteristics of crab spiders are the ambush of prey as opposed to trapping prey; the inverted V-shape under the cephalothorax; and the sideways movement of certain species in the Thomsidae family. It is of interest to note that any member in the population could vary appreciably in colour.

Wikipedia article concerning Crab Spiders available from: https://en.wikipedia.org/wiki/Thomisidae
Britannica regarding Crab Spiders available from: https://www.britannica.com/animal/crab-spider
Information regarding Misumenoides is available from: https://en.wikipedia.org/wiki/Misumenoides


What is this weird spider? Today while we're cleaning our storage room I saw this strange looking spider and I'm not even sure if this is a spider, it has two claws folding inward to its mouth and two long weird limbs, it is about 2 inch long and rarely move on its place. Is it poisonous or dangerous to us? What should I do with it?

It looks like a species from the Arachnid order Amblypygi (Tail-less whip scorpions), which are closely related to Thelyphonida (Whip Scorpions). As part of Arachnids, both of these taxa are related to spiders and scorpions, but belong to a separate order.

Even if they look scary, they are harmless to humans, even if they can sometimes bite.

According to this checklist/site only three species are listed from the Philippines, so if you want to determine it more closely, it might be useful to start from this list. The list includes: Sarax brachydactylus, Phrynus grayi and Charon grayi.

Here is an example picture (from wikipedia):

Charon grayi (giant whip-spider) from biotagua.org:


Does my nearsightedness come into play when creating light outlines in the distance? After looking at a light and closing your eyes, you see an outline of the light. I was curious how my nearsightedness would come into play. I look at a light in the distance without my glasses on and close my eyes, would I be able to distinguish the light shape better than if directly looking at the light?

Not likely.  The afterimage you see when you close your eyes is an effect dependent upon which light-receiving cells in the retina (rods and cones) saw light when your eyes were open.  The blurry image you saw when your eyes were open has the same size and shape as the afterimage you see when you see when you close your eyes.  Because the afterimage has less detail, perhaps you would be less distracted by detail and be able to pay more attention to shape, but it seems unlikely that would noticeably help your idea of the shape.


How different is an introverts brain different from an extroverts? How is an introverts brain wired differently than an extroverts? Just to give you an example. On an average, the processing that goes on in an introverts brain is greater than in an extroverts [citation needed].

What part of the brain affects personality traits such how introverted someone is? How is this part of the brain different in either it's physical entity or it's activity between extroverts and introverts?

I am not sure if this answers your question, but according to the article "The Difference Between Introverts and Extroverts" (Gallagher, 1999), the main differences between introverts and extraverts are where the main brain activity occurs (as seen by positron emission tomography (PET) measurements).  The full PET study is in the article "Cerebral Blood Flow and Personality: A Positron Emission Tomography Study " (Johnson et al. 1999).

The conclusion of the Johnson et al. paper states:

  This study revealed a pattern of increased blood flow in the frontal lobes associated with introversion. ... in the present study, there were more cortical regions associated with introversion than with extraversion. ...in the present study, extraverts did show lower blood flow in several regions in the behavioral inhibition system, namely, the frontal lobes and the hippocampus.

Some images of brain activity is included in a more recent article "Differences in regional brain volume related to the extraversion–introversion dimension—A voxel based morphometry study" (Forsman et al. 2012).  Forsman's article looks at activity in  the white and grey matter of the brain.

I hope this helps.


In which order did the cells of the immune system evolve? Thinking about how complex the interactions between different types of immune system cells (T-helpers, T-Killers, Phagocytes, B-Cells etc.) are, it's fascinating how they all combine to get the desired effect.

However, I assume that they didn't all evolve simultaneously!  Is there any way to tell which immune cell developed first or any theories to that effect?  Perhaps that question is too specific, in which case was it humoral or cell mediated immunity that developed first?

You may find this paper helpful - unfortunately I'm still months off a campus so can't access it.

As I'm lucky enough to have access to that article, I'm going to extract whatever I can find to answer your question.

To begin with, innate immunity must have evolved first - we can see it at almost all stages of evolution. According to Cooper & Herrin, ever since aerobic respiration gave rise to multicellular organisms which in turn needed protection from invasion by single-cell organisms.

They state that around 500 million years ago, the first adaptive immune systems evolved in vertebrates, but do not explain how although they attempt to. Instead, they explain why we are not able to discern at the moment how this evolution came about. The main reason given is that it is unknown when some key cells evolved (namely natural killer cells and dendritic cells) Additionally, mice and humans evolved two different kinds of natural killer cell receptors relatively recently while sharing a common ancestor only quite a long time ago.

Apparently jawed and jawless vertebrates have also evolved two different kinds of adaptive immune systems. They both seem to rely on the same mechanisms but on a different molecular and genetic basis. Cooper & Herrin conclude that at the current level of research, we are not able to determine the evolution of our immune system.

Source: How did our complex immune system evolve?

Personally, if I'm allowed to give in to the temptation of speculation a bit, I would go by a similar strategy as the evolution of Krebs cycle - look which bits make sense even without the rest. There is of course the major obstacle that the cells of the immune system require an entirely new branch in haemopoiesis: all innate immune cells (aside from natural killer, NK cells) derive from the common myeloid progenitor, whereas all adaptive immune cells (and NK cells) derive from the common lymphoid progenitor.

I think this may even be a first hint: NK cells are innate immune cells but they derive from a different lineage at the highest level - they may have evolved as the first lymphoid cells after the myeloid innate immune cells. The next closest related cell is the cytotoxic T cell (CD8+, aka Tc), which utilises the exact same killing mechanisms (perforin+granzymes and Fas ligand) and attaches to other cells in almost the same way as the NK cell (immune synapse). It is also independent and can kill on its own, as long as it recognises its specific antigen. This is the main difference and also a very large step - the generation of the specific T cell receptor. Once the specific T cells receptor is developed, the step to helper T cells (CD4+, Th) is not far, although these perform a relatively bystander-like role in the immune response, steering the other immune cells from behind the scenes and not directly effecting any killing of the pathogen. Therefore I would guess that before helper T cells, B cells evolved, which are capable of producing antibodies. Antibodies themselves are very similar to the T cell receptor (not in gross structure but in the underlying genetic domains and their processing), so a 'detachable' antigen-specific T cell receptor may have evolved and ultimately caused the development of a new cell type. Once all these components are present, it is necessary (or beneficial) to control which cell types are the most active and in which way they act at the site of infection. This is exactly what helper T cells do, by steering the local immune response either into a Th1 (cytotoxic) or a Th2 ('humoral', anti-parasitic) response direction.


How do we know which Eulerian path corresponds to the DNA sequence? Bioinformatics textbooks explain one method to reconstruct the whole DNA
sequence from multiple reads. The method builds a graph and finds a Eulerian path in it. The Eulerian path corresponds to a DNA sequence.

However, the graph can contain more than one path. How do we know which path corresponds to the actual sequence?

If the DNA sequence contains repetative elements, and your reads are not long enough to resolve them, you won't know if you have the right path.  Usually you split your results into contiguous regions whose sequence you are confident in.


Interpretation of picture of human chromosomes Does this picture show sister chromatids or homologous chromosomes? If they are homologous then what is YY? If they are sister chromatids then do homologous chromosomes ever appear like this (with the centromere)? Do sister chromatids exist only in prophase-I to anaphase-I of meiosis?

The picture can be a bit misleading because it represents 22 autosomes (autosome = non-sexual chromosome) while there are 22 pairs of autosomes (so the homologous chromosome is not represented). And it represents the whole pair of sexual chromosomes (the individual is a male).

homologous chromosome

For each autosome represented, there is another one which would be its homologous chromosome.

Sister chromatids

As you can see, each chromosome looks like an X. The right and left side of this X there are chromatids (two chromatids per chromosome here). The chromatids are attachedf by the centromere.

Note

Please note that 1) chromosomes looks like they are represented here only during the metaphase (when they are condensed). 2) A chromosome is not always made of two chromatids. Sometimes it is made of single chromatid only. It depends on the moment in the cell life cycle.


Fold Coverage of sequence read? What does it mean when N-Fold coverage of read of sequence? Details will be much appreciated if a link provider with brief explanation.

Fold coverage is often derived with respect to a genomic locus, not a read. In sequencing experiments, fold coverage of a genomic loci (coordinate along a reference assembly) will be the number of aligned reads that overlap the position.


Can a woman give birth to twins with different fathers? Is it possible for a woman to conceive from two different men and give birth to half-siblings?

Yes, this is possible through something called heteropaternal superfecundation (see below for further explanation).

Of all twin births, 30% are identical and 70% are non-identical (fraternal) twins.

Identical twins result when a zygote (one egg, or ovum, fertilized by one sperm) splits at an early stage to become twins. Because the genetic material is essentially the same, they resemble each other closely.

Typically during ovulation only one ovum is released to be fertilized by one sperm. However, sometimes a woman's ovaries release two ova. Each must be fertilized by a separate sperm cell. If she has intercourse with two different men, the two ova can be fertilized by sperm from different sexual partners. The term for this event is heteropaternal superfecundation (HS): twins who have the same mother, but two different fathers.

This has been proven in paternity suits (in which there will be a bias selecting for possible infidelity) involving fraternal twins, where genetic testing must be done on each child. The frequency of heteropaternal superfecundation in this group was found (in one study) to be 2.4%. As the study's authors state, "Inferences about the frequency of HS in other populations should be drawn with caution."


What is this white-winged insect from Hong Kong? When we were travelling in Hong Kong, near a bushy temple, we spotted some white-wing insects which we had never seen before. I sense it's a type of moth, but I have no idea what classification it is.

Tiny to 3-5mm
Mostly white on its body
Moving slowly
High volume in one area
Not so sensitive to external threats, e.g. no escaping when you try to hit them.

I think these are planthopper nymphs. I can't be sure of the species, but Ricania speculum looks rather similar:

(image source)


Is there are evolutionary explanation for why humans and primates are ticklish? How might it have evolved? Tickling is a rather interesting phenomenon: When humans or apes are touched in certain areas like the armpits or sides, we respond with laughter AND frantic attempts to stop the assault. Obviously our ticklish areas tend to be very vulnerable, so it makes sense that we would want to protect ourselves, but why do we respond with laughter? How might both of these reactions to tickling have evolved? Do they have the same evolutionary purpose or different ones?

Tickling probably evolved from a defense mechanism but then gradually changed into a more social action, as explained in Provine, 2005 (PDF):

  The neurological mechanism of tickling probably evolved from a reﬂex defense mechanism that protects our body’s surface from external, moving stimuli, probably predators or parasites. Our response to tickle is more varied and complex than the typical reﬂex, but it has some stereotypic, reﬂex-like properties (i.e., we laugh when tickled, struggle to escape the tickler, huddle, fend off the tickling hand). Although you can be tickled to laughter by a machine (Harris, 1999) (PDF), most everyday tickle is yet another social context for laughter and a form of communication.


Why is GTP, rather than ATP, used in nuclear transport? Why is GTP used for nuclear transport and not ATP, given that ATP hydrolysis is used to drive most cellular energonic reactions?

Disclaimer

Although this question appears to be either unclear or unanswerable (or both), and shows no evidence of research on the poster’s part, I have chosen to address one aspect of it to emphasize a general concept. This, despite the fact that my knowledge of nuclear transport processes is minimal.

Brief Answer

GTP, rather than ATP, is used for nuclear–cytoplasmic transport via importins and exportins, because this process involves one of a large family of ‘G proteins’ that — as their name implies — operate through the use of GTP. Whereas ATP is generally used to drive endergonic molecular reactions, the hydrolysis of GTP in G-protein cycles can be thought as a device to terminate a molecular process. Whether G proteins adopted GTP rather than ATP merely by chance or for a biological reason is a matter of speculation.

NTP hydrolysis — for fun or profit?

It would appear that the question relates to protein-transporting ‘importins and exportins’, which I learn from the Wikipedia article on nuclear transport are regulated by the small G protein, Ran. When complexed to GTP, Ran facilitates the export of proteins by exportins, a process that is terminated by hydrolysis of GTP to GDP. The GDP-bound form facilitates the import of proteins by importins, a process that is terminated by GTP displacing the GDP.

So if we consider the role of the hydrolysis of the nucleotide triphosphate — here GTP — it is clearly not to supply thermodynamic energy for an endergonic process such as muscle contraction, light generation or a chemical reaction with a +ve ΔG:

Rather, it is to produce a conformational change in a protein which allows the termination of a process. This termination is generally through the GDP-bound form of the G protein (grey) interacting with some other protein (black):

This diagram is deliberately simplistic so that the general features of G-protein action can be seen. However, I think it illustrates the same point made in Berg et al. Section 15.6. Other examples are signal transduction of hormone action via cyclic AMP and binding of aminoacyl-tRNA to the ribosome.

Why do G proteins use GTP?

This ‘choice’ of GTP in the original ancestral G protein could have been mere chance, that was subsequently reflected in other G proteins that arose through gene duplication and divergence. That would imply that, at least, it was not disadvantageous. Or as the oldest G proteins are perhaps those involved in protein biosynthesis — a process still catalysed by a ribozyme — the choice of GTP might have reflected an RNA base-pairing interaction in the ‘RNA world’.

Alternatively one might suggest a biological rationale for separating two types of energy-requiring processes — perhaps by regulation of the enzyme that catalyses the conversion of ATP to GTP, dinucleoside-phosphate kinase. However I am not aware of any evidence to support this idea.

Hydrolysis of GTP in other contexts

As mentioned in a comment by @Roland, there are instances where GTP is used to drive endergonic reactions (phosphoenolpyruvate carboxykinase) in a manner analogous to the use of ATP, but this is quite different from hydrolysis of GTP in G proteins. I do not believe that any convincing rationale for this has been propounded, nor for the similar exceptional use of UTP in glycogen synthesis and CTP in phospholipid synthesis. This question has been discussed in another post.


Is it technically possible to make someone see something when their eyes are closed? I'm writing a little article and need any information about how human vision works and latest
technologies and discoveries around. Actually its not a professional article. Its for a group of my friends.

In fact I'm looking for any possible way to make someone ACTUALLY see when their eyes are closed. I don't know maybe convince some of brain cells that a real pulse is coming from eyes, but in reality its coming from a computer; or something like that.

I call it a virtual vision, myself.

Do you guys know if there's any professional article, discoveries or technologies available about this topic?
I'm very very interested in this topic by the way.

Yes, this is most certainly possible and already being done. As long as the visual cortex of the brain (in the occipital lobe, i.e. at the back of your head) is functional, the correct stimulation will produce visual perception.

In cases of blindness caused by malfunction of the retina, meaning that the rest of the visual pathway is functional, this is the most promising approach to restoring vision. See Visual prosthesis and the TED talk on it.

"Virtual vision" as in projecting a whole field of vision (reflecting the real surroundings) is the big ideal target that this technology is aiming for. Of course as soon as they manage to make a working prosthesis for blind people, someone will probably try to make it non-invasive and easily usable for commercial exploitation.


How exactly does long-term tension (over months) build up in the ligaments, tendons, muscles? And is there any basis for believing that massage relieves that tension?

Tension is not a quantifiable thing, rather an abstract concept to describe feelings of stress in muscles.  I think I see what you are getting at but I would separate it into two questions.

"Is massage provably beneficial to muscles under physically induced stress?"

Emphatically yes, however there are so many different types of massage, some are more medically viable than others.  Most massage stimulates muscles to encourage a release of tightening, much like exercise does, though I would assume that there's also a psychosomatic that plays a significant role as well due to human contact.

The other question, more the point "Are massage therapist's claims about relief true?"

Some are and some aren't.  Unless it's by a medical professional (prescribed physical therapy for instance) they can claim whatever they like.  "Reiki contributes to your body balance and wellness by attuning your energy"  This can not be proven, but not really disproven either, so they can claim it all they want though it's purely anecdotal (if not outright fabrication on the part of less ethical individuals.)

In summary: Massage has tangible benefits, but if the claims of the therapist sound too good to be true, they probably are.


How do I calulcate the amount of concentrated stock solution to add to get the correct dilution? For example, how much loading buffer (6X) do I need for my PCR reaction with a volume of 25 μl?  What is the general way to calculate it?

For any question regarding volume and concentration, you should consider the equation $C_1V_1=C_2V_2$. We can use it to derive a general equation for the addition of concentrated stock solutions. We want to find the volume of stock solution ($V_1$) to add so that its final concentration is 1X. Here's what we know:

The initial concentration of stock solution, $C_1=X$
The final concentration of the solution, $C_2=1$
The volume of solution we are diluting the stock into, $V_s$

So the equation becomes:

$$XV_1=V_2$$

We don't know $V_2$, but we do that $V_2=V_1+V_s$. Subbing that in:

$$XV_1=V_1+V_s$$

Solving for $V_1$:

$$XV_1-V_1=V_s$$
$$V_1(X-1)=V_s$$
$$V_1=\frac{V_s}{X-1}$$

Then you simply need to sub in your values:

$$V_1=\frac{25μL}{6-1}$$
$$V_1=5μL$$

So you should add 5 μL of your 6X loading buffer to the 25 μL solution to get a 1X final concentration.


What was the evolutionary benefit of enclosing hemoglobin in cells? The ancestral solution to oxygen transport is with hemoglobin (or, similar proteins) dissolved in blood (or, "hemolymph", but, basically, dissolved in water. ) What was the advantage of enclosing the oxygen-transport proteins in cells?

If you enclose the globin in a cell you can achieve a high concentration of the globin, which makes for a faster, readily usable pool available, and it is not subject to degradation (via proteases, or other mechanisms) as if it was just dissolved. In addition, all other functions of the globins (pH regulation, CO2 metabolism, etc) will be more tightly controlled if the globin is on the same site (i.e., inside a cell), instead of being mixed in a milieu. All of that has probably more to do with the evolution of the entire circulatory system, as a whole, and only sequentially as the 'enclosure' of globins in specialized cells. You can find some more details here.


What is this long, thin and segmented insect I found in my house in India? Found this inside my house, along the wall, there were few going somewhere few distance from each other.

I suspect it is a centipede but didn't found similar images on Google. What is this?

Location: Mysore City, India.

Size(only which I saw): the one in the image is about half centimeter, and the smallest one was less than 1/4th of a centimeter.

Color: the one in the image is kind of brownish I guess and the smallest one's are nearly white (pigmentless?)

We assumed this thing is kind of larva of cockroach or big white ant. Is this fully grown insect or still it is a baby? These were behaving like ants do.

UPDATE:

Based on a comment by ArthurJFrost reminding me of the existence of a group of insects I totally forgot about, AND based on a closer examination of the cerci and what appears to be external mouthparts in the image of the OP's specimen, I think this insect might actually be a webspinner!

These insects would be also about the right size, with the described and shown body plans, but also with short (but non-pincer-like) cerci and external mouth parts as in the OP's image. Female webspinners are wingless [source], as well, as the OP's image also appears to be.

See, for example, the black webspinner (Oligotoma nigra) from New Mexico, USA from bugguide.net:

 Source: bugguide.net

See also here for additional images of Oligotomidae species. (by the way, O. saundersii is the type species of Oligotomidae within the Indian subcontinent).

@ArthurJFrost, since you are more the expert than I on hexapods, PLEASE PLEASE write up an answer detailing how we might all feel more confident knowing that the webpsinner (and not the dipluran) is the better answer. Visually it appears to be the case to me, but I think you'd be able to point out some specifics for us all to learn from!

I will certainly default to you to write up the "official" webspinner answer since my update here on my post is simply to direct away from what I now think is an incorrect answer. I would gladly link to your answer to further emphasize that you came up with this answer.

OLD ANSWER: [Informed guess, but I think it's wrong!]

Based on the thin body plan, extended, segmented abdomen, lack of wings, and pair of posterior cerci, I was immediately reminded of a dipluran (or "two-pronged bristletail").

 Sourcce: Wikimedia

It would be good to know the size of your specimen since most diplurans are smaller than 10 mm  (though some can reach 50 mm!). A better photo would also be appreciated, since diplurans typically have antennae with beadlike segments, and I cannot tell if that's the case in your photo. I will note that many diplurans have much longer and even filamentous cerci, but others (like your specimen) have shorter cerci.

I am not sure why a dipluran would be inside your house, however, since they live in soil or leaf litter. [source]

Other organisms to rule out:

Snakefly (Agulla adnixa) -- no cerci (vs. yours)
Centipede -- too many legs (vs. yours)
I can't rule out earwigs since I am unfamiliar with the species in India. However, your specimen looks longer, thinner, and possessing smaller cerci than the earwigs I am more familiar with. [A clearer image of the thorax would help to determine if wings are present or not, which (if present) would rule out diplurans altogether and suggest it might be some earwig species I don't know).


pI and pH relationship in context of ion exchange protein purification I am confused about relationship between isoelectric point and pH in context of ion exchange protein purification. Why we cannot use this method for protein with pI below 7? Thank you very much for any tips.

Have a look at this table, it really depends on the buffers you use:

The table is from this website, which is definitely worth reading when you are interested (or work) with ion exchange chromatography.


What could cause hairs to gray at the tips but not the roots? I have noticed that some of my sporadic gray hairs are gray at the tip side but oddly, not near the roots.  Some are even only gray in the middle.  I find all of this very counter intuitive, and I assure you nobody is secretly dying my hair.

How does the graying process work, and how is it that this can be happening?

Interesting question, I am not sure if I have a definite answer, but at least some ideas:
The pigment in the hair is made by specialized cells, the melanocytes. The make the pigment (eumelanin=dark and pheomelanin=red/yellowish) which is then deposited into the growing hair. They are located at the bottom of hair bulb and usually die at the end of each hair cycle. To have the hair of the next hair cycle colored as well, this melanocyte population in the hair bulb needs to be replenished. This is done by melanocate stem cells, which live in the hair bulge and which start to reproduce and differentiate in melanocyte which then migrate down to the hair bulb. There is an excellent article following this process:

Mechanisms of hair graying: incomplete melanocyte stem cell
maintenance in the niche.

The hair later gets grey (low pigment) and white (no pigment) when these melanocytes are not, or not fulley replenished in later hair cycles. Why this happens, there are a few hypothesis.

First, its possible, that with age the melanocyte stem cell population (which not only need to replenish the melanocytes, but also need to maintain its own population) is getting smaller and disappears over time. This process would explain gradually graying over time. See this reference:

Melanocyte stem cell maintenance and hair graying.

Another possibility is the presence of reactive oxigen species (ROS) which occur naturally in melanocytes. Over time, the enzyme which intercepts this ROS (catalase) is getting less active or present in the cells and thus oxidative damage is getting bigger, damaging the melanocytes and their ability to make pigment. It would actually bleach itself...

Senile hair graying: H2O2-mediated oxidative stress affects human
hair color by blunting methionine sulfoxide repair

Melanin has also an important role in intercepting ROS, so in this process less and less pigment is made (as the damage accumulates) and this also leads to hair, which is less pigmented for exogeneous oxidative stress:

Towards a "free radical theory of graying": melanocyte apoptosis in
the aging human hair follicle is an indicator of oxidative stress
induced tissue damage.

It could be possible (and this is a wild guess) that the phenomenon of the tips graying first is situated by this. Hair less protected against exogeneous oxidative stress (smoke, UV etc.) so the melanin is "used up" during this until the hair greys at the tip, since its the oldest and most exposed part of the hair. This article by Tobin gives also a nice overview:

The cell biology of human hair follicle pigmentation


What does "genus VI" mean in mycology? This Guidebook is called "How to identify mushrooms to genus VI". Some other editions/versions of it say "Genus III" or "Genus I". What does this mean?

This is a multi-part series of books, with each volume numbered with roman numerals I, II, III, IV, etc meaning 1, 2, 3, 4, etc, followed by a subtitle, in this case the subtitle is "Modern Genera."

There is no meaning to "Genus VI", the title of the book series is "How to Identify Mushrooms to Genus" which indicates it will help you identify mushroom genus but will probably not bother with differentiating species of the same genus (even that is quite a lofty goal).

The authors could have instead called this book "How to Identify Mushrooms to Genus; Volume 6: Modern Genera" to convey the same meaning.


How does cerebrospinal fluid circulate in the central nervous system? Cerebrospinal fluid (CSF) is produced in the choroid plexus of the lateral ventricles and in the 4th ventricle of the brain.  CSF then circulates through the ventricles of the brain and the subarachnoid space of the meninges.  CSF is returned to the venous system via the arachnoid granulations connecting the subrachnoid space with the superior sagittal sinus at the superior portion of the neurocranium.

What circulates the CSF such that it can return to the venous system against gravity?
In other words, why does CSF not all just pool in the caudal cistern?

There are several points here.

Arachnoid granulations are not the only "sinks" for CSF.

Even though it is true that most of the CSF is eliminated from ventricular system and subarachnoid space through these granulations, there are also suggestions that there are also other potential mechanism of shunting CSF into the venous system:

Cranial nerves leaving CNS go through dura mater and these holes are not sealed, so it is suggested that some CSF can just go along the nerves and then accumulate in the lymphatic nodes in submucus.
Dura mater is mostly perforated at the area of lamina cribrosa, that basically separates the nasal holes and our brain. Leaking through multiple small holes here CSF is accumulated into the lymphatic submucusal nodes, found in abundance here. This way is considered to be primary CSF drainage way in newborns who don't have a well developed granularities in (sub)arachnoid space.
Spinal nerves, especially in the upper part of the spinal cord, also leave unsealed holes and the presence of lymphatic nodes adjacent to the places where these nerves leave the verterbral column also make them a potential place for CSF drainage.

Arachnoid granularitis do not only drain, they are capable of active CSF uptake.

CFS is not just "circulating" here going from the place of its origin in lateral ventricles to venous system. The granularities are here to actively resorb this fluid, meaning that they effectively take it up forming vacuoles and then excrete it to the venous system. Constant uptake leads to the pressure gradient (see also below!) that acts as a driving force for CSF.

Venous system has generally low pressure, thus sucking the CSF up to drainage points.

Speaking about drainage we also should consider the fact that the venous system has a pressure lower than the atmospheric pressure and much lower than pressure in any middle-sized arterial vessels. This is reached by having elastic walls and by transmitting the negative pressure from the mediastinum during the inhale, when the diaphragm and the thorax expand. This negative pressure propagates mostly to the connected vessels, including sinus system. Due to the elastic wall other parts of venous system can accommodate this negative pressure constrict their lumen, but not the sinus system which has a hard external framework formed by dura mater and bones. That is here we can measure the lowest pressure and this is the pressure that sucks CSF in into the venous system.

I hope that answers your question.


How suddenly does lactose-intolerance onset? How quickly can the loss of lactose tolerance onset in an adult?

Such as being able to process lactose normally to having notice symptoms associated with the inability to process lactose.

I am not asking how long it takes to digest food, but rather how long it takes for lactose intolerance to become noticeable (hours, days, weeks, months, years).

Disclaimer: I am not medically qualified, and this answer must not be construed as being medical advice of any kind.

Primary adult hypolactasia is the most common cause of lactose intolerance. The majority of the world's population have this phenotype.

In these individuals, at weaning, there is a reduction in the level of the enzyme lactase, which is responsible for digesting lactose to galactose and glucose in the small intestine. Undigested lactose can create symptoms via osmotic effects (causing diarrhoea) and because it is metabolised by bacteria in the colon, producing gas and thus abdominal bloating.

About 35% of adults have a genetic variant in an region upstream of the lactase gene which results in the expression of lactase continuing into adult life. These individuals are lactose tolerant. This trait is most common in Northern Europe.

According to references cited in

  Ingram, CJE et al. (2009) Lactose digestion and the evolutionary genetics of lactase persistence Hum Genet (2009) 124:579–591

(I have removed citations from the passage for clarity.)

  "most lactase non-persistent individuals can tolerate small amounts of lactose (as in tea or coffee), and some can consume a lot without ill effects. Variation in the composition of the gut flora between individuals, as well as a psychosomatic component may account for some of the interindividual variation in symptoms."

The clear implication is that there is a lot of variation in the tolerance of lactose amongst those lacking the lactase persistence trait. Given the contribution of the gut flora to the symptoms these could presumably vary as a result of, for example, antibiotic treatment. Also I imagine that the effects of undigested lactose could be synergistic with some other gut disturbance.

Added in response to comment from the OP:

In someone with the (common) genotype that corresponds to 'no persistence of lactase' the possibility of showing symptoms will be present from a young age. Apparently there is a lot of variation in the severity of symptoms. If an adult suddenly exhibits symptoms then I am suggesting that this could be due to an interaction of non-persistence with some other gut disturbance - I imagine this could happen quite quickly. Alternatively I suppose that a change in diet could trigger symptoms.


What did pangolin scales evolve from? Were they developed anew or a heritage from fish?

Pangolin scales are certainly not retained from fish. Pangolins are within the clade Pholidota (Tree of Life page for Eutheria) and their nearest relatives are anteaters, sloths, and armadillos.

According to the University of California Museum of Paleontology, similarities between pangolin and armadillos are the results of convergent evolution. So the pangolin scales are a new feature that arose somewhere on the lineage leading to pangolins.


Introductory text for primatology I'm looking for a book that provides a good overview of primatology, one aimed more at researchers rather than a popular science book. Ideally, I'd like something with an ethology/ecology angle with an eye towards phylogeny.

My preference would be for an e-book.

I've had some experience with Karen Strier's 'Primate Behavioural Ecology', and it's solid. It's a nice overview with (obviously) a strong ecology/ethology bent. I don't think it comes in ebook though.

Here's the Amazon link.


How does NHEJ cause indels? I was reading up on CRISPR-cas9 and how it works and I am having trouble wrapping my head around how NHEJ to repair the DSB can cause indels to occur. Shouldn't the NHEJ just stick the two strands of DNA back together?

I believe I read somewhere that if other agents cause a DSB, such as certain chemicals, they can also damage / cleave nucleotides ; the damaged nucleotides would have to be removed and overhangs filled in by polymerase before the ligation, which could result in the errors that NHEJ is famous for.

Since cas9 does not cause such damage, how can it result in an indel?

Thanks.

This is a very interesting question and I had not thought about it before. I am reiterating the background of your question.

Background

Cas9 cuts the both the strands of the target DNA at the same location thereby making a blunt end cut. Usually sticky ends and microhomologous ends lead to indels because of exonucleolytic clipping and addition of extra bases by pol-µ. The question is how do indels arise during NHEJ mediated re-ligation of blunt ends.

NHEJ may not always lead to indels. Most blunt end cuts can be repaired without error. Some non blunt cuts are also perfectly re-ligated; the best example for this is VDJ recombination. The binding of Ku proteins is essential for a perfect re-ligation (canonical NHEJ/C-NHEJ).

However, there are some variant non-canonical pathways which include alternative-NHEJ, backup-NHEJ and microhomology mediated end joining (MMEJ) (Bétermier et al. 2014). Some studies also refer to all of these pathways as alternative-NHEJ or altNHEJ. These alternative pathways involve resection of nucleotides by exonucleases such as Mre11 to produce overhangs. Imperfect alignment of these overhangs prior to ligation leads to indels. Sometimes non-templated addition of nucleotide happens by the action of terminal deoxyribonuclotide transferase (TdT). Pol-µ can also add random nucleotides at the 3' end (Lieber 2010).

In general, the propensity of DSBR via alternative NHEJ pathways would be higher when Ku activity is lower. Even with a moderate Ku activity, there is always some likelihood of alternative pathways in action. Moreover, it is to be noted that sticky end ligations are more efficient than blunt end ligations.

   Reproduced from Bétermier et al. 2014


How does the cell cycle affect stem cell fate? I keep reading about the stages of the cell cycle affecting stem cell fate, however I do not understand how. After all, any cell will have to pass through the whole of the cell cycle, and go through every state.

If you are referring to cells that are differentiated in adults:
Some somatic cells in multi-cellular organisms are post-mitotic, that is, the cells cannot divide, or said in other words, they don't enter in S phase. This cells are said to be in G0 phase, because they keep synthesizing proteins but the won't replicate their DNA.
Another thing we could say about cell cycle having something to do with cell division, is that in G1 and G2 (and , of course in G0) different cell types, produce different proteins. ie: a skeletal muscle cell, produces lots of proteins associated with the contraction, but neurons not so much.

If you are referring to the first cell divisions in a multi-cellular organism's development, then:
in cleavage, the cells are dividing synchronously, and they avoid some cell cycle stages, like g1 or g2 (in cleavage, the cells are just dividing and replicating their DNA; the protein synthesis happens with mRNA inherited from the mother). In this stage, there is no cell growth at all. After some cell divisions, they have to start synthesize mRNA  and, because of that, they start to divide asynchronously. Eventually the cells (for this and also for many other reasons) get differentiated.

I hope this answer is useful :)