How well can humans detect vitamin-richness? Humans do prefer fatty, sweet/starchy and salty. And fatty foods are rich in vitamins. How well can humans detect vitamin content apart from fattiness of food? Can humans choose the vitamin-richer of otherwise identical peanut butter, cheese or chicken leg?

Based on what I could search I guess that humans (and other organisms) usually do not have strong sensory mechanisms for micronutrients (Miyamoto et al, 2013).

There are some reports on sensing of metal ions, especially zinc and copper, by some organisms, including mammals (Bird, 2015; Ballou and Wilson, 2016). However, I haven't come across any study that talks about vitamin sensing.


Book recomendation: cell cycle regulation I aim to study cell cycle regulation, can some of you suggest a good book or website that systematically explains the topic.
It should include-

Detailed account of Cyclin and cdks involved in different stages of cell cycle
Spindle assembly checkpoint
DNA damage checkpoint
Special roles of Rb and p53 proteins in cell cycle regulation

Robust texts covering such 4 listed points with rigour include the following selection:

Molecular Biology of the Cell
Molecular Cell Biology
Cell Cycle Regulation
The Cell Cycle Principles of Control.

& even a review of the latter here.

HTH


Cytoplasmic determinants - protostomes and deuterostomes Cytoplasmic determinants are spread unevenly in the egg, and so when embryo starts forming (cells start dividing), the determinants are also unequally divided between cell. This unequal distribution later plays a major role in differentiation and gene regulation.

Protostomes undergo determinate cleavage. Their cells' fates are determined very early in development, whereas deuterostomes undergo indeterminate cleavage. So, if you take away a cell at early stage of development, it can be replaced.

Now if we compare the division of cytoplasmic determinants in protostomes and deuterostomes, what I said in the first paragraph seems true (to some extent) for only protostomes.

My questions:

Do deuterostome oocytes have even distribution of cytoplasmic determinants initially and  divide unequally only after certain number of divisions?
Are there any studies showing correlation between the stage at which determination happens in deuterostome and beginning of unequal division of determinants?

The two distinct types you have mentioned in your question (determinate/indeterminate cleavage) are actually called autonomous specification and conditional specification, respectively.

In the case of the former one, if we were to remove a blastomere, it would still produce the previously determined type of cells, while in the case of conditional specification the cells, which are going to be produced, depend entirely on the neighbouring ones. The latter's ability to alter their fate is called regulation.

As for answering your questions, cytoplasmic determinants are spread unevenly in deuterostomes as well, as otherwise no axis could be developed.

You might be interested about this answer as well.

I've used the following book as source: Gilbert, S. (2000). Developmental Biology [ online version ]


Would ovoviparous to viviparous mutation have been gradual? How would that work? It seems unlikely that an ovoviparous ancestor of mammals long ago could have had a viviparous offspring in a sharp one-generation dividing line, but what would be the gradual steps between egg birth and live birth? Are there any examples of answers to the first question today? It seems that marsupials are a different thing altogether, not something in between egg laying and live birth (no modern mammal's ancestors aren't believed to have marsupial-style birth in their evolutionary history, right?)?

I happen to have seen a talk by an anthropologist who was working on this (i can't reference them here i'm sorry to say - forgotten her name).  I can only give an example from their work...

If you look at old world and new world primates, there is a large difference between the gestation time.  If you look at the table in the link, lemurs have half the gestation time that humans and gorillas have.

What I can recall is that the lemurs placenta lacks many of the structures that primates have (see section 5).  The lemur placenta is supposed to be primitive and a lot more like an egg sac which was internalized as opposed to a more articulated womb that primates have.  So her thesis was that eggs would start out being internalized and subsisting only on their own internal structures, still isolated from the mother, then later placental structures would come about that nourish the fetus and enable it to enjoy longer gestation and better development pre-partum.

The stage I'm describing is only the divergence between primitive wombs and 'more advanced' wombs in the sense that they were capable of supporting the fetus for 9 months rather than just 4.  That development happened over about 30 million years.  The divergence of mammals is thought to have happened about 270 million years ago.

So the rough answer would be hundreds of millions of years for the whole shebang, but internalized eggs and live birth would be a relatively smaller amount of time.


building intelligent structure with random evolution requires series of non useful steps In order to build an intelligent design such as a bridge or a mechanical watch, you need a series of non useful steps.

As far as I understand, in random evolution theory, the "intelligence" involved is the process of natural selection.

The problem with this is that natural selection requires that each step be advantageous right away. If I want to build a bridge, I need many steps which would be disadvantageous until the final product which would be advantageous. This would be like trying to write a computer program where each line of code must be advantageous to the program. An intelligent design just cannot be done like this.

How does modern biology deal with this problem? To say it all happened at once, is not possible since the probabilities against this are simply outside the capabilities of a random system. Furthermore even if by some freak monumental event it happened, it would need to happen again many times since there is a huge diversity of intelligent designs in life forms such as lungs in birds vs gills in fish, or sexless reproduction in bacteria versus male/female reproduction in animals (which are fundamentally different).

(Also, as side question has there been ANY experiment demonstrating that such a thing is even possible? I mean for example, to have a computer simulation of random self-replicating molecules, then having an intelligent human being picking out the best version and eliminating the others, then repeating, etc. until you have an intelligent design.)

What you say is true, but the answer as to how modern evolutionary theory understand this considers other ideas about living things which seem to allow so called 'neutral traits'.

Neutral traits being those phenotypes which seem to have no particular relationship to fitness. Toungue rolling is an often mentioned example.  Some folks argue that there is only adaptive changes and phenotype, others like Gould and Lewontin argue that some traits can be the result of pleiotropy.

So first of all this sort of discussion can tell us that the question is argued both ways in a convincing enough way that it is not resolved in biology - some argue quite confidently that all traits are selected for and things like flagellar motors and upright ambulation and eyeballs evolve because of and experiencing constant evolutionary pressure.  Others argue that these genes that produce these things are doing something else useful while they are becoming these later more useful traits.

The common twist here is plieotropy.  That the genes that are producing the phenotype one is observing is also participating in one or more other biological traits that may is being positively selected for.

A more interesting example of how this works is the domesticated silver fox experiment. Foxes which have had domestication bred into them (just to show that it can be done by selection) lose their red color and their ears are softer and fuzzier.  Nobody tried to select for these traits, but they come associated with each fox that is domesticated.  Are these traits plieotropic or only very tightly linked?  So far they have not been exhibited separately.  In any case I think its fair to say that the experiment didn't care about the color of the fox - only its meekness towards people.  These traits come along for the ride.

So it might be with any other desirable genetic trait.  If a gene becomes closer to producing a lung from a gill, if that gene is sticking around it must be because there is positive selection for that trait, even if the lung like gill is not particularly useful for that fish.

Sorry but I actually disagree that it is obvious that non-useful steps must be had for any such complicated trait.  If that were true then you would have a point, but not every biologist would give that to you.

It might be a bit surprising that such discussions are and continue to be matters of faith in science, but I hope you don't dismiss it because of this either.  All sciences do assume some things that make their view of the world make more sense.  But there are also other components of these theories which are consistently observed and understood that demand them... until they don't.

I don't give really any credence whatsoever when someone says 'this is a widely accepted theory by the scientific community'.  This in itself is not a scientific statement, but more the hope that someone else has one somewhere.  But a refutation must also take under consideration what is being refuted.


qPCR : Cross-contamination while sealing plate I'm trying to do realtime PCR on a plasmid and I have my positive and negative controls close to each other along with a no-template control. I add 1 ul of my template last into the 96 well plates (on the side wall of the well, to be precise) and I seal the plate with optical adhesive seal (applying pressure with hand) and centrifuge afterwards.

While sealing I have noticed that the template drop I add on the side of the wells is being wicked up and is likely spreading into the neighboring wells. I notice amplification even in wells where I added water instead of the template

Has anybody notice the same or has any suggestions for how to avoid this? Do you add template into the liquid in the well or onto the side wall?

I can't say this happened to me before (but also don't do qPCR all the time).

In principle it should be fine to add the template to the side of the well, since this also lets you visually confirm that you did add the template. However, if you are having problems do consider adding the template to the liquid.

As another way to avoid this problem I would try to first put the adhesive foil lightly on top and then push it down/fix it with something sturdy that has a straight edge (there are special plastic things for this, but a tip-box can also work).


What is the inlet/outlet speed of air going in/out of our mouth during inhalation/exhalation During inhalation, your alveoli expand, creating a pressure difference between the atmosphereic pressure and our lung sacks and therefore air will flow into the repspiratory airways.

I am trying to find what the (I guess average) speed of this flow is, and therefore estimate the pressure difference. I have spent some time online trying to find this, but I have not got a definite number yet. It should be an order of magnitude of 1 m/s ?

Quick clarification firstly, the main change in thoracic volume that causes inspiration is not as a result of the alveoli expanding - they have no smooth muscle lining therefore are unable to spontaneously contract.  They do have some elastic fascia however their expansion is passive. The change is mainly as a result of the diaphragm contracting to become flatter, increasing the space that the lungs can occupy.  The external intercostal muscles also raise the ribs (in adults) which further allows for inspiration.

Figure One: Inspiration and Expiration(1).  "Rib muscles" refers to the external intercostal muscles.

With that being said, the value I think you are looking for is peak expiratory flow.  Peak flow is a common medical measurement that is often taken in the management of patients with respiratory conditions, either as part of their management plan or acute assessment.  Peak flow is a measurement of the maximum speed that a person can exhale at.

As the comments on your question suggest, this varies dramatically between person to person.  Ignoring any pathologies - such as asthma, chronic obstructive pulmonary diseases (COPD) or nerve damage to the diaphragm/intercostal muscles - peak expiratory flow varies primarily with age, gender and height.  These variations are summarised in charts of expected peak flow that are used, amongst other things, to grade the severity of an asthma attack (and consequently how aggressively to manage it).  Charts resemble the following:

Figure Two: Normal values for peak expiratory flow used in UK hospitals - The EU Scale (2)

So if you pick the height, gender and age that you feel is appropriate for your question, you can then read off peak flow in litres per minute.  Then you would need, I think, to work out the area of the aperture (in your case the mouth) to get a speed in metres per second?

Medina B. Brenda's A&P eportfolio: objective 48 & 49: inhalation and exhalation [Online]. 2011 [accessed 2012 Dec 11]. Available from URL: http://blm1128.blogspot.co.uk/2011/04/objective-49-contrast-inspiration-and.html.
Häggström M. File: normal values for peak expiratory flow - EU scale.png [Online]. 2009 [accessed 2012 Dec 11]. Available from URL: http://en.wikipedia.org/wiki/File:Normal_values_for_peak_expiratory_flow_-_EU_scale.png.


Were early human beings (about 100 - 200 K years ago) far more promiscuous than we are now? I found that many friends of mine are quite easy in sexual relationship. Ex, I knew a lot of girls went to the night club & met a stranger & brought home to sleep  with him even she had never known his name. The next morning, the guy left her & she starts to do the same way to get another guy maybe in 3 days or so.

So that triggered my thought. I wonder "Are early human beings (about 100 - 200 K years ago) far more promiscuous than we are now?"

My hypothesis is "Yes", that is "Early human beings are far more promiscuous than we are now". So how i came up this? Cos Human came from Chimpanzee right?, so if we want to know early human, then we could study Chimpanzee. The early human & Chimpanzee could have some similarities.

There is a research saying that "Chimpanzees are far more promiscuous than humans" http://www.nature.com/news/specials/chimpgenome/interactive/chimp_interactive_graphic_pf.html

So, that proved my hypothesis.

Also, when human evolved, they started to realized that promiscuousness wss not healthy & not good for society so they started to develop some regional/society (ex,  monogamous relationship) codes to prevent that.

Do you approve my hypothesis?

My hypothesis is "Yes", that is "Early human beings are far more
  promiscuous than we are now". So how i came up this? Cos Human came
  from Chimpanzee right?

No.

  Also, when human evolved, they started to realized that
  promiscuousness wss not healthy & not good for society

I'm sorry, what ancient society are you claiming cracked down on male promiscuity?


Amino acid compatibility The (human) genetic code encodes 20 amino acids. They form a protein using peptide bonds. Each amino acid has a carboxyl group (COOH) and an amino group (NH2) that can potentially form a peptide bond.

Source: The Culture of Chemistry

Does this property of amino acids means that each amino acid can form a peptide bond in any combination? In other words, are there certain amino acid doublets in existence that never pair up?

It seems like you may be thinking along the lines of DNA, where adenine pairs only with thymine and guanine with cytosine.

Unlike DNA, amino acid chains are single-stranded...

...so there is no pairing of compatible types like there is in DNA. Neighboring amino acids in the chain can be in any combination (as you say, because each has a carboxyl group and an amino acid group), just as neighboring nucleotides in DNA (ie those next to, not across from, each other) can come in any order.

In practical terms, the functional groups of amino acids have different chemical properties (hydrophobic, hydrophilic, aromatic), therefore some pairings are probably more commonly found than others. But in principle there is no restriction on who is next to who.


Seizures and blood pressure A seizure is basically a synchronized firing of neurons as opposed to the more common unsynchronized firing taking place during normal neural activities. However, I am uncertain if the exact technical definition of a seizure restricts this synchronized nerve activity to the brain only .

I wonder whether a wave of synchronized firing can propagate up to or occur in the area of brain controlling the blood pressure level and hence affect the blood pressure of the individual going through a seizure? Or can the impact of a seizure propagate to other areas and hence affect other functions like cardio-vascular system and hence the blood pressure? Or can neurons connected to heart, but not necessarily present in brain, exhibit synchronization as in a seizure and thereby affect the blood pressure of an individual undergoing seizure?

Summarizing my question is: can seizures affect blood pressure?

Yes, seizures can affect autonomic function including blood pressure. Such symptoms can even result in death. Note though that not all seizures are the same: there are many different types with many different causes, and they can affect different parts of the brain. There can also be different effects before, during, and post-seizure.

The effects described seem to be more related to overall discharge rates rather than synchronous firing in the periphery per se. The autonomic nervous system does not directly control heart rate, for example, but rather modulates the rate. The heart beat or vasculature would not entrain to any sort of seizure activity, for example, because the neurotransmitters involved in autonomic regulation of heart rate and blood pressure are comparatively slow-acting relative to the rate of seizure activity (essentially those functions are taking a moving average of neural input, rather than responding specifically to each impulse).

The relationship between autonomic function and seizures need not be unidirectional, either; circulatory changes can also be triggers for seizures.

References

Devinsky, O. (2004). Effects of seizures on autonomic and cardiovascular function. Epilepsy currents, 4(2), 43-46.

Nei, M. (2009). Cardiac effects of seizures. Epilepsy currents, 9(4), 91-95.

Penfield, W., von Sántha, K., & Cipriani, A. (1939). Cerebral blood flow during induced epileptiform seizures in animals and man. Journal of Neurophysiology, 2(4), 257-267.


Do marine deep sea life forms exhibit circadian rhythms? If so, what entrains them? I've been reading a lot about circadian rhythms, when suddenly this question popped into my head: do circadian rhythms exist for deep sea organisms (3000 ft / 1000 meters+)?

For land mammals, the entrainment of circadian rhythms is done through exposure to light (retina or other photosensitive elements), but in the deep ocean there is no light. How are circadian rhythms maintained there - what acts as an entrainment signal? Is it the moon, currents, etc.?

A research paper that recently came out suggests that deep-sea life does have a circadian rhythm, but it is regulated much differently than it is by us surface dwellers. We see light, we eat and digest, and the suprachiasmatic nucleus in the brain (our "biological" clock) keeps track of it and eventually establishes a rhythm of the circadian variety.

Most living things at the surface have some sort of circadian rhythm - the mechanisms vary, but they are present and can be readily observed.

In the deep sea, the mechanisms are quite different since they can't see any light, but the rhythm is still established. When these animals (squid in the research) eat a certain type of bacteria containing a light organ, the presence of certain proteins within that organ actually trigger a change in the gene transcription responsible for encoding the protein controlling the circadian rhythm. Thus, when the squid eats, it ultimately determines what the rhythm will be. The entrainment itself actually happens by means of the light organs consumed in the bacteria.

As far as where the bacteria ultimately get there bioluminescence, there is still research to be done, although I would presume there is a mixture of downward bacterial migration and chemical generation contributing to this.

Link to the article: http://mbio.asm.org/content/4/2/e00167-13


Is happiness or pleasure an evolutionary programming for survival? I think that whenever we feel some kind of happiness or pleasure it is always related with improving our chances of survival, that might be temporarily or in long term, might be of only of an individual or his/her relatives or all human beings or all living beings as a whole.

I find that a sense happiness or pleasure is linked with the survival (might not be true as it's based on personal observation).
 We crave for things like attention & being cared, beauty & physical health, power (& money). Attaining them gives us a sense of pleasure, and these things improves the chances of our survival. People having power & money dont die out of scarcity. People having beauty & physical health get to pass their genes more often(keeping whole human history in mind). Dogs developed their behaviour around humans so as to get more attention & care thus improving their chances of survival. We also feel happy helping other people, we feel happy making more friends.
  But there is no simple answer to this one as we also have tendencies to hurt ourselves and some people derive pleasure in hurting others.

So is pleasure or happiness evolutionarily programmed into us to better our chances of survival?

Our current understanding is that pleasure is one of the major ways your brain gets "you" to do things, it is the basis of positive reinforcement of behavior and associative learning. It can almost be thought of a a tag for an individual behavior that says "do this again/more". That pleasure alone can motivate animals to do things has been understood since way back in the Skinner box experiments where a wire to the pleasure center was inserted in rats and said rats would keep doing whatever behavior they associated with stimulation via the wire foten to the exclusion of all else. The basis of our learning could be summed up as do things that elicit pleasure, don't do things that elicit pain. tying many complex behavior to a single signal seems to make it easier to control and even prioritize very complex behavior, just do whatever yields the most pleasure, of course humans and many other animals have many more competing emotions and other factors, like metacognition. But for simpler animals it is easy to see how this system is efficient, it is easy to tag new behaviors or experiences into this system, at its simplest form just connect (possibly inhibitory)a few neurons triggered by the behavior or memory of the behavior to the pleasure center.

Of course it is not perfect, few things that evolved are, behaviors that are not beneficial can trigger the system, especially novel or extremely rare behavioral options, especially ones created by technological advancement, drug addiction being a great example. Evolution is very poor at preparing organisms for novel conditions like the modern technological world. And the our brain did not evolve under conditions where cocaine (as an example) existed. Just because something is pleasurable does not mean it is beneficial.  The full range of behaviors that can elicit pleasure would be well beyond the scope of a single question but it is quite clear pleasure itself is an evolutionary advantage, it is one of the major reasons we learn to eat, drink, reproduce, and make social connections.

Happiness, is more difficult, mostly because it is a poorly defined term in biology, it is unclear if it is distinct from simple pleasure.


What would happen if brain neurons did not reduce their sensitivity to neurotransmitters after prolonged exposure? From my understanding, neurons decrease their sensitivity to neurotransmitters by reducing the amount of receptors on the cell membrane in response to sustained neurotransmitter activity. One explanation I heard is that cells do that to protect themselves from damage.

This makes me ask - what kind of damage could be caused by sustained neurotransmitter activity in the brain, if cells did not reduce their sensitivity? Can a brain survive/thrive if neurons always had the same number of neurotransmitter receptors?

Short answer
As far as I am aware, neurotoxic effects of chronic excitatory stimulation are not prevented by receptor trafficking.

Background
I think the question assumes that 1) neural damage related to continuous activation (excitotoxicity) is preventable by 2) the dynamic regulation of receptor numbers on the neuronal membrane. As far as I can see, these two processes are unrelated.

Excitotoxicity is

  ...the ability of glutamate or related excitatory amino acids to mediate the death of central neurons [...] for example, after intense exposure. [...] Excitotoxicity has substantial cellular specificity and, in most cases, is mediated by glutamate receptors. On average, NMDA receptors activation may be able to trigger lethal injury more rapidly than AMPA or kainate receptor activation, perhaps reflecting a greater ability to induce calcium influx and subsequent cellular calcium overload (Choi, 1992).

Hence, it is the influx of toxic amounts of Ca2+ that induce cell death. Not much Ca2+ is needed to accomplish this. For example, a status epilepticus (a sustained epileptic seizure) can lead to hippocampal damage, due to persistent excitation and glutamate release (Meldrum, 1991). Epileptic seizures lasting longer than 5 minutes are regarded as dangerous in this sense and after 30 minutes they are potentially fatal (often not directly related to excitotoxicity though) (Cherian & Thomas, 2009). In this short time span regulation of cell-surface receptor densities are unlikely to play a substantial role. For example, serotonin-specific reuptake inhibitors need 2 weeks to lower the amount of 5HT1A receptors (Tylee & Wolters, 2009).

Dynamic regulation of receptors. The regulation of the number of receptors is linked via feedback loops. A great example is the way glutamatergic AMPA receptors are regulated through endocytosis (Fig. 1).

Fig. 1. AMPA receptor trafficking. Source: Anggono Lab.

AMPA receptors are the principal receptors that mediate most of the fast excitatory synaptic transmission in the mammalian brain (Purves et al., 2001). The dynamic trafficking and proper synaptic targeting of AMPA receptors are crucial in determining the strength and plasticity of excitatory synaptic transmission. This dynamic regulation may also impact learning and memory processes. The process of receptor trafficking is, as far as I know, typically not associated with emergency rescue operations to prevent excitotoxicity. Nonetheless, these mechanisms, are essential to sustain an adaptable brain capable of learning, forgetting and restructuring itself.

References
- Cherian & Thomas, Ann Indian Acad Neurol (2009); 12(3): 140–53
- Choi, J Neurobiol (1992); 23(9):1261-76
- Meldrum, Epilepsy Res (1991); 10(1): 55-61
- Purves et al., Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates; 2001
- Tyllee & Wolters, BMJ (2007); 334(7600): 911–2


Why are men stronger than women? What are the evolutionary explanations for why women are physically weaker than men (on average), and is this difference adaptive? See figure one here.

I suppose that something puts pressure on men to be physically stronger than women, but I don't see what it can be. Why the discrepancy between the sexes?

What are the evolutionary explanations for why women are weaker than men (on average), and is this difference adaptive?

All of the theories surrounding this fact are speculative; it would be difficult to prove "why" men are, on average, stronger than women.

One contributing theory is Female-Choice - basically that women had (or has) the ability to be more selective when it comes to choosing a mate. Over time men will reflect the preferences of women (taller than them, stronger than them, facial hair qualities, etc.). This is superficially supported by casual studies like this study from OkCupid where the "attractiveness" curve for men is down-shifted, meaning women think the average man looks below average in attractiveness and implying those who are viewed as average ( actually the top 20% of men or so) would have better reproductive success. Men, in the same casual study, had a nearly perfect bell-curve associated the attractiveness of women, implying that men are excellent at deducing whether a women is below average in attractiveness, average, or above average in attractiveness.

Another contributing theory is Male-Male Competition. Basically men, at some point (and still might) compete with other men to win over women. The bigger, stronger man would presumably win in a fight and eliminate his competition - directly preventing the production of offspring by the weaker male. The male-male competition also holds true in a more speculative theory in that the winners of wars literally raped their way to reproductive success.

It is worth noting that men, on average, are only about 30-40% stronger than women due to the larger muscle fibers in men (as cross-sectional area determines muscle strength, not volume). With training the difference (kg for kg) is reduced to 15-20%.

Ultimately why women are weaker than men (or men are stronger than women - whichever way you prefer to put it) doesn't have a solid answer beyond "because the stronger, taller men have reproduced".


circulating microRNAs are functional? In plasma and other body fluids, miRNAs can be found. They not only originate from dying cells but also from active secretion and are usually 'packed' into vesicles/lipo-proteic structures (i.e. exosomes) protecting them from the action of ribonucleases. Thus, miRNAs in plasma are very stable, offering diagnostic opportunities.

My question is whether they may also have a functional role. Exosome transfer between cells has been demonstrated, so it is likely that miRNAs can be secreted by one source cell and reach a target cell, similarly to how hormones works. However, this has not been quantitatively assessed. Is the concentration of miRNAs in plasma known? Is it sufficient to hypothesize functional regulation of gene expression in target cells?

See papers by D Bianchi for reports of miR levels in blood of pregnant humans, both of maternal and fetal origin.

A review by Steer and Subramanian offers a number of examples pertaining to your question.

Lastly, Vickers, Palmisano, et al. (2011) show that some miRs are present in the HDL-cholesterol particle and that those levels differ between normal and familial hypercholesterolemia human subjects.


Can a cell culture insert plate be used with a vacuum manifold? There exists 96 well plate setups for use with vacuum manifolds. Is it possible to use 6/12/24 plate inserts with the same setup?

This company sells a vacuum manifold for 24, 48 and 96 well plate formats.


Enzyme Assay - pectinase During assaying an enzyme at high temperature, the substrate (Pectin) is degraded by the high temperature rather than by enzyme, so, how can I minimize degradation of the substrate by the temperature?

Pretreat the enzyme at high temperature before carrying out the assay at the standard temperature –  Alan Boyd


Bee (?) identification I live in Michigan.  I just saw a bee that I think I've seen before, but only this time was I so struck by its uniqueness and - for lack of a better word - scariness.

I'll describe it.  It was maybe an inch and a half long.  Maybe bigger, maybe smaller (I'll admit that I was hurrying to get away from it).  It looked like a queen bee, but longer and slightly thinner.  However it had wings that were very profoundly orangish-red.  Like burnt orange maybe.

I haven't been able to find any matching pictures online.  It is theoretically possible that it was covered in pollen, and I am incorrect about what I think I saw, but assuming it wasn't (as I do believe this isn't the first time I've seen this guy or one of his friends), does anyone have any clues as to what this could be?

EDIT:  PHOTOS

After considerable patience. I was able to capture some photos of this guy.  One of these photos is post-processed a little to emphasize the color.

A couple things about these photos.

They were extremely difficult to take because the bee never stops moving.  I don't know if this behavior is useful for identification, but he is always in the same place (in front of one house), and he flys back and forth between a small crack in the sidewalk (a nest?), and between 5 and 10 feet away.  He moves like a dragonfly (that's the best way I can think to describe it), and he doesn't stop - he'll seem like he is going to land, and then flies off.  This morning was an exception.
These photos do not fully capture the depth and vividness of the redness of his wings, nor do they adequately convey just how large he is.

Nice pictures! From the back pattern, size, and antennae shape, I'd say this is very likely a Cicada Killer wasp (Sphecius speciosus), cf., for instance, this picture taken at a similar angle to yours.

There are many good resources online about Cicada Killers, including this page from the MSU Extension Office, and the Wikipedia entry Sphecius speciosus.

It would be interesting to see if you could find the distinctive burrow (photo / video) of your resident wasp!


What is a sex-biased gene? How do you define a male-biased gene and a female-biased gene as they are found in the abstract of this article.

In the linked paper, the authors discuss this as sex-based gene expression that evolved by sex-specific selection. The expression is not limited to one sex (which are sex-limited genes). Sex-biased genes are expressed by both sexes, but differently between sexes.


How long will norovirus live? I hope this is the right place to ask. I subscribe to several Stack Exchange threads, and regard them as the best internet forum for genuine and credible answers.

I spent last evening talking to friend, at an Amateur Radio Club, who told me he has recently recovered from the norovirus. I was demonstrating an oscilloscope to him, and he also handled the handbook. All this is now in the holdall I used to carry it to the Club. I took all the precautions I could, like washing my hands and not getting them near my lips, nose etc. So, my question is: how long should I wait before opening my holdall, to be sure any infection there is dead?

Well, for him the virus is already likely at minimum levels within his body. If he's recovered (pass the fever phase) then his immune system has already dealt with the majority of the viral bodies in his system, since the peak of the immune response comes after the peak of the viral infection density (ignore B):

How much of the virus was left in his system to actually spread is hard to guess. Sometimes infections never truly go away, but merely become undetectable by conventional testing. However, if we're to assume that there's at least some norovirus left to transfer to you then you should realize that the greatest chance for exposure has already come and gone.

The moment you were in the same room together, talking in close proximity, shaking hands (if you did), or generally being close is the most likely source of any infection you could have picked up. However, while most virii don't survive well outside of the body, the norovirus notably bucks that trend. The Hawaiian Department of Health (PDF) notes that the virus can definitely survive outside the body for several days on hard surfaces (though it will not grow), can survive being frozen, and that it only takes about 100 viral units to cause an infection (which could fit a few thousand times over on a grain of salt). Scientific American also notes that norovirus can survive for months or years in sources of drinking water.

What you've already done is pretty much what you should do to avoid infection. You've washed your hands, refraining from mucous membrane contact, etc.

Ultimately how long you should wait depends on where the norovirus currently resides. A week should be sufficient if all of the norovirus is contained on the book or on other surfaces that you're not making contact with. However, if it's already had contact with your skin or mucous membrane, then you're either already fighting it off or you're about to become ill. Unfortunately it's a lot easier to expose yourself than contain something you can't see, as the Mythbusters have done a good job of showing (Video).

In all likelihood if he was still infected enough to transmit the virus to other people by the time you two started handling the same equipment and you didn't use gloves, you've probably been exposed. However, exposure doesn't automatically mean you get sick. If you're not sick within a week afterwards, you've successfully fought it off. So, congratulations, perhaps!


What is the primary energy source for sprouting plants? To what extent are young plants powered by the potential energy stored in the seeds and when does solar energy take over? Are there other energy sources involved?

I was observing sprouts in a germinator [is this a word?], pushing up the lid after being left alone over three-four days. As this is a considerable amount of work (for such young plants) I wondered how long the plant can access the original energy stored in the bean/seed and how it compares to the amount of energy it can get. As you can see in the picture, the sprouts have only access to water and some sunlight.

I suspect the potential energy it draws somehow decreases monotonically (perhaps linearly, quadratically, exponentially?) over time, while the solar energy pics up.

Is this mental model correct?
I'd appreciate an answer that a non-expert can understand.

I think these were radish sprouts, but my question is more general.

This depends largely on the plant, some seed stores can last a very long time, but a few general trends can be discussed.

sprouting plants run off stored carbohydrates in the seed, they are using respiration, photosynthesis begins as soon as they are able and they will switch over to it as quickly as possible it is however gradual as the plant never stops using respiration it just starts using photosynthetically produced sugars instead of stored ones. The stored energy will run out so the faster a plant can stop relying on it the better, so even a small production is helpful, you yest it is a gradual process, even if it is a fast gradual process ins some plants.


Why doesn't glucagon promote glycogenolysis in muscle? Insulin stimulates glycogenesis in both liver and in muscles. Epinephrine stimulates glycogenolysis in both liver and muscles. But glucagon stimulates glycogenolysis in liver only.  Why is this so?

Glucagon needs glucagon receptors to have an effect on the tissue or organ in question, and your answer can be found there.  Glucagon receptors are found in the liver, like you say, but they're also found in other tissues like intestinal smooth muscle, and brain tissue (http://www.glucagon.com/glucagonreceptor.html) - but, crucially, not in skeletal muscle.  So glucagon-stimulated glycogenolysis isn't actually restricted to the liver, it's also found elsewhere.  Liver-based glycogenolysis has a significant role in blood-sugar control though, so it's often only the liver that gets mentioned.


Problems in optimisation with applications to biology? I will soon have around 8 weeks to do a research project of my choosing  as I am finishing my undergrad in computer science.
My experience is mostly in optimisation algorithms (mostly combinatorial/discrete optimisation).

I have an interest in applying computer science to biology (mostly human biology).
I would like to ask if anyone knows optimisation problems with applications to biology which would benefit current research.

Although I have read a lot about biology in my free time, I am not too knowledgeable about the current state of the research and so it is a bit hard for me to find a good topic.

Some examples to spark the discussion are string problems in genetics (alignment problems), and community detection in graphs (to find proteins in the same functional group).

Thank you!

Maximum likelihood phylogenetic trees. The trees are easily scored but the tree space is so large that finding optimal phylogenetic trees is extremely difficult. There's some research but there haven't been very many actual breakthroughs, so it's probably a pretty rich field.


Extract bacteria from compost? I'm working on a project where I need to find certain cellulolytic bacteria. I was looking at this list : http://webcache.googleusercontent.com/search?q=cache:CrtQ9T6K7m8J:www.wzw.tum.de/mbiotec/cellmo.htm+&cd=1&hl=nl&ct=clnk&gl=be

How could I selectively separate one of the bacteria types that I had in mind from that list?
So how would I have to extract the bacteria from the compost?

A first (and obvious) approach is the use of cellulose agar in order to isolate all the celluloltic bacteria in the sample. Be careful, however, since the nutrient requirements of some of those microbes may be higher and then they won't grow with only cellulose (they may need some other compounds, like a nitrogen source). Be careful with fungi, too.

If you have the proper equipment, it would be ideal to extract DNA and analyze the environmental rRNA 18s sequences. With this, you should be able to know if your bacteria is present in your sample. If so, proceed with the previous steps.

Once you had a set of suspected colonies, you must proceed with more specific culture media (wich would depend of the exact bacteria you're looking for. For example, if you're looking for Clostridium, you should try to grow your sample in an anaerobic jar and test the ability to reduce sulphur). With this approach, you may reach a point where you can't differenciate similar species. At this point, mollecular characterization is the best option, with the use of rRNA 18s again. Note that the mollecular approach, while relative expensive, can be performed in every step, so you can combine cultures and DNA analyses at will.

Lastly, if you're looking for an specific bacteria, it would be useful to know wich one is, so the community can give you more accurate responses.


DNA Analysis (AncestryDNA) A recent1 AncestryDNA commercial highlights a customer who discovered that she was 26% Native American.

Credit: ancestry.com/dna

You can see the full commercial here.

My question is, how can this be?

What combination of parents' race lineage would dictate that a person is 26% Native American (or any other race for that matter), and how many generations back would one have to go to achieve these numbers?

1. Recent to me, I don't watch much television.

These tests don't actually tell your ancestry, there is no way for a genetic test to do that because there is too much genetic variation among populations, as well as between.

Instead, the test is reporting, based on the polymorphisms observed, an estimate of their ancestry based on sharing those polymorphisms with others from a group. How do you know what polymorphisms an Asian or Native American has? Well, you do tests on a bunch of Asians and a bunch of Native Americans and use the similarities between them compared to other groups to form a 'profile' for that group. However, even an individual with a perfect geographical pedigree can share polymorphisms with other ethnic groups.

Wikipedia has a section on this:

  Many companies offer a percentage breakdown by ethnicity or region. Generally the world is specified into about 20-25 regions, and the approximate percentage of DNA inherited from each is stated. This is usually done by comparing the frequency of each Autosomal DNA marker tested to many population groups.[2] The reliability of this type of test is dependent on comparative population size, the number of markers tested, the ancestry informative value of the SNPs tested, and the degree of admixture in the person tested. Earlier ethnicity estimates were often wildly inaccurate, but their accuracies have since improved greatly. Usually the results at the continental level are accurate, but more specific assertions of the test may turn out to be incorrect. For example, Europeans often receive an exaggerated proportion of Scandinavian.[10] Testing companies will often regularly update their ethnicity estimate, changing an individual's ethnicity estimate.

In summary: ethnicity testing is at best to satisfy a curiosity. There is no way that genetic testing can identify your geneology perfectly, and in fact it is pretty meaningless to do so, because interbreeding between geographically distinct populations happens all the time.


What species is this lizard? A small green lizard (20 cm in size). It was found in the direct neighboorhood of a house, in a small village in the Hungarian hills south of the Balaton lake. It was found in the middle of the day.

Our first guess would be Lacerta viridis. Is this correct?

By the picture and the official distribution it looks to be as you said a Lacerta viridis.

Some references and distribution here:

https://www.iucnredlist.org/species/61530/12507156
https://commons.wikimedia.org/wiki/Lacerta_viridis
http://reptile-database.reptarium.cz/species?genus=Lacerta&species=viridis

In Western Europe we have a brother specie Lacerta bilineata.

Example in Geneva:

The distribution maps shows that Lacerta viridis is mainly present in Easter Europe (including Hungary) and Lacerta bilineata is present in the Western Europe.

Both species are similar and the male get the throat blue generally during the breeding season.

This site have also a description of the specie.


Since the matter in the brain is recycled every few days how does consciousnesses work? Since parts of the brain are recycled every few days does that mean that materialistic theories of consciousness don't work?

That was an interesting read, and I saw nothing to support your statement that "brain parts die every few days".

Neural plasticity demands that some synapses degrade as new ones are formed. But there are (an estimated) 100+ trillion synapses (some put it an order of magnitude higher) so, really, a few here and there means little. It's when there is wholesale loss that problems arise.

A strong argument for a materialist theory of consciousness is that as neurons involved with memory die, so does memory. This is evident in the transition that occurs in early childhood allowing for the formation of long term memory as well as the degradation of short-term memory and other brain functions in people with, say, Alzheimers.

Hippocampal Neurogenesis Regulates Forgetting During Adulthood and Infancy Science 9 May 2014


Why White Blood Cells (WBCs) do not react to foreign bodies like sperm? Why do the white blood cells allow foreign bodies like sperm to exist inside body cavity without any reaction?

White blood cells function is to fight against foreign bodies (from the text books).

Majority of white blood cells in general are present only within blood vessels, lymph vessels and lymph nodes. In addition various organs have locally adapted specialised immune cells. For example brain has microglia, Liver has kupfer cells, etc... Specialised immune cells are present along the mucosal linings which are named differently in different regions - Peyer's patch in the jejunum and ileum, tonsils in oral cavity, adenoids in the nasopharynx, etc...

As sperm do not enter blood vessels, only local mucosal immunity will act on them. There is a local immune response to the sperm in the vaginal mucosa. However, the immune response to the sperm is transient. Several hypotheses have been put forth to explain this:

The seminal plasma suppresses the immune response. This is supported by the fact that sperm, if introduced without seminal plasma, do elicit an immune response--however this suppression seems to be inconsistent
Insemination might activate a sequence that results in active immune tolerance to paternal antigens (antigens present in sperm)

For details see here:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782486/


What is the molecular mechanism of odorant transduction signaling pathway? I have read a few papers on the topic of odorant signaling pathway. The following papers are listed as examples. However, I found that there is not a clear pathway representation of the odorant signaling pathway, through which the involved genes and regulations should be known. Is there any paper I have missed?

Menzel, R. and P. Benjamin (2013). Invertebrate learning and memory,
Academic Press.
Leal WS: Odorant reception in insects: roles of
receptors, binding proteins, and degrading enzymes. Annu Rev Entomol
2013, 58:373-391.
Kaupp, U. B. (2010). "Olfactory signalling in
vertebrates and insects: differences and commonalities." Nat Rev
Neurosci 11(3): 188-200.
Vosshall, L. B. and R. F. Stocker (2007).
"Molecular architecture of smell and taste in Drosophila." Annu Rev
Neurosci 30: 505-533.

Information available on this is huge. I will pin point main points. Generally this signalling will involve four components viz. receptors, transduction machinery, perireceptor processes and downstream processing of chemosensory information.

Receptors
First step is to receive signal (here odorant or chemicals). Following figure shows comparison between primary chemoreceptor neurons in vertebrates, insects, and nematodes.

These neurons constantly undergoes birth-maturation-death and process is well studied in many model systems.

Signal transduction

After stimulus is received, it needs to be transfer inside cell for further processing. In this case, generally transduction happens via GPCR signalling. These neurons use two widely used signalling cascades. Following figure shows main components in this signalling ( (a):vertebrate olfactory receptor neurons (b): lobster olfactory receptor neurons),

Perireceptor Processes

These process are important for receptor activation and transduction. They can be any type like mechanical or biochemical.

Downstream processing

There is huge information available at the level of pathway. Following figure represents main components in two model systems.

For finding genes, you have to search in specific part of this process (like this is good example of receptor genes in human).

I would strongly recommend reading chapter 4 of "The Senses - Comprehensive Reference". All above information is taken from this book. Another good open source reference is The Neurobiology of Olfaction, this reference has all things you need for free.


How can I resuspend a cell pellet without harming the bacteria? When using a preculture with Ampicillin in my protein expression, I have to get rid of the preculture medium to avoid carrying over too much beta-lactamases that will destroy the ampicillin in the main culture. To do this I pellet the cells and resuspend.

Which methods of resuspension are best suited if you need the bacteria alive afterwards? I'm not sure how much force I can apply without harming the bacteria, and resuspending very gently takes a very, very long time.

Which methods can be used to resuspend bacteria alive, and which ones are the fastest?

Assuming that you are talking about E. coli: As long as you are resuspending the cells in a suitable liquid, e.g. fresh medium or buffer, then from my experience you don't have much to worry about - the cells are very robust. I've found that different strains and growth conditions give pellets with very different qualities - some will resuspend quite well with vortexing. If the pellet seems clumpy then trituration is something that I always found to work - pipette up and down until the pellet breaks up.

If you were going to do some kind of physiological measurement with the resuspended cells then it might require some checking, but if you only intend to regrow and induce expression I would say that giving the cells some time to recover in the new medium (check that absorbance is increasing) before inducing expression should be enough.


How did evolution support sports, fun, entertainment etc We know that many animals entertain themselves by playing games. But sports actually increases risks of death,or at least accidents. So why did evolution choose it? And why did evolution decide to make us look for entertainment every now and then?

This answer can be from many different perspectives! I'll try to blend them all together as much as possible.

First of all evolution did not choose to make us love sports. Evolution made us social animals. And sports is just one of the tools we use for that purpose. Think about it, because if evolution gave us sports, then you will play sports, your kids will inherit that bit of experience from you and they would be that much better than you. But no, we all start from level 0 when we try to play any games or sports. This is because, sports is primarily a motor memory

So why are we social?

This study back in 2014 was one of the first to suggest that memory can be heritable. It generated a lot of attention and the authors themselves suggested that their findings were standing on a very capricious footing and required further validation.

This point is valid because evolutionary forces require mechanisms by which features/mechanism which bestow advantages towards the survival of the species are positively reinforced. In this case social behaviour is the function.

Do not go googling the word Social behaviour, for some reason the wiki article looks only at dogs and cats. That is unpragmatic, because we also have the same function.

I will broadly breakdown social behaviour into

Accommodation of non-aggressive behaviour from individuals in neutral territory.
A means to communicate

But, you may ask how does social behaviour benefit you? Well the answer is simple, increased survival capacity, and better chances of propagation.

Such studies exist in crows, which have studied social behaviour. Indeed, if you start to consider studies in behavioural biology, you would find that there are instances where female mosquitoes do not just mate with any male mosquitoes, even in this case you can call it a very rudimentary form of socialising.

So in your case sports is a tool which allows us to accommodate and communicate with others in neutral territory.

You can take a look at this which better explains the social aspects of sports


Do transcripts always start and end with exons? I realized that in all cases of "RefSeq Genes" annotations of hg19 I looked at spliced transcripts start (and end) with an exon. From the annotation there is no evidence of any sequence upstream or downstream of these exons that remain in the nascent RNA.

Does this reflect the biology or is it just a consequence of the spliced read mapping? In other words: Do transcribed regions upstream of the first exon and downstream of the last exon exist in nascent RNA?

These regions, if they exist, cannot be called introns when those are defines as 'spliced sequences between exons'. How would one call them?

Most (almost all, AFAIK) mRNAs and lncRNAs start with exons for the reasons already mentioned by David. In a typical splicing event, the nucleotide that is 5' to the splice donor site (lets call it pre-donor) and the one that is 3' to the acceptor site (lets call it post acceptor) are joined together and the intronic sequence between them is removed.

If you look carefully at the mechanism, you'll notice that the pre-donor (i.e. the 3' end of the first exon) renders a nucleophilic attack on the phosphorous of the post acceptor (i.e. the 5' end of the second exon) which leads to the release of the intron.

   Image courtesy: http://mips.helmholtz-muenchen.de/proj/yeast/reviews/intron/spliceo_splicing.html

Therefore there is always an exon preceding an intron, in the transcript.

However, RNA processing can occur via a different mechanism in which the ends are just chopped off. This happens in tRNA processing, where RNAseP chops off a portion 5' to the mature tRNA region, called the leader sequence (see the figure below). I am not aware of such a mechanism happening in the case of mRNAs but a possibility certainly exists. One possible reason for mRNAs not having this kind of mechanism is because their 5' end is capped (co-transcriptionally) and cleavage of the 5' would lead to loss of cap and destabilization of the mRNA (all guesses, though). Similarly, the 3' of mRNAs is polyadenylated which also renders stability to them. Many lncRNAs are also capped and polyadenylated but there are exceptions (mRNAs too).

Since this mechanism is not very common, there is no systematic name for the excised ends. For the case of tRNA, it is simply called the "leader" sequence.

   Image courtesy: Leigh & Lang, 2004


Term for trait that is advantageous to a population only as long as it is rare I remember reading about a concept—in evolutionary biology or natural selection, I think—whereby a particular trait is advantageous to the population or species but only so long as that trait is only exhibited by a minority of the population. That is, the population is more likely to survive if the trait's existence and expression is maintained, but only if that expression is limited to a small percentage of the population. If the trait becomes too common, the selection advantage of having it will decrease, and the fact that most of the population has it may even negatively impact the survivability of that population.

I can't recall where I encountered it. It may have been in the context of reading about ADD, Aspberger's/Autism, neurotypicality, introversion, or mania/OCD. I want to revisit the topic and learn some more about it, but Google is failing me.

Can anyone tell me the name of or term for the concept I'm thinking of?

Frequency-dependent selection is the term you are looking for, I believe. Positive frequency-dependent selection encompasses traits that become more advantageous as they become more common. Negative frequency-dependent selection encompasses traits that become more advantageous as they become rarer.


Clarifying distinction between genetic recombination , translocation. and transposition Having thought about the distinciton between these terms I have come up with the following definitions, are these correct?
Translocation describes the relocation of a chromosomal segment to a different position in the genome.
Recombination is the same except:

it usually describes a non-pathological process involving balanced, reciprocal relocation of homologous DNA segments. Translocation is its accidental counterpart.
Translocation usually related to endogenous DNA. Recombination is a broader term that can describe the incorporation of external DNA in bacteria such as transformation or transduction.
The term can be used even more broadly to include independant assortment, which also effectivley acts to "Reshuffle" genetic material.

Transposition:

essentially a special case of translocation which occurs as a result of transposase enzymes acting on mobile genetic elements.

Thanks for your help!

Translocation is a mutation . Others are not necessarily .
By the way do not confuse those 3 terms with transversion and transition mutations.
Translocation refers to 2 concepts :

In protein localizing during/after transcription

wikipedia
article

A type of mutation in a chromosome

Chromosomal Translocation
(this is about the latter)

Translocation describes the relocation of a chromosomal segment to a
different position in the genome.

To some extent yes. Also It is a type of mutation . It does not happen normally and it is a result of malfunctioning proteins, mutagens etc. More importantly Translocation happens

a) between two nonhomologous chromosomes
b) between one chromosome and itself (it moves to a different locus
of the same chromosome)

See : Campbell biology 9th.ed.2011 Chapter 15 figure 15-14
you can say that
Translocation of DNA segments between homologous chromosomes has a specific name ("duplication"). Keep in mind that most of the times we do not consider a movement of DNA to a homologous DNA a "translocation" as noted above.
Recombination is a new combination of 2 DNA . Two DNA s become one. I believe the difference between Translocation and Recombination is that Translocation usually involves a huge amount of DNA (a lot of genes) compared to Recombintation ( probably not more than 10 genes or so)
I also agree with your statements on recombination. Here's more :

it usually describes a non-pathological process

Recombination happens in several ways. We have recombination resulted from DNA repair, recombination from Cross-over during meiosis, artificial lab DNA recombination (in vitro) and also recombination by some viruses during infection ( Recall Lysogenic cycles and retroviruses) or other vectors.
Therefore recombination CAN happen in pathologic and non-pathologic procedures.
See: Molecular Cell Biology Lodish et al 8th ed Section 5.6 "DNA repair and Recombination"
See T. L. Orr-Weaver and J. W. Szostak, 1985, Microbiol. Rev. 49:33.

Transposition:
essentially a special case of translocation which occurs as a result of transposase enzymes acting on mobile genetic elements

Correct. Still I'm quite sure that we DO NOT use the term "Translocation" but instead "Recombination" for transposition.
a special case of Recombination which occurs as a result of transposase enzymes acting on mobile genetic elements.
Transposition involoves 2 or 3 genes and also it is not a type of mutation. So it is not a translocation.
See: Molecular Cell Biology Lodish et al 8th ed Section 8.3 "Transposable (Mobile) DNA Elements"


Hardy-Weinberg applied to three alleles and stimation of allele frequencies I have this equation:
Corresponds to HW in equilibria with three alleles:

$(p+q+r)^2=1$

Expanding the square results:

$p^2+2pq+r^2+2pr+q^2+2qr = 1$

I need to separate homozygous and heterozygous, that means:
$2pq+2pr+2qr=1-p^2-q^2-r^2$

How I can use a equivalence similar to $(p=1-q) or (q=1-p)$ in two alleles to resolve the last equation?

Everybody said it already, but there is none.  The original HWE equation ($(p+q)^2=1$) works because you've got two variables and two equations ($p+q=1$) to work with (in reality, these are just one equation and one variable, since $q=1-p$ so $p+(1-p))^2=1$).  Now you have three variables and still only the one equation ($p+q+r=1$) which is, mathematically, impossible.

You need go out and measure some frequencies.  In particular, you need to measure two of them - I'd choose two of the homozygous types for convenience's sake.

This basically summarizes everything nicely for ya: http://www.bio.miami.edu/dana/dox/trinomial.html


How does vitamin C increase iron uptake? I've read that vitamin C increases the iron uptake in the human body. How does that work, physiologically?

Vitamin C both enhances iron uptake, and affects iron metabolism:

  in addition to the known ability of dietary ascorbate to enhance nonheme iron absorption in the gut, ascorbate within mammalian systems can regulate cellular iron uptake and metabolism. Ascorbate modulates iron metabolism by stimulating ferritin synthesis, inhibiting lysosomal ferritin degradation, and decreasing cellular iron efflux. ... Importantly, this iron-uptake pathway is of particular relevance to astrocyte brain iron metabolism and tissue iron loading in disorders such as hereditary hemochromatosis and β-thalassemia. Recent evidence also indicates that ascorbate is a novel modulator of the classical transferrin-iron uptake pathway, which provides almost all iron for cellular demands and erythropoiesis under physiological conditions.

--The active role of vitamin C in mammalian iron metabolism: much more than just enhanced iron absorption!


What are the key differences in giant and large unilamellar vesicle preparation processes? I have to study my peptide's folding on membrane mimetic (model membrane) by circular dichroism spectra. Now I'm looking for suitable methods for preparation of vesicles: LUV, SUV, GUV- large, small and giant unilamellar vesicles.

I have studied several methods but I am having a hard time grasping the key factors that affect the resulting vesicle size (LUV, SUV, GUV, etc.)

Any pointers are greatly appreciated.

Giant unilamellar vesicles (GUVs) are made by methods like hydration of phospholipid membrane generally by use of some solvent , use of electric current, combining small vesicles etc.
large unilamellar vesicles (LUVs) are made by methods like evaporation with low concentration of phospholipid, dialysis etc.
Small unilamellar vesicles (SUVs) are made by methods Injecting solution spontaneously, microfludic methods etc. There are many methods reviewed extensively (just search in pubmed you will get lot of them)

Now coming to your question, factor which affect sizes are depends on method you are using. I will list out few, rest you can check in references of each method I gave above. Most of times these methods will have all kinds of vesicles. Success of these methods relies on which method gives you highest proportion of vesicle size you desired.

Microfludic method - total flow rate, ratio of solvent to aqueous phase (Kastner et al 2014)
Electric method - rate of application of electric field (Angelova and Dimitrove 1986)
Hydration method - amount of phospholipid, evaporation rate (Lasic 1988)

Besides all of this, basic physics behind this explained here like energy difference shown below
(Image taken from (Lasic 1988))


Does digit 1 have an extensor sheath? Extensor digitorum and extensor digiti minimi both insert into the extensor hoods of digits 2-5 (or just 5 in the case of e. digiti minimi).  In every source that I can find, extensor pollicis longus & brevis insert directly into the base of the distal and proximal phalanxes respectively.

Does this indicate that the thumb does not have an extensor sheath as the remainder of the digits do?

From $n=2$ textbooks, the results are equivocal.

Moore et al. (2013)

There is no mention of an extensor expansion associated with the pollex.
EPL and EPB are listed as inserting on the distal and proximal phalanges, respectively.

Rohen et al. (2010) (p. 394)

"Extensor expansion of extensor of thumb" The label points to the middle of the diaphysis of the proximal phalanx. It's odd that extensor is singular here, given that there are two extensors.

However, Abdel-Hamid et al. (2013) present data from dissection of 95 limbs.

Extensor pollicis longus:

  "EPL tendon was attached to both proximal (PP) and distal (DP) phalanx through the extensor expansion in 94.7% of specimens (Figs. 1A, B; 2A). In 5.3% of upper limbs, the EPL tendon was attached to the DP through its extensor expansion (Fig. 2B; Table 2)."

Extensor pollicis brevis:

  In 55.8% of upper limbs, [EPB] was attached distally to the base of the [proximal phalanx] of the thumb (Fig. 1B). While in 41%, EPB tendon was attached to the extensor expansion of the thumb at the level of the base of [proximal phalanx] (Fig. 2A). However, in 3.2% of specimens its tendon was inserted into the extensor expansion of the thumb at the level of the base of [distal phalanx]."

And the answer appears to still be equivocal.

Abdel-Hamid GA, El-Beshbishy RA, Abdel Aal IH. 2013. Anatomical variations of the hand extensors. Folia Morphol 72:249–257.


In myosin II are regulatory and essential light chains calcium binding proteins or sites of phosphorylation? According to my medical physiology by Rhodes and Bell their description is as follows:

  the essential light chain is necessary for myosin stability, and the other chain called the regulatory light chain is phosphorylated during muscle activity and serves to modulate muscle function*

However, according to molecular biology 4th edition:

it states that the light chains both exert their function via Calcium binding, they make no mention of phosphorylation.

So do light chains regulate myosin by calcium binding, phosphorylation or both ?

The answer is both, the regulatory light chains , regulate myosin by phosphorylation which  can be dependent or independent of $\ce{Ca^2+}$.

Medical Physiology:

  The activity of the myosin regulatory light chain is in turn regulated through phosphorylation by $\ce{Ca^2+}$ -dependent and $\ce{Ca^2+}$ -independent kinases.

Source claiming calcium is essential for phosphorylation in tarantula skeletal muscle:

  Contraction is modulated in many striated muscles by $\ce{Ca^2+}$-calmodulin dependent phosphorylation of the myosin regulatory light chain (RLC) by myosin light chain kinase.

Calcium independent phosphorylation of regulatory protein by MLCK4:

  We find that MLCK4 is also expressed abundantly in cardiac muscle, and structural analyses indicate that it is a $\ce{Ca^2+}$/calmodulin (CaM)-independent kinase, in contrast to $\ce{Ca^2+}$/CaM-stimulated cMLCK.


Evolution of autophagy and apoptosis Autophagy and apoptosis are both necessary for survival of a multicellular organism. I have some information on evolution of autophagy and apoptosis.
However, the key difference between the pathways struck me as - autophagy is for self survival whereas apoptosis is for survival of the population. Given this, is it logical to assume that autophagy evolved earlier than apoptosis ?

Edit1:
I thought of a reason for autophagy to precede apoptosis. Since apoptosis requires mitochondria for its initiation and was acquired as endoymbiosis, I assume that:
$1)$ The primitive organisms taking up primitive mitochondria were eukaryotes.
$2)$ These were already sophisticated enough to have preliminary autophagy.

Firstly, it is important to note that, while autophagy's primary role is to 'shut down' the cell in hopes that reduced function will aid its return to homoeostasis, there is evidence of it being used as a primary method of programmed cell death in certain animals, where periods of massive cell elimination are required (e.g. insect metamorphosis). Source (Nature Review)

Your question is somewhat difficult to answer, as there is fairly limited research in the area, to my knowledge. For extrapolation purposes, it's also necessary to establish what we should consider as autophagy and apoptosis in simple organisms - how similar do the mechanisms of the processes have to be in a rudimentary form in primitive organisms to qualify as such? There is evidence of an apoptosis-like process, as well as autophagy in a range of protozoan bacteria. PLOS article (Evolution of apoptosis-like programmed cell death in unicellular protozoan parasites, Kaczanowski et. al) (Metamorphoses of Malaria: The role of autophagy in parasite differentiation, Isabelle Coppens) Additionally, based on genomic investigations, macro-/micro- autophagy are likely to be present in all non-parasitic primitive eukaryotes. (Origin and Evolution of Self-Consumption: Autophagy
Timothy Hughes and Tor Erik Rusten)

Based on some reading I did during my first degree, it is likely that both apoptosis and autophagy both developed from a precursor process that was present in prokaryotes (some bacteria, such as Myxobacteria, undergo a type of programmed cell death). An older nature article extrapolates that, based on prior research, it is likely eukaryotes came to possess the rudimentary processes of apoptosis (and likely autophagy) through the absorption of multiple strains of bacterial genomes. (Origin and evolution of eukaryotic apoptosis: the bacterial connection, E V Koonin and L Aravind)

Ultimately, I feel it's difficult to state which developed first, if, indeed, they did so separately. Assuming they originated from the same initial mechanism, which seems likely, there is a distinct possibility of them developing alongside each other. If this is the case, it's a bit of a 'chicken and egg' situation - at which point would you consider apoptosis apoptosis? There is evidence of both occurring in yeasts, as well as protozoa, so assuming these processes are indeed precursors to what we observe in multicellular eukaryotes, simultaneous development seems most likely.

Please excuse me posting the names of some articles, rather than links - I have limited use of them at the moment.


Why is funnel web spider venom so lethal to humans and not so much for other mammals? According to the information from this article,

  People and other primates are exquisitely sensitive to funnel web venom but, intriguingly, other mammals such as mice, rabbits, guineapigs, dogs and cats are relatively immune and often survive 100 times the human lethal dosage.

Why is the funnel web spider venom so much more lethal for humans and primates than other mammals?

First, we need to understand that neurons have special proteins embedded in their membranes called ion channels. These allow dissolved ions such as sodium, potassium, and calcium to pass from one side of the membrane to the other. Neurons use these channels to control their electrical activity.

Peptide neurotoxins such as the one produced by funnel spiders (robustoxin) work by having a shape and charge configuration that is complementary to ion channels, and thus they will bind to these channels and affect the way they operate (often by simply blocking the channel). Robustoxin seems to operate by removing sodium-channel inactivation.

There is a bit more information about the primary toxin on the Wikipedia page for delta atracotoxin. The intended target of this toxin seems to be insects, where it interferes with potassium and calcium channels. In mammals it interferes with sodium channels, but it seems to be particularly potent in primates. Why are some species affected more than others?

Not all ion channels are built the same. From species to species, we see a huge array of genetic differences that affect both the shape and functional properties of these proteins. Ion channels which happen to have a shape and charge configuration that is highly complementary to robustoxin will adhere to it more firmly, and thus be more affected by it.

So did we just get unlucky and happen to have sodium channels that perfectly fit robustoxin? That seems to be the most likely answer, given that Australia probably has no native spider-consuming primates. Perhaps someone else can suggest other arachnid predators that might be an intended target for robustoxin?


Chromosomomal walking I'm having a great deal of trouble understanding chromosomal walking, especially in regards to this article:

Control of male sexual behavior and sexual orientation in Drosophila by the fruitless gene.

I can get the fact that you can use recombination frequency analysis with chromosomal markers to assess the relative position of a gene, but I'm just stumped as to what it exactly it means when they say that they cloned the gene using DNA segments flanking the two insertions (fru3 and fru4) as a basis for the chromosomal walk.

How to perform a chromosomal walk

I believe that the first publication to describe this approach was Bender et al., Science, 1983.  In that paper they explain how they "walked" along the chromosome to reach the Bithorax Complex (BX-C).

This approach requires two reagents:

a cloned DNA fragment that you have mapped to a defined genetic interval, and possibly to a cytogenetic interval as well (this is only possible if the organism in question has cytogenetic tools).
a genomic library of larger cloned DNA fragments.

Step 1. Use the DNA fragment to screen the library and isolate genomic clones.

Step 2. Purify each genomic clone and prepare enough DNA to construct a restriction map of the foreign insert (N.B., Bender et al., actually used heteroduplex mapping--an EM-based technique--as well) in each clone.

Step 3. Isolate a suitable DNA fragment, devoid of repetitive DNA, from one end of the clone that extends the farthest along the genome in the direction in which you wish to "walk".

Step 4. Congratulations, you have taken one "step." Now use the new DNA fragment as a probe and screen the genomic library again.  Each time you screen the library you will recover all of the genomic clones that hybridize, or overlap, with the fragment you are using as a probe.

Step 5. --> go back to Step 2. above.

Each time you take another "step" you are isolating cloned DNA that is taking you closer to your target (the gene of interest).  For the very first step you will not know which clone is extending in the desired direction (typically) so you need some type of complementary assay to decide which end of the overlapping clones' restriction map is the direction you want to pursue. In other words, you need to align the physical map to the genetic map. In Drosophila one can use  in situ hybridization to polytene chromosome squashes to visualize where the genomic clones are derived from in the genome, and this lets you pick the correct clone at that first step.

Periodically during the walk you will need to test the new genomic clones by in situ to find out when you are getting close to your target (or if you have even walked past your destination).

Ideally you will have some chromosomal rearrangements that alter the physical and genetic maps, and let you unambiguously determine when the chromosomal walk has reached, or entered, the locus.  Alternatively, a strong loss-of-function mutation in your target gene might be a deletion or deficiency that causes a RFLP, and isolating genomic DNA from such a mutant will let you use a Southern Blot to confirm that you have reached the gene.


What is the best file format to store gel images? I store many gel images which are included in my Latex notebooks. The geldoc software normally produces TIFF files, however, Latex only accepts PNG or JPEG.

If I am going to store only a single copy of my DNA agarose gel images, which format is a good idea? PNG, or JPEG? Is there a good reason to keep one copy in TIFF and one copy in another format for every gel?

Always keep the raw data files! This is always a good idea for scientific data, and the only exception should be if the raw data is prohibitively large and it is not feasible to store it completely. This is not the case for gel images, so I would always keep the originals, and then use a cropped and edited copy in a suitable format for documents.

The original image has the full amount of data, any conversion can potentially destroy data. For example, some imaging systems produce images with more than 8 bit color depth. Converting to another format will in many cases reduce the color depth to 8 bit as many programs and some image formats like JPEG don't support higher color depths.

JPEG is lossy compression, I would always prefer PNG. You might have to use JPEG at some point because of the file size, but that should be at the latest point possible.


Did my wildlife camera take a picture of a lynx? A wildlife camera took a photograph of an animal. Unfortunately this is the only picture my camera collected. This picture was taken in the central interior of British Columbia, Canada. The distance from the camera to the subject is a few meters, and the height of the camera off the ground was probably about 40 - 50 cm.

Is this animal a lynx? It looks like it might have those fine tufts on its ears and a reduced tail.

Lynx or Bobcat
Without a clearer image or a better sense of scale I cannot say which. Their silhouette is just too similar.


How do some plants grow in salt water, while others die? My question is basically out of curiosity and comes from observing how certain plants (such as mangroves or salt cedar) can grow in seawater. If this gives the plant an advantage, why haven't all plants that grow in coastal areas developed a salt tolerance? How can the plants keep from intaking salt, while absorbing other soluble nutrients through the roots?

A few things you have to realize when you ask 'why hasn't species x evolved trait y':

What is the cost of evolving this trait? If you gain one trait, you lose another (or others). Everything in evolution is a tradeoff: that's why you're not nine feet tall, you'd be able to beat up all your enemies great, but it would take so much food to sustain you, it wouldn't be worth it.
Not every trait can be easily evolved. When you're starting as a freshwater plant, there are many, many, many, many mutations that have to occur for you to become salt-tolerant. Every one of those mutations would have to give a fitness advantage to be positively selected. The chances of this happening are low, which means if it happens at all, it would take a long time.
Who knows, perhaps these plants are, slowly, becoming more and more salt-tolerant and you're seeing them at an intermediate point in their evolution. Everything is evolving all the time, if these plants were not in a salty environment until recently, mutation and selection haven't had time to work their magic.

Update from comment:

  Can you flesh out a little on "How can the plants keep from intaking salt, while absorbing other soluble nutrients through the roots?"

Sure! I'll give you the simple answer first: there are different mechanisms for absorbing salt and for absorbing nutrients, so they can function largely independently.

Now the longer explanation: Salt and nutrients don't just diffuse (much) through cell walls, they have to be transported across by what are called transmembrane proteins. Think of the cell membrane (a layer inside the cell wall) as basically something like a layer of oil (it's called a lipid bilayer) -- you know oil and water don't mut, and for the different ions in salt (sodium ion and chloride), neither do oil and salt or oil and many nutrients so they get sort of escorted across that barrier by big proteins that form sort of a tunnel through it.

There's a different transport protein for different substances; the salt ones will only let salt through, and in fact there are different ones for letting salts in and letting salts out, and for the different ions (sodium and chloride) in salt.

Update from comment:

  This makes me wonder how salt harms most plants, if it can't get in except by 'invitation'

Quite a bit of salt can diffuse in, the molecules are small enough (unlike most nutrients) to pass through the membrane via the channels that let water in. Every living creature has a quite sophisticated setup of "ion channels" to pump salt out. If suddenly its cells are in a very salty environment, these pumps can't keep up.

Update from comment:

  So if salt can diffuse in, what do salt-tolerant plants have that other plants don't?

Mostly, if I recall correctly, three things: They will have enzymes that have evolved to work in higher salt concentrations, they will have cellular functions to "sequestrate" salt, i.e. store it in organelles called vacuoles instead of leaving it where it can harm other organelles, and of course they will expend more resources on ion pumps to get the salt concentration in the cell to an acceptable level.


Microinjection intestinal organoids I am attempting to microinject small intestinal organoids, using the Eppendorf FemtoJet 4i microinjector and Femtotip capillaries, and have come across several issues. This is a new set up in our lab, and I am first to attempt it so I apologise for the basic questions.

When attempting to fill the Femtotip capillaries using a needle or Western blot tip the liquid backs up and does not fill the capillary, leaving a large air bubble. Is this a common issue with the Femtotip capillaries? Are there other methods for filling (that do not require specialised microloader)?

When I attempted to use a tip where I had let the liquid be pulled to bottom by gravity, I had issues with leakage out of the tip bottom. Just to be absolutely clear, is it necessary for the entire tip to be filled with liquid prior to injection (no air bubbles)?

Finally I would be grateful for any advice on injection pressure and time used for organoids.

Thank you

I found that using the Femtotip loaders gives a continuous block of liquid, which can then be moved to the end of the tip by injecting several times. It is fine to have a air above the liquid at the tip.


Thermal ratchet model Two models have been proposed to explain how ATP hydrolysis by mitochondrial hsp70 drives protein import.In the thermal ratchet model (Figure 12-28A), the emerging chain slides back and forth in the TIM23 translocation channel by thermal motion. Each time a sufficiently long portion of the chain is exposed in the matrix, an hsp70 molecule binds to it, preventing further backsliding and thereby making the movement directional. Thus, a hand-over-hand binding of multiple hsp70 proteins translocates the polypeptide chain into the matrix.

What does thermal motion mean here? I will be obliged if somebody could explain it.

To repeat @Malijam comment, by thermal motion it is referring to the "random giggling" of molecules.

Temperature difference is nothing but a change in the frequency at which molecule move randomly. This movement has no specific direction. If a given molecule is prevented from moving into one specific direction (due to attachement to another molecule) but allowed to move into another, then the molecule will move directionally pushed by nothing but its thermal kinetic. This create a so called thermal ratchet.


Does tea have its effect if you have a sleep after drinking it? If I drink tea, then go to sleep for a while, when I wake up, will the effect of tea still be on me (the refreshing effect)?

Does it depend on the duration of sleep?

Caffeine is the stimulant in tea. It has different effects on different people, but if you can sleep right after drinking it, it probably isn't strong enough to have long term 'refreshing effects', And yes, the duration of your sleep does matter. If you sleep for 12 hours, much more caffeine will filter out of your blood stream than after a 1 hour nap.

Some info on how caffeine works, from here:

  Caffeine, a component of tea, coffee and cola, induces wakefulness. It binds to adenosine A1 and A2A receptors as an antagonist, but the receptor subtype mediating caffeine-induced wakefulness remains unclear. Here we report that caffeine at 5, 10 and 15 mg kg-1 increased wakefulness in both wild-type mice and A1 receptor knockout mice, but not in A2A receptor knockout mice. Thus, caffeine-induced wakefulness depends on adenosine A2A receptors.


How to calculate the number of folds present in a protein Suppose I have number of PDB files of proteins. How can I get the number of folds present in these proteins? Is the fold count derivable from the PDB files? If so, how?

There are various ways that you could do this.

CATH is a hierarchical classification system
SCOP is another such system with a different hierarchy
PTGL is the protein topology graph library
Tops motif will scan PDB files and match patterns against it

How you actually apply these tools or lookup within these systems is documented on their websites. However, it depends on what you want to do - look up published structures, or new experimental data.

I should point out that writing software from scratch to determine the fold of a protein may be tricky.


Is the common house gecko poisonous to touch? I live in India. Sometimes some common house geckos came in house and my family members kill them and I feel very bad (I even cried once ). They told me that It is very poisonous and toxic. If they fell in food or water, the water or food becomes toxic and would kill you. They told me that if you want to save them then catch them and release somewhere else but should I touch it?

I just saw a man on YouTube who handled it like it was no big deal?
I am talking about this gecko :-

They are completely harmless. There are no poisonous lizards in India, and only one species of poisonous lizard in the world (Heloderma suspectum, from Mexico and SW U.S.). A gecko's skin is not toxic. They don't inflict a painful bite. The best way to hold a lizard without harming it is by the base of a hind leg.


What kind of fish is this? What sort of fish is the big one in this picture? I saw it in an aquarium so I don't really know anything about its habitat.

Its a Giant Gourami, Osphronemus goramy.
The giant gourami (Osphronemus goramy) is a freshwater species  believed to be native to Southeast Asia, and has been introduced to other parts  of the world.
This species is commercially important as a food fish and an aquarium fish.

(Source: tropical-fish-keeping)
Reference: fishbase


I just had my genome sequenced. Can someone tell me what these different file formats are? I just had my whole genome sequenced and now I want to play a bit with bio-informatics. However, the documentation is quite scarce on the file standards used.

These are the files I have been given (the "raw" data):

Can someone explain me with some detail what is each file format, and for what are they used?

Transcribed list of file-formats from the picture:

  Indel (TBI)
  Indel (VCF)
  SNP (VCF)
  SNP (TBI)
  CNV (TBI)
  CNV (VCF)
  BAM (BAI)
  BAM
  FASTQ R2
  FASTQ R1

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more.

Your genome has a sequence that is unique to you, gifted to you by your parents and by small changes from random chance.

Your genome is pretty close to what is called the reference genome, which gets updated — infrequently1 — as sequencing platforms, pipelines, and algorithms change.

The reference genome is the "standard bearer". All other individual genomes are compared against it. This lets everyone compare apples to apples when trying to say something about the genome, in the aggregate or "big picture" view.

The files associated with the VCF format specify places in your genome that differ from the reference genome — and how they differ. These differences include:

Indels — insertions or deletions of DNA, as compared with the reference.
SNPs — single bases that differ from the reference.
CNVs — repeated stretches of DNA that differ from repeats in the reference.

The specifics of each of these classes of variants can be associated with various diseases or other attributes that make you unique and interesting. More on that later.

Each of these VCF files in your dataset has an associated TBI file. This is an index file, which helps you to quickly retrieve elements of interest from these datasets using a command-line tool called tabix.

If you are looking for differences within a specific genomic interval — say, all the differences on chromosome 4, from bases 123456 to 567890 — then you can pass that interval to tabix along with your VCF file of interest, and it will return all the indels, SNPs, or CNVs within that range, if there are any within that interval. This subset is VCF-formatted, so by knowing the format, you can get more detail about those differences.

The BAM-formatted file collects all the individual sequencing reads in a form that is mapped or aligned to the reference genome, along with some summary information to tell you how those reads differ from the reference genome.

As with the VCF files, this BAM file has a BAI index file to go along with it. Like tabix, you can use the samtools command-line tool to extract the set of reads over your genomic region of interest, if you want to examine them further.

Both tabix and samtools are available from the same author. If you have questions about these tools, the Bioinformatics Stack Exchange site is a great place to ask questions3. Lots of bioinformaticists  there have a great deal of experience with those toolkits and can help answer more specific questions.

The two FASTQ files are the raw sequence data coming off the sequencer, along with quality data. The sequence reads in these two files are paired for higher quality and longer reads, which makes the sequencing platform faster, cheaper, and better.

I walked a bit backwards, here, on purpose.

The raw FASTQ files are starting material for making the BAM file. The BAM file is then, in turn, used with variant calling software (example) to generate the variation (VCF) datasets.

Why walk backwards through these datasets?

Most people don't care about the raw FASTQ data, except perhaps to do manual alignment or check data quality. What is often more interesting or useful to most is how one's genome differs from the reference, which is captured in the variation data.

Those differences, in aggregate, are how companies like 23andme sell a product2 that tells you that you are more related to so-and-so population than so-and-so population, or whether you are more or less likely to have some disease or other odd, interesting phenotypic trait.

1. Even when new versions of this reference genome are released every few years or so, if you know what original reference genome was used to generate your BAM and VCF files, you can redo analyses based on that knowledge. There is likely some metadata associated with your sequencing results that you can look up to find this out, or you can ask the sequencing center from where you obtained these results.

2. For a bit more context, in this answer to another SE question, I talk a bit about SNPs and how they are used for testing association with so-called Mendelian disorders, diseases caused by single base changes, which may be of interest to you given what motivated you to get your genome sequenced, in the first place: https://biology.stackexchange.com/a/88839/5075

3. You can ask questions about them here, too, but you'll make certain people grumpy. Better to go to the other SE site for that.


relationship between cytokines This is for a mathematical research. I am building a model to identify severe dengue patients through the interaction of cytokines S1P,IL1b,TNFa,PAF and IL10.
For this I would like to know if there are any relationships among these cytokines. That is for example: when PAF increase S1P should decrease. or when IL10 increase Il1b too should increase likewise.
There are seperate articles on the individual effect of these cytokines but I couldn't find any that exhibit any kind of relationship among these cytokines.

Probably you used bad keywords. It is called cytokine (or interleukin) network what you are looking for. There are several articles in the topic.

For example:

Cytokine patterns during dengue shock syndrome
Multiplex cytokine profile from dengue patients: MIP-1beta and IFN-gamma as predictive factors for severity

You can find here more:

https://scholar.google.com/scholar?q=cytokine+networking+in+dengue


What type of distribution should binding affinities fit? I've been averaging Ki values from the PDSP Ki Database, and I can't help but to wonder: how I can determine p values for the binding affinities, so I can exclude anomalies in the data if need be?

P-values reflect how well the data fits some background model. This background model should reflect some assumptions you make about the data. What assumptions do you think would be reasonable in this case? For example, do you assume high values are more likely to be incorrect?

Throwing away outliers like kmm suggested is probably not a good idea, because it means you will remove $K_i$ values which are very high or very low. It is not clear there is much biological justification for that, since we know some $K_i$s can be low and some can be high, but it doesn't tell us they are wrong.

The bottom line is that without making some assumption about what the values should look like, you can't identify what incorrect values look like.


Blood circulation - How to expand blood capillaries? Do blood capillaries expand? If yes, through what means can it be done? And can warm water also be used to expand blood capillaries?

Capillaries are the smallest blood vessels. They are unique in that:

They don't have any muscular component like arterioles or venules do.
They are lined by a single layer of endothelium  (cells lining blood vessels are called endothelial cells) overlying the basement membrane.

Due to these reasons the capillaries are very permeable facilitating nutrient and gas exchange.

The capillaries don't expand as they do not have muscular or elastic components. However exposure to heat do increase the circulation. This is due to the following facts:

Exposure to heat dilates the pre-capillary arterioles - this would inevitably cause improved capillary circulation in capillaries that are already open.
Increase in pre-capillary flow opens up collapsed capillaries. In the human body roughly only one-fourth of the capillaries are open during rest1. As the pre-capillary arterioles dilate, the collapsed capillaries open up thus further improving circulation.

To improve capillary perfusion:

Temporary improvement can be achieved by activity (exercise), exposure to warmth, emotions (flushing is due to vasodilation), even exposure to cold causes vasodilation after the initial vasoconstriction
Permanent improvement of capillary circulation can be achieved by increasing capillary density. Capillary density refers to the number of capillaries present in 1 cm2 area. Capillary density can be increased by consistent anaerobic (isometric and to some extent isotonic) exercise.

References:

1: Boron and Boupaep text book of medical physiology, 2nd Edition, p.467

For more:

http://corporate.dukemedicine.org/news_and_publications/news_office/news/6597
http://www.ncbi.nlm.nih.gov/pubmed/8852622


Ebola immunosupression and infection I was wondering... If Ebola attacks immune cells and causes immunosupression, then shouldn't we see death in Ebola patients due to secondary infection?

Yes, we should. But Ebola doesn't completely immunosuppress us, or there would be no survivors.

Ebola kills by overwhelming the body before enough antibodies are formed to fight it.

If you're one of the survivors (as about 40-50% are, more with good care), you'll have antibodies to Ebola in your blood which might help someone else infected with Ebola.

If you're not one of the survivors, it's still likely you'll have some antibodies, but the shock your body goes into from all the dead cell products in your blood (which - overly simplified - causes a cytokine storm -> leaky capillaries -> fluid balance problems -> end organ failure -> death).