Are there genetic causes underlying the difference in circumference of the upper arm and foream? Is there any genetic reason for the difference in size between the upper arm and lower arm (i.e., the forearm)?

In most women, it seems that the upper arm is larger in circumference than the forearm. However, in males it seems to vary - some men (like myself) have an upper arm with a diameter smaller than their forearm, while for example in body builders the opposite may be true, as they often have large biceps.

The first answer explains that proximal limb segments do more "work" * using quotes to be careful w.r.t. technical definitions of work. Genetically, this is correct--it's the ancestral condition for tetrapods. It is also worthwhile to answer why it's beneficial for why proximal segments get bulky to do this work, instead of their distal counterparts -- i.e. why did natural selection favor this arrangement in the first place.

There is a biomechanical reason for distal limb segments to be less massive than proximal limb segments, especially in tetrapods: That moving masses farther away from the center of rotation, when force is applied between the center of rotation and the mass, takes a LOT more force.

Let's consider the arm from your example. We'll treat the forearm as a "load" which is supported by the upper arm and shoulder.

In this case, the whole arm is a Type 3 lever, with the force applied (by upper arm and shoulder) inbetween the load center of mass and the fulcrum (joint). Image from https://alexeinstein.wordpress.com/2014/09/03/lever-of-human-body/:

 In the picture, it's showing the hand (could be a weight in the hand, too) as the load, but for an empty hand the center of mass of the lower arm is probably slightly more proximal (but not more proximal than the muscle insertion).

In order to support the load that is the lower arm, the torques about the joint need to be balanced. So the torque produced by the muscles (by force AF in the diagram), needs to equal (or for bicep curls, exceed) the opposing torque produced by the mass of the load.

Torque is the product of the rotational force acting perpendicular to the lever and the distance along the lever to the fulcrum. (Reference is Wikipedia, but there's no argument about the definition of torque.)

Lets make up some numbers, and work through the example. Say that the weight of the lower arm (R in the diagram) is 10. And the distance from the center of mass to the elbow is also 10. Then, the biceps in this image needs to produce an opposing torque of at least 100. But the insertion of the biceps is very near the fulcrum, say at a distance of 1. So it needs to produce 100 times the weight of the load to create a balancing torque. For most joints in the body, the muscle insertion is nearer to the joint than the load--so the muscle will ALWAYS need to produce more than the load. So you can see how having a lighter forearm would be of benefit.

Now let's consider the whole arm, relative to the shoulder. I drew a picture for us. Suppose we only need 10 muscle mass to do day to day moving of things. Let's imagine a world where that 10 muscle mass is in the lower arm. If we have an upper arm of length 10, and a lower arm of length 10, and we hold our arm perpendicularly in front of us (so the center of mass of the 10 muscle mass is approximately at the middle of the lower arm(15 length from the shoulder), the weight of the arm is generating a torque of 150. This needs to be matched by the rotator cuff muscles, and it's a lot. The shoulder girdle insertion is quite close to the joint (let's say 2 length from the shoulder), so these muscles must produce 150 Torque / 2 length = 75 force perpendicular to the arm -- which means even more force overall, because the muscle is not acting perpendicular to the arm. That's a lot of force. (PS: red is showing lines of action of forces)

Now, suppose instead we put the 10 required muscle in the upper arm. (Another drawing for you.  We'll say the center of mass of the whole arm is now probably just before the elbow, at length 9 from the shoulder. The whole arm is producing a torque of 10 * 9 = 90 at the shoulder. The shoulder girdle muscles (with the same insertion distance of 2) must produce 90 Torque / 2 length = 45 force perpendicular -- much less. This holds in general--for a type 3 lever, the muscles will always have to do more work if the load is farther away from the joint.

Thus, placing muscle mass distally means the center of mass of the entire limb s farther from the body -- which means the body must produce a lot more force to support the mass than if the load is closer to the body. This is the same reason why it is easier to carry a heavy backpack in your arms than at the end of your arms. On an evolutionary time scale, it makes sense that the bulk of muscle mass has been placed closer to the center of mass.


Question about the consequences of non-random mating and allele frequencies I just began studying population genetics, and I don't understand something that is written in my lecture:

Consequences of non-random mating:

More homozygote and less heterozygote individuals in the population
Allele frequencies are constant (not in case of negative density dependence)
Genotype frequencies change

What I don't understand is the second point. If the genotypes' frequencies change, shouldn't the frequencies of alleles change as well? Furthermore, I don't really understand either how this is supposed to be linked to a negative density-dependence case...
Any help is welcome! :)

Out of context at least the small piece of text you cite is very poorly phrased and partially wrong.

First, you should have a look at Solving Hardy Weinberg problems. Take your time and read that post... Done? Good.

  More homozygote and less heterozygote individuals in the population

This is wrong as non-assortative mating might be disassortative mating where individuals are attracted to individuals of different genotypes.

However, it is true that population structure will cause excess of homozygotes. This is called the Allee effect. The loss of heterozygosity due to population structure is equal to twice the variance in mean allele frequency among those populations. These details sounds a bit too advance for your needs though so I won't go any further.

  Allele frequencies are constant (not in case of negative density dependence)
  Genotype frequencies change

Constant over what? Change over what? Not over time necessarily (at least not unless some other assumptions are being made).

I guess what is meant is that if in a given generation mating is not random (due to population structure for example), then you expect the same allele frequency as if it was random but not the same genotype frequency. If it is not clear why, you should probably reread the post "Solving Hardy-Weinberg problems"

Much further discussion in both english and french on @AlissaDeschamps misunderstanding can be found here.


Is the barcode COI sequence the sense or antisense strand of DNA? Is the COI sequence commonly used for DNA barcoding the sense or the antisense strand of DNA?

When the barcode sequence is generated by Sanger sequencing, it is sequenced in both strands, and presented in sense strand.


Where in this photo can I find archaea? This photo is from Guide to the Six Kingdoms of Life under Archaebacteria:

It's not obvious to me where I can find archaea in this photo, although the website seems to indicate it's clear.

Question: Where in this photo can I find archaea?

It's probably the yellow bacterial mats, which are rich in life. The mats are a stratified ecology which varies with distance from the surface, so they are rich in many species of algea, procarote and eukariote. In Yellowstone,  the bacterial mats can range in color including brown, green, yellow and orange. They are different to precipitated minerals.

You can say "The photographer contains archaea"! So, no need to search very far.

Here is a pic of an bacterial mat habitat: https://www.sciencedirect.com/science/article/pii/S0717345817300738

You can see in some videos. Ideally we would have a a biology video demonstrating the stuff at Yellowstone to show if it's squishy, slimy, spongey, has growth rings, colord layers, cross sections... although it's only tourist videos for the moment.


NADH shuttles - Why cytosol? Why is the malate-aspartate and the glycerol-3-phosphate shuttles located in the cytosol and intermembrane space?

The krebs cycle happens in the matrix so why wouldn't they push electrons from the matrix and into the intermembrane complex for oxidative phosphorylation??

The electrons for shuttling are mainly generated in the cytosol from glycolysis. NADH can easily pass the outer membrane, but must be shuttled over the inner membrane. It is important to consider that the electrons must be fed to oxidative phosphorylation from the matrix of the mitochondrion, and not the intermembrane space.


Succulent weed identification There is a succulent-looking weed growing in a crack in my driveway. What is it?

Conditions: Dry, full sun, asphalt & gravel, no competition.
Date: 2018-07-16
Location: Toronto, Ontario, Canada
Size: 40cm x 40cm x 2cm

This is Common purslane, Portulaca oleracea. It is used in salads, although it contains oxalic acid and there are poisenous plants resembling Purslane, see comment below.
https://en.m.wikipedia.org/wiki/Portulaca_oleracea


Does anybody know which plant (or tree) is this? Thus one has teased me a lot. This is just a small plantlet, the actual one went about 5 feet in height before we had to cut it. Whenever we cut it, it grew back within weeks. And soon small plantlets grew near it in a radius of about 3 meters. Today, we called 2 men to take off its root. They dug a hole about a foot deep and discovered that its roots had spread all across our garden. All the people we asked gave us different speculations of what plant it could be, but nobody was sure. Does anyone here know about it?

Data:

It has lots of thorns, even in its roots!
This plant is about 25 cm in length.
Its leaves are about 4 mm long and 1 mm wide.
A compound leaf is about 1.5 cm long.

Location: Northern plains region, India

The plant scientific name is Prosopis juliflora. It is widely found in our country (India) which is a major problem because of its impact in agricultural land. It can withstand any harsh climate also.

Initially it was introduced to our country around 1950s to be used as firewood under drought situations. But later it became a major threat, since it absorbs as much as water (approx 4 litres of water to produce 1 kg of biomass) from the soil which spoils the cultivable land and also this plant grows very fast and spreads easily as weed which also causes a major problem to the underground water table.

The government also realised its mistake later, but still this is found in most of the places in our country, particularly in the southern part of India.

You can find further details from the below links:

https://www.hort.purdue.edu/newcrop/duke_energy/Prosopis_juliflora.html
http://www.cabi.org/isc/datasheet/43942


How far in can non-extremophiles live, in Earth? I am a high school student. I'm doing a project where I need to find a planet in our galaxy that might be habitable. Then I need to create an organism that could live on that planet and justify everything about it Ex: Sight, whether or not it can see and why or why not / Touch / Smell / Respiration / Central Nervous System / Cell Count... My final outcome must have these and a lot more.

I just need to justify and explain where it lives on the planet I have chosen. I found a planet (Kepler-422b) which was described as being one of the most Earth-like planets, in terms of size and temperature, yet found. Since it is very Earth-like, it made my job a bit easier. But the planet orbits a red dwarf star that is cooler than our star, and this planet is -40 degrees Fahrenheit (80 degrees cooler than earth) so my organism will have to live in the ground of the planet and rely on the core for warmth. But I do not know how deep organisms can go into the Earth. Can someone please help me? I have done a lot of research and spent a lot of time trying to find this but extremophiles are the only organisms listed.

Thank you so much for helping me.

An extremophile is defined as a microorganism, especially an archaean, that lives in conditions of extreme temperature, acidity, alkalinity, or chemical concentration. Like the Tardigrade. Im sorry I did not make this clear initialy

Welcome to Biology.SE and what a great project, it sounds fascinating!

A few years back there was an expedition that drilled down to the deepest layer of the ocean's crust. Down there they found hundreds of different species of bacteria (mostly Proteobacteria) surviving largely on hydrocarbons and other minerals found in the rock. The deepest (that was sequenced) was found 1391.01 mbsf (meters below sea floor) and survived at a temperature of about 102°C (215°F). Like I said, there were several species sequenced, so you could really use any of them that match your needs as at least a start to your organism.

This is the deepest point I know of that we have found life, and, considering your project, I don't think you have need to go much deeper. I assume Kepler-422b has liquid water (obviously not at the surface, but perhaps a few miles down)? If so, there is a chance that the water goes relatively close to that depth already.

I hope this helps and good luck!

CDB

Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974637/

Edit: If you are looking for a multicellular organism that survives deep enough underground to rely on core warmth, I suggest Halicephalobus mephisto, a nematode living about 1.3 km underground at about 32°C (90°F). This is still considered an extremophile, however it is multicellular with a digestive tract, nervous system, etc. I apologize for the confusion in my initial answer and thanks to jamesqf for noticing my mistake. If you are not content with any extremophiles (even multicellular) please let me know and I will do my best to find something else. Again, I am very sorry for my error.


What is dendritic processing good for? Can - on a very coarse level - the functional role of dendritic processing as a whole (at least one of possibly many functional roles it might play) be described as rewarding spatially coherent synaptic inputs when creating action potentials?

This would make sense, when the mapping of neurons to synapses was neighbourhood preserving (in the sense of topology): the efferent synapses of two neurons in close vicinity (in other parts of the brain) sit in close vicinity on the dendritic trees of their common target neurons.

Then it would be desirable, that when a group of $n$ neurons in close vicinity to each other (e.g. a nucleus) projects to a subtree of the dendritic tree (i.e. synapses in close vicinity) and those neurons are firing at the same time, this should evoke an action potential in the target neuron, but not, if $n$ synapses spread randomly over the dendritic tree are active at the same time. To achieve this could be the (or one) function of dendritic processing.

As I said: this is a very coarse level of description, and to be taken with some grains of salt.

(The whole question would break down if there is no such neighbourhood preserving mapping from neurons to synapses.)

References

I've read the following articles (but maybe not carefully enough to be able to pin them down to the short form above):

Buonomoano/Maass, State-dependent computations: spatiotemporal processing in cortical networks
Stuart/Spruston, Dendritic integration: 60 years of progress
Poirazi et al, Pyramidal Neuron as Two-Layer Neural Network (this article comes closest to the spirit of my question)
Magee, Dendritic integration of excitatory synaptic input

Action potentials are always based on coherent synaptic inputs. So dendritic processing means rewarding specific coherent subsets of synaptic inputs.

So to me it makes more sense to frame dendritic processing as allowing neurons to detect several different patterns (alternatively or at the same time).

In that case each dendritic spike encodes a different pattern. This allows a neuron to play roles (or maybe the same role) in several different contexts (or possibly in different combinations of contexts). If this is the case the neighbourhood mapping you describe doesn't have to exist (though it still might).


Is it possible to deduce facts about a person's parents just by studying his/her genome? As an example, suppose Anne had abusive parents. Is it theoretically possible to deduce this from her genome even if she didn't inherit this quality (of being an abusive parent)?

Not the kind of complex phenotype that you describe (because nobody knows for example if/how "being abusive" is written in the genome), but yes, some things can be determined.

The easiest is through sex chromosomes.

For example: if you look at the X chromosome of a man, you can tell for sure that it comes from his mother (because the Y can only come from the father, quite logically) so any allele that you see there is also part of the mother's genome - but since she has a second copy, maybe it does not translate into a phenotype.

Sometimes you can even guess the phenotype of one of the parents: if you study a woman's X chromosomes and see that both have alleles that cause color-blindness (encoded on this chromosome) it means that the only X chromosome of the father has this allele, so the father is probably color-blind.

See: https://ghr.nlm.nih.gov/condition/color-vision-deficiency


Are seedless fruits considered life? From school, I remember that for something to be considered life, it must be able to reproduce.  With the creation of seedless fruits (such as watermelon), would this be considered life as they don't have seeds so they can't reproduce?

Definition of life

The definition of what is alive and what is not is not a matter of biology but a matter of philosophy. Most definitions are based on:

Physiology

Existence of a metabolism

Evolution

Ability to reproduce and have heritable traits

Ecology

Ability to respond to the environment

There are plenty of possible definitions of "life". Note also that behind the complexity of defining what is alive there is the issue of defining the unit (the individuality if you want) on which the concept of life applies.

Your definition of life

You suggest a quick and simple definition so let's consider it.

  to be considered life, it must be able to reproduce

If you talk about the watermelon tree

If this is your definition, then Citrullus lanatus is definitely alive as it is able to reproduce (otherwise we would not be able to cultivate them).

If you talk about the watermelon fruit

Now you may ask is the fruit itself alive. Then, using your definition again, I suppose the answer is no because a given seedless watermelon will not be able to give birth to other seedless watermelons (even via the make-up of a watermelon tree).

Note that following the same logic one could argue that one's head is not alive either as one's head does not reproduce. Only your gonads do. Your dog might not be considered alive either. A castrato (singer) would not be alive either. A woman, after menopause, cannot reproduce either! Arguably, a cloud replicates or a fire replicates and could eventually be considered alive following your definition. So really, as you can see your simple definition hardly fit your intuition of what should be called alive.

My opinion on your definition

Personally, I am not a big fan of your definition but again it is nothing but a matter of preferences. I don't like that your definition is unclear because there are plenty of limit cases and because there are plenty of cases we would want to call alive that we can't anymore (like a woman after menopause for example!) Every definition of life would eave limit cases but with your definition, it really easy to find these limit cases.

Is this question about Biology?

No, it is not. It is a question of philosophy.

Other interesting post on Biology.Stack

You might want to have a look at why isn't a virus alive.


How's the membrane potential restored to resting state after hyper polarisation? I have known for so long that Na+/ K+ pump restores the membrane potential. But as it pumps in 2 K+ for every 3+ Na+ moving out how can it make the membrane potential less negative when the net result is one positive charged ion moving out?

The Na,K-ATPase restores negative membrane potentials.  When a cell is hyperpolarized, leaky K+ channels take care of that. Leaky K+ channels are always open. Generally, K+ has the tendency to diffuse back out of the cell along its chemical gradient through leaky K+ channels, after been pumped in, making the cell's inside more negative. However, in the reverse situation, where the cell is hyperpolarized, they may flow inwards, along the electrical gradient.

Note that while the Na,K-ATPase is indeed the driving force behind the membrane potential, it is not the direct consequence of the ratio of Na+ being pumped out and K+ being pumped into the cell. It is the leaky K+ channels that determine the membrane potential largely, together with the Na+ channels being permanently closed, except when an action potential is generated.

Suggested further readings
- What keeps the resting potential of neurons constant at -70 mV?
- If the average resting potential of a neuron is -70 mV, why is there such a high ratio of potassium ions inside relative to out?


Can birds touch their wing tips together either in front or behind (not above and below)? Can the tips of a birds wings touch so that it would form a ring if view from above or below? I suspect it might be a bird of prey and at the moment it is picking something up from the ground but I can't find a good photo.

Black herons (Egretta ardesiaca) can overlap their wing tips in front of them while doing what is known as canopy feeding.


Element of promoter responsible for expression power of gene I know that there is a classification of promoters like: strong, medium and weak. This shows how a promoter affects gene expression levels. So my question is: what part of the promoter affects it?

For example I want to raise or lower the expression of some gene, so, what part of promoter I need to edit or maeby I can just replace it with another promoter?

Tldr; In an in vivo context the answer is going to be dependent on DNA sequence and context.

Simplistically, Eukaryotic genes promoters can be segmented in to several parts. The first, a core promoter region where RNA pol II will bind. This isn't capable of a robust transcriptional response on its own and relies on proximal promoter regions, or more specifically transcription factor binding to the proximal promoters. Proximal promoters are usually 100 or so base pairs upstream of the transcription start site and will bind proteins that will assist in Pol II binding and activation (or silencing). Enhancers (and Silencers) are conceptually similar to proximal promoter regions with the exception that they can be a looooooooooong way away from the transcription start site in sequence space. See here:1.

So, if you just wanted to drive expression of a transgene in a cell line in the lab there are plenty of established cloned promoters and enhancer regions known to work such as SV40 or Gal4. This would be an example of "replacing the promoter". That's exactly what it is and why these sequences were chosen to be cloned.

If you are asking which regions are specific to activate or repress a gene in vivo and/or in context then it will be, of course, context dependent and you'll have to find out yourself if someone hasn't already. Generally, these regions of effect will be binding sites for sequence specific transcription factors  which interact with the core transcriptional machinery (or bind other proteins that do) to effect the rate of transcription. So, if the sequence is what can induce an effect, how can you find it? You can search for these sequence specific sites by analyzing your sequence of interest with a slew of computational tools for potential binding sites and directly assess any hits ability to increase/decrease expression as isolated units when cloned upstream of an appropriate reporter construct. I guess you could even go as far to CRISPR single base pairs in or out to "edit" any hits. Alternately, you could use a purely wet bench technique such as promoter bashing to similar effect - performing serial deletions to find out which part of your promoter is important for strong/medium/weak effects or activation/repression.

The Stark Lab developed a cool genome-wide approach looking at the ability of DNA to drive expression. Although, something worth bearing in mind is that in a normal in vivo situation everything is context dependent - one piece of sequence may be reliant on another close by (like the core promoter requires proximal promoters) or it may require one or more pieces of DNA that are distant in sequence space to be close by in 3D space (like distal enhancers).

People have also taken completely synthetic approaches to making promoters .

This would be easier to answer if your question was more specific.
HTH.


Understanding Research Paper Differences I'm doing a high-level research which led me to the following paper - https://www.researchgate.net/publication/280389511_Quality_of_life_of_patients_with_chronic_lymphocytic_leukaemia_in_the_Netherlands_results_of_a_longitudinal_multicentre_study

As it's mentioned there are many groups of testing and comparison in the research, which are: the general population, total patient group and three groups of CLL patients.

I'm a bit confused about the definitions' differences between "the total general population" and "the total patient group".

I appreciate every advice / help.

This study enrolled 144 CLL (chronic lymphocytic leukemia) patients ("total patient group"). They further grouped these patients into 3 groups according to the treatment they were receiving.

When they refer to "general population" they are referring to norm scores:

  For each patient, an individual norm score was
  derived from age- and gender-matched scores of the general population on the EQ-5D [28] and EORTC QLQ-C30
  [29]. These two studies, as reported in Refs. [28] and [29],
  used a panel consisting of more than 2000 Dutch households, representative of the Dutch-speaking non-institutionalised population in the Netherlands.

So these scores are not part of the current study, but they are estimates from a survey of the wider population rather than patients who have CLL (you can assume they do not have CLL). "Total population" doesn't mean "all CLL", it means "all Dutch-speaking non-institutionalized people".


Can neurotransmitter concentrations in the synaptic cleft add up if there are several impulses in quick succession? When an electric signal reaches a chemical synapse, the signal is transmitted using neurotransmitters. Afterwards, the neurotransmitters are removed from the synaptic cleft. My question is whether it happens in a normally functioning brain that neurotransmitter concentrations in the synaptic cleft add up if there are several impulses in quick succession? If so, does this serve any purpose? Or is the time between two impulses always long enough for all of the neurotransmitter to be removed from the synaptic cleft?

Edit: To further clarify (as the currently only answer does not really adress my issue), I am aware of the principle of summation, however I do not know whether this is actually caused by multiple neurotransmitter emissions "adding up" in the synaptic cleft or whether the postsynaptic membrane can just somehow remember if there was an increased amount of neurotransmitter recently.

To describe it graphically: According to this article, the concentration of serotonin in the synaptic cleft during a single impulse looks somewhat like that. Now when there is a quick series of impulses, does the neurotransmitter always get removed before the next impulse as on the right side of the following image, or can it add up as on the left side? And if it does add up, does this actually serve the purpose of temporal summation or some other purpose?

The answer by bpedit is a good explanation of temporal/spatial summation, which can be partly a postsynaptic phenomenon (due to membrane time constants or second messenger sytems, for example).

Your specific question is about whether extracellular neurotransmitter levels sum over time. This definitely occurs regularly with "neuromodulatory" neurotransmitters like serotonin (others that behave similarly include dopamine and norepinephrine/epinephrine). "Faster" neurotransmitters like glutamate and GABA are cleared more quickly, though there are complicating factors there as well that are outside the scope of this question.

Although the summation has been shown many times, I looked quickly for an example and found the paper by Bunin and Wightman, 1998. Figures 2-6 all show extracellular serotonin concentrations that are elevated for seconds after release (let me know in the comments if you can't access this paper at your institution), and they show the changes in extracellular concentrations with multiple stimulus pulses (see in particular Figure 3).


How does chromosome number get halved in meiosis I? In meiosis 1, it is said that chromosome numbers become halved in the two daughter cells. For example, in a 2n human cell there are 46 chromosomes. During meiosis 1, the cell will undergo interphase and probably the S-phase, where chromosome number becomes duplicated. Now the cell is 4n (i.e. 92 chromosomes). During anaphase 1, 46 chromosome out of 92 would go towards one pole and 46 would go opposite. Thus the resulting two cells will have 46 chromosomes in each. So why should we say that, in meiosis 1, the chromosome number is reduced? I say that S phase shouldn't occur in meiosis 1 but rather it should occur in meiosis 2. Is my reasoning incorrect?

If you consider sister chromatids to each be a chromosome, meiosis I, rather than halving the chromosome count, separates the homologous chromosomes, which result from sexual reproduction, from one another. Meiosis II then separates the sister chromatids from one another resulting in the final halving of chromosomes.

On the other hand, many if not most biologists don't consider the sister chromatids to be individual chromosomes until they are segregated during meiosis II. In this sense, meiosis I does reduce the chromosome count to half.


Why are H+ ions pumped out instead of in during cellular respiration During cellular respiration in both mitochondria and aerobic prokaryotes, the Electron Transport Chain pumps H+ ions out of the matrix or cytoplasm to create a H+ concentration gradient. This forces the H+ ions back into the matrix or cytoplasm forcing ATP synthase into action.

I was wondering, however, why the H+ ions are pumped out of the matrix or cytoplasm, instead of into it. For aerobic prokaryotes, and the early mitochondria (which were prokaryotes living on their own) pumping the H+ ions out of the matrix or cytoplasm means pumping them into the outside world, a very uncontrolled environment. There is nothing to prevent the H+ ions from diffusing out, making the pumping completely inefficient, if not pointless. Wouldn't it make more sense to pump the H+ ions into the matrix or cytoplasm, where the H+ ions cannot diffuse, resulting in much higher efficiency?

Mitochondria pumps out the H+ perhaps just because there is no disadvantage of it. Once they've evolved such a machinery with complex network; they weren't threatened to evolve any opposite-system.

Any opposite system too; would not plausibly disadvantageous; and really happens in case of chloroplast; another sort of cell-organelle.

1: image from Plant Biochemistry, by Hans Walter Heldt, 3rd Edition.

2:  picture including all chloroplast membranes.

But if any organelle used cytosol as the H+ pool; probably that would made cytosol acidic as wel disrupt metabolic processes on cytosol. (usually the cytosol have very mildly alkaline pH.)

  Reference: Plant Biochemistry by Hans Walter Heldt, 3rd Edition, Academic Press.


Can anyone identify what type of bug this is? Can anyone identify what type of bug this is?

From a rummage around Google images for "black and red striped bugs", your insect looks a bit like:

Mylabris syriaca

Hycleus ornatus, although yours has different antennae.


Reptiles are a paraphyletic group because? Here is a question I am trying to find the answer to

Reptiles are a paraphyletic group because... ?
A) They include worm lizards, which have no limbs
B) The group doesn’t include birds
C) The group doesn’t include mammals
D) Not all of them have three- chambered hearts

I’m a bit confused about the reasoning. I know a paraphyletic group does not have all of its descendants so if birds were to be included it would become monophyletic. So is B the answer? Could anyone help explain it better?

I think the question's phrasing is arguably a little wobbly, typically as to the nature of what someone would mean by the term "reptile". But I think you understood what your teacher was expecting. I agree with you, answer is B.

Reptilia is a clade (clade = monophyletic group) that encompasses all species that we traditionally classify as reptiles + all birds. Hence, our traditional definition of reptile makes up for a paraphyletic group as birds aren't included.

Related post: If dinosaurs could have feathers, would they still be reptiles?


Can electricity be harvested from the soil around plants? This is a rehash of a question I originally wrote on Skeptics which got moved to Physics, but I'm really after an answer from a biological perspective.

A device called the E-Kaia is making news by claiming to harvest enough electricity from the soil of a pot plant to charge a phone. They claim they can draw 600mA from the soil, which actually wouldn't charge most smartphones in the 1.5 hours they claim in the article (thanks Physics.SE!).

Is there really electricity in the soil around a plant? I can't imagine there being 600mA there for the taking in the soil of a huge tree let alone a pot plant. Maybe it isn't electricity in the soil but some other kind of energy or chemical that can be extracted to generate electricity - it sounds like the lemon battery experiment, which relies on a chemical reaction.

And surely, even if there was electricity there, extracting all of it would damage the plant?

Electricity may be indirectly generated from plants through the use of a microbial fuel cell, in which biologically-catalyzed chemical reactions are used to drive an electrochemical cell.

A non-technical description of the technology can be found here.  The basic idea is that plants produce organic compounds, which are broken down by soil microorganisms to produce carbon dioxide, electrons, and hydrogen ions.  Ordinarily the hydrogen ions and electrons combine with oxygen to form water, but there are various ways to divert the electrons to travel through an electrical circuit before the oxidation reaction takes place.  This flow of electrons (electricity) can be used as a power source.

This technology is still in its early stages but the process has been demonstrated in some laboratory proof-of-concepts:

Strik, David P. B. T. B.; Hamelers (Bert), H. V. M.; Snel, Jan F. H.; Buisman, Cees J. N. (2008). "Green electricity production with living plants and bacteria in a fuel cell". International Journal of Energy Research 32: 870–876. doi:10.1002/er.1397.
De Schamphelaire, Liesje; Van den Bossche, Leen; Dang, Hai Son; Höfte, Monica; Boon, Nico; Rabaey, Korneel; Verstraete, Willy (2008). "Microbial fuel cells generating electricity from rhizodeposits of rice plants". Environmental Science and Technology 42 (8): 3053–3058. doi:10.1021/es071938w.

The E-Kaia company has not released enough information to say whether their product is in fact a plant microbial fuel cell, a simple earth battery, or a mere scam.


What is meant by "complexity of carbon sources"? My biology book states

  "life on earth depends upon carbon based molecules, most of these food sources are also carbon based. Depending upon the complexity of these carbon sources, different organisms can then use different kinds of nutritional processes"

Please explain this statement.

Consider all the different types of carbon molecules one can find on earth.

Proteins.  Sugars like cellulose and starch.  Alkanes like methane and tar.  CO2.  Alcohols.  A boatload of variety.

Now think of how each one is used or can be used by an organism.  I will chow down on a potato.  And some alcohol. Termites eat cellulose.  Anaerobic bacteria use methane.  Plants eat up the CO2.

One carbon nothing eats is CaCO3 or limestone.  I am not sure why.  Oh - also diamond.  Not many things can metabolize a diamond.  Although maybe they don't get the opportunity to try...


Is there any organism that is born with all the nutrients and resources needed for their entire lifetime? I understand that adult mayflies have no mouth, but they do take in oxygen through openings in their exoskeleton.

Is there any organism that does not need to ingest any type of nutrition and does not need to take in something for cellular respiration?

You may need to clarify your question: As written, this would be the biological equivalent of a perpetual motion machine. No such organism could reproduce without either violating the first and second laws of thermodynamics, or ultimately evaporating into nothingness as it divides.


Genetic engineering for experimenting at home? I am just wondering whether it is possible to carry out small scale genetic engineering at home, without any sophiscated tools.
Ive searched google and found this http://explorebiotech.com/the-7-important-molecular-tools-used-in-genetic-engineering/
So i am wondering whether these tools are easily acquirable and how feasible it is to be done at home maybe as a hobby.
Also my budger is probably about 200 USD so my hopes arent that high.

Doing genetic engineering experiments at home is generally referred to as either "biohacking" or "DIY Bio". There's a number of forums out there filled with hobbyists who are doing that sort of work in their homes and garages, and discuss how to do such things in a hobbyist environment. With those terms (and the info in the Wikipedia article), you can probably find those forums on the internet. (Suggestion: look for ones where the regulars emphasize safety and appropriate conduct - not only is it better for you, it's a sign that the regulars know what they're talking about.)

However, 200 USD might be a little small to set up a decent (and safe) "biohacking" space in your own home. Possibly a better bet is to see if you can find a local "makerspace" which has a biology component. Makerspaces are places where, for a small fee, fellow enthusiasts pool together to purchase equipment (and space) to do various projects. Most makerspaces are geared toward the computational/mechanical (e.g. building robots), but there are some out there which have biotech equipment. Your mileage may vary, though, and you're likely to have more success in finding a decent makerspace in a large city than in a small town.

A final caveat is to make sure you research your local laws to figure out what is legal in the jurisdiction you're living. Especially with laws targeting illegal drug production, there are locations where possession of basic scientific equipment by normal homeowners is criminalized. There's also regulations about waste disposal and material storage that you'll need to follow. Also, in most jurisdictions accidents/damage from home labs are penalized much more harshly than, e.g., cooking accidents. Know what's legal/illegal in your jurisdiction (and by your homeowner's insurance) before attempting to set up a home lab.


Are self pollinated plants genetically different? Gametes in pollen grain are formed during meiosis in the anther. And meiosis produces genetically different gametes. When the pollens grains are carried to the stigma to fertilise the egg cell of the different/same flower from the same plant, doesn't it produce genetically different flowers even though it is self pollinating because of the variation in gametes?

Yes, it does.
In Meiosis there is genetic recombination (by recombinase) in the Meiosis-1. So even though it is self pollination, there is significant genetic variation.
Still for higher degree of variation cross pollination is exhibited.
It should be noted that cross pollination has greater evolutionary significance.
Few plants exhibit self-incompatibility to supress self pollination (in monoecious flowers/plants).


Why can all animals swim in water without learning to swim but humans cannot? I had a question since I was a child. I was always curious about the fact that all animals can swim in water. They don't need any training or to learn swimming. But humans need to learn to swim. Why ?

I am a technical person and not in biology after my 10th year in school. Can anybody please shed some light on this question?

While I am not sure I buy your assertion that all mammals know how to swim, I would say that humans are at least as good as dogs when swimming. If you drop a human in water we will instinctively flap around and try too keep our head out of the water in about as elegant a way as a dog. The main problem for humans is panicking. Someone who does not know how to swim is likely to panic and not manage to keep their head out of the water. Remember that humans float in water, if you keep calm you should be able to keep your head above the water line easily enough.
Dogs can't swim as such, they simply do the same motions in the water as they do on land. There is no different action happening, they don't instinctively do a breast stroke.
In addition, human infants actually have a couple of instincts that make them "swim" (source):

The Diving Reflex
The diving reflex, or bradycardic response, means that infants whose heads are submerged in water will naturally hold their breath. Their heart rate will also slow down while they are underwater. This reflex disappears after about six months of age.
The Swimming Reflex
Newborns placed stomach-side down in water will move their arms and
legs in a repetitive "swimming" motion. This is known as the swimming
reflex. This reflex, too, begins to fade at about the six-month mark.

That is no better and no worse than any other non-aquatic mammal can do. Try dropping a cat in water* and telling me she is a graceful swimmer :).
* Don't, that's not nice.


What is the difference between "genetic" and "hereditary"? What is the difference between the adjectives "genetic" and "hereditary"?

From dictionnary.com

  Genetic:
  pertaining or according to genetics

  Hereditary:
  passing, or capable of passing, naturally from parent to offspring through the genes:

Note: I selected the pieces of definitions that I found most relevant to the current discussion.

Genetic information can be passed on to offspring. As such, I understand the confusion you may have.

When the adjective "hereditary" does not apply

By its definition the adjective "genetic" can be used in multiple situations where the adjective "hereditary" could not. It is specifically obvious when the term "genetic" is used in the context of a whole population. Indeed, not all genetic patterns are inherited especially when referring to population-wide patterns. Also, the adjective "genetic" focuses on genetics and not necessarily on its characteristic of being inherited.

Example

Consider for example the concept of "Genetic signature of selection". A genetic signature of selection is any pattern in the genetics of a population that can be used to infer past selection invent. These patterns include
 - high population divergence around the specific site
 - loss of heterozygosity (and polymorphism) around the selected site
 - modification of the site-frequency spectrum
 - genetic - environment covariance

Further information

Please note that the concept of heritability might have an unexpected definition for some layman. You might want to read Why is a heritability coefficient not an index of “how genetic” something is?.

When the adjective "genetic" does not apply

There are non-genetic information that can be transmitted from parents to offspring (or even between unrelated individuals).

Examples

Niche construction inheritance or epigenetic (esp. in the broad sense) modifications are examples of non-genetic inheritance.

Further information

You will get more information about non-genetic inheritance (and its role in evolution) in this answer.


Why does hair grow after trimming but remains at a constant length after a while? Some hair especially body hair regrows after trimming but stops growing after a while. What is the mechanism behind control of hair growth and how is the length limit determined?

Hair grows from the follicle; there is no way for the follicle to determine if the hair tip is trimmed or not. This is unlike plant shoot/root growth that happens at the tip. Also there is no signaling from tip to follicle.

Hair growth has four stages: Anagen (Initiation), Catagen, Telogen (resting) and Exogen (falling off). Initially the primary follicle is formed during development of the skin, after that the hair growth continues in a cycle. In other words the old hair shaft is replaced by a new one. The period of the cycle (or how fast it happens determines the final hair length); the faster is the cycle the shorter will be the hair (you may note that certain people have a very short head hair even when they do not trim). This is because the old shaft doesn't get time to grow before it is shed and replaced by the new one.

From: Stenn & Paus (2001)

From the same source

  Because there is a limit to the time a follicle stays in anagen, there
  is also a limit to the length of its product, the hair shaft. The
  anagen phase has been divided into six subphases (64, 359). Except for
  the last subphase, anagen VI (the duration of which dictates the shaft
  length), the length of the anagen subphases I–V does not differ
  substantially between follicles from different regions (490, 565).
  […]
   Because the actual length of a hair follicle does not appear to
  dictate the length of its shaft (rather the duration of anagen
  determines hair shaft length), it is tempting to speculate that the
  subcutis offers optimal growth conditions…
  […]Although influenced by environment (light, temperature, and
  nutrition) and systemic (endocrinological factors) parameters, it is
  generally believed that there is considerable innate local control of
  hair shedding; each fiber grows to a specific length, for a specific
  period of time, before being shed


What is the name of this plant with many purple blooms with orange inner parts? I have photographed the following plant in Pittsburgh, PA. It has many blooms and every bloom is very small (about 5mm diameter), purple on the outer and orange in the inner. You can see it here:

What is the name of that plant?

This looks pretty much like Buddleja davidii to me. They are available in a range of different colors, see this image from the Wikipedia:


Will climate change affect flower population? There is a flower population elevated 1000 meters above sea level.  If climate change causes a 12⁰C increase in temperature over the next 10 years, what will happen to the flowers?

Its really hard to say for any given field of flowers and its hard to separate temperature from so many other factors that are accompanying climate change.

For example, rainfall is changing as well as CO₂ levels.  The pH of the rain may change because CO₂ becomes a mild acid when its absorbed into water.  The speed at which the seasonal temperatures vary and how cold is the minimum temperature and how hot is the hottest day will cause parasites and infections which kill plants to appear.

To be sure the heat is important, but the timing maybe just as important.  The temperature is causing earlier blooms and later growing seasons.

Each different species is responding differently, but odds are that nearly any given field of flowers is going to feel it.  The temperature is important, but its sometimes hard to guess if its the specific culprit in changes.


Where to download gene list of human genome? I am looking for a place where I can download a full gene list of human genome. Either by HGNC symbol or ensemble ID as long as it is usable on the consensusPathdatabase. Up until this point I have only found fasta files which include a bit too much information and unfortunately not in the format I would like. I am not in the biology field myself so if I am asking for something unreasonable call me out on it!

Reason for this is I am trying to stress test an application that uses the output tabular forms from the gene set analysis tool on consensusPathbase. The stress test on the entire human genome seemed to be the best option as a bigger data set than that will probably not occur.

Thanks in advance

The database you are looking for is ensembl [Yates (2016)].

Go here and chose  Customise your download. There you can select a dataset (e.g. genes and then specify human genes - currently uses build GRCh38; you can also go the same way here to do the same for hg19/GRCh37).

After chosing your dataset, you can click on Attributes to specify what to include in your download (HGNC symbols, IDs, regions, GO terms, and a ton of other stuff), click on Filters to apply filters to your choices (only genes from a chromosome, region, and a ton of other stuff).

Then click Results and download your selection in a format of choice.

(Hint: click Count first and use it as a a sanity check to see if the number of selected genes fits your expectation.)


Do skull bones have pain nerves (nociceptors)? I recently attended an awake brain surgery  for deep brain stimulation and it seemed to me that only the skin surrounding the drilled hole got local anaesthesia. I know that the brain itself does not have nociceptors, but what about the skull? And how does this compare to other bones in the body? Would you feel a hole being drilled in your skull? Would you feel your leg being chopped off if the surrounding tissue was numbed?

Yes, bones can be innervated. I say "can be" because although I'm not certain that ALL are, I know that most are. "Innervation" is your key word to learning more about the presence or absence of nerves reaching to any body part. Googling "are bones innervated" yields plentiful results, but the short answer is yes.

If you were to chop your leg off with surrounding tissue numbed, you would still feel it for this same reason.


Was Darwin aware of the difficulties behind the concept of species? Introduction

The concept of species is a very old concept that suffers from not being a natural category. There exists no single definition that would categorize living beings into groups and that would fit our intuitions of what a species should be.

Many of such problems in definitions are revealed in the field of evolutionary biology. For more information about the difficulties behind the definition of the concept of species, have a look at

How could humans have interbred with neanderthals if were a different species?
This post on ring species.

Question

Did Charles Darwin comment on this problem?
If yes, did Charles Darwin comment on the reason why he chose to keep using the term "species" instead of simply "lineage"?

The whole point of Darwin's theory was that transition from one species to another is extremely slow and gradual. There are plenty of quotes in "Origin of Species" stating this, and also affirming that there is no clear boundary between species and subspecies, or "races".

Quotes from Origin of Species > Variation under Nature (Chapter 2)

Quote 1

  Nevertheless, no certain criterion can possibly be given by which variable forms, local forms, sub species and representative species can be recognised

Quote 2

  Several experienced ornithologists consider our British red grouse as only a strongly marked race of a Norwegian species, whereas the greater number rank it as an undoubted species peculiar to Great Britain. A wide distance between the homes of two doubtful forms leads many naturalists to rank them as distinct species; but what distance, it has been well asked, will suffice if that between America and Europe is ample, will that between Europe and the Azores, or Madeira, or the Canaries, or between the several islets of these small archipelagos, be sufficient?

Quote 3

It is here the most definitive quote I managed to find and partially answers to your second question.

  From these remarks it will be seen that I look at the term species as one arbitrarily given, for the sake of convenience, to a set of individuals closely resembling each other, and that it does not essentially differ from the term variety, which is given to less distinct and more fluctuating forms. The term variety, again, in comparison with mere individual differences, is also applied arbitrarily, for convenience sake.


What is cross-immunoreactivity, and how does it impact vaccine development? What I understand about cross-immunoreactivity is that the antibody induced by one specific antigen is also fairly effective against another antigen. How would this be used for vaccine development?

Moreover, cross-immunoreactivity is related to epitopes. And how is how is cross-immunoreactivity defined among epitopes? Are variants of a specific virus hypervariable region some kinds of epitopes? What does antigenic convergence have to do with cross-immunoreactivity? Any comments or directions to further references are greatly appreciated.

Cross-immunoreactivity is just as you stated where an antibody that is specific to one antigen may recognize another antigen. I don't think this term is widely used as I see cross-reactive or broadly reactive more often. With regards to vaccines against viruses, cross-reactive immune responses are very important to establish an immune response that is effective against varying strains. Using Influenza as an example, an antibody that recognizes the HA protein of the H3N2 strain and also recognizes the HA protein of the H1N1 strain would be cross-reactive. If we had a vaccine capable of this we would not have seasonal flu.

Epitopes are specific regions on the antigen that are recognized by T cells or antibodies. They are the specific area on the protein structure that is recognized. Thus, for a response to be cross-reactive that specific structure must be present on both antigens. Epitopes could be located in any region of the protein, viruses will often have a region that is highly antigenic and highly variable to trick the immune response into focusing on the highly variable region rather than the more conserved regions.

Antigenic convergence is related to the sequence space available to the virus. Since viruses have limited space  for genes the amount of possible variation is limited as a single point mutation can have a large effect on the virus. Taking this into account some predictions could be made on how the virus might evolve. If the virus is evolving in such a way that there might be conserved epitopes, those epitopes might be important for cross-reactivity. Here is a paper on antigenic convergence in Hepatitis C. http://www.nature.com/articles/srep00267

This is a paper focused on flu, but it outlines the ideas surrounding cross-reactive antibody responses.
http://www.ncbi.nlm.nih.gov/pubmed/26175732


Can a human smell through the ears? The title does, prima facie, appear absurd.

Performing a swallowing action whilst pinching the nostrils shut gives the impression of listening through a bucket filled with water around the head; audible sound levels are perceptibly reduced. Some humans may encounter a similar sensation blowing their nose - hard.

This makes sense give the ears connect to the mouth/nose through the eustachian tubes. Can an odour make its way to the olfactory sensors through the ears?

A quick diagram to point out to people who may not know what Eustachian tubes are (#2).

In order for the aromatic molecule to reach the olfactory bulb, it would first have to get through the Tympanic Membrane (#22) [a.k.a. - Eardrum]. The Tympanic Membrane is water/airtight unless pierced.

So, while it's plausible that an aromatic molecule could travel through the Eustachian tubes and enter the pharynx areas, there isn't any way to get into the middle-ear in the first place unless the Tympanic Membrane has been compromised.

In a healthy and intact individual, the answer should be No.


How does protein enter bloodstream? If a hemophiliac patient injects his factor 8 through the veins directly into the bloodstream to provide the body with clotting factor... Why don't they just make the drug as a pill and have the liver do its job with extracting protein and dumping it into the bloodstream?

Proteins will be digested through a number of proteases in the stomach and intestines (pepsin, trypsin, etc) into their constituent amino acids. The amino acids are then absorbed in the small intestine. So any specific proteins you try to put into a pill will be digested into amino acids before being absorbed. If you somehow manage to defeat the digestive enzymes, the protein will simply pass through the digestive tract without being absorbed--the intestines don't have the capability to allow larger polypeptides through.

If you think about it, this is probably a good thing. We don't want random proteins from our food running around in our bodies. It would likely kill us in short order.


What makes the neurons of the auditory nerve with such high-speed? What makes the neurons of the auditory nerve with such high-speed? So the most labile are the fibers of the auditory nerve, in which the frequency of the generation of PD reaches 1000 Hz, while for skeletal muscles, it corresponds to 200 pulp / s, for smooth - 10-20 imp / s.  Motor nervous ending can be transferred to the skeletal muscle and at all no more than 100-150 excitations in 1 s

High Speed vs High Frequency
For starters, what you are describing is a high frequency signal, not necessarily a high speed signal.  High speed signals are caused by myelination (a sheath of fat deposits that encases neuron fibers), and by minimizing the number of actual dendrite/Axon junctions you need to pass through to get from point A to point B.  In this respect, the nerves responsible for muscle control tend to be very long and have similar myelination to the cells in your ear; so, muscle control neurons would if anything transfer a signal faster than the more densely packed neurons in your ear.
Now to Answer the actual question: Why the Higher Frequency?
No one nerve in your ear actually needs to transmit a signal at a higher frequency than those nerves used by muscles.   Instead you have a number of different nerves detecting for different audio frequencies, and your brain then receives a combination of signals that tell it that various Audio Frequencies are being detected 1.  Each of the hairs in your inner ear tapers from the base to the apex such that the apex begins being stimulated by low frequencies, but the base only begins being stimulated by higher frequencies 2.
Each auditory nerve fiber is actually a cluster of nerves that work together at different frequencies to create a more complex signal. This results in a number of parallel signals that is interpreted as a complex (high frequency) signal.
Here is a simple diagram showing how low frequency signals can merge to make a higher apparent frequency.


Do fish increase or decrease pH of aquarium water? If I understand it correctly, aquarium fish produce NH3 as their waste product and CO2 due to respiration. Producing NH3 increases water pH due to its equilibrium with NH4+. Producing CO2 decreases pH due to its equilibrium with H2CO3 and its equilibrium with HCO3-. My question is: Which of these effects is more important in most common aquarium fish? Do fish increase or decrease water pH?

Like a glass of beer going flat, any excess CO2 that your fish produce will quickly and irreversibly escape into the atmosphere. Thus, at least in terms of the pH battle between NH3 and CO2 that you describe, NH3 would win.

boilerplate "science is complicated" disclaimer

That said, it's likely that the total environmental effect that fish have on a tiny non-circulating volume of water will be much more complicated than the interaction between two basic chemicals. For example, say one of your fish sheds some scales and they start to rot. All sorts of things would be happening at that point which could affect the pH.


What does static electricity generated by plastic combs do to our hair? It is said that wooden combs should be preferred to comb hair as compared to plastic combs. Reason is that plastic combs generate static electricity.

Question: What does static electricity do to our hair that it is said that we should use wooden combs to prevent that electricity generation?

Is it bad for hair? Does it get generated always when we comb hair?

The motion of the comb against your hair remove electrons from the hair and deposits them on the comb. The positively charged hair and negatively charge comb now attract each other due to their opposite charges. You can read about this is any introductory Physics text, the topic is "static electricity". I doubt any harm is done to your hair, the issue is that it may be difficult to get your hair lying perfectly flat because of this attraction. This effect is more pronounced in low humidity.

If you want to see an exaggerated example of this, rub an inflated rubber balloon several times, quickly in the same direction, against your hair. Then bring it back near your hair while observing in a mirror.

Edit: I hesitated adding this because folks on this particular SE are sticklers for references. My source for the following is a workshop I attended at Chico State University circa 1990. This workshop was taught by a couple PhD Physics professors to enrich Physics teachers in electircity and magnetism.

When you dry clothes in a drier, static electricity is generated resulting in "static cling". But the cling that persists after a load is done is only part of the story. Constantly, at least once clothes are sufficiently dry, electrons are being stripped from one type of material by another. These electrons snap back from where they accumulate to where they were removed. This results in microscopic "sparking" that causes an ever-so-sight amount of wear on the cloth. So, the professors went on, the use of fabric softening anti-cling tissues minimizes this and prolongs the life of clothes. My take is that this is subtle and is more likely to be evidenced by the quality of appearance of the surface of a garment after many washings than it prematurely falling apart. I don't know for sure how significant this is, especially if you replenish your wardrobe regularly.

So, this may also apply to hair. But, unlike a particular garment, hair is constantly replenishing itself. (Well, not on my head.) So I seriously doubt this static discharge damages hair to any measurable extent. Perhaps if you were to run a comb through your hair for a couple hours every day you might see an effect. Bottom line for me, I use anti-static tissues, fragrance free; typically I get 20 years of use from my washable items and consider the tissues cheep insurance.  But I use plastic combs on what remains of my hair without any worry.


Identifying the origin of replication of an unannotated *E. coli* plasmid I have attempted a few searches for a list of origins of replication for plasmids in E. coli, but I was only able to find a list of origins, but not their individual sequences. The available plasmid maps are often extremely vague on where exactly do the origins start or end, and in any case it would be extremely tedious to collate a list of origins in order to determine the exact origin of replication of a plasmid.

Is there a database of origins of replication available anywhere that would allow one to perform BLAST searches on the plasmid sequence in order to obtain the compatability group of the plasmid, in cases where the plasmid's origin of replication is not specified?

Plasmapper Is quite good a recognizing common origins of replication. You will have to look up compatibility yourself. It is what I usually use when confronted with unnannotated plasmids.


Which strand of a gene specifies a protein? A gene is a segment of DNA (I hope double stranded) and each strand when transcribed form a mRNA and after being translated a protein. As from each gene there are two proteins that are being formed. Now how do these two proteins determine the expression of the gene?

I may be wrong. Please explain if so.

If a piece of DNA were to be transcribed on both strands, at the same time, the transcription complexes would collide and inhibit each other, like steric hindrance.

If you could overcome this interference and synthesize primary transcripts from both strands, it follows that the two RNAs would hybridize to each other and form complementary RNA-RNA hybrids.  These dsRNAs are very poor substrates for translation by the ribosomes. This was the initial mechanism proposed for anti-sense RNA to down regulate gene expression.

In many, if not most, EUKARYOTIC cells, a dsRNA will trigger the siRNA/shRNA/miRNA response mediated by Dicer et al. leading to degradation of both RNA strands.

So in virtually all instances, only one strand will be transcribed, and encode a mRNA with a significant ORF.


What is the function of cystine, cysteine, and cysteine protease? I am not a biologist, and I have a probably dumb biological question. For some purpose, I need to understand the function of the CTNS gene, and here is the definition of it:

"This gene encodes a seven-transmembrane domain protein that functions to transport cystine out of lysosomes.

I did not know what cystine is, and when I checked Wikipedia, I see that "Cystine is the oxidized dimer form of the amino acid cysteine."

What I understand is lysosomes digest a bigger peptide, and cystine is created as a result, and it is taken out of lysosomes by the enzyme produced thanks to the gene CTNS. My question is, where does cystine go and what is it used for after leaving lysosomes? And is it ever broken further into monomers of cysteine?

I also read about a term "cysteine protease". What is its relation to cystine?

I'm not sure as to what level of detail I should answer this question, but I will try to give you as much information as I can that I think will be relevant to.. whatever it is you are doing.

Cysteine proteases

Are a class of enzymes that degrade proteins, and utilise cysteine-residues as part of their catalytic mechanism.

Cystine

Is, as you said, a cysteine-dimer.. Which basically means two cysteines stuck together.

These are often formed in the intermediate steps of a cysteine protease's catalytic mechanism.

But also, during protein degradation within the lysosome, cystine can be released as a free molecule. When this happens, it will be transported in to the cytoplasm, to be processed via anabolic pathways into various products, such as glutathione (an antioxidant).

So, basically, the function of your seven-transmembrane (7TM) transporter protein is:

To make accessible to the cell, the digested products of proteins (or, amino acids).

Cystine is an amino acid. Cysteine is also an amino acid. These can all be used by a cell to create new molecules, such as proteins, or antioxidants, or vitamins or cofactors, etc., so many things. And can indeed be broken down in to cysteine.

The function of the CTNS gene, is to provide the cell with the genetic information used to synthesise the 7TM-transporter protein.


Coalescence time: Is it different for haploids and diploids in population genetics? I'm trying to model Cyanobacteria cells divergence in 2 populations with mutation rate $-\mu$ and I need to verify my model with a valid theory. I don't have much biology background and all the theories I can find are either valid for haploid population or mating populations. All I need to know is a theory for coalescence time/divergence for a haploid population without mating. So far I have this:

$$T = 2\times N \times d\\
D = 2 \times \mu \times T$$
in which N is the number of diploid individuals, d is the number of subpopulations (in this case 2), T is the coalescence time and D is divergence. Can I apply this to my case even though it's defined for diploid population?

Thanks

Coalescence time: Is it different for haploids and diploids in population genetics?

Short answer

The coalescent time is twice as high in a diploid population than in a haploid population

Long answer

Imagine you sample at random one chromosome. Then, you sample a second one and you ask the question, what is the probability that they coalesce in the previous generation. This probability is $\frac{1}{PN}$, where $N$ is the population size and $P$ is the ploidy number (1 for haploids, 2 for diploids). The probability that they do not coalesce is therefore $1-\frac{1}{PN}$. The probability that the two chromosomes coalesce $t$ generations ago is the probability that they don't coalesce for $t-1$ generations and then coalesce. That is the probability that the two chromosomes coalesce $t$ generations ago is

$$P(t) = \left(1-\frac{1}{PN}\right)^{t-1}\frac{1}{PN}$$

You might recognize here a geometric distribution, where the probability of success is $\frac{1}{PN}$. In order to simplify the math, let's assume that the population size is very large. In such case the above formulation is well approximated by

$$P(t) = \frac{1}{PN} e^{-t\frac{1}{PN}} $$

You might now recognize the exponential distribution with rate $\frac{1}{PN}$. We can now compare the mean expected time to coalescent of a diploid population and a haploid population.

The mean of the above exponential distribution is simply $PN$. Therefore, the expected time to coalescent is $2N$ in diploids and only $N$ in haploids.

Details of your post

In your post you talk about structured populations. The calculations are a little more complicated in structured populations and I don't remember on the top of my head how they work.

You talk about divergence $D$. I don't know what you mean by divergence. From coalescent results you can compute the expected heterozygosity, the number of pairwise differences, and even the whole site frequency spectrum. You can as well make those calculations for the structured coalescent model.


Can I tell my antioxidants intake based on nutrition facts labels? The recommended daily intake of fruits and vegetables is 5-10 portions (url), in order to meet the "required antioxidant levels" (dark-leaf green vegetables, berries, cruciferous vegetables, ...).

Can I measure my antioxidant intake based on nutrition facts label, instead of counting vegetable portions?

Adding up the total intake of vitamins A, C, E and magnesium may not be representing because they are not necessarily the "major players" (additional significant players are CoQ10, alpha-lipoic acid, l-carnitine, acetyl-l-carnitine, n-acetyl cysteine).

Well yes, you could get this information from food labels, since the recommended daily intake of vitamins is well established. But there is really no need to worry about dietary "antioxidants" (usually vitamins A, C and E, and carotenoids). If you eat a reasonably balanced diet, you are getting all the vitamins you need. Thankfully, vitamin deficiency is very rare in the western world today.

There is a lot of hype around "antioxidant" dietary supplements, but there is no convincing evidence that high levels of these vitamins in your diet has any beneficial effect at all. Randomized clinical trials have failed to show any effects whatsoever of antioxidant supplements on chronic diseases, and excess intake may even increase overall mortality.

Non-vitamin compounds like carnitine are not necessary in the diet at all, since they can be synthesized by the body in sufficient amounts. In general, the fact that a compound is a "major player" in cellular metabolism (in oxidative defense or other wise) does not mean that you have to consume it. For example, the TCA cycle intermediates are arguably the biggest "players" in human metabolism, but none of them are necessary in the diet.


Measure of environmental impact on phenotype Let me begin by disclaiming that I am nowhere near a biologist by competence or education and that I am simply interest in some of its fields of study as a matter of general curiosity. So excuse my ignorance.

I've been recently pondering the concepts of genotype and phenotype. This page succinctly summarizes the difference between the two.

I was curious if there are scientific measures, and how accurate they are, for the impact of environment on the phenotype of a specimen. Hypothetically, if the environment had no effect, the phenotype would be 100% determined by the genotype. But, in a simple approximation, phenotype = genotype + environment. Does modern biology have a measuring system for how much the environment affects the ultimate observable features of an organism, on top of what its genotype does?

In between a long comment and an answer...

For a review of the theory behind the causal variables of phenotype, one might want to have a look at Biology Why is a heritability coefficient not an index of how “genetic” something is?.

One can investigate the impact of a specific environmental variable onto the phenotypic variance but the environmental as a whole is typically computed as whatever is left when other sources of phenotypic variance have been explained. As such you might want to read about estimations methods for heritability and maybe esp. the post How do heredity and regression to the mean work with respect to intelligence?.


Can you identify this flower? I have found this plant in my garden. I watered it, and now it is blooming. I have no idea what plant it is. Could someone help me to identify this plant? My geographic location is the Indian subcontinent.

I am not sure but I think it is water leaf plant ( called sambar cheera ).If you see other pictures, the leaf and flower color matches but I am not sure as I do not know how the flower looks when it is bloomed ( in your picture).
You can see this site http://papanasini.blogspot.in/2012/02/cylon-spinach-sambar-cheera.html

I got a picture of the above-mentioned plant from my house, unfortunately, it is not having flowers and I will get back when it will have one.

Hope this helps!


How do electrons destroy DNA bonds in radiation? Malignant tumors can be treated by radiation therapy. Most commonly it's radiotherapy with photons, or protons and so on. The common denominator for both types is that the radiation creates electrons inside the body via different effects.

What I haven't quite understood is how these electrons destroy the DNA bonds in the tumor and how this aids in killing off the cancer cells? Is it due to the generation of heat, or otherwise?

I think you have a fundamental misunderstanding of the chemical reactions involved in radiation therapy. Neither photon based or proton based therapies "create electrons", but they do cause ionization by adding enough energy to existing electrons around atoms so that the electron is ejected from the atom, creating an ion or free radical, which can then undergo chemical reaction.

Photons, typically gamma rays, X-rays, and high energy UV, typically interact with water molecules and produce free radicals, including the dangerous hydroxyl radical. The hydroxyl radical can interact with proteins and DNA and damage those molecules, but has a very short half-life. Molecular oxygen can help increase the damage by reacting with the hydroxyl radical to produce Reactive Oxygen Species, ROS, which can also damage DNA or protein. However, many tumors have low oxygen concentration that reduces the effectiveness of photon based radiation therapy.

To overcome this, many patients receive proton based radiation therapy. Protons are much heavier than photons (I guess infinitely heavier than a photon, since photons have no mass) and therefore scatter to a much smaller extent. They just sort of plow through tissue and knock electrons out of orbitals as they collide with molecules such as DNA or protein. They don't rely so much on free radical generation or ROS, so low oxygen levels don't reduce their effectiveness.

The goal is damage the DNA to induce double strand breaks which are hard to repair in fast growing cancer cells. Because they grow so quickly, they are already stressed and their DNA repair machinery is less effective than in healthy cells. If their DNA can be sufficiently damaged, the cell will die.

For more information about these processes, please see these wikipedia articles on Radiation Therapy, Radiolysis, Linear Energy Transfer, and Free Radical Damage to DNA.


Are these spinach leaves? I often buy baby spinach from the store, and sometimes, in a few bags of spinach I also find these leaves:

They have a different shape than the spinach leaves, they are a lighter green, and they taste differently. The bag doesn't say that "it may contain traces of" other plants, so are these some part of the spinach plant? Or are they something different? Why do they often come together with the spinach leaves? I haven't found any other kind of leaves (besides spinach) in the bags except those in the picture.

Those are the cotyledons (seed leaves) of spinach.

For comparison, here's a picture of what spinach sprouts look like:

Source: https://wimastergardener.org/article/spinach-spinacia-oleracea/


Modern understanding Darwin's "correlation of variation" In Variation under Domestication, Darwin makes several references to the concept of "correlation of variation":

  I will here only allude to what may be called correlated variation. Important changes in the embryo or larva will probably entail changes in the mature animal.

And:

  Some instances of correlation are quite whimsical; thus cats with blue eyes are invariably deaf.

In the chapter's ending, he also calls this "correlation of growth":

  Variability is governed by many unknown laws, of which correlated growth is probably the most important.

I gather that this is Darwin's humble way of admitting that there are many unknown unknowns, at least as far as correlation is concerned.

But, since 1859 until present day, what did we find out about this quirky aspect of evolution? Are all cats with blue eyes deaf?

One must not confound a phenotypic variance-covariance matrix (usually called $P$) and a genetic variance-covariance matrix (usually called $G$) for a set of phenotypes. The mutational variance-covariance matrix is also a common concept (usually called $M$). There are a lot of papers on the evolution of the G-matrix (and related matrices).

In the abstract of Roff (2000), you can find the equuation

$$\Delta\bar z = GP^{-1}-S$$

, where $\Delta\bar z$ is the vector of mean responses, $G$ (often just called the G matrix) is the matrix of additive genetic variances and covariances, $P$ is the matrix of phenotypic variances and covariances and $S$ is the vector of selection differentials.

You will find much more by just googling "evolution of G-matrix"


Can an exotic species be also endemic? While talking about the evolution and conservation of dingoes in Australia, someone asked an interesting question:

  Can I define the dingo as an endemic species?

That question, despite apparently simple, deals with some terminological conflicts and I must confess that I was not able to say yes or no at the moment.

The context:

As everybody knows, the dingoes (Canis lupus, but for some people Canis dingo1) were introduced in Australia by human beings, between 4,000 and 12,000 YBP. That being said, it's acceptable to define the dingo as an invasive, exotic species. Using Campbell's2 definition:

  Invasive species: a species, often introduced by humans, that takes hold outside its native range.

However, some researchers argue that the dingoes, being isolated in Australia for a relatively long time, have a unique genetic profile. As this is controversial, let's suppose, just for the sake of the argument, that they do have a unique, distinctive genetic profile (and that they became a distinct species).

That being the case, the dingoes may be defined as endemic. Quoting Campbell again:

  Endemic: referring to a species that is confined to a specific, relatively small geographic area.

I have taught biology for many years and I must confess that, for me, endemic and exotic were always opposite, mutually exclusive terms. However, in this case (and many others), it makes sense to say that the dingoes are exotic and endemic.

Maybe one can say that, from the moment the population became a distinct species on, it stopped to be exotic and started to be endemic, which would keep the two terms mutually exclusive.

My question

So, my question is: can a given species (or population) be defined as exotic  and endemic simultaneously?

PS: I'm not asking for opinions, which would make this question off topic  for SE Biology. I'm asking for rules and guidelines in the use of the terms, preferably with references.

I think this partially depends on the timeframe. Endemism is usually divided into paleoendemism and neoendemism (see e.g. Kier er al in PNAS for use of both terms). Here, neoendemism is referring to the result of recent adaptive radiations that have led to new endemic species. This is then in contrast to paleoendemism, which refers to previously widespread species that are now confined to isolated areas.

Neoendemism is clearly related to your question, but whether dingos should be labelled as neoendemic depends on if it can be seen as a unique subspecies. If it is, it might be more suitable to view it as neoendemic and not exotic (nothing prohibits neoendemic species to be ecologically "problematic" to the previous fauna though).

In the literature (from what I've seen), neoendemism is usually used to describe historical events though (the result from adaptive radiations etc), so timeframe is obviously important (see e.g. Mishler er al, 2014). Even so, all taxa that has led to neoendemic species (through adaptations to local conditions) was by definition exotic at one point in time (e.g. when the most recent common ancestor of the Galapagos finches colonized the Galapagos islands). The same goes for the relatively recent adaptive radiation of Drosophila on Hawaii.

To me, neoendemic and invasive are not mutually exclusive terms, while the division between neoendemic and exotic may depend on time since colonization and whether the population now forms an independent taxon (e.g. subspecies) instead of a subpopulation still connected to its host population. I cannot find a reference or definition to support this interpretation right now though.


How to find mutations related to disease for a protein? I have done research on the protein (CYP3A4). I have its function, purpose and diseases (breast cancer, prostate cancer, testicular cancer, lung cancer). I am however having trouble finding the mutations of the protein and how it correlates with the diseases, specifically breast and prostate cancer.

I think I understand what you are asking so I will make a little guide to find what you need:
NOTE  the mutations you are searching for are probably on gene level so you can search your protein on Uniprot and then use the gene name to search on DisGeNET, you typ in the gene you are searching for:

Then you hit the search button and this will give you a result like this:

You can see that this site uses a sort of text-mining, in other words it is searching for the gene name associated with disease in articles. The score is an indication for how good the text-mining "worked". As mentioned in the manual:

  We have developed a score to rank the gene-disease associations
  according to their level of evidence. DisGeNET gene-disease
  association score takes into account the number and type of sources
  (level of curation, model organisms), and the number of publications
  supporting the association. The score ranges from 0 to 1.

Then you have to click the browse details... in the down right corner. This will guide you to another summary page like this:

(NOTE I omitted a lot of rows to avoid huge images in the answer, so there will be more rows in your result). Because you were interested in prostate cancer I will click on Prostatic Neoplasms:

You can click on the 3 to obtain the 3 articles where the combination of the CYP3A4 and Prostatic Neoplasms was found. This will give you a list like:

As you mentioned in your question

  "where do I find such papers"

You can easily click on the PMID this will guide you to the article, for example the first article:

  CYP3A4 polymorphisms--potential risk factors for breast and prostate
  cancer: a HuGE review(link).

I think this will help you to find the papers related to the protein + disease, you can further read the papers to find mutations which cause these diseases.


What's the smallest flier that migrates? Painted ladies and monarchs migrate hundreds of miles (~1.61 hundreds of kms).

Are there long distance fliers that are significantly smaller?

Dual question: Are fliers' migration distances strictly a function of size? Or are there any fly-sized 1000-mile migrators?

The marmalade hoverfly (Episyrphus balteatus) flies to Southern Europe and back every year.

It's difficult to track and find them compared to birds and butterflies, here is a study witch citations: https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1570-7458.2007.00568.x?purchase_referrer=scholar.google.fr&tracking_action=preview_click&r3_referer=wol&show_checkout=1

it is now known that large numbers of E. balteatus migrate South during the autumn period. Therefore, it has been sug-gested that a comparable migration to the North helps tore-establish E. balteatus populations in northern Europe during the spring. There are many records to show that some hoverfly adults are active so early in the spring that they could not possibly be long-distance migrants. Nevertheless, although some adults remain active late into the autumn, few authors have managed to find females in overwintering sites

studies have suggested that E. balteatus migrates in large numbers during late summer and autumn to the Mediterranean area and only return to central and northern Europe during the following year(Aubert et al., 1976; Gatter & Schmid, 1990; Kehlmaier & Martínez de Murguía, 2004; Hondelmann et al., 2005).

https://www.sciencenews.org/article/flying-insects-tell-tales-long-distance-migrations


Question about enveloped RNA virus viral genome I am a newbie studying campbell biology. just a quick question about virus.
When viral genome(RNA) expose itself in the host cell, why does the host cell not eliminate the genome since it apparently not belong to the cell ? Is there any mechanism that the host cell can detect and eliminate the viral genome as in the step 2,3 in the figure below ?

Thanks in advance !

Your image illustrates the replication cycle of a negative-sense single-stranded RNA virus, where the viral genome needs to be "inverted" by an RNA polymerase into mRNA before being translated by the host. There are many examples of (-)ssRNA viruses, including filoviruses (Ebola, Marburg), paramyxoviruses (measles, mumps), orthomyxoviruses (influenza), rhabdoviruses (rabies), deltaviruses (Hepatitis D), and others.

These (and all) viruses evolved alongside their hosts, and consequently the hosts evolved various protection mechanisms. One primitive component of the so-called innate immune system in humans and other organisms (going back at least to plants) are proteins known as pattern recognition receptors (PRRs) which bind to conserved motifs found in microbes, including possible pathogens. The types of molecules recognized by these PRRs include certain types of carbohydrate moieties like LPS, peptidoglycans and other components of bacterial cell walls, fungal glucans, bacterial peptides, some types of microbial nucleic acids (such as single- and double-stranded RNA, more on this in a bit), chitin, and others.

One class of PRRs are the Toll-like receptors (TLRs), named after the Drosophila Toll protein. They recognize a wide variety of microbial patterns and activate downstream signaling to stimulate an immune response, including production of pro-inflammatory cytokines and anti-viral interferons. In our case, two of them are particularly important - TLR3 and TLR7. TLR3 recognizes double-stranded RNA, which occurs transiently during (-)ssRNA virus infection when the negative-sense genome is being copied to positive-sense mRNA. However, dsRNA is much more common in retroviral infections. TLR7 recognizes single-stranded RNA in endosomes, which would occur after macrophages, dendritic cells, or B cells consume dead virally-infected cells.

Unfortunately for the host cell, once it has been infected there isn't much that can be done to save it. Viruses evolved to hijack the cell's machinery and make more copies of themselves. This hijacking is generally one way, so the only way to fight the infection is to kill the cells producing the viruses. This is, for example, why you often get a sore throat during an influenza or rhinovirus (one of the most common causative agents of the common cold) infection - epithelial cells lining the throat get infected, and are killed by the immune system to prevent the spread of the infection. This leaves a "raw" area that must heal over time.


Supercomputer Vs Human Brain With supercomputers doing calculation in petaflops ($10^{15}$ Calculations per Second), have we crossed the speed of Human Brain?

I will just show the statistics of last attempt to mimic the brain process.

In 2011 fastest computer in Japan was launched:

K computer OR SPARC64 VIIIfx 2.0GHz

Features:

Manufacturer:    Fujitsu
Cores:   705,024
Linpack Performance (Rmax)   10,510 TFlop/s
Theoretical Peak (Rpeak) 11,280.4 TFlop/s
Power:   12,659.89 kW
Memory:  1,410,048 GB (16GB RAM per CPU)
Processor:   SPARC64 VIIIfx 8C 2GHz (88,128 CPUs, 8-core each)
Operating System:    Linux

It's currently world's 4th fastest supercomputer.

Source: Top 500 Supercoputers

Image Source: http://wondergressive.com/wp-content/uploads/2014/01/WG-k-computer.jpg

Now,

  An 83,000-Processor Supercomputer Can Only Match 1% of Your Brain

  ...The most accurate simulation of the human brain to date has been
  carried out in a Japanese supercomputer, with a single second’s worth
  of activity from just one per cent of the complex organ taking one of
  the world’s most powerful supercomputers 40 minutes to calculate.
  Researchers used the K computer in Japan, currently the fourth most
  powerful in the world, to simulate human brain activity. The computer
  has 705,024 processor cores and 1.4 million GB of RAM, but still took
  40 minutes to crunch the data for just one second of brain activity...

  Source: http://gizmodo.com/an-83-000-processor-supercomputer-only-matched-one-perc-1045026757

Human Brain:

  Do we have brain to spare?

  by David A. Drachman, MD

  Within the liter and a half of human brain, stereologic studies
  estimate that there are approximately 20 billion neocortical neurons,
  with an average of 7,000 synaptic connections each.1 The cerebral
  cortex has about 0.15 quadrillion synapses—or about a trillion
  synapses per cubic centimeter of cortex. The white matter of the brain
  contains approximately 150,000 to 180,000 km of myelinated nerve
  fibers at age 20, connecting all these neuronal elements. Despite the
  monumental number of components in the brain, Szentagothai estimated
  that each neuron is able to contact any other neuron with no more than
  six interneuronal connections—“six degrees of separation.”

Image Source: http://www.nature.com/polopoly_fs/7.2933.1329907514!/image/far-to-go.jpg_gen/derivatives/fullsize/far-to-go.jpg

Why Brain beats Supercomputer?

  Why is it so hard for computers to reproduce what your grey matter
  does as a matter of course? Volume. The human brain consists of about
  200 billion nerve cells (neurons) that are linked together by
  trillions of connections called synapses. As the tiny electrical
  impulses shoot across each neuron, they have to travel through these
  synapses, each of which contains about 1000 different switches that
  route that electrical impulse. In total, one human brain could contain
  hundreds of trillions of these neural pathways. It's like a Choose
  Your Own Adventure book that stretches from here to Jupiter.


Where does extra blood come from to fill your muscles during exercise? Let's say I go to the gym and lift some weights an hour.  During this time my arms will grow due to the "pump" -- the extra blood rushing in to feed the muscles.  For example, I've measured about 2-3 centimeters increase just in the diameter of the upper arm (bicep+tricep).

But where did this blood come from?  Also, if my arms got bigger, since I'm the same weight that means some part of my body must have gotten smaller, right?

The blood comes from the body's reservoirs:

spleen (mostly erythrocytes) [1]
liver [2]
veins (probably the most important blood resevoir as they contain 50-60 % of the volume) [3]

In pathological situations, if hypovolemia occurs, blood can also come from:

splachnic vascular bed [5]

But what attracts the blood into the muscle? The phenomenon is called active hyperemia:

  Active hyperemia is the increase in organ blood flow (hyperemia) that is associated with increased metabolic activity of an organ or tissue. An example of active hyperemia is the increase in blood flow that accompanies muscle contraction, which is also called exercise or functional hyperemia in skeletal muscle. Blood flow increases because the increased oxygen consumption of during muscle contraction stimulates the production of vasoactive substances that dilate the resistance vessels in the skeletal muscle [4].

References:

The human spleen as an erythrocyte reservoir in diving-related interventions. Kurt Espersen, Hans Frandsen, Torben Lorentzen, Inge-Lis Kanstrup, Niels J. Christensen. Journal of Applied PhysiologyMay 2002,92(5)2071-2079;DOI: 10.1152/japplphysiol.00055.2001
Lautt WW, Greenway CV. Hepatic venous compliance and role of liver as a blood reservoir. Am. J. Physiol. 1976 Aug;231(2):292-5. PubMed PMID: 961879.
Michael J. Gregory, Ph.D. The Circulatory System. Licensed under CC-BY-NC-SA-3.0
Richard E. Klabunde, PhD. Cardiovascular Physiology Concepts. Active Hyperemia. Available from http://www.cvphysiology.com/Blood%20Flow/BF005.htm (accessed 03.08.2014)
Blaber AP, Hinghofer-Szalkay H, Goswami N. Blood volume redistribution during hypovolemia. Aviat Space Environ Med. 2013 Jan;84(1):59-64. PubMed PMID: 23305001.


How to supply oxygen to a culture vessel? I'm reading this paper:
https://www.jstage.jst.go.jp/article/jpsa/51/3/51_0130043/_pdf

From day 17 of the culture period until hatching, pure oxygen was supplied at a flow rate of approximately 500 ml/h through the previously installed plastic tube.

What kind of hardware is used to achieve this ? I would like to test this method, but I don't have access to laboratory equipment ( meaning .. I'm not going to buy expensive equipment for this hobby project..)

I'm used to incubate eggs inside an incubator, and day 17 is approximately the day when they start chirping, and sometimes hatching, so it's my understanding that at this point the chick starts to use its lungs, and breaks the shell in search of oxygen.

Also I don't understand the airflow in this setup: when I supply 500 ml/h of oxygen, where does the displaced gas go ?

Gases are supplied to culture vessels by design. Flasks, for example, may have filtered caps that allow gas in, or microplates with lids that have enough room under the lid to allow a gas exchange interface with the culture medium. Of course with these traditional culture vessels you need to make careful consideration about fill volume, since the gases won't penetrate 100% through the culture medium.

In the case of your paper they cut a large hole in the side of the cup and plugged it with cotton, then fed a small plastic tube through into the cup. They attach a gas line and feed oxygen through the tube. The cotton plug is where the gas will escape back out without letting contaminants in, as the cotton plug acts as a filter. The system seems to have no other outlet, so it makes sense.

In order to control a gas flow rate, you need a regulator of some sort to act as an output control.


Do the bacterial species X, Y, Z code for proteins A, B, C? My PI has assigned me a task to gather evidence to determine whether or not a list of particular species of
Campylobacter and Helicobacter code for a list of several proteins.  To put it simply I’ve been asked, “Do species X, Y, Z code for proteins A, B, C?”  The genomes of these bacterial species have been fully sequenced and I am able to retrieve the FASTA files for each of them.  I am having trouble deciding on the proper method to screen these genomes for the genes.  I have been given the names of the proteins, i.e. VgrG and HCP, but the amino acids sequences listed on databases are annotated to different species of the bacteria.  I seem to be stuck in a grey area and am having trouble connecting the overwhelming amount of resources available on the NCBI website.  I have not found a specific guide to perform this task - Could you please provide me with a solution to my problems?

First of all, don't reinvent the wheel, search for annotated homologs first. Assuming you don't find them, the next step is:

Collect the sequences of your query proteins (not genes) from one species in a multifasta file.
Run a tBLASTn with those sequences against the genomes of all the other species of interest.
Analyze. Look for HSPs with a certain level of sequence identity. The details of what threshold you choose will depend on your data, I can't help you  there.

While the tBLASTn approach is going to be more sensitive, an easier method that can find gene structures and not just HSPs is to use exonerate:

exonerate -m p2g proteins.fa genome.fa

Finally, for a more sensitive search than either of the above, useful for finding more distant homologs, run a Psi-tBLASTn of your proteins against the genomes of interest.

In all of these approaches, the tricky bit is to choose the right threshold. Unfortunately, there is no golden rule here. It all depends on how closely related your species are and how similar the homologs. You will have to try a few different ones before you can choose the right one.