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How a vegan can consume all the needed varied proteins / amino acids?
I would like to ask if there are some proteins that the human body needs and can being endowed only from meat?
According this:

Other protein sources, such as fruits, vegetables, grains, nuts and
  seeds, lack one or more essential amino acids. Vegetarians need to be
  aware of this. People who don’t eat meat, fish, poultry, eggs, or
  dairy products need to eat a variety of protein-containing foods each
  day in order to get all the amino acids needed to make new protein.

How a vegan can complete these missing proteins?

this might be better for the cooking exchange.https://cooking.stackexchange.com/ Otherwise this borders on medical advice or at least nutritional advice.

Proteins are made up of amino acids. It isn't particular proteins that are necessary in diet, but particular amino acids. For humans, these come primarily from breaking down the proteins in foods we eat.
Essential amino acids are the amino acids that humans cannot synthesize; other amino acids can be synthesized from these, but they do not need to be part of the diet. Not all sources of protein have sufficient quantities of all of the essential amino acids. When people refer to a protein source as "incomplete" they mean that particular source is low on one or more of the essential amino acids.
Meat products are typically "complete" because they contain all of the essential amino acids together. Therefore, if you subsisted on various foods but only got your protein from one animal source, you would be okay.
Some plant products do not have all the essential amino acids in large concentrations. However, if you combine protein sources from different "incomplete" plant sources that together cover these deficiencies, there is no disadvantage compared to a single "complete" source.
You also have a fairly substantial reserve of amino acids in the form of all the proteins in the body, which are constantly broken down and recycled. The daily protein intake is just a tiny fraction of the total amino acid content in the body.
Here is a paper that talks about some of these issues, and addresses some of the myths about balancing proteins. The quick summary is that problems develop if you get your sole protein from a source that is low in a particular essential amino acids over a long time period, but there is no need to ensure every meal contain all the amino acids.
It is possible for people on unusual protein diets, such as vegans, to develop a particular amino acid deficiency. There are many many guides on the internet for protein sources to mix to avoid this problem. A common combination is a legume (beans, peanuts) and a grain (wheat, rice). There are also some vegetable sources that provide complete protein nutrition - soy, for example, mostly works as long as it is not truly the only source.
References:
Young, V. R., & Pellett, P. L. (1994). Plant proteins in relation to human protein and amino acid nutrition. The American journal of clinical nutrition, 59(5), 1203S-1212S.

Does the human body know to construct all the needed proteins from the 20 amino acids? That sounds impossible. Why not to use the consumed proteins? Or it's impossible for them to penetrate the plasma membrane?

That's exactly the information contained in DNA: information on which amino acids to assemble and which order, and both directly and indirectly, how much of each protein to make. That's actually much simpler than trying to detect and incorporate foreign proteins. Foreign proteins could also be harmful, and they vary far too much between different organisms. This is how biology works from bacteria to plants and animals. Think about how similar cars are, and yet, if you have an engine from a BMW and a transmission from Toyota, good luck putting them together in that Ford body.

You probably meant "how can a vegan consume all the needed amino acids".
Proteins are made of amino acids chained together in a dehydration reaction. Digestion breaks the proteins, allowing the amino acids to be reused.
The most obvious and easy way to get all the amino acids: meat.
For vegans, rice and beans is a common way to get all the needed amino acids. Even today it remains a staple in many poor countries where meat isn't always readily available.

If you can add a source or two, and possibly an example, then you'll get my +1. Your answer is accurate and to the point, but IMO you should elaborate and support your statements a little more.


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What is the ratio of head to waist and waist to floor of the human anatomy?
I'm trying to find the ratio of upper body to lower body. That is, the ratio of the length of the waist to the head over the length of the waist to the floor.
It's been harder to track down a readable outline of the ratios of the human body than I expected.

Since I can't comment, I'll answer using the answer above - given the image shown, the 0.52/0.485 ratio is comparing the top of the head to the inseam relative to the inseam to the floor. Notice that the image given shows the waist at between 0.53 (the practical waist that most of us use when we wear clothing) to 0.630 (the anatomical waist, the narrowest point on the torso above the hips). That's actually the only number you need - subtract that from 1 and you have the other number. In short: above waist ~= 0.37 of total height, 0.63 below waist. The previous answer gave a reasonable image, b

@TPStacker: Simple observation would suggest that there is no such ratio.  Some people have long legs compared to their torso, other people have short legs.  That would seem to be true of other body proportions as well.

The study of those measures is called anthropometry. Typing anthropometry on google image returned this

This is definitely not a peer-review source and might eventually be a good approximation only for white males (or whoever they considered to take these measurements on) but if we believe this image, then the ratio head-to-waist over waist-to-floor is $\frac{0.52}{0.485} = 1.072$.

Perfect! And thanks for the additional comments on likely assumptions and approximations. And for the help with the correct term to look for.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Predators on the Galapagos
I understand that in many isolated islands, such as the Galapagos, there are no large predators. I find this observation interesting because it has been suggested that the lack of predators unleashes the evolution of new and bizarre species.
However, as new species evolved there (and increase their size, with respect their ancestors), why no small predator species evolved into a large predator species? Or can new predators evolve from herbivorous animals?
This may be a difficult question, because we may not  know the natural history in such great details. More specifically, I wonder if, in general, there is some pressure against the selection of predators or if there are counter examples which show that small isolated islands evolved their own apex predator.

Larger predators need a large range on which to find potential prey. An island might be bigger than the normal range of a predator, but too small to support a large enough breeding population (because of inbreeding, and because a brief lack of food, disease, or other insult could wipe out the entire population, rather than just a few individuals).

Interesting point. Are there fossil evidences of extinctions in islands due to that? Of course let us exclude humans and their pets and pests.

Not such a simple and clear pattern
What you are talking about is called insular dwarfism. The process is not as straight forward as you seem to think it is. It is not systematic that insular islands evolve toward reduce sizes. In fact, the opposite of insular dwarfism, insular gigantism (which is related to Foster's rule) has also been observed.
In any case, there seems that islands often bring selection pressures of size but the causes are numerous. I think wikipedia does a descent job at screening over the existing explanations.
Wiki > insular dwarfism > Factors influencing the extent of dwarfing

For both herbivores and carnivores, island size, the degree of island isolation and the size of the ancestral continental species appear not to be of major direct importance to the degree of dwarfing.4 However, when considering only the body masses of recent top herbivores and carnivores, and including data from both continental and island land masses, the body masses of the largest species in a land mass were found to scale to the size of the land mass, with slopes of about 0.5 log(body mass/kg) per log(land area/km2).[7] There were separate regression lines for endothermic top predators, ectothermic top predators, endothermic top herbivores and (on the basis of limited data) ectothermic top herbivores, such that food intake was 7 to 24-fold higher for top herbivores than for top predators, and about the same for endotherms and ectotherms of the same trophic level (this leads to ectotherms being 5 to 16 times heavier than corresponding endotherms).[7]

Wiki > Insular gigantism > possible causes

Large mammalian carnivores are often absent on islands because of insufficient range or difficulties in over-water dispersal. In their absence, the ecological niches for large predators may be occupied by birds, reptiles or smaller carnivorans, which can then grow to larger-than-normal size. For example, on prehistoric Gargano Island in the Miocene-Pliocene Mediterranean, on islands in the Caribbean like Cuba, and on Madagascar and New Zealand, some or all apex predators were birds like eagles, falcons and owls, including some of the largest known examples of these groups. However, birds and reptiles generally make less efficient large predators than advanced carnivorans.
Since small size usually makes it easier for herbivores to escape or hide from predators, the decreased predation pressure on islands can allow them to grow larger.1[a] Small herbivores may also benefit from the absence of competition from missing types of large herbivores.
Diagram displaying the change in size of weta species in two ecosystems. The size and population of wetas are affected by predation. Rats introduced on the mainland began to prey on wetas, reducing their population; wetas shrank in response. On an island isolated from predation, such as Little Barrier Island, wetas have a dense population and have grown to a massive size. Insular species of giant wetas are the only ones not facing extinction. As wetas grow over time, bird predation declines.[citation needed]
Benefits of large size that have been suggested for island tortoises include decreased vulnerability to scarcity of food and/or water, through ability to survive for longer intervals without them, or ability to travel longer distances to obtain them. Periods of such scarcity may be a greater threat on oceanic islands than on the mainland.4
Thus, island gigantism is usually an evolutionary trend resulting from the removal of constraints on the size of small animals related to predation and/or competition.5 Such constraints can operate differently depending on the size of the animal, however; for example, while small herbivores may escape predation by hiding, large herbivores may deter predators by intimidation. As a result, the complementary phenomenon of island dwarfism can also result from the removal of constraints related to predation and/or competition on the size of large herbivores.[6] In contrast, insular dwarfism among predators more commonly results from the imposition of constraints associated with the limited prey resources available on islands.[6] As opposed to island dwarfism, island gigantism is found in most major vertebrate groups and in invertebrates.
Territorialism may favor the evolution of island gigantism. A study on Anaho Island in Nevada determined that reptile species that were territorial tended to be larger on the island compared to the mainland, particularly in the smaller species. In territorial species, larger size makes individuals better able to compete to defend their territory. This gives additional impetus to evolution toward larger size in an insular population.[7]
A further means of establishing island gigantism may be a founder effect operative when larger members of a mainland population are superior in their ability to colonize islands.[8]
Island size plays a role in determining the extent of gigantism. Smaller islands generally accelerate the rate of evolution of changes in organism size, and organisms there evolve greater extremes in size.[9]

Dwarfing refers to species evolving towards a smaller size. This is not the case of Galapagos where predators didn't become smaller... Is seems that they just didn't arise!

There actually are some terrestrial predators on the Galapagos Islands. Notably, there are four species of birds of prey on the islands: the endemic Galapagos hawk (Buteo galapagoensis), and three other birds with a wider distribution, the osprey (Pandion haliaetus), the short-eared owl (Asio flammeus), and the barn owl (Tyto alba). This is actually pretty typical for islands, even Hawaii and New Zealand have a number of native bird of prey species, even if they lack predatory terrestrial mammals or large terrestrial reptiles.
In a broader sense, the reason why there aren't a lot of predators on small islands is because there aren't enough resources for them to sustain a breeding population. A carnivorous animal on average requires ten times as much resources in the environment to support them than a herbivorous one due to energy that is lost from plant to herbivore and herbivore to carnivore, which results in carnivores either existing at very low densities across islands and easily going extinct. This is thought to be one reason why carnivorous mammals rarely successfully disperse to islands: they do disperse, but the islands they arrive on can't sustain them.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

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Cat herpes and behavior
We have 2 cats, aptly named "Fatty" and "Tiny".
"Fatty" is a 6 year old house cat that hasn't seen the outside world in years.
"Tiny" is a cat we rescued about 45 days ago and she's roughly 2.5 months old.
Tiny came in with what looked like an eye infection, a million fleas and intestinal worms.
We kept the cats isolated until Tiny could be seen by a veterinary doctor. She had treatment to kill fleas and worms and we just washed her eye and it cleared quickly.
Soon after Fatty started to develop a cough; the doctor at the clinic said it was some cat flu, probably brought over by Tiny and she got some antibiotics.
If the flu is a virus, I question the antibiotics.. but we went through anyways.
Now we're a month and a half later and Fatty has completely lost her voice and she articulates sounds that are like 'krr'; she is unable to make any normal cat sounds anymore.
The doctor said it may be cat herpes that was introduced by Tiny; if this is the case, she'll never 'speak' again. In the meantime, Tiny is doing very well.
The most striking change is in her behavior; at first she didn't accept Tiny, now they are friends, but she has become slow, uninterested in any form of play, doesn't really purr anymore, doesn't come close to us and walks away when we pet her.
So, my question is: if she had the herpes virus, which is very common in stray cats where we live, can it have any effect on her brain that would explain a huge change in behavior? (her blood test is normal)

I'm so sorry to hear this. I hope it's just a temporary adjustment. You might have more luck with this on Pets.SE.

yes; I was a bit on the fence since it's about a specific virus.. but it's about cats :) I followed your advice and posted in Pets as well.

https://pets.stackexchange.com/q/17764/11132


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Is this a stag beetle?
Just saw this beetle on my window.
The coin is an American dime.
Location is Shenandoah Valley,
in central Virginia, U.S.A.

This is indeed a Stag Beetle (Family Lucanidae); in particular a member of the genus Lucanus.  Looking at the bugguide.net page for the genus here your specimen is most likely Lucanus capreolus, though Lucanus placidus also looks possible -- the two species are very close in appearance, though the former does seem more likely based on distribution.  Consulting The Generic Guide to New World Scarab Beetles here confirms that L. capreolus is featured here -- the femora (the first long segment in the leg, and the first we can see -- look at the right front leg) are bicolored (darker at the tips) -- the femora of L. placidus would be solid dark brown to black.


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What is the name of this plant has dazzling look like leaves?
I am living in India. My neighbours are growing this plant and they even don't know what it was, but its leaves really dazzled me.

Google Image search has an option to upload a photo to it and it will show you matches. You could find these plant names that way too. Not just by asking on this forum.

It is Jatropha podagrica also known as Buddha Belly.
It comes under succulent plants.

Source: flowersofindia.net


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Why nerve fibre is infatiguable?( is my conjecture correct?)
According to this:

A nerve fibre cannot be fatigued, even if it is stimulated for a long time. This property of infatiguability is due to absolute refractory period.

How is refractory period related to infatiguability?

My attempt: If there were no absolute refractory period, then there will not be closure of Na+ ions into cell, so there will be temporary deficiency of Na+ at that location, now if a new action potential arrives at that point then , due to lack of Na+ there will not be further conduction of it.
Is my conjecture correct?

What exactly is your question? Is it why nerves don't get tired, or whether your conjecture is correct?

Is my conjecture correct?

Then it seems my awnser isn't what your looking for,  but the conjecture is not  quite right. It isnt a lack of ions, but rather the sodium gates are inactivated (and cannot open) that causes a absolute refractory period.

I really don't understand the reason for down vote.

If you study the electrical function of the nerve, it does exhibit attenuation to repeated signals, and there are various electrical stabilization times for the stasis within and outside the nerve to reach a balance after stimulation. ou should read about nerve disorders and nerve fatigure research to get an idea of how they malfunction. this is not recent but it could be interesting: http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.1906.sp001147/pdf

One can imagine that each action potential causes a small amount of $\ce{Na+}$ goes inside the cell, and a small amount $\ce{K+}$ goes outside the cell, thus weakening the electrochemical gradient of both ions. If each action potential has (approximately) the same flux of $\ce{Na+}$ and $\ce{K+}$ then higher frequency of action potentials means more flux, thus a quicker depletion of the electrochemical gradients. The absolute refractory means there is a maximum firing frequency.
Thus the Sodium-Potassium pump only needs to be able to "recharge"  the maximal possible depletion of ion's gradients. If there was no absolute refractory period then theoretically the action potential frequency could be faster than the Sodium-Potassium pump can keep up. A abnormally fast firing rate in theory could deplete the potassium gradient and sodium gradient thus would result in a fatigued neuron.
Edited to add in reference to the conjecture:
Absolute refractory periods are cause by sodium gate inactivation, thus no matter how much current one adds the sodium gates will not open until sodium inactivation ends. However, over long periods of time (in seconds) and in the absences of a ionic pump, the lack of sodium (and potassium) gradients will cause fatigue.
However, "fatigued" neurons may not act like one expects.

Hopefully, the edit clarifies.

You mean lack of gradient? because Brayn Krauss comment on this question says so https://biology.stackexchange.com/questions/62826/what-is-the-energy-cost-of-an-action-potential

Yes I do mean lack of gradeint. I will edit for clarity when I return to my desktop.

How do you define the side effects of fatigue neuron?

@LéoLéopoldHertz준영  thats a complicated question, and the linked paper gives some possible side-effects such as hyper-excitablility. It's counter-intuivite so I left it out, and gave a link for the more interested reader. Perhaps a separate question would be good?

@xelo747 No, I do not think so. It is part of the topic here. Please, add a section about it in your answer stating some of the factors.

Nerve fibres cannot be fatigued even when stimulated continuously because the nerve fibres primarily conduct impulses that do not involve any type of energy expenditure

Can you elaborate on this? We're looking for fully-fledged answers with detailed explanations, and with supporting references.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.


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How long can you store tissue on 4°C before B-cell extraction and culture?
We receive tissue regularly and extract B-cells for culturing, studying differentiation and survival with diffenet stimulation conditions. However, often the tissue arrives late afternoon and might be put in FCS at 4°C overnight before cell aextarction. I'm not sure however if such storage would impact the viability or functionality of B-cells later on during the culture.


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Microalbuminuria in inflammation of urinary tract

Albumin is excreted into urine (albuminuria) in nephrotic syndrome and in certain inflammatory conditions of urinary tract.$^1$

How is inflammation in urinary tract related to increase in albumin excretion? I know that microalbuminuria will result when albumin filtered is greater than its absorption( which takes place in nephron, not related to urinary tract).

My attempt : After some research I found this, which states cause of microalbuminuria in children may be causing infection in glomerulus, leading to increased permeability of glomerular basement membrane.
So, will it be correct to say that UT inflammation is not causing directly microalbuminuria?

UT infection in glomerulus causes inflammation of Glomerulus which causes increased permeability of glomerulus that directly cause increased filtration  of albumin. So, more is excreted as well.

in a nut shell, its indirect effect?

Direct effect.  Inflammation caused increased permeability which itself means protein filterablity.

inflammation is in ut which is not a place where filtration takes place. re read my question.


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Bacteriophages and their role in genetic editing?
I know how plasmids and restriction enzymes work to change the dna of a bacteria cell, but I do not really understand how a bacteriophage works to edit the genome of a cell. Is it related to crispr since its a virus which inserted genetics in bacteria? Also, is it during the lysogenic or lytic stage that the bacteriophage alters the DNA?

Putting CRISPR to one side (since that is the bacterium editing its own DNA) where have you got idea that phage do have an effect on their host's genome? Do you have any sources that you could cite?

Yes, I think its called transduction.

https://en.wikipedia.org/wiki/Transduction_(genetics)

That Wikipedia page looks quite comprehensive and answers your question about lytic or lysogenic cycle. What specifically is puzzling you? Bear in mind that transduction isn't really something that phages do 'purposefully', it is rather an example of the old adage in E coli genetics: 'anything that can happen will happen'. The trick is to find a way to detect the event by selection or, as a last resort, by screening.

Why do you think a bacteriophage "edits" the genome of a cell?

Why do you think a bacteriophage "edits" the genome of a cell?

I mean I read someone it is manipulated in genetic editing. It obviously doesn't just edit the genes willingly for humans' benefit ...

As explained in the Wikipedia page that you have linked to, transduction is the name given to a particular phenomenon whereby phage can be used to move bacterial DNA between cells.
Depending upon the phage, some aberrant or infrequent process can result in the packaging of host cell DNA into a phage particle during a lytic cycle. The resulting defective phage particle is still infective however, and when it infects a new host cell it injects the bacterial DNA that it is carrying. This DNA can then recombine with the host DNA.
So, for example, if the second host was a lacZ mutant but the parent host was lacZ⁺, then it would be possible to select lacZ⁺ in the second host.
Transduction was an important tool in E. coli genetics. Phage P1 can be used for general transduction, which means that any piece of DNA can be moved. As I said in my comment: anything that can happen will happen.


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How to interpret figure on somatic mutation frequencies
In paper Mutational heterogeneity in cancer and the search for new cancer-associated genes, Figure 1 defines:

Somatic mutation frequencies observed in exomes from 3,083 tumour–normal pairs. Each dot corresponds to a tumour–normal pair, with vertical position indicating the total frequency of somatic mutations in the exome.

Is the figure representing with each point a tumor/normal pair because somatic mutations (differently from germline mutations) are assumed to not be present in the normal sample?


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Overnight bacterial culture
I am working now to prepare an overnight bacterial culture. My question is should i pick only one colony of the bacterium streaked plate in order to make an overnight culture and what will happen if i picked two or three colonies?. I am working to make a deletion mutation in one bacterial starin using the phage transduction method. The technqiue said that i should make an overnight culture in 20 ml of the medium. So, i wondered if it would be two low if i pick only one colony in such amount.

Broadly the answer is 'yes, work from a single colony' but can you give a few more details of your experiment so that the potential pitfalls can be explained?

I am working to make a delation mutation in one bacterial starin using the phage transduction method. The technqiue said that i should make an overnight culture in 20 ml of the medium. So, i wondered if it would be two low if i pick only one colony in such amount.


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Phasing haplotypes
I'm new to this area (but not to programming & algorithmics) and I want to help a friend to solve a problem (I don't need source code, I just want to understand the problem itself).
He needs a cycle to phase haplotypes ("I need find haplotype pattern(s) from SNP string"). He also said "The method is simple, I need to compare homozygot combinations (AA, BB) in sequence with haplotype chains. And ignore heterozygot pairs (AB) at their right positions."
An an input he has a SNP string and a bunch of haplotypes strings (array).
Any help is greatly appreciated.
Thank you!

Rather than re-explaining the basics of haplotype phasing, I will refer you to useful documentation.
One of the first works on haplotype phasing has been perfromed by Andrew Clark. You can find here a nice slide presentation detailing the problem.
Useful discussion is going on here on Biostars.
I suggest you to use of the several approaches that have already been developed: my favorites are Beagle and fastPHASE.

Thank you. I managed to do it in PHP (really great on working with strings)


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Combination of different antibodies
How can I know if I can combine anti Cenp-C and anti Rod1 antibodies? I want to use them to label those protein and analysing cells by fluorescence microscopy.
*Cenp-C is kinetochore protein and Rod1 is localized on the kinetochores or spindle microtubules during cell division.
Can I just combine them if they are from different animals? how can I know they will not have cross reactivity?
Thanks

What exactly do you envisage as the potential problem? What do you mean by 'cross reactivity'?

I dont know if the the proteins they recognise can be too similar cause they belongs to the same complex so one ab can regonize a similar ag but not the one I want.

If they are made in different animals you should be fine.  You could do a western with those antibodies though, to double-check.  Looks like Cenp-C is about 106kD and Rod1 is about 60kD.  So on a western, if you see bands at both those sizes with one of the antibodies, you have cross-reactivity between those proteins.  And if you just see the specific band you're looking for, you're good.

Ok thanks. The fact they need to be from different animals is because the secondary antibody would not be specific? I never studied any course of immunology so I am not sure.

Secondary antibodies are made to bind to any antibody from a particular animal.  If both your primaries are from the same animal, the secondary will bind both of them, and you won't know what signal comes from what protein.  If you don't care about distinguishing Cenp-C and Rod1 in your IF, then it doesn't matter.  If you do want to be able to distinguish them (ie, have Cenp-C localization red and Rod1 localization green) then the primaries need to be from different animals so you can use two secondaries.


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What's the smallest animal with hemoglobin running in its veins?
What's the smallest known animal with hemoglobin running in its veins?
Here I mean an animal that on its own is able to produce the hemoglobin that is running in its veins. For that reason this excludes mosquitoes that have filled themselves with blood from another creature, for example.
With smallest I mean either by mass or by spatial dimensions. Either would be interesting.

Smallest by mass?

thanks @AlanBoyd, I have now updated that in my question:-)

What kind of googling have you done? It sounds like a "homework" question to me (not that it comes from actual homework)

The scope of the question is still unclear. Some definitions of 'haemoglobin' include proteins found in invertebrates and even in microbes. By using the expression 'running in its veins' do you aim to exclude such organisms?

Why do you want to know this? What will it tell you? Anything other than an entry in the Guinness Book of Records?

Why veins? Why not arteries?

It depends how different from human hemoglobin it can be and still count as hemoglobin.  Here is a cool evolutionary tree of globins.

http://www.mhhe.com/biosci/genbio/enger/student/olc/art_quizzes/genbiomedia/0329.jpg
Here is the worlds smallest fish.  Fish have hemoglobin similar to that of humans.
from Wikipedia:  The world's smallest fish is Paedocypris progenetica1 from Indonesia, with mature females measuring 7.9 mm (0.31 in).

But I think bloodworms are even smaller. They have hemoglobin too.  It is evolutionarily more distant from us but they use it for the same reason we do.

from https://www.prestoninnovations.com/img/media/Seq-7.jpg
http://www.allaboutworms.com/the-basics-of-blood-worms

Blood worms are red because their blood plasma contains haemoglobin,
  like human blood. Also spelled “hemoglobin,” haemoglobin increases its
  ability to take up oxygen. The larvae commonly burrow in the
  oxygen-poor mud bottom of pools and rivers, so haemoglobin is of great
  value to the larvae.

If you are going to allow very distant relatives,  I think this snail is even smaller than the smallest bloodworm.  Less than 1 mm.  Molluscs have hemoglobin too.

from https://www.slideshare.net/fmoretzsohn/texas-seashellsmore-than-you

Paedophryne amauensis, the world's smallest vertebrate by length, 7.7mm. The coin by the way is an American dime.


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Does Rüppell's Griffon Vulture Have Greatest Vision Acuity? (Small Carrion Spotted at 10 km+?)
Synopsis:
Some sources seem to imply the Rüppell's (griffon) vulture (Gyps rueppelli) can see objects at a distance in excess of 10 km -- roughly three times the commonly asserted vision distance of an eagle.
What studies have been done on eyes of this species and can any experts comment on the accuracy of this assertion?
Also, do we know whether their eyes perceive a similar color range to that sensed by human photoreceptor cells?

Background
Wikipedia's List of birds by flight heights lists the flight height of Rüppell's (griffon) vulture (Gyps rueppelli) as the highest known bird flight height at 11,300 m (37,000 ft).

The claim appears based on this ornithology journal article [PDF]
 ("Collision between a Vulture and an Aircraft at an Altitude of 37,000 Feet") detailing a collision over Abijan, Ivory Coast.  This is a coastal city...

...so can be estimated to be approximately at see level, inferring this is a height above ground (roughly).
The article adds:

Vultures use their excellent eyesight to scan the landscape below from a relatively static aerial position. Instead of flying over a larger distance, they use elevation to expand their field of vision. If they spot a meal down below, the climb has an immediate payoff.

That piqued my interest, as I came across this while trying to track down what the maximum known distance an animal could see was (per a separate discussion of fantasy vision capabilities).
Human vision is according to quantitative testing limited to "~2.6 km (1.6 miles)" [synopsis], likely varying mildly based on physiologic variability.
A Wikipedia entry on eagles ("Eagle Eye") states (citing a book on eagles as its source):

The eagle eye is among the strongest in the animal kingdom, with an eyesight estimated at 4 to 8 times stronger than that of the average human. An eagle is said to be able to spot a rabbit 3.2 km away.

The statement is a little bit tenuous on the sourcing, but impressive if reasonably accurate.
The note in the list of highest flying birds, though, makes it sound like this high-flying vulture could be able to detect faint objects at a distance of 10+ km!
That in turn suggests this bird to have perhaps the longest range vision acuity of any known species, with a vision range perhaps three times that of an eagle or more.
If so, the record for animal vision would not be "eagle eye", but rather "vulture eye".
Granted, it might also all be bunk; the internet is a very inaccurate place hence why I came here to StackExchange seeking quantitative evidence in support of this claim.

Humans can't see distant objects?  On a clear night with dark skies (all too rare these days) I can make out the Andromeda galaxy, 2.5 million light years away.  If you want something that doesn't produce its own light, Saturn at 1.2 billion km is easily visible.  On Earth, I can see individual trees on mountains 20 km or more away, and on one of those rare clear days, can see Mt Shasta from the summit of Mt Rose (near Reno), about 250 km.  I think what you really need to ask about is angular resolution...

I think the limitations that may have been missed due to my wording is 1) size of the of the object 2) an object that is not a light source.  Your terrestrial examples are impressive and of interest, but deal with objects signficantly larger than those discussed (see MIT candleflame discussion) in this thread and attached links.  Likewise Andromeda to my understanding is a somewhat different example than the one discussed here as it's much larger in relative angular vision than a distant mouse at 1 km+.  Maybe you're right on the angular vision term... is that the proper terminology here?

And how would I quantify how small a range would be implied for this vulture to improve the question?  Feel free to edit my question jamesqf if you feel that putting this in angular terms would improve the clarity!

You might ask whether this vulture has the greatest visual acuity.  The problem is that you don't specify what sort of objects it sees at 10 km.  Large objects, as per my examples, are no problem to see at much greater distances.  A dead (since it's a vulture) critter?  But what sort?  The eagle can spot a rabbit; can the vulture spot a dead rabbit at greater distance?  Then there's the issue of camoflage: I sometimes don't see rabbits until I almost step on them, but can track them at some distance if they're moving.

Thanks, when I get some time I may reword this further per your suggestions in hope of eventually getting an answer.

Tweaked the title @jamesqf ... is that clearer?

I think, but I'm not sure, that one way carrion feeders such as vultures find food over large distances is by observing other vultures closer to the source. Some south American vultures also have a keen sense of smell, and can find carrion on the forest floor.


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What enzymes I shall use for preparing single cell suspension from cardiac tissue for flow cytometry?
Can anyone suggest which enzymes I shall use for preparing single cell suspension from cardiac tissue. I will be looking at both cell surface and intracellular antigens involving cardiomyocytes and fibroblasts.


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Identifying a lone bone found newar Rowena Crest, Oregon (USA)
I was wondering whether anyone knows how to identify what animal the following bone belongs to.  I assume it a femur, but it seems rather short and squat.  The following photos show two views of this bone and I've placed a 15cm ruler in the frame with the bone.

Can't be sure about the species, but I agree with @kmm's answer that this is a humerus. The condyles (i.e., the "trochlea" and "capitulum" in the case of the humerus) are clear giveaways on the left side of the picture.

www.boneid.net provides a great searchable database of identified bones

Did you ever figure out what animal that belonged to? We found the exact same bone (just the other side) in the Adirondacks of upstate NY

My guess is that it's a relatively young cow humerus. The strongly grooved trochleas are more characteristic of a humerus than a femur, which usually just has two condyles. The deep pit is where the olecranon process (your bony elbow) goes. The proximal end is missing, which indicates that the growth plate was not fused, suggesting juvenile.
And I guess cow because cows are very common and have robust bones compared to other artiodactyls.
Here's an image pulled from the web:

It is not necessarily young, it looks like it has been out in the weather a while, the end could have been gnawed or weathered. Just based on size and the shape of the condyle it is either bison or cattle, and cattle is far more likely.

@John Young means the animal was of earlier than full-grown age when it died (based on the size), has nothing to do with how long it's been outside. Limb bones of cattle are sold for people to give their dogs, by the way.

@BryanKrause based on size I could see it, although cattle can vary quite a bit by breed no it is not a great metric to go by.

I'm not sure why (or how) the bone of a cow/buffalo would get where I found it.  There are certainly no cattle that graze any where near there.   Also, there are no gnaw marks on the bone either, so it doesn't seem like the sort of thing that had been given to a dog.  Could it be something more likely to live in the area like a wolverine or bear?  Though, still the size just doesn't seem right for those suggestions.

There are cows everywhere in the US, and they escape and get everywhere else. There is no state in the US where you cannot find cattle. And no, it does not look anything like a bear or wolverine bone.


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Radiation dangerous or not?
I've always been told that most electronic devices such as WiFi/phones/laptops and such emit a non-ionizing radiation which is completely fine as it does not damage human DNA. I've been googling and i see people arguing about it but there seems to be no evidence to back up the fact that it's not damaging. I'm just curious is what I'm saying correct? or can it damage the human body as i see people mention it can lead to pretty serious health problems.

WIfi and phones emit radio waves, you you might want to ask about that specifically, all non-ionizing radiation is too big a spectrum to cover in a meaningful answer.


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Identification of insect
I am trying to identify this insect on a hibiscus plant. Google googles is unable to identify it.

Google "Japanese Beetles".

Can you please specify where you found the insect?

Found in toronto canada

It's a Japanese Beetle Popillia japonica - they are invasive in most of North America and some of Europe now.
https://en.wikipedia.org/wiki/Japanese_beetle

They are spreading rapidly west in the United States and many areas are reporting the largest numbers ever observed, for example:
http://www.wisconsinrapidstribune.com/story/life/2017/07/19/japanese-beetles-invade-central-wisconsin/490140001/
http://www.omaha.com/living/japanese-beetle-swarms-are-worse-than-ever-this-year-and/article_77257d36-6c28-11e7-839a-877ff3c8538b.html
For control around your plants, it is recommended to manually remove them; brushing or placing them in water with some dish soap works well. They tend to congregate with other individuals of the species, so if you take them off your plants that will tend to limit the numbers that join them. However, they likely do the most damage to gardens etc as larvae, and there doesn't seem to be a good, specific way to control them at that stage.


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What is the name of this biting bug?
I just was bitten by a bug!!! It is 3mm long and has large pincers. Here is a photo:

I live in Colorado. Any help identifying it would be great.

It's a larva of a green lacewing (Family Chrysopidae). Yes, they can bite hard but you're not its intended victim and they're not only harmless but beneficial as they're aggressive predators of aphids and other soft bodied plant pests. I can't be specific to what species of lacewing as they look fairly similar.
Another larva that looks very similar to yours.

Source from BugGuide.net
What the adult looks like (remember,they're an entire insect family so there are differences but not to most people).

Source also from BugGuide.net

Wow! Thanks for the quick identification. Glad I caught it and released it ;)

That's rather interesting. The larva itself seems terribly threatening, while the lacewing looks cute!

That's a larva of an insect from the Order Neuroptera, probably from the Family Chrysopidae. Their common name in English is green lacewings.
Here is a larva very similar to your specimen:

Source: https://www.cedarcreek.umn.edu/insects/newslides/023neurop2line.jpg
Here is another one, also from the Family Chrysopidae (the colour pattern is not quite the same, but you can see the resemblance):

Source: http://bugguide.net/node/view/803060
And here is the imago (adult), for comparison:

Source: https://en.wikipedia.org/wiki/Neuroptera#/media/File:Crisopid_July_2013-9a.jpg

When I gathered my links to post an answer, there wasn't one yet. But you obviously beat me to it!

Doing it on my phone with quick breaks to look after lemon muffins I was making. Multi-tasking. :)

Have to use phone (tablet charge was low & computer sadly has a glitch & can't be accessed till fixed). Using SE app but still frustrating.

No, Geraldo, I think you might've misunderstood me. I wasn't trying to be the first. At the time I saw the question, no one had answered. I knew what it was but also knew I couldn't simply give an answer without references. There are other times species ID is a puzzle to me so I see if I can figure it out as a challenge to myself but don't bother answering since I'm sure someone will later. It's not a contest for me. I'm not that sort of person. I'm not at all competitive. Did you think I was trying to be first? If so, I apologise. My comment about you beating me was made light-heartedly.

FWIW, I don't think the app shows the "1 new answer to this question" in real time like the site does. I'd assume innocence (especially since @Jude insists that was the case).

Maxathousand, that information makes all the difference. I didn't know that because, on the mobile, I use a browser (which, by the way, also don't show "1 new answer" in real time). It's explained now. @Jude, let's clean this up, I'm deleting all the comments.

Thanks for understanding, maxathousand. There wasn't any answer. That's why I answered. When someone's already answered, I don't add an answer - it's redundant - which is why I didn't understand Geraldo. Good idea to have these comments deleted and I'm going to delete my SE app too.


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What do white blood cells do with FOREIGN white blood cells?
White blood cells or leukocytes are known to fight invaders, infections or basically anything foreign. They also contain DNA (while red blood cells don't). But what about foreign "white blood cells" received in a transfusion or sexual intercourse (as semen, not sperm, holds "lymphocytes" which are a type of white blood cells, they can "possibly" enter the blood circulation, not quite sure).
Anyways, my question is:
1) Do white blood cells "fight" the foreign white blood cells and kill them off? OR is that something cleaned by the spleen itself? (considering WBC lifespan is 13-20 days so they die off their own). So do they "get" attacked by the host's WBC or do they naturally die off their own?
2) Does the body detect them as "foreign"?
3) I've also heard about the "extracellular DNA" phenomenon. Which is, the ability of DNA to exit a cell (while it's dying) and float in the extracellular (non-cellular) environment. The DNA is degraded during a cell death but it can definitely exit a cell and float non-cellular in the environment. This is also true for the cell's RNA. This is labelled as an "extraceullar DNA/RNA" or a DNA/RNA without a cell. So that being said, can the DNA of foreign leukocytes or white blood cells that do not belong to the host (having a completely different DNA, of course) exit it's cell during it's death and become extracellular DNA? Is that even remotely possible? Also, can that extracellular DNA (keep in mind, the DNA is a fairly stable molecule) ever remain in the circulation or the human body for life? Perhaps in the bloodstream? or in one of the organs? or in a biofilm? (considering exDNA is a component of a biofilm) Does that even have the "slightest" possibiliy of happening? For it to remain there for life?
1) If it is, wouldn't the body (the immune system or WBC) ever "react" or "act" on eliminating the "foreign DNA" of another person that's floating around? Or is that something which will remain for life OR be eventually faded away? I'm well aware of enzymes such as DNAses/RNAses (enzymes responsible for DNA and RNA degradation) but do they do that in the blood? And that being said, "sometimes" in a biolfilm they don't.
2) And even if it gets stuck in a "biofilm" (assuming it's possible?), would it "EVER" degrade eventually or remain there for life? OR CAN/WILL the "biofilm" holding such extracellular components degrade eventually or will it remain for life as well? (can they remain there forever?).
3) A simple way to explain this would be if I insert hundreds of "foreign DNA" (strands, not cells) into your blood stream, what would happen to them?
4) Can it get "stuck" or get glued to an organ or it's cells and remain there for life somewhere out in the deep where they won't be found? Since I'm not an expert in molecular biology I don't understand. In other words, can it EVER remain there for life with "ANY" slightest 1% possibility with all the possibilities I've explained or any other possibility of it remaining there for life? And same goes for the RNA. Having someone else's DNA and RNA scares the shit outta me. And having that for the rest of my life, makes me really uncomfortable.
My question is for both the DNA and the RNA.
I don't want "assumptions" or hypothesis please. Please answer if you're an expert in microbiology/molecular biology, others, etc. And are well aware of what I'm talking about. I will greatly appreciate it.
Also, this is a tricky one! (I completely don't understand this)
The molecules secreted by these "foreign" white blood cells after their death would provide structural and biochemical support to other cells so wouldn't a part of his trace (his molecules) would remain in other cells forever once they consume it? Or the molecules get replaced on a cellular level itself if I'm not mistaken? Wouldn't his molecules be a part of my body forever?
Please answer if you're an expert in microbiology/molecular biology, others, etc. And are well aware of what I'm talking about. I will greatly appreciate it. I don't want assumptions or hypothesis only whatever is known, proven, researched & concluded as a fact. :)
Thanks guys,
Marry

Please shorten your question body. Your question body has some unnecessary sentences.

It might be good for getting answer of your question that you don't restrict the job to specialist in molecular biology. Most of the people are here not specialist, but they are enthusiast and can provide good answers.

Okay, you have a lot of questions there. I'll try to give some answers, but if you want more details or background knowledge I'd recommend you to read /study more about immunology (none of your questions are actually about molecular biology or cell biology).
2) Foreign cells are generally recognised by the immune system, based on the HLA molecules on the cells: all cells that do not have the exact same HLA molcules are recognised as forgein and attack by the immune system (cells without HLA are not human and by 'default' foreign). Since there are many different variants of the HLA class I gene and humans have usually 6 different ones, its very unlikely that a cell from someone else would not be attacked (that's why it's so hard to find matching organ donors).
1) Foreign cells are attacked by the immune system, the spleen's purpose is to remove/recycle old blood cells from the body itself. Depending on how the immune system recognises a cell (e.g. by antibodies or diretcly by immune cells) different strategies to fight the foreign cell are activated.
3) There are certain receptors on some immune cells that can recognise extra-cellular DNA or RNA. This recognition is not sequence specific und usually causes an inflammatory reaction, because extra cellular DNA is a sign of either cell damage (by necrosis) or invading pathogens. After the immune system recognised such 'invading' factors they are usually taken up and removed by macrophages.
Generally speaking all of this only happens if foreign cells or DNA manages to get into your body (e.g. if you would inject it). It's very unlikely that DNA or cells can pass into your body unless you have open wounds. (White blood cells usually only are able to pass the endothelium of blood vessels, not other kind of barriers)


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How to keep Paraffin Sections from falling apart?
I've been trying to make 5 uM sections of injured mouse spinal cords and stain the tissue with Luxol Fast Blue and H&E. At first I was removing the bones from around the spinal cord, but the tissue just fell apart after I got it on the slide. I think because it had been severely damaged.

I thought I might be able to hold the tissue together better if I kept the bone, so I took a spine and decalcified it with 500mM EDTA for 1 week and tried again. But the bone tissue just pulled away from the spinal cord.

These were some of my better images. I have many others that are even less intact. I see the tissue fall apart on the slide during the drying step, after I put the section on the surface of a water bath and catch it on the slide. I have seen some sections spread all the way across the slide. I suspect it has something to do with water getting trapped under the paraffin section and not drying correctly.
How can I improve the procedure to keep the tissue in 1 piece?

What is your dehydration protocol? What are you using for a fixative? How experienced are you with histology generally? Brain and spinal cord can be tricky tissues to work with. My initial bet is on the dehydration being incomplete. Also a nice attempt on the decalcification and using the bone as a scaffold - I don't have a good sense on whether this is likely to cause other problems, but it seems most typical for people to dissect the cord out rather than keep it in situ. And as you noticed, it's going to be hard to keep the tissue anchored within the bone after the shrinkage of fixation.

@BryanKrause Fixation is done by transcardial perfusion of 10 mL PBS followed by 10 mL of 4% PFA. The spines are removed and stored in 4% PFA for 1-3 days, then 500 mM EDTA for 1 week, then back into 4% PFA until I have time for paraffin embedding, usually just overnight. I need to double check the dehydration protocol, it's done by a machine with multiple buckets and I was just told to put the samples in the basket and hit start. I'm pretty sure it's 70%, 90%, then 100% Dryzol followed by paraffin, but not sure about the time for each step. Total time is 24 hours.

@BryanKrause I have no experience with histology. My advisor just sort of dropped me into a project a year ago and expected me to learn animal surgery, gait analysis, histology etc with almost no training or supervision. Needless to say, this has been a slow project.

That's why I asked about your experience with histology - I think it's fairly typical to get thrown into a project like that, whereas professional histologists have a ~2-year professional degree program. Not to mention you are working with some of the most difficult tissues. I would try to find a histology expert that works in your department in another lab to help you out a bit (I myself am a novice at best). Your PFA is made fresh, right? No methanol?

I'm not familiar with "dryzol" but if you are dehydrating in ethanol some people use several sequential baths in absolute ethanol at the end (again, this should really be absolute ethanol, 100% ethanol, not "reagent ethanol" or some similar alcohols mix that has methanol or isopropyl in it).

The PFA is purchased premade. Dryzol is a mixture of ethanol, methanol, and isopropanol, not sure of the ratios.

Let us continue this discussion in chat.


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Do all plants grow roots when separated from parent?
Recently I bought my very first plant.
I thought it was doing well because it remained green, sometimes a yellow leave but all of my acquaintances which do know about plants told me not to worry, and remove the yellow leaves.
Until yesterday,
suddenly
a branch of the plant fell off,
I looked at it and it had rot through the whole stem of that branch and broke off.
Quite displeased of course,
Now, the branch is still alright, I guess, the leaves are still green,
now what am I supposed to do?
For now I planted the branch in the pot of the main plant,
I'm intending to get a separate pot for the branch and plant it again,
But I wonder, do all branches of all plants grow roots when put in ground?
If not it's not worth the effort to buy another pot of course,
Could someone help me out?

Dear respected person,
I am not a professional botanist, but I adore gardening, and would like to help you as much as I can from my humble garden experience.
As far as I have experienced, not all plants have stems which root when put in the ground. For instance, I have a plant called Bouganville Tom Thumb (I apologise for any spelling error). I once decided to clone this Tom Thumb variety by cutting its stem off and then burying its base in potting soil. I even tried rooting hormone powder (from a gardening store) but it did not root, even after a whole month.
On the other hand, I had a plant called Petunia whose stem I cut off on purpose to maintain the plant's shape and threw the stem into the soil. The stem shriveled, and I thought it died and left it there. However, to my surprise, I found the stem all fresh after 2 weeks only to find that it had rooted into the soil from side of its stem. Another plant called Jade Plant can be cloned by putting its leaf in soil.
I think it really depends on the type of plant whether its stems will root or not and how long the stem will retain its rooting potential after being cut.
If possible, you can try the following. Put the cut stem in a small plastic pot (they are very cheap) with soil and see if it roots (leaves will begin growing). If it does, transfer it into a larger pot later once it has grown. Wait for it to grow big enough to spread its roots thoughout the pot, then shift it into a big pot.
I believe if a plant roots, then all stems of that plant will root. Plus, congratulations on your first plant.

Hey Taimur, thanks a bunch for your in depth answer and the kindness it radiates... I'll surely follow your advice, I do hope the separates branch will survive, thanks for your elaborate answer and I wish you much fun with your gardening endeavors!!! Best regards, S.

Plants vary wildly in their ability at vegetative propagation. Not all plants grow roots naturally when cloned. Many plants have very slow response time to make new roots, and the branch dies long before the roots arrive, even in good normal conditions, so that it can only clone with very artificial environment.
You will find guides how to propagate your plant by searching google for clone+plant name... Lots of practical information is available online, it normally involves: 1/propagating by cutting new buds and putting the fresh branch underground while still attached to the plant
2/cutting new branches and taking off some of their leaves so they dont dehydrate, they evaporate passively drawing from roots, and putting them in controlled humidity for a week/months. the roots can take anywhere from a few days to many weeks to become visible, depending on species, i.e. conifer vs most broadleaves.
here's an interesting text on the subject:
https://gardening.stackexchange.com/questions/30685/are-all-plants-able-to-be-cloned


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Are transcription factors some kind of eQTLs?
Cause of working on Allele-Specific expression, working I am trying to know more about expression quantitative trait loci (eQTLs). based on definition, eQTLs are loci that control the expression level of other genes by Cis or Trans effects. Transcription factors are also proteins (product of genes) that control expression level of other genes. So the question is that, are transcription factors some kind of eQTLs? (or eQTLs are some kind of TFs?)

No, eQTLs and transcption factor are very different things.
Like you described TFs are proteins that control the expression level of genes.
eQTLs are nothing that is physically present in the cell. An eQTL is the conceptual influence of an allele-specific DNA locus (a SNP) on the expression of a certain gene. Explained with an example this means that some with the allele AA has a different expression in 'gene 1' than someone with the allele TT. The eQTL does not even imply any causality, merely statistical association of the allele state with a change in gene expression. (Of course one possible causation for the change in gene expression is that the allele influences binding of a TF to that locus.)


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My Queen ant has laid eggs but has not dropped her wings, is this ok?
My Queen ant has laid eggs but has not dropped her wings! I caught this Queen in England, I've had her for three days and she's laid eggs already but I was expecting her to to drop her wings first as she needs the wing muscles to feed her brood. I don't yet know the species of the queen but I'm suspecting it's a camponotus queen but I'm not sure, the queen is 1cm long and 4mm wide, the gastor is bigger than the thorax and she is black. (I haven't got a recent photo of the queen because I am currently away on holiday and will be for the next month. (My mum is still at home though so that's how I know there are eggs and the queen still has her wings)).Is there a species of ant that never drop there wings or don't drop them for a long time?

You might have better luck asking some of your questions on a forum specifically for ant-keeping. Not so much that your questions are off-topic here, but we have a relatively small community and it might be quite some time before someone with the relevant expertise comes across these questions.


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Names for effects of sleep deprivation on the brain & body
When staying awake for a long period (3 or 4 days), some weird phenomena can occur. In my experience, it was always triggered by thinking too deeply and has in other occasions too.
Do these things have names at all?

The brain is a complex dynamic system; if you perturb it outside of its normal functioning parameters (for some examples: severe brain damage, psychadelic drugs, sleep deprivation), odd behavior can result. Note that sleep deprivation for ~2+ weeks kills rats. The rest of your question is too much based on personal health and experience to be on-topic here at Biology.SE.

“Deprivity”? Oh, I see, very clever pun on “depravity” and “deprivation”!

@BryanKrause, I completely disagree. The question of whether there are formal names for the mental changes the OP experienced during sleep deprivation seems to be fine.

@Michael_A Tried to make the question actually about that to keep it on topic, and retracted my close vote.

@BryanKrause, Nice. I thought the original description was a good attempt at describing the phenomena; it's a hard thing to describe. I agree that more words often make discerning the question harder.

During extreme sleep deprivation you can briefly fall asleep, this is known as a microsleep. The disorientation that you experienced can be referred to as  Hypogogia.
Hypogogia covers a range of effects including visual and aural hallucinations as well as having thoughts that are experienced as seeming logical during the microsleep but illogical once you're awake.


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What is this growth on a Rosa rugosa stem?
I saw many of these on my big old Rosa rugosa bush yesterday. What are they?

Please provide your location and an approximate size of the specimens. Thanks.

I have this on my Rosa rugosa as well. I first noticed them 2 years ago and it is spreading to many of my plants. I think it has killed several of them. I am going to cut them back below this growth and see if that helps them survive. I am in Cape Cod , MA.

This looks like a gall. At first I thought that it was the common rose bedeguar gall, also known as Robin's pincushion gall which is caused by Diplolepsis rosae, a small wasp. However, there is a related wasp, the spiny rose stem gall wasp Diplolepsis spinosa, which attacks Rosa rugosa so I imagine this is what you have here.
Incidentally, you are probably wondering what bedeguar might mean. According to the OED it derives from a French word bédégar which in turn comes from the Persian bād-āwar ('wind-brought’).

This is a stem gall induced by the cynipid wasp Diplolepis spinosa. It has moved from the wild rose Rosa blanda in eastern Canada and Rosa woodsii in western Canada, onto the introduced Rosa rugosa. The bedegular or Robin's pincushion gall is induced by Diplolepis rosae. Both the host dog rose and D. rosae have been introduced from Europe. The mossy gall of D. rosae is induced on leaf tissues - even though the gall looks like it comes from stem tissues.

This is a great, informative answer, but it would be helpful to have a citation.


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Does catching a cold give you an "effective" advantage against future colds?
By effective advantage I mean that if I catch a cold now and then recover fully, does this actually reduce my probability of catching a future cold. I understand that the body can build up anti-bodies and such, but pathogens also have the ability to mutate and I would assume that anti-bodies levels decrease over long periods of time. I am not a biologist! So feel free to correct my poor assumptions.
Thus taking those factors into account, are there models or data to argue that catching a cold gives me a future advantage over avoiding the cold altogether?

Short answer: no.
The "cold" is a common term for symptoms caused by dozens of different viruses. Even the canonical "cold" virus (rhinovirus) has large numbers of strains.
Exception to the short answer: Getting a cold might be effective against similar strains of the same virus.
Most of the time, future colds will be due to a different strain or a different virus. Best protection is to block unused/vulnerable receptors in the nose.

Can you cite something so I can read more? A Wikipedia article or two would be fine.

Read the "Rhinovirus" and "Common cold" articles on Wikipedia.


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Population-biology, migration-patterns, & ethology of the Big Five (elephants, rhinos, lions, leopards, & buffalo) in S. Africa's winter months?
I know that animals are unpredictable, but I also know that there are seasons in which the wildlife are more active. Now, August in South Africa is still their winter season, which is emerging into spring, and I was wondering what the population-biology, migration-patterns, and ethology of the Big Five (black rhinoceros, African elephant, water buffalo, African lion, African leopard) are like in August?
Now that's quite a variety of animals (some migrate, and others don't), but I'm essentially wondering: are the wildlife less active in August (because it's winter) or do they stay pretty active all-year round, even in the winter months (because of the warmer climate)? Are the migratory animals present in the winter time in Kruger National Park?


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Is it theoretically possible to create two humans by splitting one human in two?
There have been cases where a person has had one of their brain hemispheres removed, and they ended up living a fairly normal life. Could it be possible to split a normal person down the middle and create two people, each with a brain hemisphere? Machines could be used to replace organs that can't be split, like the heart.
I'm assuming there would exist some very advanced technology to prevent excessive blood loss and other problems with splitting a person down the middle.

If you split a human early enough (in the first weeks after fertilization), you can get monozygotic twins.
Other than that, you are in the field of science fiction and we cannot safely answer such question on a science website. I am not sure your question will be accepted in its current format but you may try WorldBuilding.SE.
And if you like fantasy novels, I recommend The Cloven Viscount by Italo Calving! You will definitely not learn much about biology in this book though.

Given how some parts of the brain control the opposite hemisphere of the body, and how this is not consistent throughout the entire brain, you would have to do a lot more than split someone in half down the middle.
Importantly, in split-brain patients only the cerebral cortex is hemisected, and only at a particular (though significant) point of connection, called the corpus callosum. It would not be possible to do this through the entire brain.
Especially in adult humans, some functions become lateralized, as well, so each "person" would be capable of different functions.

I see, the hemispheres would need to be swapped after separating them so a hemisphere stays with the side of the body it controls.

@Thomas It's not possible to separate in that way. Things are too intertwined. You can refer to it as a sci-fi possibility, but in the real world it isn't even close, not even with the most expert surgeons or even futuristic robotic abilities.

In split-brain patients, only corpus callosum is hemissected because its the only point where thetwo hemispheres connect. IMO spliiting hindbrain into hemispheres wouldn't be very logical...

@another'Homosapien' That's actually not true - there are the anterior and posterior commissures, and there are some other indirect pathways between cerebral hemispheres. The corpus callosum is just the bulk of the connectivity. But yes, there  is no sense in splitting the hindbrain, nor parts of the midbrain.

Although there have actually been some cases where a human have survived with half-a-brain after one hemisphere was surgically removed - the remaining hemisphere took up the slack.   http://mentalfloss.com/article/70120/how-removing-half-someones-brain-can-improve-their-life

@BaardKopperud The extent of the ability of the brain to compensate depends a lot on age. The most extreme examples in that article are for people who lost a hemisphere at a very young age. Also remember that the cerebral cortex is only a portion of the whole brain. An important one at that, but a lot of function is possible without any cortex at all, so it's important to keep that in mind.


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What is the relationship between DNA molecules and the chromosomes?
Regarding the human genome, if the DNA molecule is two continuous strands, with each gene occupying a segment in it, and there are 46 chromosomes each with some genes, where is the physical boundary of each gene?
My understanding of a molecule is a collection of atoms bound together by covalent bonds thus giving the substance its properties.
My reading so far gives me the understanding that the nucleus of a cell contains DNA, whose molecule is that famous double helix. At the same time, I read that the genes are packed into 46 chromosomes. This got me confused. How is the DNA molecule split into 46 parts?

I don't really understand what you're asking.

Ehh! Can you make it clear what you are asking.

Isn't DNA one molecule?

What research have you done to try to answer this question from available sources on the internet or in books? If you had completed the introductory guided tour you would be aware that you need to demonstrate such prior effort. This question is standard introductory material that can be found in numerous places on the internet.

Yeah, DNA is one molecule, but its nearly impossible to pack one such long molecule into chromosome. So, its split into 23 parts, and each part has a duplicate with it. I suggest you should keep studying...

To cite @canadianer, I don't really understand what you're asking but the following may help you.
Genome composition
First of, in the genome of most eukaryote (incl. all plants, fungi and animals), in general, genes constitute only a small part of the genome. Typically, in humans genes occupy 26% of the genome (24.5 for introns and only 1.5 for exons).
What does a genome look like?
Introduction
You say

Isn't DNA one molecule?

I think this question shows an important misunderstand you have. Note that I will only talk about the nuclei of eukaryotes below.
DNA is a type of molecule, which is constituted of two anti-parallel strands. In the human genome, we have 46 chromosomes, that is 46 independent DNA molecules. Now, these exact numbers vary depending on the moment in the cell cycle you want to consider but this is a story for another time.
A little more advanced
Below is a karyotype of a human allowing you to visualize the chromosomes. The 46 chromosomes we have go by pairs (pair of homologuous chromosomes) and on the image, they are numbered by pairs, the last pair being the sex chromosomes. By the way, can you identify the sex?

Note now that, depending on the moment in the cell cycle you want to consider, each homologuous chromosome may be constituted one 1 or 2 DNA molecule, each of them being called a chromatid. Chromatids are physically attached by the centromere. Two physically attached chromatids are called sister chromatids.
More information
For the moment, I threw some vocabulary at you but it was probably a bit hard to follow. You can get more information at the posts

Chromosome and chromatid numbers during cell cycle phases
The human has 46 double chromosomes or simple chromosomes?

or simply an intro course to genetics such as the following three courses by Khan Academy

Classical and molecular genetics
DNA as the genetic material
Central dogma (DNA to RNA to protein)

Thanks, so it's 46 different DNA molecules and not just one DNA molecule in the cell nucleus.

Indeed, there 46 double-stranded DNA molecule in a human cell nucleus (although this number may be doubled depending on the moment in the cell cycle).

Actually, each double-helix is two DNA molecules, if you define molecule as atoms held by covalent bonds (as is typical). Each strand of the double helix is a separate molecule, but the two strands fit together so well that the (non-covalent) hydrogen bonding holds the two very long strands tightly together.

There are actually even more strands in the cell as a whole since mitochondria have their own strands. these strands are small short loops that do not contain many genes (~40 genes by many estimates)

@mkgrebbs. Sure, this is why I said double-stranded DNA molecule assuming hydrogen bounds are sufficient to consider the two strands together a single molecule. I avoided this discussion to avoid further complication given how introductory was the OP's question.

@John Indeed, this is why, I said in a human cell nucleus. The OP might be aware that there is DNA in the mitochondria as he says  in the cell nucleus himself. Again, I wanted to avoid further complications here (even more so that DNA is not organized into chromosomes in the mitochondria).


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Alternative conditions for Liquifactive Necrosis
A person is beaten on the head hard enough to swell the whole front part of the head. The body is thrown into the river and recovered after about 36 hours. Is this condition enough for liquifactive necrosis to occur? If not, what could have caused it?

Damn that's an image... Lemme check it out actually...


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What is the reason for occurence of introns in eukaryotic mRNA?
After transcription of the Template strand of DNA, in prokaryotes, the translation process begins immediately. But in eukaryotes the mRNA transcript has both non coding (introns) as well as coding (exons) sequences. So they undergo Post Transcriptional processes i.e. Splicing, Capping and Tailing.
From where do non-coding sequences arise in eukaryotic mRNA? I'm guessing its from Heterochromatin (found only in eukaryotes). Is this correct?
Also the process in prokaryotes seems to be hassle-free and simultaneous. But what is the reason for such a complicated process in the more evolved eukaryotes?

No organism is more evolved than any other. That aside, no one knows why introns exist, but we do know that they presently play roles in gene regulation and generating protein isoforms

Please note that you are required to some research of your own before posting here. Not only could you have searched this site to find that your question has been posted before, but you could have searched Wikipedia or the web in general. I see you have not completed the guided tour as you lack the corresponding badge. Please do so if you intend to use this site.

@David My apologies sir for not having done my homework. I wasn't duplicating anyone else's work. Its a genuine thought and i was too overwhelmed by it and posted it immediately. I could have done everything you said. I regret it.

No big deal, just explaining how the site operates. Nobody is accusing you of duplicating anyone's work — that's a standard message generated by the system.

Oh thank you so much sir. I'm totally free of the burden of an accusation:)


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Why doesn't local anesthesia affect muscles?
While having a dental surgery, I've got this question that why I can still talk, open/close my mouth, move my lips and so on while I can't feel anything at all in my mouth?
If the local anesthesia interrupts the alert that goes through brain, how is the muscle still functional? Is it some sort of one-way interruption which only disables the alert that go "from" the nerve "to" the brain? Or are there different nerves for this task?

Why isn't anyone just saying that local anesthetics block sensory neural pathways, not motor neurons? There are two differing neurons, motor and sensory. Is not that the bottom line? This is what I assumed, but ended up confused after reading the answers provided.

@michelleb this is because local anesthetics block both sensory neurons and motor neurons. They block a specific receptor site inside $Na^+$ channels found in all axons, preventing propagation of an action potential. All neurons need this channel in order to send signals, so it's not a matter of a difference in the physiology of a sensory vs. motor neuron, it's about the anatomy of the specific nerves involved.

@Nicolai's answer is not entirely correct.
Background
The most common local anesthetics are all the "-caine" drugs - like novocaine, lidocaine, - and even cocaine has some of the same pharmacology, as well as other effects (in movies this is why cops might rub some white powder on their lips - if it's cocaine, it will make their lips tingle; this is not standard training for non-movie police; also not advised for drug sellers or purchasers, because for exactly this reason cocaine is often cut with other -caines or other compounds that give a tingly feeling).
What all of these drugs do is to block voltage-gated sodium channels. These are the channels that propagate action potentials through axons and excitable dendrites. Other local anesthetics that aren't used in the clinic, like tetrodotoxin from pufferfish, block the same types of channels. At sufficient concentrations, local anesthetics block all nervous activity: unlike @Nicolai's answer, they do shut down nerves (as a brief note for terminology: nerves are bundles of axons containing many many individual fibers).
So back to your original question: how come the muscle isn't impaired during dental surgery?
Geometry of innervation of the face
Take a look at this picture of the nerves innervating the facial muscles and the muscles themselves: https://bmc.med.utoronto.ca/cranialnerves/wp-content/images/c_07/Facial-vii12_labelled768.jpg (note: I wasn't able to find a good image that has a license allowing me to reproduce it here; if someone finds one and wants to edit it in, please do - thanks!)
They mostly come in from the sides of the face, and so they are further away from the site of local anesthetic injection. The muscles themselves also extend further away. It may be that the muscle is partly anesthetized, but you don't realize it.
Limited diffusion and location of injections
Diffusion of local anesthetics is limited because they actually act inside cells, and only the unionized form can diffuse across cell membranes. Once inside the cell, the tend to be ionized and therefore get "stuck". Therefore, they don't typically diffuse nearly as far as other compounds of similar size, especially lipophilic compounds.
The nerve endings that sense pain, on the other hand, have to be at the surface of the skin/mucous membranes. That is, they are exactly where the local anesthetic is being injected. The objective of local anesthesia is often to inject enough to affect only those surface tissues, trying to spare the deeper tissues.
Effects on nerves
However, it isn't too uncommon to overdo it and to paralyze the underlying muscles or nerves. Even nerves far away can be affected, for example see this paper discussing cases where the local anesthetic travels near the eyes and impairs eye movement. There are also other non-dental procedures where block of a particular nerve is the intended result: this can be seen as an alternative to general anesthesia. One example is the use of an epidural (essentially into the space around the spinal cord) injection during childbirth or surgery. The extent of paralysis depends on the dose, however, and usually the intent is to avoid major paralysis and use other drugs like opiates to assist in preventing pain.

Sorry to say, but this isn't exactly correct either. In dental procedures, nerve bundles are usually the target of the anesthetic block. Similar to digital blocks in laceration repair. We block either side of the base of the finger, yet the finger can still move quite easily.

So to be clear, the neuron itself is not paralyzed? One quick question, If we do a LA on inner ear, is it still able to send crucial feedbacks to the brain? By the way, thanks for the long and nice answer :)

@anongoodnurse Thanks! Today I learned... Feel free to edit my answer or add your own. Is that always how things are done for dental procedures? Presumably those nerves are separate from the ones that control the muscles. Or is it just because the different fibers have different thresholds? My experience is in rodent surgeries, where we just inject under the skin. I thought the nerve endings were particularly vulnerable. For the finger, isn't part of that because the actual muscles that move the finger aren't in the finger itself?

For dental procedures, yes. Topical (mucosal) anesthesia is just to pierce the mucosa and get to the deeper nerve bundle. And yes, (that was a stupid example, sorry) the muscles that control finger movement are in the forearm, but other sensations can still be felt (e.g. pressure.) I think it's the type of nerve fiber. IV lidocaine can decrease pain (or, e.g., the cough reflex during a crash intubation) but doesn't cause paralysis because of differing nerve types. Interesting, too, is the effect on cardiac muscle. Btw, been reading about tinnitus; very interesting. Thanks for that.

@anongoodnurse Started reading some papers where people studied dose-dependent effects of lidocaine so I can improve my answer. Ran into some authors I know personally...oops.

@BryanKrause - Ahhaha! I've done that too. Luckily, we can't be experts in everything.

The answer to this question boils down to 'because local anesthesia does not interrupt the nerves themselves'.
From the wiki article on local anesthetics (LA):

All LAs are membrane-stabilizing drugs; they reversibly decrease the rate of depolarization and repolarization of excitable membranes (like nociceptors). Though many other drugs also have membrane-stabilizing properties, not all are used as LAs (propranolol, for example). LA drugs act mainly by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane, in particular the so-called voltage-gated sodium channels. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited.

This means that the LAs don't actually shut down nerves. What they shut down is the ability of nerves to sense mechanical movement. Because mechanical movement on the cellular level is a bit different from what we usually associate with it, this means that in an area affected by LAs the nerves can not report feelings of pain, touch or temperature [actually also spicy taste] to the brain. All other nerve functions (including muscle control) are not affected

Thanks for the answer. It's also interesting that how we can talk under LA effects just like normal situation. Was wondering if we can walk normally if our feet or head is under LA effect too?

@JackJohansson You should still be able to walk in theory, but it will feel very 'wierd' and you will have higher chance of stumbling, because all sensory feedback from your moving legs is missing. E.g. you will not feel the moment your foot hits the floor, so you're brain may not automatically adapt the position of your foot to 'roll' it over the floor.

This is also why people under LA do more damage when they bite their tongue, they can't feel it and can't feel the position of the tongue well.

This answer is incorrect for the most part.

the quoted text and your assessment of it are incompatible, voltage-gated sodium channels are not for sensing mechanical movement.

@Bryan's answer isn't totally correct.
Short Answer: There are different nerves. Motor neurons and sensory neurons are not identical and anesthesia affects them differently.
When dentist inject novacaine they are targeting the V3 or V2 nerve trunks, where both sensory and motor neuron bundles are in close proximity. Take a look at this illustration for clarification
https://operativeneurosurgery.com/lib/exe/fetch.php?w=400&tok=5831b0&media=trigeminal_nerve.jpg The injection site is usually near the jaw at the side of the face, this allows the whole side of either zone be sufficiently numb. So it must be a difference in the physical makeup of the neurons.
Some of the differences between motor and sensory neurons are: Motor neurons are long, multipolar, and contain efferent fiber, sensory neurons are short, unipolar, and contain afferent fibers. Myelin is a protective sheath of proteins and lipids that protect and insulate the nerve fibers. Myelination is the process in which myelin is formed over  the nerve fibers. But afferent and efferent fibers undergo different types of myelination. Progression of anesthesia is related to the diameter of affected never fibers, conduction velocity, and myelination. The difference in myelination between the two types of fibers is the main reason anesthetics mostly affect sensory neurons.

Welcome to Biology.SE! This looks like a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and leaves non-experts with no way to follow up on your answer. ——— This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site.


text:
Comparison of examples in incomplete dominance and Co dominance
When we consider examples of incomplete dominance we take that of FOUR O CLOCK plant -
We say that alleles for red and white colour of flower are not completely dominant against each other. Hence in hybrid progeny we
Say (as in standard textbooks) that pink colour appears due to "expression of single gene for pigmented flower which produces only pink colour (quantitative inheritance )"
In codominance concept we take example of SHORT HORNED CATTLE which again appears as same case white and red cattle produces roan coloured hybrid progeny but due to "juxtaposition of small patches of red and white colour hair"
The same principle can be applied to four o clock plant too. Suppose pink colour of flower is too due to juxtaposition of red and white coloured elements.
Then where is the difference between the two concepts?
Further the thing which puzzled me more was that - "initially cattle example was considered to be in complete dominance. Later it was CORRECTED to codominance "
Also incomplete dominance is also known as "mosaic dominance" but actually mosaic happens in codominance.
Kindly clarify my doubts

Mosaic dominance
I think your confusion comes from the statement

incomplete dominance is also known as "mosaic dominance"

I had never heard of mosaic dominance before and I could not find much on this concept. I found a few papers but they either referred to mosaicism (see below) or they did use this term only a few times without defining it. There is an entry for mosaic inheritence in the online medical dictionnary though (here). The definition they give is

inheritance in which the paternal influence is dominant in one group of cells and the maternal in another.

It is a little vague to me as 1) the phrasing is a little unusual and 2) it does not specify the underlying mechanism. If anything, it feels like a synonym of codominance and not of incomplete dominance.
Mosaicism is a thing in genetics but it is mainly unrelated to the concept of dominance as it refers to genetic polymorphism among cells within an organism.
Where did you read about mosaic dominance? Can you please give a direct quote?
If anything, mosaic dominance sounds like a synonym of codominance and not a synonym of incomplete dominance.
Codominance vs incomplete dominance
Outside the above issue, I think you pretty much define these two terms through your examples. You might want to have a look at the post (although it is a post who did not get much attention)

How is incomplete dominance different from codominance?

In short, codominance implies that the specific phenotypic effect of each allele is being visible in the heterozygote, while incomplete dominance implies that the heterozygote has a phenotype that is somewhat intermediate between the two homozygote phenotypes.

Well thank you very much for the answer. There is no direct quote on mosaicism but it is written like this-"incomplete (partial or mosaic) dominance is the phenomenon where none of the two contrasting alleles ir factors is dominant. "

But there is still one doubt does pink appears due to expression by single gene for pigmented flower, if yes how did that gene form? Or it is mixed effect of red and white colouring proteins as written above , if this is true then why it is not included in codominance


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If action potential is "all or nothing" then how are finely tuned signals sent from one neuron to another?
If the action potential is an "all or nothing" phenomenon, then how is one type of neurotransmitter secreted rather than another? Let's say, for example, if a neuron received an excitatory post synaptic potential that initiated a graded potential that initiated an action potential, what specific signaling cascade or mechanism would denote the release of one excitatory neurotransmitter (say nor-epinephrine) over another (say dopamine) ?

https://www.ncbi.nlm.nih.gov/books/NBK10818/

@JM97 That link is very misleading in the context of this question. See my answer.

how is one type of neurotransmitter secreted rather than another

Most neurons release a single major neurotransmitter. JM97 commented a link about cells releasing more than one, but that is talking about "extra" neurotransmitters are short peptides, different from the major neurotransmitters like glutamate, GABA, acetylcholine, dopamine, norepinephrine, etc - I think that link is very misleading in the context of your question. Those cells don't choose one or the other, they release their primary neurotransmitter plus the peptide.
However, there are lots of different neurons and lots of different TYPES of neurons, so some release one type of neurotransmitter, others release another. Typically this is denoted by refering to cells as "___ergic": GABAergic cells release GABA, glutamatergic cells release glutamate, etc. Those specific cell types express the proteins necessary to synthesize their neurotransmitters and transport them into synaptic vesicles, ready to release. The actual signalling cascade that results in vesicle release is pretty much the same across different neurons: the difference is in what is packaged into those synaptic vesicles.

if a neuron received an excitatory post synaptic potential that initiated a graded potential that initiated an action potential what specific signaling cascade or mechanism would denote the release of one excitatory neurotransmitter (say nor-epinephrine) over another (say dopamine) ?

Simple: if the action potential is fired by a noradrenergic cell, that cell will release norepinephrine on all of its targets. If the action potential is fired by a dopaminergic cell, that cell will release dopamine on all of its targets. They are different cells.
In contrast to outputs, which use a single primary neurotransmitter, individual cells can receive inputs from many types of neurotransmitter. So a dopaminergic cell could receive GABAergic inhibitory inputs and also receive glutamatergic excitatory inputs, but it will only release dopamine on its targets.
If you have a network, and you wanted that network to release more dopamine on average, you would increase the synaptic weights of the excitatory inputs to dopaminergic cells: that is, increase the amplitude of EPSPs in those cells (you could possibly also reduce the inhibition).
In the title of your question, you asked how "finely tuned signals" can be sent. Tuning of signals isn't just about which neurotransmitter is released, but rather which cells that neurotransmitter is released on to. Individual cells can both receive 1000s of inputs and send outputs to 1000s of other cells. The patterns of those connections and the patterns of active cells are what determine the "message" - this is called "encoding".


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Can you identify this climbing plant?
In my house there's a strange plant that I see growing for years now. I believe it is a climbing plant. Do you know how is this plant named? Is it poisonous?
Location: Greece
Altitude: 800m.

if you don't get answers here, this question would also be on topic on Gardening: https://gardening.stackexchange.com/

Do you have any idea what the flowers look like? A picture would be fantastic, but color, size and/or number of petals would also help a great deal.

we have this all over the place in france. it tends to wilt as the summer goes on, it has annoyingly hairy leaves which are a bit weird. red briony https://upload.wikimedia.org/wikipedia/commons/2/23/Bryonia_dioica_%282144983672%29.jpg they used to put it on the bandages of lepers, you know those who lose fingers and limbs to consumption.

Based on the fruits, leaves and tendrils, it looks quite like Bryonia dioica (which is toxic). It is almost certainly something from the same family (Cucurbitaceae, which often make such tendrils and usually have similar leaf shapes) and could even be the same genus, Bryonia, which is present in the Mediterranean region (there's even a cretica species). Based on images found on the internet, leaf shape seems variable (more or less indented).


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Definition of Cis-eqtl
I have simple question, do cis-eQTLs use the SNPs that are within 1 Mb from the gene's TSS on the same chromosome ?

Kind of.
What you describe is a cis-eQTL, but the exact distance (1Mb in each direction, 1Mb total, ...) and the definition of the location of the gene (TSS, transcript borders, ...) depend on whoever calculates a cis-eQTLs and are not universal.
The 'cis' part just means the SNP is somehow near the gene, there is no defined limit on the distance.


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Protein expression in K. lactis system
I am trying to express a protein in K. lactis Protein Expression Kit (E1000S - NEB) in the way that the protein is secreted into the medium. I know that I can get some protein but it is not active. As the protein is secreted into the medium, I am not sure if doing expression for 24 h at 30°Cis a good idea. I am wondering if there are people here with some experience in this protein expression kit and, if so, what are the conditions for protein expression that worked well for you? Did you use ammonium sulphate precipitation to purify the protein from the medium or some other method?


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Is it possible to separate either father or mother chromosomes from a sperm?
If we were to use a flow cytometry, can it separate either the father or mother chromosomes from a sperm?

Welcome to Biology.SE. I thought I understood the question but after our discussion in the comments under my answer, I see that I actually don't understand what you mean. Can you please expand your post to clarify your question? In the meantime, I am voting to close as unclear.

There are no "mother chromosomes" in a sperm since the sperm comes from the father.  If you mean the mother of the sperm donor, there are no "mother chromosomes" because each chromosome is in general a mix of DNA from the father and the mother.

@mgkrebbs but we have 46 chromosomes from both father and mother right?So the sperm should contain 46 chromosomes can you seperate the another 23 chromosomes from the sperm?

If we were to use a flow cytometry, can it separate either the father or mother chromosomes from a sperm?

A sperm is haploid. It contains either Y or X but not XY or XX.
Sperm sorting is the process of sorting sperm cells based on specific trait of interest. Whether the sperm is carrying a X or a Y chromosome is definitely of interest to many.
There are a number of methods for sperm sorting (see wiki > sperm sorting > methods), one of which is indeed flow cytometry. Flow cytometry is typically used to separate X bearing sperms form Y bearing sperms. You should typically have a look at Beltsfield Sperm Sexing Technology (Johson et al. 1999).

I'm actually asking can we seperate those xy or xx chromosome that carry genes?

I mean the autosomes from the father or mother chromosomes

I don't understand.... Do you mean whether we can separate sperms carrying the grandmother haplotype or the grandfather haplotype? Note that segregation and recombination make that gametes carry some mixture of the two grandparents haplotypes. (Here by grandparent, I refer to the parents of the male producing the sperm). Btw, is there any reason you talk about sperms and not ovules?

I asking is it possible to empty all the chromosomes genes from the father or mother from the sperm to have either father or mother chromosomes?

The expression chromosomes genes is unclear and suggest that you don't really understand what a gene. I am still a bit unsure of what you are asking but you can't tell what chromosome come from which grandparent (whether in a sperm cell, in an ovule or in a zygote), the main reason being that recombination shuffled them up together.

if we use flow cytometry can seperate the autosomes and the sex chromosomes of the father or mother from the sperm?

I am not sure what you call mother and father. I suppose it is what I call grandfather and grandmother, right? The answer (but I am not sure I understand what you're asking) is 'no' because it makes no sense due to recombination. Even if there was no recombination, you could not because the only eventual difference between maternally inherited and paternally inherited chromosomes are epigenetic modifications (which flow cytometry won't help you to distinguish).

You are repeating the same question over and over but I still don't get it! Try to write more than a one line question. Give some context and maybe I will be able to understand what you're trying to ask. I think your question makes no sense (but might be wrong) but I can't tell what is your misunderstanding as long as you limit your phrasing to a single one liner question.

Sorry you seem confused,I will ask one more time Can sperm sorting empty either all the father or mothers genes from a sample of sperm?

I will answer one more time then :) Assuming that by mother and father you are referring to the parents of the male who produced the sperm (but you still have not explained what you actually meant by mother and father), then the answer is 'no' 1) because, obviously, flow cytometry is not able to brake and recombine chromosomes to undo what recombination just did and 2) the only potential markers of whether a chromosome comes from the 'mother' or the 'father' is a few epigenetic differences that can't be detected via flow cytometry. I'm out repeating that now! Good luck Daniel!

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