text:
Why do we get sleeply after we eat?
After we have eaten, we feel cold and sleepy. I think it's because the maximum blood supply is transferred towards the digestive system so that digestion is done, and therefore the brain to does not get adequate blood supply. Am i right about this?
Also, why do they suggest to take a short walk after dinner especially?

Who are "they" advising naps after lunch and walks after dinner?

"...that's why we feel cold and sleepy too because the brain to does not get adequate blood supply." That's a very, very common myth, but it is a myth.

@Roland my grandmothers? Maybe the OP knows them ;-)

After we have eaten... the maximum blood supply is transferred towards the digestive system so that digestion is done, and therefore the brain to does not get adequate blood supply. Am I right about this?

This is a very, very common myth, but it is a myth. Because blood flow and oxygen delivery to the brain is critical for survival, cerebral circulation is one of the most tightly regulated systems in the body. Blood is not shunted from the brain to the gut for digestion.

In a normal physiological state, total blood flow to the brain is remarkably constant due in part to the prominent contribution of large arteries to vascular resistance.

Eating, sleeping, walking, etc. are all normal physiological states. If we had blood shunted away from our brains after eating, we'd literally collapse after every meal.

In normotensive adults, cerebral blood flow is maintained at ~50 mL per 100 g of brain tissue per minute, provided CPP is in the range of ~60 to 160 mmHg.

As eating alone doesn't normally cause our blood pressure to rise or fall, cerebral perfusion is constant regardless of what is or isn't in our digestive systems.
Blood flow to the gastrointestinal system (or GI tract) is also regulated, but the flow varies widely:

Estimates of blood flow (in ml /min × 100 g) to the quiescent gastrointestinal tract of dogs and cats range from 15 to 100 for the stomach, 35–120 for the small intestine, and 10–74 for the colon. Somewhat lower values for resting blood flow to the stomach, small intestine, and colon have been reported for man.

So, the basic answer is that, yes, blood flow to the gastrointestinal tract varies, but blood is not shunted from the brain in favor of the GI tract.
So why do we get sleepy after a meal?
Sleepiness after a meal is caused by the level of peptides in your brain called orexins (aka hypocretins).
In 1998, two groups of researchers simultaneously discovered 2 small neuropeptide hormones that regulate, among other things, wakefulness and feeding behavior.
One group discovered them while searching for molecules that could bind to "orphan" receptors, that is, a brain receptor with an unknown "binding" molecule (called a ligand). They found that the prohormone prepro-orexin was found in a very small area of the hypothalamus which had been implicated in the regulation of feeding behavior and energy homeostasis; this suggested the possibility that the neuropeptides might be involved in the regulation of food intake. When administered into free-feeding rats' brains, one of these peptides (orexin A/hypocretin 1) stimulated food consumption in a dose-dependent manner (with attention to light and dark periods, i.e. the circadian rhythm), with a lower dose increasing rat feeding about 2-fold, and the higher dose inducing a 3+-fold increase in feeding compared to rats injected with a solution without the peptide (the other stimulated feeding to a lesser degree). The effect persisted for 4 hours. Furthermore, fasting rats produced more than twice as much orexins as rats feeding freely. For this reason, the molecules were names "orexins", after the Greek word orexis, which means "appetite". They speculated that the orexin-secreting neurons might somehow be modulated by glucose.
At the same time, another group of researchers using a completely different approach found that the same group of hypothalamic neurons were stimulated by a peptide hormone similar in composition to the gut hormone secretin. They identified the same prohormone and its two peptides, naming them hypocretins for "hypothalamus" and "secretin". They found that at least one of the peptides had a neuroexcitatory activity in specific areas of the brain (they mapped effects in the hypothalamic neurons, the posterior hypothalamus, the septal nuclei in the basal forebrain, the preoptic area, the paraventricular nucleus of the thalamus, the central gray, the locus coeruleus, the colliculi, the laterodorsal tegmental nucleus, and the nucleus of the solitary tract) suggesting that the peptides acted within the central nervous system as homeostatic regulators with a role in nutritional homeostasis.
Scientists have not decided on whether to call them orexins or hypocretins yet, so both are used. They are found in all vertebrates.

Mammalian orexin A sequences thus far identified (human, rat, mouse, pig, dog, sheep, and cow) are all identical, whereas the sequences of orexin B show some differences among species. From Orexin/Hypocretin: A Neuropeptide at the Interface of Sleep, Energy Homeostasis, and Reward System, Natsuko Tsujino and Takeshi Sakurai
In 1999, a group of scientists found that narcolepsy (a sleep disorder characterized by extreme daytime sleepiness) was caused by a lack of a hypocretin/orexin receptor 2 gene in certain dogs, therefore establishing that they play a very important part in the regulation of wakefulness.*
Since then, an enormous body of work has shown that orexins/hypocretins (O/H from here on in) are involved in the regulation of a wide range of behaviors, including wakefulness and vigilance (needed to find food), systems that regulate emotion and reward (including drug-seeking behavior when stressed and eating for pleasure - "consumption beyond homeostatic needs" - leading to obesity), and more.
What does eating have to do with sleepiness?
Several studies report that the firing rates of O/H neurons are influenced by serum glucose, triglycerides and amino acids.
In English: You are awake (O/H is being secreted by O/H neurons in your hypothalamus). You eat. Your serum glucose rises. The elevated glucose causes depolarization of inhibitory neurons that hyperpolarize O/H neurons decreasing the amount of O/H. released. Result: wakefulness decreases.
Control of Cerebral Blood Flow
The Gastrointestinal Circulation.
Comparing these two papers - the first and second references - is a wonderful example of the completely different methods used by scientists to investigate unknowns and up with the same basic conclusion.
Orexins and orexin receptors: a family of hypothalamic neuropeptides and G protein-coupled receptors that regulate feeding behavior, Cell 92 (4): 573–85
The hypocretins: Hypothalamus-specific peptides with neuroexcitatory activity Proc. Natl. Acad. Sci. U.S.A. 95 (1): 322–7
The Sleep Disorder Canine Narcolepsy Is Caused by a Mutation in the Hypocretin (Orexin) Receptor 2 Gene
The role of orexin in motivated behaviours A Nature Neuroscience Review
The role of orexin-A in food motivation, reward-based feeding behavior and food-induced neuronal activation in rats
*Human narcolepsy - caused by a destruction of O/H neurons - also is associated with metabolic abnormalities, including increased frequency of non-insulin-dependent diabetes mellitus and increased body mass index.
Hypothalamic Orexin Neurons Regulate Arousal According to Energy Balance in Mice
Orexin/Hypocretin: A Neuropeptide at the Interface of Sleep, Energy Homeostasis, and Reward System

A plus one seems so insufficient. Where did you find the time for this answer?

@AMR - That is so kind of you! :) Actually, I wrote most of this answer for another SE site. The myth of blood being diverted from the brain after eating is so prevalent, and the reality so much more interesting that I really like sharing about it.

What would be interesting (to me at least) whether napping after meal is beneficial for digestion etc.


text:
Do mutant alleles result from mutation of the wild type?
The allele that encodes for the most common form of a phenotype in natural population is called a wild type allele and all the rest of the alleles encoding forms other than the wild type are called mutant alleles. Do they result from mutations of the wild type allele?

Hey there, is there any particular reason you keep reverting the changes to the question's tags?

Please stop reverting edits. These are edits that experienced users in the community deem are relevant and appropriate. The question and the answers provided fit the tags that have been added. Tags are used to identify a question and make it easier for others to find when searching. It also drives how the question is indexed on Google, so there are specific reasons that they are added beyond the interest you have in the question.

Please review the Help Center on How do I ask a a good question, especially the section on Make it relevant to others and Keep an open mind.

The determination of whether an allele is wild-type or mutant has to do with the frequency that it is observed within a population.
In genetics, a wild-type allele can be defined as

an allele, or DNA variant, whose frequency is more than 1% in a population.
an allele that dictates the most frequently observed phenotype in a population.

Genetics; From Genes to Genomes, Fifth Edition, Hartwell, et. al.
A mutant allele is then defined as

an allele, or DNA variant, whose frequency is less than 1% in a population.
an allele that dictates a phenotype seen only rarely in a population.

Genetics; From Genes to Genomes, Fifth Edition, Hartwell, et. al.
So mutant in this respect only means that the phenotype is seen less frequently in the population.
There is a sequence difference in the alleles, which leads to a phenotypic difference, but if the mutant allele provides an evolutionary advantage that ends up being selected form then it will eventually become the most representative allele in the population and will then be the wild-type.

No, not necessarily!
The terms might be confusing I agree. The most common allele (the wild type allele) might be a mutant of one other type of allele (one mutant allele) present in the population.
The reason we call the least common alleles the mutant alleles is that beneficial mutations are rare compared to neutral or deleterious mutations. If at a given locus most mutations are deleterious, then the mutant alleles will never reach a high frequency. However, if at a given locus a beneficial mutation occurs, then this beneficial mutation will likely rise quick quickly in frequency and therefore there is only a limited time frame under which the most common allele is actually a mutant of a least common allele. In consequence, we tend to call the least common alleles "mutant alleles". This name is often a good fit to the reality but not necessarily.
Note by the way that there are other sorts of selection regime occurring at a given locus that may maintain polymorphism at relatively high heterozygosity such as any form of balancing selection.

source: Stack Exchange

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

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
Do snRNAs exit the nucleus or not?
In Molecular Biology of The Cell (Alberts, et al., 2015), it lists the various RNAs that are trafficked through the Nuclear Pore Complex (NPC) into the cytoplasm.
The list includes snRNAs, but I have seen it stated elsewhere that snRNAs don't leave the nucleus, that they are made there and perform their function there.
Is MBOC's version correct and snRNAs leave the nucleus, or are the other sources correct and the snRNAs are made, remain, and function in the nucleus?

After transcription of some UsnRNAs, the RNAs leave nuclei first. After assembly of various proteins and modification on the RNAs in cytosol, the RNAs come back to nuclei. In addition, it has been shown that mature U6snRNP shuttles between nuclear and cytosolic fractions in yeasts, if I remember correctly.
http://openi.nlm.nih.gov/detailedresult.php?img=2582628_gkn658f1&req=4

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


text:
Can we artificially increase human growth using HGH?
Robert Pershing Wadlow was a man who lived in the first half of the twentieth century. He had hyperplasia of his pituitary gland, which caused him over-produce human growth hormone (HGH), and as a result, he grew to nearly 9 feet (2.75m). He had difficulty managing his body size and died at age 22, with no sign that this growth was slowing down.
HGH can be used for medicinal purposes, and it seems that doctors prescribe it for conditions like chronic underdevelopment and HGH deficiencies.
Putting aside ethical or government regulation issues, is it theoretically possible for someone (like a "fully grown" adult) to artificially grow beyond their genetic potential by providing them with regular doses of HGH? If not, what was different about Wadlow's case?

Do you mean grow someone from scratch ( :-) ) or just substantially increase their growth?

@HDE226868 lol... Increase their growth (or generally prevent them from ceasing to grow).

You have to note that Robert died at a young age. Usually when the puberty hits and androgens are being produced at appropriate levels the growth plates of the bones would fuse and the person would cease growing.

@CRags That's true, but he was well past puberty, and bone plates usually fuse around 20 (if I'm not mistaken). It could be that if Robert had lived a few years more, he would have slowed down, but unfortunately there's nothing to suggest either way.

It varies but growing at 22 years is not unheard of.

If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.

It's very slippery question. Because some doctors give a prescription for HGH when you genetically have not enough of this hormone. So Wadlow's case was something unique. Otherwise, it's always better to go for diagnoses it in clinic and read an article like thisabout HGH deficiency testing.

You asked

... is it theoretically possible for someone (like a "fully grown" adult) to artificially grow beyond their genetic potential by providing them with regular doses of HGH?

For an adult, the answer is no. Human growth means skeletal lateral growth, which is indeed mediated by human growth hormone. But during normal human development bones ossify in the process, and in human adults the bones are completely ossified and can't grow in length anymore.
From the cancer.gov site on Bone development and growth:

When cartilage growth ceases, usually in the early twenties, the epiphyseal plate completely ossifies so that only a thin epiphyseal line remains and the bones can no longer grow in length

Further reading: NEJM Osteogenesis: The Development of Bones
This point is usually reached around the early twenties in humans. The case mentioned in your question is different because in this case, the human growth hormone was "given" before this process had finished and thus the bones grew longer. He was 22 when he died, so we will never know if he would have finished growing in his mid- to late twenties.
Giving adults (that don't suffer from an HGH deficit) more human growth hormone has been done and does not result in lateral growth, but it does result in increase in lean body mass in both young adults and the elderly


text:
Why are some human injections intraperitoneal?
In humans, what benefit do intraperitoneal (IP) injections(old/cheap rabies vaccines, or cancer related injections) offer versus traditional intramuscular injections?
For example, where I live, the rabies are not administered right away after a bite because of the associated discomfort(cheap IP injections) or cost(newer intramuscular injections) they represent versus the low probability of a dog having rabies and the long incubation period(instead, the offending dog is observed carefully for 10 days to decide, or the vaccines are administered in the fourth day if not found). So, since speed of action doesn't seem to be an important factor, what are the benefits of IP injections?

Likely has to do with how the injection will drain into the lymphatic system. http://cancerres.aacrjournals.org/content/24/10/1700.full.pdf and  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2515477/

@AMR Interesting, mainly because in the cancer case, it seems that the main purpose seems to be that the fluid flows through the same channel as tumoral agents.

Remember that the adaptive immune system resides in the lymph, waiting to be activated... Though the rabies vaccine has been around longer than we have known about the intricacies of the lymphatic immunity. Pasteur invented the Rabies vaccine around 1885 and the lymph system role wasn't elucidated until many decades later. https://en.wikipedia.org/wiki/Timeline_of_immunology Maybe they just got lucky, they saw it worked, and well "if it ain't broke, don't fix it."

This might have some answers to your question. http://www.ncbi.nlm.nih.gov/pubmed/20156151

@chubakueno we almost never give anything intraperitoneal in humans (I've never given an i.p. injection to a human) - this is done for rodents, dogs and other smaller animals. I see the article above from AMR - though that is for intraperitoneal chemotherapy which is given through a special surgically placed catheter (not injected) - what injection are you talking about specifically that you think is i.p.?

@AMR Thanks for the links, they explain why IP injections are given for cáncer or peritonitis very well. Alas, I don't have Access tu PubMed articles, but thanks anyways.

@VanceLAlbaugh Rabies vaccines are the only ones that remain to be explained. In fact, I was asking this question because I was bitten by an street dog recently so I went through the process, and the public center for rabies gave IP injections(and some older people also talked to me about those). I got treated by a private clinic with IM ones, but IP ones took my attention.

IP injections are used for a variety of reasons:

The peritoneum provides a large surface area for absorption of drug (compared with intramuscular (IM) or subcutaneous); can thus inject a larger fluid volume.

Easier to inject that intravenous.

For some chemotherapy, such as ovarian cancer, IP injection is used to attempt to localize the drug near the tumor (it's through a catheter, rather than with a syringe and needle).  Essentially the goal is to provide chemotherapy to the abdominal region where cancer has spread rather than systemically.

 It is commonly done in animals, such as mice, because it is difficult to find a vein in small creatures.

https://en.wikipedia.org/wiki/Intraperitoneal_injection
http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-treating-chemotherapy
http://www.ncbi.nlm.nih.gov/pubmed/20156151 courtesy of @AMR
http://cpharm.vetmed.vt.edu/VM8314/Administration.htm

Nice answer +1. An additional point is that s.c. and i.m. only allow for small volumes to be injected, even in large animalia like humans. Plus, i.v. may result in a surge of drug in the body. I.p. allows for injection of large volumes, even in small animals, with a slowly-sloping absorption curve which may, or may not, be beneficial.

The reason IP injections are common in mice is not for lack of veins, it's for convenience' sake. The tail vein, for example, is fine for injections, but it's so narrow that injections need to be in very small volumes and at very low rates to avoid blowing out the vein. The vein also needs to be expanded by bathing the animal in a heat lamp while restrained, all of which takes time and equipment, and is stressful for the animal. IP injections are easy: scruff, tip, inject, pull out, back in cage.

@MattDMo Completely agree, IP is much easier and less stressful on animal and researcher!

@chubakueno it is important to realize that in humans we do not give routine injections intraperitonally - that only happens in animals. In fact, we intentionally do not insert needles into the peritoneal cavity for fear of potentially damaging intra-abdominal structures. However, if a patient has a peritoneal dialysis catheter or other intraperitonal access, we will administer things like antibiotics for a peritoneal infection or chemotherapy- but this is not for routine administration.


text:
Why is the swelling of bread when placed in water not considered to be caused by osmosis?
Why is bread swelling up when placed in water not considered to be caused by osmosis?
Is there a property of water that should make it leave the bread instead of enter?

I'm not sure what your last sentence means. The bread is absorbing the water.

Osmosis refers specifically to the diffusion of water across a semi-permeable membrane.

The phenomena that you are describing, where bread, which is a porous material, similar to a sponge, absorbs water, is the absorption of water by capillary action.
As @Joel mentioned, osmosis is specifically the flow of a fluid across a semipermeable membrane, such as the plasma membrane of a cell or dialysis tubing, that occurs in such a way as to cause a flow from an area of low concentration to an area of high concentration. This flow eventually leads to a state of equilibrium when the concentration on both sides of the membrane is the same.
The wikipedia article on Osmosis gives this definition:

Osmosis is the spontaneous net movement of solvent molecules through a semi-permeable membrane into a region of higher solute concentration, in the direction that tends to equalize the solute concentrations on the two sides. It may also be used to describe a physical process in which any solvent moves across a semipermeable membrane (permeable to the solvent, but not the solute) separating two solutions of different concentrations. Osmosis can be made to do work.
- Wikipedia: Osmosis

- By OpenStax College [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons
The bread is not selectively permeable, and it will continue to absorb liquid until it is fully saturated. This isn't actually an equilibrium, because additional water would do nothing to change the concentration on one side of the bread or the other. If you added more water to one side of a semipermeable membrane in equilibrium, by Le Chatelier's principle, you are will force the reaction (in this case, you change the concentration) to one side, then the liquid would again flow from the area of low concentration to the area of high concentration.
Capillary action is the result of water flowing into the small spaces, such as the air bubble that form in bread when it bakes, in the absence of a force "pushing" it into those spaces, or against the force of gravity. The liquid accomplishes this through intermolecular forces that cause adhesion of the molecule to the surface of the material that is absorbing it and cohesion of the molecules in the liquid keep them associated to one another, and as the liquid moves into the spaces, it is able to pull the other liquid molecules along into the space.


text:
About acetyl-coA in the Krebs Cycle of respiration
In respiration, Krebs cycle starts with acetyl coenzyme A which is made from pyruvate.
However, it is said that the cycle keeps repeat it self with oxaloacetate turning back to citrate and cycle starts again, so why is acetyl coenzyme A constantly supplied to the cycle?
According to that logic, shouldn't there be no need for acetyl-coA after the first round?

Pyruvate transfers an acetyl group to coenzyme A.
The acetyl group from acetyl co-A is the molecule that provides the 2 carbon atoms that get added to oxaloacetate to form citrate, and as you said, citrate starts the cycle over again.
Without coenzyme A, pyruvate cannot transfer the acetyl group to oxaloacetate to form citrate so without coenzyme A/acetyl co-A, the process would stop.
This is a slightly busy version of the diagram, but it does let you see how molecules in the cycle are formed and where carrier molecules interact with the molecules in the cycle.

- By Narayanese, WikiUserPedia, YassineMrabet, TotoBaggins [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons


text:
Why is binding energy the difference between ∆G catalyzed and ∆G uncatalyzed?
I think the title explains it pretty well -- I'm confused on what 1) exactly binding energy is 2) and why it's the difference. Like in this diagram:
my teacher sort of said it was the energy the enzyme uses to make interactions to the substrate, but that doesn't really click for me.

A catalyst does not change the free energy i.e. ∆G of the net reaction. It only changes the activation energy. The catalysed reaction can be expressed as a series of many reactions and the overall ∆G can be expressed as a sum of that of the individual reactions.

yeah I know that. where was binding energy in your explanation?

binding can be considered one of the reactions (binding-unbinding reversible reaction). So totally there would be two reactions 1. binding and 2. conversion

There's two binding energies in your diagram, and it's the difference between them that's the critical point in understanding enzyme catalysis and the difference between $\Delta G$ catalyzed and $\Delta G$ uncatalyzed?
$\Delta G^R_{bind}$ is the binding energy of the enzyme-substrate complex. That is, it's the difference between the energy of the apo-enzyme and substrate in the non-bound form ("$E+S$") and the enzyme and substrate in the bound form ("$ES$").
The other binding energy is $\Delta G^T_{bind}$. This is the (theoretical) binding energy of the transition state. That is, it's the energy difference between the enzyme-transition state complex (here labeled "$T_{uncat}$", for some reason; it probably should be "$ET_{cat}$") and the apo-enzyme and the unbound transition state ("$E+T_{uncat}$").
Now remember that free energy is a state function. A free energy change ($\Delta G$) is simply the difference between the free energies of the starting state and the ending state - it doesn't depend on the path you take to get there. (The absolute free energies of any given state are unmeasurable, but you can infer information about relative free energies by measuring the $\Delta G$ of transitions between them.)
The two equations at the bottom are derivable from this definition of free energies as a state function. You know that the free energy difference between the $ES$ and the $E+T_{uncat}$ state is the same regardless of the path you take. So if you go first through $ES$ the free energy change ( $- \Delta G_{bind}^R  + \Delta G_{uncat}^\ddagger$) will be equal to that if you go through "$T_{uncat}$" ($\Delta G_{cat}^\ddagger - \Delta G_{bind}^T$) - you don't necessarily need to have physically realizable reactions for the state function property to hold. The second equation is then simply a rearrangement of the first.
In looking at the rate of catalysis, you're primarily interested in how big a free energy change it is to the relevant transition state from the previous state. (This is a basic principle of Transition State Theory.) To speed things up, the enzyme needs to make that energy change smaller - that is, to make $\Delta G_{cat}^\ddagger$ smaller than $\Delta G_{uncat}^\ddagger$. If the enzyme binds the substrate and the transition state equally well, $\Delta G_{bind}^R$ and $\Delta G_{bind}^T$ are the same, and $ES$ and "$T_{uncat}$" are lowered by the same amount, such that $\Delta G_{cat}^\ddagger$ and $\Delta G_{uncat}^\ddagger$ are equal: no catalysis.
But if instead $\Delta G_{bind}^T$ is greater than $\Delta G_{bind}^R$, then the "$T_{uncat}$" state is lowered more than the $ES$ state, making the gap between them ($\Delta G_{cat}^\ddagger$) smaller than the gap between $E+S$ and $E+T_{uncat}$ ($\Delta G_{uncat}^\ddagger$): the enzyme thus speeds up the reaction. This is what that second equation is saying.
This sort of thermodynamic analysis is what leads to the "transition state stabilization" hypothesis of how enzymes work: enzymes speed up reactions because they bind to the transition state more tightly than the substrates or the products.
(P.S. You may be wondering why we have the enzyme hanging around in the uncatalyzed reactions. This is simply a bookkeeping measure to make sure we're using the same reference state for the very start of the reaction ($E+S$). In the uncatalyzed reaction the enzyme doesn't change, and so doesn't really contribute to any free energy change.)


text:
What is known about the coding sequence of Factor H in the human genome?
Factor H is a protein coded in 20 domains.
My question is whether these domains form some kind of repeat cluster in the human genome. Basically, I'm interested in the coding sequence from an assembly point of view: Is the coding region fully resolved? Apparently there is only one copy of the gene per haplotype, but are coding domains maybe similar to each other or repetitive in themselves?

As clearly stated in the WP article:

The molecule is made up of 20 complement control protein (CCP) modules (also referred to as Short Consensus Repeats or sushi domains) connected to one another by short linkers (of between three and eight amino acid residues) and arranged in an extended head to tail fashion.

So in your terminology yes, it is a repeat cluster. Each of those 20 domains will be similar to the others, although not identical.

The ensembl entry, which was easy to get to from the Wikipeda page, shows that the protein is one gene with 20 domains
http://uswest.ensembl.org/Homo_sapiens/Transcript/ProteinSummary?db=core;g=ENSG00000000971;r=1:196651878-196747504;t=ENST00000367429

I don't see how this answer adds anything to what I already mention in the question. The question is whether those domains form a repeat cluster in the genome and whether the full sequence has been resolved in the human genome.

@BlindKungFuMaster your question said "a molecule made up of 20 proteins"; the answer says "one gene with 20 domains". Those are enormously different things.  If Factor H is a single protein and not 20 proteins, then obviously it forms a cluster (called a gene).  What makes you think it is formed by 20 proteins (a claim that isn't substantiated by your wikipedia link)?

The key word in my question is "repeat". Yes, it is one big protein and yes its domains are clustered. If you read my question carefully, you'll see that I mention that it is coded by a single gene. My question is whether these coding domains are "similar to each other or repetitive in themselves". Whether you'll call the parts proteins or not is not substantial to the question, but I'll change it just in case.


text:
Through which mechanisms did the Drosophila Histone Cluster evolve?
The Drosophila Histone Cluster is a gene cluster that contains more than a hundred copies of a sequence that encodes several histone proteins. These copies are very similar.
My question is what mechanism are known that could have played a role in the genesis of this cluster?
I'm aware of the possibility of recombination, which might expand the cluster on one chromosome, shortening it on the other. Are there any other mechanisms to expand or change the cluster and are there telltale signs left by these mechanisms in the genome sequence?
Given that in most species histone genes aren't clustered, it would be weird to assume that recombination is the only mechanism to duplicate these sequences. Also, at one end of the cluster bits and pieces of histone genes are mixed with other sequences, a bit like all the broken copies got pushed to one end. It would be interesting to have an explanation for this pattern.

Isn't this explained via gene duplication events? Or am I misunderstanding the question?https://en.wikipedia.org/wiki/Gene_cluster#Gene_duplication_and_divergence

Yes, but there are different gene duplication events. I already mentioned recombination. Is retrotransposition a possibility for histones? Can replications slippage account for 5000bp duplication? Or what is the max length for replication slippage? Is recombination the only mechanism that results in back to back copies?

It's an interesting question, though I don't think your claim that histone genes aren't clustered in most organisms is correct. On the contrary, both yeast and humans also have histone clusters. Given the evolutionary distance between these species, it would seem reasonable to expect that this phenomenon is quite ubiquitous.

This is the best review I have seen with a comprehensive discussion on gene duplication and amplification mechanisms (and it is also quite recent). It seems like there may be no definitive answers to your question in the literature--perhaps because of a paucity of viable experimental models that would allow one to test various hypotheses.
Also @canadianer is quite correct. Most metazoans with sequenced genomes have some kind of clustering of their histone genes (as well as multiple copies). In Drosophila embryogenesis the early zygotic cell-cycles are extraordinarily brief, on the order of 20 min as I recall, which means the fertilized egg is essentially a bag of DNA polymerase replication complexes.  Therefore there is a very high demand for histone proteins.  The gene amplification you describe is one way to achieve high concentrations of histones in a short time-frame.
Note that not all metazoans undergo this rapid burst of synchronous nuclear division, and therefore not all species have such a high copy number of core histone clusters.

Thank you, that is an interesting tidbit and what looks like a nice overview.  I upvoted so you should get the bounty if nobody else comes along, even if I forget to accept the answer. But I'll probably do that later today anyway.


text:
What is the length of the centromeric repeat sequence in a human?
I'm looking for the lengths of the centromeres of human chromosomes.
The best I could come up with so far has been: The length of individual centromeric arrays was found to range from an average of 680 kilobases for the Y chromosome to 3000 kb for chromosome 11.
Here they say that "Human centromeres are located at repetitive alpha satellite DNA arrays that compose approximately 5% of the genome." Which unfortunately is not the same as saying the centromeres compose 5% of the genome. (Or maybe it is? Biologists to the rescue!)
Ideally an answer would contain the length of the centromere in each chromosome, but a precise percentage for the whole human genome would be good enough.

No specific length for centromeres. Actually in a real chromosome in a cell, centromeres are usually very condensed sequences of DNA, they are winded and folded (if you know about the DNA structure). Thus you cannot measure the length of the centromere unless you decondense the chromosome first.

My question is about the length in base pairs. My understanding is that you can sequence centromeres, you just cannot assemble them. But the sequencing reads might be enough to give an estimate of the total base count.

@BlindKungFuMaster There's not much genes in centromere region. So it is hard to design a RNA primer for sequencing. Sequencing cannot be done on the entire DNA molecule due to the the vulnerability in the structure of macromolecules. By the way, why does total base count matters? What triggered this question? And what do you mean "cannot assemble them"?

My question is in the context of whole genome assembly. I wanted to know how much of the human genome cannot be reconstructed, when treated as a DeNovo Assembly. The centromeric region is a big chunk of the unassembled regions in the human genome, I just wondered how big.

There is no fixed length of human centromeres.
As the paper you cited says in its introduction, there are array-length polymorphisms in centromeres. A polymorphism can be described as two or more forms of the same DNA sequence existing; which one you have depends mostly on which one you inherited from your parents. There are also polymorphisms that are created by imprecise DNA duplication during meiosis. Array-length polymorphisms can be explained by the latter.
As the DNA in centromeres is highly repetetive, it can happen that during replication, the number of repeats is decreased or increased. This leads to many different copy numbers in different individuals. Therefore, your answer cannot be answered with a specific number.

I would settle for an average number, a range, or the specific number of a specific individual.


text:
What is the length and number of the parts of a conformational epitope?
I am interested in the question whether exposure to protein A might create antibodies that also bind to protein B.
I am wondering whether, if the antigen of protein A is a conformational epitope, it would still be possible to predict (or at least guess at) the reaction against protein B with only a sequence comparison.
This might be possible if the subunits are long enough and if there are enough of them, which is why I ask about their length and number.

You seem to be using the word "subunit" in a manner that conflicts with that used with respect to protein structure. Do you mean short stretches of primary structure that contribute to the epitope?

Yes, I guess that's what I mean. I took that term from the definition of conformational epitope at wikipedia: "A conformational epitope is a sequence of sub-units (usually amino acids) composing an antigen that come in direct contact with a receptor of the immune system."

I found this paper that analyzes 111 antigen-antibody x-ray crystal structures.
They find that in their dataset that "the large majority of Ag structures (86.5%) have CRS ranging from 20 to 229 aa." CRS stands for contact regions span which they define as "the minimum contiguous amino acid sequence containing all CRs of an Ag or Ab and represents the size of a complete structural epitope or paratope, inclusive of CR and the minimum set of supporting residues required for proper conformation." further on they mention that "The average and median CRS of all 111 Ag structures is 125 and 95 aa, respectively." and "the majority of the structures do indeed have epitope CRs that are clustered together in short, contiguous stretches ranging from 2 to 12 aa, longest contiguous sequence of CR being 5"
I hope this helps.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
PCR that worked previously is now only showing primer dimers and a smear on gel
PCR amplification of a promoter sequence for gel extraction worked beautifully using Phusion HF enzyme with GC (higher error but less picky) buffer. However, DNA concentration from the gel extraction was too low, so I need to do it again. Now with all the reaction parameters the same it is not working. So far I am using the same Phusion enzyme stock and buffers, the same primers which worked before, the same proportions, and the same thermo-cylcer set up. I have extracted fresh genomic DNA to amplify from thinking maybe the DNA had degraded with no luck. I make a mastermix fresh before each reaction by combining the Phusion enzyme, nuclease free water, dNTPs from a 10mM stock, and the GC buffer mix. Any ideas would be appreciated.

Did you scale up the reaction to get more yield?

Yes, I have gone up to 50ul reactions and load 20ul samples onto the gel each time for the gel extraction.

Don't do that. You change the characteristics of the reaction - bigger volumes heat up and cool down slower. Instead of doubling the reaction volume, rather do two reactions. This usually works better.

When I scaled up I did use thermo fishers tool to recalculate the proportions for the mastermix.  I will keep this in mind when trouble shooting in the future though. Thanks

Have a look at this answer here at bio.se. That's what I have in mind.

You can try performing the reaction again using the purified promoter sequence from the first amplification as template. With the low error rate of polymerases like Phusion, the chance of an error occurring for a ~1kb amplification is low enough to not be a significant issue.


text:
Why do tattoos persist if body cells are regularly renewed?
I am not quite sure if it is true, but I read somewhere that within 7 years all the body's cells are replaced with new ones. I am not quite sure if it is cells or atoms.
If it is then why do tattoos persist for so long? If the cells which were impregnated with the dye have been replaced, then why do the tattoos still remain?

That's not true - some cells turn over quite quickly, others take months or years, others never replicate.

It's a damn pity that that's not how it works, wouldn't have minded getting a tattoo if I knew it would fade in 5 years time and have disappeared entirely in another 10.

Smarter Every Day explained this quite well on their YouTube channel.

First, tattoo pigment isn't injected into cells. If you were to puncture a cell with something the size of a tattoo needle, it would die - full stop. Many cells are destroyed in the process though, mostly by tearing, which initiates the wound healing process.
So what actually happens is the particles lodge in between the cells of the dermis (the layer below the epidermis, or outer layer of skin) and new cells crowd around it as damaged cells are replaced.
Since the particles in good tattoo ink are too big to be carried off by macrophages, they just sit there. That doesn't stop them from trying, though. Macrophages take up the pigment but are unable to escape with their garbage. Fibroblasts envelope the particles, both intracellularly and within the extracellular matrix they generate. At the end of a fibroblast's life, its contents are taken up by the same process - still too big to remove.
Smaller particles will be carried off by macrophages capable of both consuming the particles and migrating into the lyphatic system, which is why some ink fades more than other kinds. Ink composed of fine particles would be expected to fade severely. New tattoos are also sharper because some of the ink that was injected is lodged in the epidermis, which is the layer that grows out and is shed over time.
In this biopsy of a tattooed mouse, you can see how the epidermis has carried some of the pigment out of the skin while much of the dermal layer's pigment has been either removed lymphatically or enveloped:

Source: Tattooing of skin results in transportation and light-induced decomposition of tattoo pigments--a first quantification in vivo using a mouse model.
Thus, over time the pigment will be moved around a bit by this cellular activity, in fact deeper into the dermal layer on the whole.
The intent of using laser light to remove tattoos is to break those particles down into smaller pieces burst any cells containing them - again initiating the wound healing process. However, unlike in previous cases, when macrophages reach the site they can now sweep the remaining particles away to the lymph nodes.

Sources

General - Tattoos and tattooing. Part II: Gross pathology, histopathology, medical complications, and applications.
Process - Cutaneous Wound Healing

Secondary sources:

Fate of tattoo pigments in skin (pdf)
How Laser Tattoo Removal Works - Smarter Every Day

It would be great if you could add citations because this does not sound quite intuitive. For instance, when you mention particle size and clearance from dermis has a connection, then add a reference for that. Also, you should add some reference for the particle size distribution of the tattoo ink. Most tattoo pigments are composed of metal salts, there is also a possibility of leaching (I am not sure how it does not happen. There are some reports on diffusion of tattoo pigment though)

Additionally, it is very strange to phrase the sentence "puncture a cell with a tattoo needle" when the tattoo needle's tip is hundreds of times larger than a cell.

Destin produced a quite nice video that could be used as a reference for this answer. https://www.youtube.com/watch?v=D0B7F5UbTOQ

-1 See my comment to March Ho's answer: the majority of the ink seems to be intracellular, albeit after a certain time. In any case, all the articles that I've read say there is no ink in the epidermis.

@WYSIWYG Metal salt leaching would be interesting, but I think some of those issues might be better answered in a separate question. Some of that information is available in the sources I have added.

@MarchHo Some people aren't familiar with the relative sizes of cells and needles, so I thought that would be important to mention.

Contrary to the other answer posted, this paper shows via microscope images that the tattoo ink is in fact absorbed into cells, and forms small intracellular round granules.

Electron microscopy of untreated tattoos revealed membrane-bound
  pigment granules, predominantly within fibroblasts and macrophages,
  and occasionally in mast cells. These granules contained pigment
  particles.

Images a, c and e are images of toluidine blue stained cells, while images b, d and f are images of unstained cells showing the tattoo pigments.
Images a and b are prior to the laser treatment, c and d directly after the treatment, and e and f 90 days post treatment with the laser.
The reason why the tattoo marks persist is not because the pigments are deposited extracellularly, but that they are deposited intracellularly.
The pigments form intracellular granules that are not broken down, and therefore in the absence of external forces such as a laser, the pigments will remain there for long periods of time.
This paper (thanks to biozic) also describes the tattoo ink being persistently found intracellularly instead of extracellularly.

Biopsies obtained from tattoos 1, 2, 3, and 40 years old differed only
  in the types of ink used. All the ink particles were found to be
  located in dermal cells. The epidermis was completely devoid of
  pigment particles. The basement membrane was continuous at the
  epidermal-dermal junction. Ink particles were found throughout the
  upper dermis but all were within the boundary of a cell membrane.

According to this TED video (which unfortunately does not state its primary sources), the fibroblasts that contain these engulfed ink particles are themselves taken up by newer fibroblasts when they die, therefore the ink particles remain in the dermis and are not removed by cellular renewal.

Several other articles confirm that the majority of ink particle are intracellular (mainly in fibroblasts and macrophage) after the skin healing process is done [http://dx.doi.org/10.1111/j.1365-4362.1987.tb00590.x]. But, according to these articles, pigments are not deposited into cells: they end up there after a complex and time-consuming process.

@biozic Can you point out where in the article does it say that pigments are not deposited into cells? The 24 hour post tattoo result clearly describes intracellular tattoo ink deposits.

Do these cells persist for a long time? Mast cells release their granules when stimulated and macrophages are chemotactic (can move around). Only fibroblasts seem static but even they can undergo apoptosis. So as the OP asked, what would happen when these cells die/move and are replaced by new cells?

@WYSIWYG See the video citation. I was unable to find a better primary source.

@MarchHo What I wanted to say is that ink particles aren't specifically deposited into cells. According to the article, when they looked at a 24h-aged tattoo, "Homogenization of the epidermis, the epidermal-dermal junction, and the upper portion of the dermis was almost complete". "Both epidermal and inflammatory cells had ink particles in their respective cytoplasms [...] Ink particles were also found in the enlarged intercellular spaces".


text:
Can the spike protein created by the Covid mRNA vaccines be created independently of the human body, and is there a higher cost to that?
How different in principle is using the bodies own mRNA to create the coronavirus spike protein differ from other methods of using genes to manufacture other drugs or proteins and is there a cost benefit to it?
Take the scheme for instance that uses genetically modified genes in goats to manufacture spider silk, as shown in this link - The goats with spider genes and silk in their milk or Yeast cells genetically modified to create morphine-like pain killer
I understand that in the case of the Covid vaccines the human body's genes themselves are not modified, but it is the principle of using the body's own cells as a manufacturer of some desired protein that I'm inquiring about.
Even without any cost-cutting benefit does the way Covid mRNA vaccines work differ in principle from other gene based compound manufacture?

I’m voting to close this question because it is not about a biological mechanism or process.

It is about a biological process which in this case uses the human body as the system of manufacturing. Whether a cost benefit is a secondary issue, but it clearly has to be a factor given the huge scale on which it is being applied.
Is the scale the only reason why Covid has enabled mRNA vaccines managed to go mainstream or is just fortuitous timing?
The scale and the economics matter.

I don't think you're looking at this the right way and taking far too literally the meaning of "manufacturing" in this sense. You're comparing a vaccine to mass production of bulk materials. The mRNA- or viral-based covid vaccines produce very little protein in comparison.

@BryanKrause I'm not acquainted with the science here, as you can see that I have only asked one question here previously.
The question can be broken into 2 parts. 1. Whether  the spike protein can be manufactured independently of the human body, 2. If it can, why the human body is being used to produce it and whether is a cost benefit to it.
I assume for the layman there is the implied assumption that the human body is the only place the spike protein can be synthesized, but seeing that is not the first time gene manipulation have been used to create compounds is what prompts the question.

@Amanda — If you want to have a discussion about how the site works please use the [meta] site rather than antagonizing Bryan (who like all moderators is a volunteer). ——— However, I encourage you to first familiarize yourself with how this site is supposed to work by taking the [tour] and then carefully reading through the [help] starting with with [ask] and [answer] questions effectively. In particular, note that Not all questions can or should be answered here. Thanks!

@vfclists Come support the SynBio Stackexchange proposal? As soon as we hit 100 people with 200+ reputation, an interdisciplinary site will be launched where questions like these are clearly on-topic. https://area51.stackexchange.com/proposals/125068/synthetic-biology?referrer=MTFmYjRhNDUzOTZkYmY1NjU0ODE5ZjczMWY0Y2RiMDFlNTQyOWI1MWZkNzQyMzRhYjk2MWU0YzAyNjE3NjA0M930KtpvebSN1XkrLHnQGy7CghuJQAyr-Me9iSdHtWfZ0

What you describe, creating the spike protein independently and delivering it, is exactly what is done by subunit vaccines, such as the COVID-19 vaccine developed by Novavax.
As already noted in @Amanda's answer, mRNA is great at amplifying a delivery, so you need a lot less to be delivered.
The manufacturing process for the vaccine itself is a lot more modular as well, since you can address a new target simply by adjusting the contents of the mRNA. It's not necessarily simpler overall, though, since there are different challenges related to nanoparticle encapsulation and delivery.
The stability is also not necessarily better than for a subunit vaccine: proteins are sensitive and unstable, but so is mRNA.  The degree of sensitivity for mRNA, however, is more predictable than for protein, since the mRNA itself is a much simpler and more regularly structured molecule.


text:
Are there any documented cases of extinction of a species of fungus?
Are there any documented cases of extinction of a species of fungus? I imagine it would be hard to detect something like this.
Edit: documented by humans when it happened and/or induced by humans.

Why should it be hard to detect?

@Jam Fungi are composed of soft tissue, which breaks down easily and quickly. The conditions to preserve such tissue occur even more rarely than the already rare conditions for fossilizing bone.

@Jam 99 % or so of funguses are below ground and more or less microscopic.

According to the International Union for Conservation of Nature’s Red List there are many endangered fungi, but none that are documented to have become extinct within the time frame of interest to you.
However, it seems likely that some fungi have gone extinct with their plant hosts — according to the IUCN there have been 133 documented extinctions of plant species. In particular, mycorrhizal1 (and other) associations between plants and fungi are prevalent and some of these associations appear to be specific (i.e. the fungus only associates with one plant species). For example, there are reported to be 28 species of fungi that only associate with the shrub Lantana camara.2
References:
1: Hoeksema, J. D., Bever, J. D., Chakraborty, S., Chaudhary, V. B., Gardes, M., Gehring, C. A., ... & Lajeunesse, M. J. (2018). Evolutionary history of plant hosts and fungal symbionts predicts the strength of mycorrhizal mutualism. Communications biology, 1(1), 116.
2: Hawksworth, D. L., & Rossman, A. Y. (1997). Where are all the undescribed fungi?. Phytopathology, 87(9), 888-891.

Yes. One example is of a fungus named Prototaxites. It was originally thought to be a tree, but it was a massive, tree-like fungus.

"documented by humans when it happened and/or induced by humans" does not really match with "approximately 430 to 360 million years ago" though

@eis I believe that the OP added that in an edit to their question after I provided my answer.

I don't think that is true - based on timestamps, edit was made 20:11:08 and you answered 22:43:23.

@eis Well, I must have missed the edit... ::shrugs::


text:
What is the evolutionary advantage with two lungs (kidneys)?
What is the evolutionary advantage with two lungs (kidneys)? Most living beings only have one heart, one stomach. Most internal organs are not doubled and if one lung fails it is not exactly quite transparent due to having an extra lung. Before modern health care one failed lung would kill the individual.
The same can probably be said for kidneys.

Evolution does not have a purpose.  As for why things evolved that way, most animals are essentially tubes.  It would seem to take very little evolutionary change - basically a few mutations to the HOX genes - to create bilateral symmetry.

The heart is two-sided, each side doing pretty much the same thing, much like the lungs and kidneys. Could easily be separate, though wouldn't work as well together. Also, you should cite sources for your claims.

Does this answer your question? Why do some bad traits evolve, and good ones don't?

most organs come in pairs in vertebrates, (the heart starts as two separate organs embryonically) the digestive tract organs are the exceptions, you may want to reframe your question about that.

Humans and most organisms have bilateral symmetry.  Anything that is on the left side of the body will be on the right also.  Not everything can be in the middle, so ... you end up with two.  This is evolutionarily labile - for example, fish generally have one dorsal swim bladder, though it is derived from the lungs.  In a similar manner, the heart is formed by the fusion of primordia on either side during development - see UNSW for a cute video.

-1. Your thesis does not stand. The heart and other organs like spleen does not have bilateral symmetry.

Bilateral symmetry is of course an approximation - biology doesn't know theory.  But it is a good one.  For example, the spleen begins from the dorsal mesogastrium (the mesentery connected to the greater curvature of the stomach), making it, conceptually, an unpaired midline organ that merely reacts to surrounding circumstances.  In some humans the situation is more bilateral

Bilateral symmetry goes much further that the internal organs, of course, so bilateralism must be deeply embedded in the genes.  (Even structures like vertebrae are symmetric.)  So the question really should be why some few organs AREN'T paired or symmetric.

As I said, "other organs" in plural, with spleen being but one example, which do not have bilateral symmetry. What is the mechanism of all the other non-bilateral symmetric organs? With respect to the spleen in particular, it just begs the question: what makes the stomach non-bilateral symmetric? You can say they just compete for the same spot and randomly eking out a space and deforming each other. Why do all of them not have two or more which can all be arranged bilaterally? Another question is why we do not have more equal distribution of people having their hearts and spleen situated

randomly on either sides of the spine.

The nodal signalling pathway is clearly involved, which can be traced back to the clockwise motion of cilia in some species.  But I have not kept up with recent developments in this area; you should find more with a little research.

@Hans the heart actually starts as two sperate organs embryonically. the only organs that do not start as pairs are the digestive organs (stomach, liver, pancreas, spleen) because the digestive system starts as a single tube.

@John: Wow, really? Does the heart start out as two bilaterally symmetrically embryonically? If so, my previous other question still remains: why do we not have equal number of people having left situated and right situated single-organ heart and bilaterally symmetrically situated two-organ heart?

@Hans the heart starts as two unconnected blood vessels. this may help https://open.oregonstate.education/aandp/chapter/19-5-development-of-the-heart/ I have a whole answer in the unclosed question about this. https://biology.stackexchange.com/questions/100928/why-do-we-have-two-kidneys-but-one-liver/100935#100935 Your questions about bilateral symmetry are great questions I suggest asking them as a stack questions (look for identical questions first) but in short is comes down to shoving 30ft of digestive tract in 2 feet of torso and the fact we are no longer laterally narrow fish.

Two of the duplicated organs work better (e.g.: also kidney) or even enable something new (e.g.: depth perception for eyes). Source

Two hearts? Two brains?

Same applies to animals with multiple hearts or brains. https://www.mentalfloss.com/article/52337/3-creatures-more-one-heart And https://medium.com/illumination/the-animal-with-many-brains-that-makes-us-rethink-intelligence-1fc5e1325bcb

@d-b: Vertebrates do basically have two brains, separate left and right hemispheres with interconnections between them.

-1 for the falsehood. 1. Why is 2 the optimal rather than 3 or 4 or more like the number of teeth? 2. It is not true for other organs like the heart and spleen.

My answer addresses OP’s question (what are advantages of multiple organs). The question  is not, why different animals all are not the same / why they occupy a given niche in the evolutionary landscape (and hence experience different tradeoffs). Additionally Mike Serfas great answer well explains the developmental possibility of two organs.

@jamesqf they also have two hearts that fuse into a single one during early embryonic development.

Eels have two lungs and so do lungfish and all vertebrates, so the design is at least 375 million years old, although vertebrate lungs have developed different air flow systems, i.e. birds and iguanas. No vertebrates have a very small and big lung as far as I know.

Rib punctures can affect one lung which fills with fluid.
Stick and tooth punctures can actually cause air to escape the lung through the chest, a condition that can sometimes be survived in th wild, but less likely with only one lung.
Pulmonary infections can cause a lung to fill with water, so having two lungs gives some extra protection.
Breathed in objects like twigs can sit inside a lung for many years and cause weakness, for example a man coughed up a twig from his lung 14 years after having breathed it in while playing in a hedge with friends.
Two lungs may also bring higher surface area and higher performance than one lung.

Most of your points are deadly in a non-civilization (i.e., for all animals except humans living in a society that offers some surplus food etc) context, even if you have a spare lung. Re the surface are, that is why lungs are "wrinkled", and that works fine with a single lung.

-1. None of your points answer the question. Regarding the last point, the fractal-like structure of each lung already increases the surface. It is not necessary to have two to increase the surface.

Actually, if your lung fills with water from a stick/rib/pneumonia, you will die irrespective of the fractal structure, which is not part of the question, but having two lungs will stop the liquid spilling into the second lung and choking the vertebrate in question, and two hemispherical spheres have a surface area of 3.14+1.4, i.e. 30% bigger.

@d-b Humans have only lived as a civilization for 10,000 years, previous to that they were hunter gatherers with very low populations because the surplus-giving crops did not exist, and they inherited their lungs from other primates and the primates from basal placental animals.... Two hemispheres have 30% more surface area to place the wrinkles on in the first place, so a 5 liter double-hemisphere lung is equivalent to a 7.5 liter single spherical lung, approximately.

Given the total volume and a geometric shape  the more isolated domain of the same size one makes the more surface area one gets in the form of $n^{1/3}$ where $n$ denotes the number of isolated geometry. So for $n=2$ there should be $2^{1/3}-1~26%$ more area. It is not clear what you are computing and where 3.14+1.4 comes from. If you split a sphere into two hemispheres, the area increases by 50%, not 30%. More importantly, it is not the outer shape and area we are looking at. It is the ultimate (inner) surface shapes, i.e, alveola sacs we are talking about,

not the exterior shape which has nothing to do with respiratory gas exchanges. One needs only more and smaller alveolar sacs. So there is no need to separate into two largely isolated domains if our objective is just to increase the gas exchange surface. You do have a point in asserting the risk diversification. That though begs more questions. Why we do not have more than 2 lungs? Why do the other organs such as the heart and spleen have only one isolated unit?

The lungs and the windpipe both lead straight into the middle of the lungs and provide better air and blood distribution than if it was a sphere. https://cdn.britannica.com/s:690x388,c:crop/20/125820-050-F1FD8A7E/veins-arteries-human.jpg Do you also disagree about the  protective effects outlined in the first 4 bullet points, and disagree with only the last one? What about the puncture, pathogen and fluid protection afforded by two lungs? The heart and spleen can't absorb pathogens and twigs and get pierced by ribs as easily as the lungs can.

Let us continue this discussion in chat.

Please check out my response to your last comment in the chat.


text:
use of adjuvants and peptides in modern vaccines?
when preparation of modern vaccines we generally use a part of the microbe or the antigen such as polysaccharides to create an effective vaccine against the vaccine. so when the preparation of sub unit and conjugate vaccine we use adjuvant? so what is the use of using an peptide in case of babies having week immune system?
Basically my question is What is the use of peptides when we are using adjuvants to enhance the immunogenic response?

I really don't understand your question, can you please clarify it? What do you mean by "effective vaccine against the vaccine" or " so when the preparation of sub unit and conjugate vaccine we use adjuvant"?

What is the use of peptides when we are using adjuvants to enhance the immunogenic response?

Ah, ok, now I understand. You should probably still rephrase your question to avoid closure because of non understanding.

In many vaccines, there are two components: One immunogenic substance, these can be parts or complete (inactivated) pathogens (for example the small pox vaccination), peptides or proteins (like the tetanus vaccination) or polysacceride components from the capsule of bacteria (for example against MenC). Against these components the actual immune response is directed. See references 1 to 3 for some more details.
Then they can (depending on the vaccine) contain adjuvants, which enhance the immunologic reaction of the body. This is done either to enhance the reaction and to get a proper immune reaction but also to be able to reduce the amount of injected antigen. So the adjuvant simply causes a general inflammatory reaction. Classically Alum (aluminium hydroxide is used here), newer adjuvants are squalen based oil-in water preparations or CpG olinucleotides (see references 4 and 5 for numerous examples on adjuvants and literature).
So what you basically do is to identify (more or less) a part of the pathogen which can serve as a vaccine and use this part for the vaccine.

Making Vaccines: How Are Vaccines Made
Designing Tomorrow's Vaccines
Strategies for designing and optimizing new generation vaccines
Dose Optimization Strategies for Vaccines: The Role of Adjuvants and
New Technologies
Vaccine Adjuvants Review


text:
Identify little green long legged bug

Discovered attempting to hide on bathroom sink handle at night, though bathroom light had been left on.
Barely reacted to attempts to capture it at all. No flying. No jumping. Just really slow crawling.
Found Eastern US. 2017/11/18

Please update question time of year it was found. If you have a better picture, please upload that, too.

looks like the nymph of some species of Hemipteran. Hold on...

The photo is not high quality, but the shape and size of the insect definitely point towards it being the nymph of some species of assassin bug (order hemiptera, family Reduviidae).
See this as an example:

Specifically, your specimen looks similar to one found in a home in Virginia.
The genus is likely Zelus, and based on it's greenish hue, I'd say it's an individual of the eastern US's most common species of Zelus, Zelus luridus (Pale Green Assassin Bug).

 Source: Christine Hanrahan

Nymphs are solid green, wingless, and with narrow bodies

The most reliable feature to distinguish this species from others is the pair of spines on the rear corners of the pronotum. These spines are long on the lighter colored individuals and shorter on ones that are darker. It can also be distinguished by dark bands on the distal ends of the femurs, but these can often be too light to be easily seen. [Source].


text:
Animal gene in plants
Usually only microbes, specifically bacteria are used to express genes of other species for various functions. But, it is possible to try and express an animal gene into a plant. Bacteria like Bacillus thuringiensis is used in many plants like cotton, to modify them to BT cotton with insecticidal properties. Can one use an animal gene to get those characteristics in the plant?

What kinds of characteristics you are looking for ? I mean you can express successfully lot of animal proteins, pharmaceuticals and antigens into plant (Julian KC 2003). But I don't think they are any way important to plants.

A few years ago plant scientists introduced a protein (afa3)in tomato from Winter Flounder, a type of fish surviving freezing conditions. The idea was to make a frost resistant tomato but I believe they did not have much success. Anti-GMO activists had a field day however with baseless claims of making tomato's smell like fish and other nonesense.

I was looking at adding a particular gene of the penguin that makes its skin thick to survive the winter, in a cotton plant. Do you think that could work?

I don't know much about pinguin skin but I know it is very very different compared to plant epidermis. It seems rather unlikely but it all depends on the gene

One example that I am aware of where an animal transgene was put into a plant was to produce the ZMapp, a chimeric, monoclonal antibody against the Ebola virus.
This is a wikipedia article on ZMapp, that gives you an idea of the process.
Other than this, I am not all that familiar with plant transgenics, other than Round Up resistance genes that were transfected from soil bacteria that developed a resistance to the active chemical in Round Up.
Hopefully other answers can provide you with more details, but these are the two examples that I know off the top of my head.


text:
How to write 100% phenotype ratio?
I am not quite sure how to write 100% out come for the phenotype ratio after using "Punnett Square". The result from the each alleles, the dominant allele completely(100%) took over the recessive allele.
How can I express my phenotype ratio?
(Let's say....Purple flower→dominant White flower→recessive)

Phenotype/ Purple flower 1: White flower 0
Phenotype/ Purple flower 4 :white flower 0
Phenotype/ Purple flower 4

I am voting to close because It is a question of language and not of biology.

You could write "ratio of purple to white flower 1:3" I suppose. Also you should clarify whether you want to express such ratio in a sentence or as a list of such ratios.

Note btw, that there are a few typos in the title of your post.

I understand the how to express the ratio of the our come of 1:3.....but I was not quite sure how I should do to express when the outcome is 100%......I guess I could do with "Purple flower4: white flower 0".....!?

...sorry about the typo....

Oh... maybe I misunderstood your question then. The question might be about basic math and not language. A ratio of white to purple of 1:4 corresponds to 25% white flowers and 75% purple flowers. Does it answer your question?

thank you for your help...yes, that is true that it is 1:4...., however, my instructor was using this ratio of 2:2:0 when we did multiple alleles....I thought there are rules about how to create "Bio ratio" using "Punnett Square".....so.....if it is 100% outcome of the genetic cross, it will be 4:0....hmmm, still little confused....

@Remi.b Just to clarify, a ratio or 1:3 (not 1:4) corresponds to 25% white and 75% purple flowers.

The phenotype ratio would be 4:0.
You did not include the complete example including the genotypes, but an example that might produce this result is:
P is a dominant allele that produces purple flowers, and pp homozygotes are white.
    P    p
  -----------
P | PP | Pp |
  -----------
P | PP | Pp |
  -----------

The genotype ratio is 2:2:0 (2 PP : 2 Pp : 0 pp) meaning there are 50% PP and 50% Pp.
The phenotype ratio is 4:0 (4 purple : 0 white) meaning there are 100% purple and 0% white flowers.
To keep things simple, you do not need to reduce the ratio to the lowest terms (in other words, the sum of the numbers in the ratio should equal the number of boxes in the Punnett Square). It would not, however, be incorrect to reduce the genotype ratio to 1:1:0 and the phenotype ratio to 1:0.

Thank you so much for your help! Especially giving an example of genotype.! I can clearly see the difference now. And yes....I should have given my example a lot more clearer....
one more worries....the way I should answer fully...is going to be...
" purple flower 4 : White flower 0" for the phenotype...? If you could help me once again....

@Runa I do not understand what you are asking now. It is a matter of preference whether you reduce the ratio to lowest terms (that is 1:0). However, from your comments it appears your instructor is keeping things simple by making sure the number of boxes in the Punnett Square add up to the sum of the numbers in the ratio, which is why I suggested the best answer is 4:0.

Yes...you are very correct...
My worries are not about the number anymore but how to express"Biology term ratio"(Thanks you as you explained, it made all clear for the number.) it is just about how to answer the question, how to write....(I was not sure if there were the big rule about "how to write the biology term of the ratio")...I guess I am little like " being-worry-too -much"...


text:
What is the probability of genetic reincarnation?
Parents pass on 23 chromosomes to their children, with a 50/50 chance for each chromosome. Considering that people of a families lived over millennia in the same region the abundance of some chromosomes in this region should be quite high. So if we for a moment neglect the occurrence of mutation the reincarnation of a genetic similar individual should just be a question of time. Therefore I asked myself how to actually calculate the probability and time span of this occurrence. (with and without mutation rates because of the complexity of the model)

And how would you define similar?

Assume there is no mutation, leave enough time and the there will be no single living individual that will differ genetically from any other. If you really want to answer how much time it takes to have a probability of say $\frac{1}{2}$ that two individuals are exactly clones of each other in a population, we need to know the population size, the number of loci, the mating system, the population structure and the level of genetic diversity to start with.

Genetic clones are not "reincarnations" – there is much more to a person than their genes. For starters there are epigenetic and environmental factors.
Also, chromosomes are not passed on whole from one generation to the next. Genetic recombination occurs which means, for example, that a mother's egg contains chromosomes that are a mixture of her parents' chromosomes. As a result, chromosomes are generally not passed on identically from generation to generation. This means that it is therefore not true to say "Considering that people of a families lived over millennia in the same region the abundance of some chromosomes in this region should be quite high". The Y chromosome in males is an obvious exception to this rule (it is passed on down the paternal line mostly unchanged).
These points aside, the chances of two people having identical genomes is so infinitesimally small and genetic inheritance is so complex that I do not think there is a sensible model to calculate it.
If you really want a number you could simplistically say that the human genome is about 3 billion base pairs. Humans share about 99.5% of their DNA with everyone else, so let's just say that to be clones two people would have to match at that other 0.5% of the genome – 15,000,000 base pairs. For each base pair there are four options: A, T, C or G. The probability that someone would match on every single of these base pairs could thus be 1 in $15,000,000^4 = 5.1 \times 10^{28}$.
That's 1 in 51,000,000,000,000,000,000,000,000,000.
To put this in perspective, since time began there has been about 108,000,000,000 people who have lived, so humanity would have to repeat it's history several billion billion times to make this remotely likely.
Calculating this number make more assumptions than I care to count. You might take off a few zeros if you are considering a highly inbred population.
It is theoretically possible that an accidental genetic clone of a person could occur, but the point is it's just not going to happen.


text:
Lack of yolk in mammalian oocytes as compared to other vertebrates?
Why do mammalian oocytes have little to no yolk? How does it compare to other vertebrates such as frogs, fish, and birds?

In oviparous animals (those that lay eggs which hatch outside the body), the eggs need to be provided nutrition for embryonic growth, which is the main function of yolk.
In placental mammals, the embryo is provided nutrition directly from the mother via the placenta.
Therefore, most mammalian oocytes do not need to develop large quantities of yolk to support the embryo in the way the eggs of most birds, reptiles, amphibians and fish do.


text:
Why don't the genetic similarities between ‘unrelated’ individuals of the same and different species outweigh the differences?
Ever since starting to learn about the concept of inclusive fitness during my BSc, I've been bugged by this questions: if inclusive fitness can account for many ‘altruistic’ behaviors, why don't the genetic similarities between ‘unrelated’ individuals of the same and different species outweigh the differences? In other words: when we consider (from a gene-centric perspective) that individuals are temporary vehicles for selfish genes, and if we also consider that the fitness effect of different genes should not be measured in the reproductive success of just single individual, should we not expect to see that genes that promote more broad-scale altrustic behaviour since we share most of our genetic heritage with other individuals?
I understand that my confusion arises from the fact that I fail to sufficiently distinguish between behavioral genes that influence altruism and whose distribution in the population is differentially influenced by different game strategies and genes that have no direct influence on this type of behaviour and are thus not under the same type of selection pressure. However, I cannot seem to manage to produce a clear-cut argument from this distinction.
I'm asking because, when I find myself in the position of having to explain inclusive fitness, I feel a bit awkward when I know in the back of my head that I would not be able to answer this basic question if it comes up.

Relatedness measures a specific type of genetic similarity. In particular, it measures the genetic similarity relative to the rest of the population. When $r>0$, the recipient carries the actor's genes at a higher frequency than the population. When $r=0$ it doesn't mean that the actor and the recipient do not share genes; it only says that the recipient carries the genes of the actor at the same frequency as the population.

I've upvoted your answer, but haven't yet sufficiently thought it through to be able to say whether or not it clears up my confusion.

Saying that we are talking about relative relatedness yield to the question relative to what?. If I am not mistaken, altruism through kin selection does not need population structure to evolve, relative relatedness can only be define relative to other (isolated) lineages. I think I am confused as the OP is.

@Remi.b Assuming that relatedness is modeled as a regression coefficient of the genetic values of the recipient and the actor, doesn't it follow that relatedness has to be relative to the mean genetic value of the population? Hope we are not talking pass each other.

Yes, I think so... Though this implies that 1) population structure is necessary for kin selection to evolve and 2) it brings the question of whether you consider a population that is differentiate enough to have partial reproductive isolation as being included or not in the regression. This is where I get confused.

@Remi.b Right, I think I understand your question. As to 2, my impression is that the boundary of the population is determined by all and only the individuals affected by the behavior in question. The population doesn't have to be partially reproductively isolated (e.g., migration can happen). Or would like to say that the populations in, say, the infinite island model are partially reproductively isolated?

partial reproductive isolation is generally defined in terms of the fitness of their offspring and not on their probability of mating together due to isolation by distance. Am I right that in absence of any population structure (in a panmictic population where a focal individual has equal probability of meeting any other individual) altruism cannot evolve through kin selection if relatedness is defined as a correlation between the genetic values of the actor and recipients? And if yes, then is it really true that altruism through kin selection can only evolve in structured population?

@Remi.b I would say "yes": altruism requires population structure for it to evolve (according to kin selection theory). I didn't know that "partial reproductive isolation" is typically defined in terms of fitness -- instead of mating. My bad...

mmhh... ok. Without population structure, there is no selection for altruism through kin selection. Ok... I guess I can accept that. I feel like there are debates o this question in the literature but am not sure. +1 thanks for the clarification. and...hum I got it wrong to say that reproductive isolation is in terms of fitness and not habitat isolation. So...definitely MY BAD $\ddot \smile$.


text:
Why doesn't one develop immunity to bacterial STIs?
Why doesn't one develop immunity to STIs such as Chlamydia/Gonorrhea and Syphilis even after the first exposure and treatment with antibiotics?


text:
Wasp? Wicked looking bug
Saw this bug this morning in Colorado. Looks like a giant wasp.

That is a horntail, family Siricidae. https://www.insectimages.org/browse/taxthumb.cfm?fam=455
They are a family of sawflies. Not technically wasps, but they are Hymenoptera.

Yeah, she looks dangerous doesn't she. However, the 'stinger' is used for ovispositing eggs in wood. These wasps do not sting.
This species is called Pigeon Tremex Horntail, Tremex Columba.
Nice pictures and very interesting information on the website below, however the images have copyrights, so I can't include them here.
http://bugeric.blogspot.com/2012/09/wasp-wednesday-pigeon-tremex-horntail.html?m=1

I haven't formally asked for a species identification (maybe I should?), but you may find this of interest and potentially amenable to an additional answer: Why do wasps have "wasp waists"? What's been optimized?

Yes, beautiful tremex!


text:
Can amount of gene share in descendants be easily calculated?
I saw on the web an explanation on how to calculate amount of certain genes in a person.
For instance: if your grandfather was French and your granny was an American then your father is 50 French and 50% American. Then he met an american woman and their child going to be 50/2=25% French and 50% American. And so on... dividing each time by two.
Is it truth?

Just so we know: how far down the rabbit hole do you want to go? That calculation is... approximately true, on average, but there are plenty of exceptions and a lot of terminology needed to make it all clear.

@downvoter can't say why somebody would downvote it.

@bashsane not too deep.

Every parent passes half their DNA onto their kids. There is a not infinite, but very high, amount of DNA. This means for the first generation it is precisely true: if Mom has 100% red genes and Dad has 100% green genes, child will have 50% green and 50% red genes. For the second generation, for people with mixed genes, it becomes true only on average. So if child has 50% green and 50% red genes, by passing on half its genes it could theoretically pass on all red genes, or all green genes. It very likely won't pass on  exactly half of each. But because there are a lot of genes, the law of averages does that in practice you can say they pass on half of each, meaning if the other parent has all green genes the resulting child will be 75% green genes, 25% red. This indeed goes on through the generations for awhile until you run into the finiteness of DNA; at some point the amounts will be small enough that they no longer follow the laws of averages, and it become much more variable whether a child gets the full complement of their parent's red genes, or none, or some intermediate amount.
This is further complicated when we aren't talking about abstract "red" or "green" genes, but "American" or "French" genes. What the heck are "American" or "French" genes anyway? The human gene pool is fairly well-mixed, with most genes being widely shared. Those that can be used to identify specific ethnic or even national origins are low enough in number that what I said earlier about the law of averages no longer applying happens earlier if you look at specific subcategories of genes. Still, it works for several generations I believe.

What the heck are "American" or "French" genes anyway? The human gene pool is fairly well-mixed, with most genes being widely shared. Those that can be used to identify specific ethnic or even national origins are low enough But there was a company in the US, you could sent it a sample of your slime and see results on the web-page, that you have 30% of German genes, 20% African...

@RS that's right, but those depend on small numbers of genes that are characteristic of certain groups - meaning people in that group tend to have them and people outside of them don't. Those groups don't map perfectly to nationality, and how well they map depends on said nationality - I've never heard of them assigning people to "American" for example, and I doubt most French people would get "100% French" either.


text:
Is there such substances that body can only send to storage (as fat)?
I watched video with statement that there are such part of substance in potato chips which body can't use ("empty calories"), that they surely will be stored as fat.
It was here on 12:23:
https://www.youtube.com/watch?v=-jCd6vIF8Co
Is she talking nonsense ?

You might want to read this. If this helps you, I might post this as an answer.

An empty calorie is still a calorie.
"Empty calories" was coined to describe foods that only provide calories without significant amounts of other nutrients. The idea is that if you're eating a lot of empty calorie foods, you're eating less food with proper nutrition. The implication is that you will not be getting the vitamins, amino acids and other essential nutrients required to sustain you in a healthy manner.
If you can store it as fat, your body can use it. Where does the fat go when people lose weight? Those calories get "burned" when there aren't enough calories in your current diet to provide energy for your metabolic needs.


text:
How does consumption of vinegar affect food chemistry?
For example: does consumption of vinegar somehow change digestion of flour (bread, cakes, pasta, puffs) ? May be there are some benefits to eat flour meal with vinegar ?

How much vinegar are you talking about? 50ml? 500? 2L? What sort of "benefits" are you expecting? And could you define "dough" - do you mean uncooked bread dough, or something else?

@MattDMo I mean bread, cakes, pasta... quantity to taste.

In the case you're talking about (just using vinegar to taste), there should be no effect whatsoever on a healthy stomach. The stomach already contains a significant amount of acid, and a little bit more from the acetic acid in vinegar won't change much, just like eating some citrus fruit with a meal (oranges, lemons, and whatnot) won't change much. Acid-mediated hydrolysis of chewed food is only the first of many steps in digestion - a significant portion is performed by enzymes and commensal microorganisms in the gut. Changing the type or amount of acid by a small amount won't affect anything significantly in the long run.
The only exception I can think of is for people suffering from peptic ulcers, whether from over-use of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs such as aspirin, ibuprofen, naproxen, etc.), infection with H. pylori, or possible genetic/developmental issues (most often seen in young children). In these cases, consuming an overly-acidic meal may aggravate the symptoms of peptic ulceration.


text:
For how long viruses survive in non-air moisture environments?
On the Internet there are plenty of information that viruses don't live long after they were exposed to air, after they starting to dry out.
But it's hard to find an information on how long viruses can survive in wet non-alive environments at a room temperature like food, oils, soap.
I understand that it varies from virus to virus, but there may be maximal (for the most survivable ones) or average values.

Depends on the virus. They have PH, and temperature requirements that can't be disrupted. If completely disrupted then the virus denatures causing it to no longer have the effect it had.

@Ark Lomas thanks for info. I know it depends on the virus, but there must be maximal (for the most survivable ones) or average values.


text:
Can anyone please help me identify this plant?
Please help me identify this plant. My aunt had one but it died due to the drought in California. She wants to get a new one but she doesn't know what it's called. The leaves are around two inches and it is seedless, though I'm not sure if it's native in California. Suggestions are welcomed!

Welcome to Biology. Species identification questions are warmly welcomed, but without knowing more details it is impossible to identify this plant. Important things to mention are: 1) Was this an indoor or outdoor plant 2) Was it a native or not 3) Where do you live 4) Did it flower, and if yes, what did the flowers look like 4) How big was it 5) How old was it 6) What was the size of the leaves? ...etc.

Thanks for the edit, but please answer all 5 questions that AliceD asked.


text:
Do micro-organisms survive and live normally in a zero-g environment?
Have there been any experiments in space regarding micro-organism behavior? Are they able to move around in a drop of water like they do on Earth? Are they able to eat and reproduce normally?
Edit: by zero-g, I mean an environment where you feel zero acceleration. Orbiting the Earth would be this since you're constantly in free fall. A rotating environment is not zero-g as the things inside will feel a "centrifugal" force pushing them into the wall (though it's actually a centripetal acceleration coming up against your intertia).

Sometimes they can even survive better in zero gravity than in Earth gravity! See Phys.org's Researchers discover bacteria thrive in zero-gravity low nutrient environment.

A team of researchers at Rensselaer Polytechnic Institute, in New York, working with Lockheed-Martin Ames Research Center has found that one strain of a common type of bacteria thrives aboard space vehicles, even when faced with minimal nutrients. In their paper published in BMC Microbiology, the researchers describe an experiment they conducted aboard NASA Shuttle Atlantis that showed that Pseudomonas aeruginosa, a very common type of bacteria, grows more dense cultures when in space than it does on Earth when available nutrients are restricted.


text:
What properties of DNA and Chromosones do birds have?
What properties of DNA and Chromosones do birds have? How many chromosones do males and females have? Are the nucleotides the same (CGAT)?
There are a lot of different kinds of birds. Maybe the DNA varies a lot among them, so I want to specify: Fowls (gamefowl/landfowl/waterfowl).

Yes. Birds do have DNA. I don't understand what you mean by the type. If you mean by geometry, I suppose they should be having all 3 A, B, Z- DNA. Chromosome number varies with species. 'Birds' is a class of animals with many many species.. so ya - you can't generalize. Sex determination also varies. Since you ask for the fowl - males are homogametic - ZZ and females are heterogametic with ZW. So in a way, it is opposite to that in humans. I don't understand why you expect birds to be that different

-1, the most basic search will confirm that birds, and indeed all life above eukaryotes, have genomes encoded by DNA.

@Michael_A Which is why I asked "what kind of DNA"---and specified the properties I'm interested in, instead of asking "do they have DNA at all?".

Then, what are the 'kinds' of DNA u r looking for?

@DrZ214, My comment is specific to these two questions. Is it really DNA, or rather RNA, or something else? Are the nucleotides the same (CGAT)? You have posed 4 questions which confuses the issue. Polisetty's question is a good one, I also don't understand what you mean by kind of DNA.

@Polisetty I specified in the OP: chromosones, nucleotides, and DNA or RNA. Those 3 things are what I mean by "kind".

Then everthing is the same. Just chromosome number varies

@DrZ214 Not to be offensive, but knowledge about DNA is probably one of the most basic things when it comes to biology. Exactly because it is basic, it is also easy to find on the internet, e.g. Wikipedia page on DNA. DNA is not RNA. DNA and RNA are made up of nucleotides. Chromosomes are condensed DNA packaged by histones and scaffolding proteins. You have contradicted your own question by listing those "kinds" of DNA. DNA has probably only two qualifiers: linear/circular, single-stranded/double-stranded.

@LiuTianyi I made some edits.

The class "Aves" fall under the kingdom Animalia. Therefore, they are multicellular eukaryotic organisms. Being eukaryotes, their genetic information is encoded in linear double stranded DNA.
What is their chromosome number? Fowls (gallus Domesticus) have approximately 36. It varies from bird species to bird species as much as it does from humans (46) to gorrilas (48). Chickens have 78, and so on.
The genetic code is universal. It is used by virtually all known organisms, save some very specific outliers.