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Why does decomposing matter emit a bad smell?
Often, when matter decomposes (such as a rotting carcass), a nasty smell is emitted.  After speaking to my teacher, it was likely due to the nitrogen compounds that leads to the bad smell.  Is this so?  Why then, do nitrogen compounds smell bad to us humans?

When bacteria and other microorganisms decompose matter, many gases are released alongside nitrogen, such as sulphur and methane. Our brains have evolved to perceive the smell of these gases as “bad” in connection to decomposing matter to protect us from eating them and being exposed to the harmful bacteria, just as we perceive certain plants as tasting bitter (the “bitter compounds” in plants are for its self defence) which could be toxic to us if we eat them.

@P.SN is it true though that brain's perceive at bad as due to smell? Also isn't bitter taste due to alkaloid poisons...So humans have evolved not to like alkali?

reframe the question, why did humans evolve to think the smell of rot is bad, AKA something to be avoided.

Since this question has no answer, I thought of taking a stab at it.

Why does decomposing matter emit a bad smell?

Due to cadaverine and putrescine. More information here: What produces the strong odor of decaying dead animals?

Why do they smell so bad? Why do we perceive those smell as bad?

Let's start from the basics. Stuffs smell because they release chemicals odorants. They are volatile and hydrophobic. Different odorants have different smell due to presence of specific functional groups. Thiols smell like garlic/rotten eggs, , nitro groups gives a sweet ethereal smell. More information here: How does the smell of a compound come about, and is it possible to define a smell?
Cadaverine and putrescine has two amine groups which gives off that rotten fish mixed with that characteristic decay smell. This compound now binds with receptor proteins present in cilia. This chemical stimulus binds initiates an electric signal in the neuron, which transmits the information to the olfactory nerve, which carries the signal to the olfactory bulb in the brain and the brain processes the signal. The olfactory bulb is part of the limbic system, which is also associated with emotions. A person recognizes the odor and give off the emotion  of "disgust" as a reflex action.

Recent studiesref also found that smell of death is somehow related with threat management mechanisms. The paper suggest that humans can identify threats via chemosignals. For instance, when people are exposed to fearful experience, they show a heightened startle reflex. This transmission of threat-arousing chemosignals is assumed to serve an adaptive function by orienting us to impending dangers. Cadaverine and putrescine are found to be chemosignals. The paper explains it more properly:

The decay of tissue can function as a "necromone" cue that signals an animal’s death to conspecifics. Alarm and avoidance behaviors (necrophobic behaviors) in response to these scents are widespread in the animal kingdom and thought to have evolved at least 420 million years ago. In fact, recent research shows that necrophobic behavior may have innate underpinnings through the activation of trace amine-associated receptors (TAARs), a group of specialized scent receptors in the olfactory epithelium. TAARs are known to detect specific chemicals that evoke behavioral responses, without the need for prior exposure to the scents. Certain TAARs respond to diamines (e.g., putrescine) by producing avoidant behaviors that likely serve to defend against immediate dangers . Thus, it is feasible that we have a chemosensory sensitivity to diamines like putrescine, given that their detection can aid survival.

ref: Wisman, A., & Shrira, I. (2015). The smell of death: evidence that putrescine elicits threat management mechanisms. Frontiers in psychology, 6, 1274. https://doi.org/10.3389/fpsyg.2015.01274

to clarify humans avoid the smell of rot, because rotting things pose a direct and indirect threat. poisonings, contamination, and places were predators and disease vectors will gather. eating rotting things will make you sick so you evolved to think they smell bad so you won't try it.


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If overcooked hard boiled eggs show these green sulfide rings, why do scrambled/fried eggs not show this?

In the image above, the dark green rings are ferrous sulfide rings, caused when the sulfur from the egg white reacts with the iron in the egg yolk when the egg is overcooked.
I was wondering, given the same circumstances, why do we not see our scrambled/fried eggs coated with this layer of ferrous sulfide?

I'm voting to close this question as off-topic because it is Food Science and not Biology in terms of SE Biology.

Although I htink David's concerns are valid, I disagree with him as our cooking stack doesn't typically attract these types of food science questions that are more focused on science vs food, and it certainly doesn't typically provide an answer that would adequately address the OP's science-leaning question. This question is probably most on topic either here or at Chemistry SE.

@QuIcKmAtHs, I recommend that you do a bit of research on your own and indicate that you've done so more explicitly here. In doing so, you should be able to convince us that this is in fact a biology-related question (regarding biochemistry) and not simply a chemistry question.

It would seem obvious, at least in part. 1) Proper scrambled and fried eggs are not overcooked, and it's a lot easier to determine when they are properly cooked when they're not in the shell.  2) Scrambled eggs are just that - scrambled - so even if ferrous sulfide did form, it would be mixed in rather than forming a visible ring - though I admit I have vague memories of greenish scrambled eggs from boot camp :-(

@theforestecologist thank you for your comments, I will take note of them.

Scrambled eggs can change color, but you perhaps haven't run into a batch that shows discoloration. It is the same chemical reaction:

Why Scrambled Eggs Turn Green
When serving a large group, a buffet can provide enough food for everyone without the need to spend all of your time in the kitchen. Breakfast is a fairly simple buffet to set up, but there are special challenges when it comes to scrambled eggs. When scrambled eggs sit for a while, they tend to turn green or gray. This is a chemical reaction that happens as hydrogen sulfide in the egg white reacts with the iron in the yolk to form iron sulfide.

Via: https://living.thebump.com/lemon-juice-keep-raw-eggs-turning-green-cook-them-8383.html

source: Stack Exchange

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

sort: votes


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Can skin acclimatize to a the humidity level?
When the outdoor temperature is low, the absolute humidity is low because cold air holds less water. When the heat is turned up indoors the relative humidity decreases and during days with cold weather it can fall below 10%. This can lead to cracked skin or lips because, I assume, dry air draws more water from the skin. So my question is, can skin acclimatize? Around here in New York, some people get cracked knuckles every winter or use moisturizer to prevent them (I use nasal saline for nosebleed prevention). If those people lived in dry climates would they have this all year around? Or does the skin (and nose) eventually acclimatize?
If I install a large humidifier in my home could that actually have adverse effects by preventing me from acclimatizing (that is, making my nose less naturally lubricated), thereby possibly causing problems when I enter other houses or buildings?

Some lifestyle things cause symptoms like high blood pressure, and thin or inflexible capillaries. for oily skin, My scalp sebaceous glands produce more or less oil depending on how often my skin is devitalized. If i shampoo every day, my scalp skin eventually makes at least 7-8 times more protective oil after one month. probably the same for the rest of the body. I didn't know you can use saline for nose. dunno if the sinuses have a lot of sebaceous glands and I don't figure you can snort almond oil. Cracked skin is protected by daily moisturizer. I had that in India doing manual laundry

@com.prehensible According to this article, the claim that scalps  produce more or less oil based on how often you shower isn't true: http://www.oprah.com/style/biggest-hair-myths-do-frequent-trims-make-hair-grow-faster/all

That's not a study, that's a self styled doctor's opinion. Doctors always disagree until they have measured the study. I'd believe that if I had an explanation of why my hair goes greasy faster when I shampoo more often... If I use soap my scalp very seldom, it becomes annoyingly oily after about 7 days. I can do that for a year. If I shampoo every day to stop it becoming greasy, my hair becomes annoyingly greasy faster and faster and eventually after about 20 hours it becomes oily versus 7 days. I've observed the effect first hand so I'd have trouble agreeing with someone who has 2nd hand.

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


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Transformation of E.coli cells
As a team of undergraduate researchers we are looking to transform two genes of interest into our competent E.coli cells. Both of these genes are in separate plasmids and we would like to put them into one E.coli cell. Is it possible for a cell to uptake two plasmids in one transformation process? If the last question is impossible, is it possible to transform a cell and then transform the colonies produced by that transformation? Thank you very much.

Do your two plasmids have two different selectable markers?

Yes, we are giving one amp resistance and one kan resistance.

I have done the second protocol (transforming a cell with more than one plasmid) before, and it works. The cells will be resistant to both antibiotics. The chemical competency procedure will have to be carried out with the original transformed cells.

Double transformation (you may want to try searches using that term) has been doable for a very long time, but the efficiency will of course be less than either single transformation below the saturation point.
As for your second question, if the cells are made competent, I think a sequential transformation should work.

The two plasmids have to have different origins of replication. Two plasmids from the same incompatibility group cannot survive together in the same cell.
This quote is from the Wikipedia entry on plasmids:

Plasmids can also be classified into incompatibility group. A microbe can harbour different types of plasmids, however, different plasmids can only exist in a single bacterial cell if they are compatible. If two plasmids are not compatible, one or the other will be rapidly lost from the cell. Different plasmids may therefore be assigned to different incompatibility group depending on whether they can coexist together. Incompatible plasmids normally share the same replication or partition mechanisms.

This is a nice definition/explanation from an OpenAccess article:

A formal scheme of plasmid classification is based on incompatibility (Inc) groups (Novick, 1987). The procedure for incompatibility grouping is based on the introduction, by conjugation or transformation, of a plasmid of an "unknown" Inc group into a strain carrying a plasmid of a known Inc group. If the resident plasmid is eliminated in the progeny, the incoming plasmid is assigned to its same Inc group (Datta and Hedges, 1971). Plasmids with the same replication control are "incompatible", whereas plasmids with different replication controls are "compatible". On this basis two plasmids belonging to the same Inc group cannot be propagated in the same cell line (Datta and Hughes, 1983; Couturier et al., 1988). Inc group identification has been frequently used to classify plasmids. The method has been an important tool to trace the diffusion of plasmids conferring antimicrobial resistance and also to follow the evolution and spread of emerging plasmids (Anderson et al., 1977).

A synopsis of the Datta & Hedges article sited above:

Classification
  In 1971, Hedges and Datta proposed a plasmid classification scheme based on the stability of plasmids during conjugation (incompatibility). The first incompatibility (Inc) groups were IncI, IncN, IncF, and IncP. Currently, 26 Inc groups are recognized in Enterobacteriaceae including six IncF (FII to VII) and three IncI (I1, Iγ, I2) variants. Major plasmid families occurring in Enterobacteriaceae are HI2, HI1, I1-γ, X, L/M, N, FIA, FIB, FIC, W, Y, P, A/C, T, K, B/O, FII, FIII, FIV. IncF plasmids are low- copy-number plasmids, often carrying more than one replicon with at least one replicon strongly conserved.

One way to think about it is: if one prepares a plasmid cloning vector to accept foreign inserts, and ligates in a "shotgun" collection of fragments from some DNA of interest. After transformation, selection and growth on plates, none of the colonies whose plasmids carry inserts ever contain more than one unique plasmid.  In other words, it may be possible for two different inserts to be inserted during ligation into the same vector backbone, but it is not possible to find a single pure colony that contains cells harbouring two different plasmids, each carrying a different insert.
If a cell gets transformed by two different plasmids from the same inc group only one plasmid will "win."
Examples of compatible ori's commonly encountered:

pMB9 (pBR322, pUC, etc., etc.,)
F (fosmids)
bacteriophage lambda (some cosmids)
bacteriophage M13 and relatives (also yields ssDNA phage useful for Sanger sequencing)
bacteriophage P1
pSC101

Here is a nice table, but I cannot vouch for its accuracy.

I've only ever done single plasmid transformations, where do I find incompabtibility groups?

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


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Are releasing-hormones and release-inhibiting hormones from the hypothalamus ever present in the blood?
Our teacher said that these two hormones are normally never present in the blood stream, and to be carfeul of it if it comes as a question. I'm not conviced to be honest, is this true?

I think your teacher means that these hormones only go from the hypothlamus to the anterior pituitary gland, where they stimulate hormone secretion. Like, for example, of the FSH or LH, who are stimulated by GnRH. GnRH is not present in the systemic sirculation, but it's definately present in the one between the hypothalamus and the APG. FSH and LH are though. I don't remember the name of the small blood-system between the hypothalamus and the APG, but I don't think it's connected to the systemic circulatory system.

Yes that was what he meant, he said that if one did a blood test and took blood samples (from places like the viens of the arms , like normal) you wouldnt find these hormones.

I would think it's true, but if you just google whether the different blood systems (systemic VS hypothalamus-APG) are connected you have your answer.

I see. Thanks, I didn't know the name of that system. I'll google it and see what I get.

https://en.wikipedia.org/wiki/Hypophyseal_portal_system got it!

This isn't strictly true. The hypophyseal portal system, like other portal systems (e.g., the hepatic portal system), is part of the systemic circulation, but has a second capillary bed. Releasing hormones act at very low concentrations. They are released in a pulsatile manner and are inactivated by enzymes in the blood, providing tight control of their activity in space and time.

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


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Can we detect the origin of a 1000 year old dead body after grave excavation?
I recently read an article saying DNA analysis has shown some of the people buried in Viking graves in Scandinavia originated from places like Persia and it is talking about something around 1000 years ago.
How accurate could this analysis be based on our DNA and the fact that we have 99.9%  DNA similarity?

Vikings travelled through the mediterranian and all rivers for trade, there are museums with roman jewellery and persian silk artefacts found in sweden. The analysis is FORENSICALLY precise... your mother has blue eyes, you have blue eyes. persians have type A1 protein, swedish have A2... they only have a 50 percent complete DNA to find a collection of A1,B1,C1 genes, to know that the human was almost entirely from zone 1.

Adding to comprehensible's answer, 99.9% similar DNA still leaves 0.1% of different DNA. Within this 0.1% would be enough differences to be able to find the differences that comprehensible mentioned. This is also how the ancestry tests that are so popular these days work.
Additionally, for that type of place-of-origin analysis, my impression is they commonly look at isotopes of chemicals found in the bones, and matching it to profiles found in other regions.
For example, let's say that an area we're interested in has high levels of isotope X but low levels of isotope Y in the water and food, which we discovered from examining the archeological record. If we find someone in that area whose bones have low levels of isotope X and high levels of isotope Y, we can conclude that this person traveled here later.

Note that 0.1% of the human genome leaves four million differences. Four million is plenty of room for identification


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What is the standard protocol for creating permanent stocks from freeze-dried bacteria?
I've received freeze-dried bacteria that I intend to use for a study I'm doing on slime mold; however, I've never dealt with freeze-dried, only frozen, bacterial cells. After reconstituting these cells in 6mL media, is it alright to split this in to halves and place one aliquot into DMSO or glycerol to make a permanent stock right away? Or is it best to plate, isolate, suspend, grow, and then make a permanent stock?

I was under the impression that glycerol stocks should be made from log phase cells. Therefore, I would definitely grow up the cells before freezing a glycerol stock.

I am not sure, if the cells would survive this procedure. I would reconstitute them first and then make glycerol or DMSO (which I prefer for easier handling) from fresh cultures.


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If a person touched an electric eel, would they sustain electrical burns as if they touched a high tension power line?
I've been wondering this, if an eel was continuously shocking someone, would they sustain electrical burns as if they touched a high tension power line due to the high voltage and amps?

Electric Eel
In the electric eel, some 5,000 to 6,000 stacked electroplaques can generate a shock of up to 860 volts and up to 1 ampere of current (1). They can also concentrate the discharge by curling up and making contact at two points along its body. When agitated, they can produce these intermittent electric shocks over at least an hour without tiring.  Eels have been known to jump out of the water to shock prey or dissuade threats in the air (2).
A shock from an electric eel is like the brief, numbing jolt from a stun gun. Normally, the shock can't kill a person. However, the eels can cause heart failure or respiratory failure from multiple shocks or in persons with underlying heart disease. More often, deaths from electric eels shocks occur when the jolt knocks a person in the water and they drown.
Electrical Burn
Electrical injury is the physiological reaction caused by electric current passing through the body, electrical burn is a specific subset of that. For high voltage (above 500V) damage can be very severe but most of the damage occurs bellow the skin. If the voltage is less than 200 V, then the human skin, more precisely the stratum corneum, is the main contributor to the impedance of the body in the case of a macroshock—the passing of current between two contact points on the skin. The characteristics of the skin are non-linear however. If the voltage is above 450–600 V, then dielectric breakdown of the skin occurs.(3) Whether an electrical burn occurs is not always clear cut in the case of electrical injury and will depend on the conditions of the skin (perspiration etc).
Conclusion
It is possible for an electric eel to harm a human even when out of the water. The extent of the harm will depend on the exact voltage, current, hertz, pulse duration, and number of contact points between the eel and human. Whether this harm will included electrical burns depends on further factors and is particularly difficult to answer if you limit 'burn' to injury with a visible skin defect.


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What happens to the complementary base when the other undergoes a base substitution mutation?
From what I know only the base pairs A and T/U, or G and C can occur due to hydrogen bonding. So if a base substitution mutation occurs, say an A is replaced by a C on the strand, does it affect only one of the strands on the DNA or does it changes the base pair entirely? Thanks.

Consider a stretch of DNA
A T C C T C
T A G G A G

Let's say that during replication a nucleotide get switched
A G C C T C
T A G G A G

Now, this does not work. The cellular machinery will find this location and try to solve it. It will either resolve it as
A T C C T C
T A G G A G

and no mutation would have happened. Or it will solve it as
A G C C T C
T C G G A G

and a mutation just happened.
You might want to read about DNA repair mechanisms.

A base substitution mutation often occur during replication of DNA. Remember that the template strand is methylated, in order to understand who will be the new synthetized strand between both.
Having this scenario, with a nucleotide substitution mutation in the 3rd position from 5' , the 5'-3' strand is the fresh synthetized.
The DNA polymerase will trait just the 5'-3' strand as something to work on : if a mutation happens the proof-reading activity of the DNA polymerase will try to cut off the wrong base, and to re-synthetize this piece of the strand.
5'- A G G T T C G -3' --> new strand
3'- T C A A A G C -5' --> template

If it isn't able to figure the mutation, it'll be fixed in the next replication process, so the mutation will be fixed into the considered DNA.


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How is the mechanism that reads dna passed?
DNA is how a species stores genetic information. Somehow the body needs to know what to do with this information. somehow the "machinery" that translates the DNA into proteins needs to be passed along with it.
Could this machinery also be encoded within the DNA? Or does it come automatically from some physical/chemical properties of dna? Or is it already present within the sperm/egg?
I am thinking if the dna somehow contains information on how to build the machinery to interpret it, we might be able to get a whole new understanding of how it works.

Welcome to SE Biology. Please read the Help on how to ask a question here. You are expected to demonstrate that you have done your own research before asking.Yours is a basic question that is covered in many biochemistry and biology texts, such as Berg. Please do some reading and then If you have specific questions post them here, explaining what you do not understand. Text book explanations of basic ideas in a subject are likely to be far more useful than the short answers here.

well, i come from a computer science background. biology is not my usual area of expertise so I don't know the right technical terms to put into google....

Ok, but if I posted a similarly naive question on Stack Overflow, I would be treated much more severely. Computing Scientists entering bioinformatics have to take the trouble to educate themselves in molecular biology. I mentioned one good biochemical resource. NCBI bookshelf also has older versions of a couple of outstanding Molecular and Cell Biology texts: Lodish et al. and Alberts et al. Use them!

Your question is very general, but it has a simple answer.
Yes. The protein machinery which interacts, reads, structures and manipulates the DNA strands is coded for in the DNA.
By way of example: one enzyme which opens the double helix is called DNA Helicase B. Once a DNA strand is accessible, another enzyme 'reads' (transcribes) DNA, called RNA Polymerase. In humans, the gene which produces helicase B is found on chromosome 12. The gene which produces one of the subunits for RNA polymerase is found on chromosome 10. These genes are essential for life; they are found in all organisms, perhaps excluding viruses, which hijack a host cell's machinery to duplicate their own DNA.
You may have also noticed that DNA by itself cannot 'read itself', it requires machinery in the form of proteins. How the first-ever replicating gene arose is an open question today. A likely candidate for the first ever gene, or unit of inheritance, is a kind of molecule called RNA, which is capable of storing information as well as catalyzing reactions (functioning as an enzyme).

The machinery that manipulates and read the DNA (e.g. helicase, rRNA and RNA polymerase) is itself coded in the DNA.
Now, of course, if you put an individual DNA in a bowl of water, that won't be sufficient to create a new organism. An egg (ovule + spermatozoid) is not just DNA and a membrane. It contains a lot of stuff that was already present in the ovule is still present after the spermatozoid made its entry. There is already a lot of nutrients and a lot of proteins, including those needed to manipulate and read the DNA.

Somehow the body needs to know what to do with this information.

No.  That's not how it works.  Chemicals interact with other chemicals according to their shape.  Chemicals do not "know" anything.

somehow the "machinery" that translates the DNA into proteins needs to
  be passed along with it.

Well, yes, in that when an organism divides, or makes a gameme, it doesn't make an empty cell with DNA floating alone.  The gamete or new organsim also gets the contents of the cytotol of the parent cell, which includes a bunch of of proteins.


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Frequent urination caused by sound of running water
I urinate at sound of running water when I brush my teeth or wash my hands . This only happens when I am home

Very simply put, its the power of suggestion. You urinate, flush, wash your hands umpteen times together each day. So when you hear the sound of running water, you naturally feel the need to urinate.
Apparently, the sound of running water also help patients with lower urinary tract symptoms urinate (reference)


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Could we back-breed birds into dinosaurs?
Do some species of birds have dinosaur DNA? Seeing as how birds evolved from dinosaurs. I presume this isn't possible as I haven't seen anything else about it on the internet but it's interesting to think about!
If we discovered that some bird species had traces of dinosaur DNA in it, could we selectively breed individuals with dino genes together repeatedly, over thousands of generations perhaps, until we eventually create a baby dinosaur? (Sort of like what the Tauros project is currently doing.)

Welcome to Biology Stack Exchange. You seem to have some misunderstandings  about what a dinosaur is: all birds are dinosaurs. To clarify things, you may be interested in reading:
https://biology.stackexchange.com/questions/35370/if-dinosaurs-could-have-feathers-would-they-still-be-reptiles
or

As I see it, you are thinking that birds (and probably all organisms) have a history log of mutations in their DNA that tell how their DNA looked 100 million years ago. AFAIK this is not so ;)

Do birds descend from dinosaurs?
First, it is confusing to say things like

Birds descend from dinosaurs
Humans descend from monkeys
Mammals descend from vertebrates
Snakes descend from animals

It is much more correct to say

Birds are dinosaurs
Humans are monkeys
Mammals are vertebrates
Snakes are animals

You should definitely have a look at the post If dinosaurs could have feathers, would they still be reptiles?.
Can we resurrect an ancestor from a modern day individual?
By looking at your genome, we can't know the entire genome of your mother. By looking at any modern day genome, you cannot fully know the genome of an ancestor. That being said, we can find DNA in pretty good conditions in fossils (ancient DNA aka. aDNA), so that there are ways to get to a pretty good aproximation of an ancient dinosaur genome without having to even consider the modern day descendents (or rather modern day most closely related lineages).
Can we resurrect an ancestor aDNA?
Bringing an extinct species back to life is called de-exctinction (or resurrection) and, if I am not mistaken, it has never been done. Candidate species for de-exctinction are species that are closely related with extant modern species so that we can use our knowledge of their biology and use the zygote of this extant species and just replace its genome. It is hard to imagine doing so with a species that disappeared in the Jurassic as it is already an important challenge with, more recently extinct species such as the wolly mammoth or the passenger pigeon.

The Pyrenean ibex was briefly resurrected, except it only survived for ten minutes. But thanks for your help!


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Have Polyphyodonts ever evolved from Diphyodonts?
The Wikipedia article for polyphyodont says this:

Although most extant mammals are not polyphyodont, mammalian ancestors were. During the evolution of Therapsida, there was a period during which mammals were so small and short-lived that wear on the teeth yielded no significant selection pressure to constantly replace them.

...which was a bit surprising at first, but makes sense. So I'm wondering - have any species evolved in the opposite direction? In other words, have there been any non-polyphyodont species which have teeth, and evolved into polyphyodonts?

Not true polydonty, True polydonty is an animals that grows endless numbers of teeth like reptiles and fish do.  Elephants, kangaroos, and manatees are sometimes called polydont but they are doing something very different, they still only grow a set number of teeth, but instead of growing them in two sets they spread them out growing them a few at a time. the total number of teeth is still the same as other mammals and once that last tooth falls out they can't make anymore. It is worth noting the teeth migrate forward in the jaw as they wear out unlike true polydont in which new teeth grow from below endlessly.In essence they are rationing that limited number of teeth.
True polydonty has never evolved from a non-polydont ancestor.

I might not be understanding correctly, but it seems like this isn't really answering the question

Polydont is a difficult term there is ture polydonts and mammals that get called poly dont but aren't.


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Chromonema and Chromonemata
A chromonemata is composed of two chromonema. Which are again composed of chromatin fibre. Thus my question is chromonemata is composed of how many chromatin fibre ?

It's the opposite: singular -> chromonema, plural -> chromonemata.

To my understanding, a chromonema is the filament of DNA constituting a chromosome during interphase; its equivalent during DNA replication is chromatid. The plural of chromonema is chromonemata.
The chromatin is the form in which DNA is found within the nucleus of a eukaryotic cell, that is in complex with proteins such as histones.


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Why is Sleep apnea only risk to males?
I was reading this article. In Risk Factors, it clearly mention "Being a male".
Why is Sleep apnea only risk to males?

you may want to learn what a risk factor means, it does not mean it is only a risk to males.

http://www.sleepreviewmag.com/2004/03/gender-differences-and-sleep-apnea/

Wikipedia actually means that being male is a risk factor for sleep apnea, which is a jargony way of saying that males have been observed to develop sleep apnea more often than females.
The article pointed out by com.prehensible suggests that this difference in the prevalence of sleep apnea between genders is due (in part) to a difference pharyngeal airway length (illustrated below), which is longer in men than in women even when corrected for (body) height.

Since the pharyngeal airway lacks any bones or cartilages for structural support, the theory goes that a longer pharyngeal airway is more likely to collapse during sleep, when breathing is reduced via mild to moderate hypoventilation (in everyone). Here's an illustration (3rd one in the set below) what that collapse looks like (source):

Another theory of this structural kind is that the pharyngeal cross-sectional area is smaller in women relative to men, but studies measuring this cross-section didn't all come to the same conclusion.
Finally, an experimentally observed difference between males and females during sleep is the so called "hypocapnic apneic threshold", which means that relative to men, women require a more substantial reduction in PETCO2 (a measurement of carbon dioxide partial pressure during expiration) before they show signs of apnea. A more prosaic way of saying this is that men's bodies are more prone to go into a state where a reduction CO2 in the expiration causes the brain to decide to stop breathing for a bit because it seems it has enough oxygen (based on the lack of CO2). This mechanism is substantially inhibited during wakefulness and least inhibited during NREM sleep (and in REM sleep it's somewhere in between).
Why there's a difference in this threshold between men and women is not known precisely, but another experiment established that giving testosterone to women increased their breathing instability during sleep. And conversely, blocking some of the effects of testosterone by administration of finasteride increased breathing stability in healthy men during sleep. Note that this is a pretty new (2013) study. Neither finasteride nor any other medication is currently FDA-approved for treating sleep apnea.
And one more thing to point out is that there are different types of sleep apnea, so the two mechanisms discussed above are not necessarily contradictory or competing; the first one (airway length and its collapse) is mostly relevant to obstructive sleep apnea, while the second one is more often discussed in the context of the so-called central sleep apnea.


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What disposition means in the context of registering clinical studies?
I was diving into the AACT database, and in the studies table I had noticed some columns containing the term disposition such as:

disposition_first_submitted_date
disposition_first_submitted_qc_date (qc means quality control)
disposition_first_posted_date
disposition_first_posted_date_type

and I do not know what disposition means in this context.
Additional information
The AACT database contains the same data as ClinicalTrials.gov, but in a relational databse, so it is a database of all clinical trials made in the US, but also has international studies.
Every row in the studies table represents a clinical study.
Here is the first 5 rows where the disposition_first_submitted_date is not null, alongside the header:
|nct_id                                                                                |nlm_download_date_description                                                                       |study_first_submitted_date|results_first_submitted_date|disposition_first_submitted_date|last_update_submitted_date|study_first_submitted_qc_date|study_first_posted_date|study_first_posted_date_type                                                                        |results_first_submitted_qc_date|results_first_posted_date|results_first_posted_date_type                                                                      |disposition_first_submitted_qc_date|disposition_first_posted_date|disposition_first_posted_date_type                                                                  |last_update_submitted_qc_date|last_update_posted_date|last_update_posted_date_type                                                                        |start_month_year                                                                                |start_date_type                                                                                |start_date|verification_month_year                                                                             |verification_date|completion_month_year                                                                               |completion_date_type                                                                                |completion_date|primary_completion_month_year                                                                       |primary_completion_date_type                                                                        |primary_completion_date|target_duration                                                                                |study_type                                                                                |acronym                                                                                |baseline_population                                                                                |brief_title                                                                                |official_title                                                                                |overall_status                                                                                |last_known_status                                                                                |phase                                                                                |enrollment |enrollment_type                                                                                |source                                                                                |limitations_and_caveats                                                                             |number_of_arms|number_of_groups|why_stopped                                                                                |has_expanded_access|expanded_access_type_individual|expanded_access_type_intermediate|expanded_access_type_treatment|has_dmc|is_fda_regulated_drug|is_fda_regulated_device|is_unapproved_device|is_ppsd|is_us_export|biospec_retention                                                                                |biospec_description                                                                                |ipd_time_frame                                                                                |ipd_access_criteria                                                                                |ipd_url                                                                                |plan_to_share_ipd                                                                                |plan_to_share_ipd_description                                                                       |created_at         |updated_at         |
|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|--------------------------|----------------------------|--------------------------------|--------------------------|-----------------------------|-----------------------|----------------------------------------------------------------------------------------------------|-------------------------------|-------------------------|----------------------------------------------------------------------------------------------------|-----------------------------------|-----------------------------|----------------------------------------------------------------------------------------------------|-----------------------------|-----------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------|----------------------------------------------------------------------------------------------------|-----------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|---------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|-----------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|-----------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|--------------|----------------|----------------------------------------------------------------------------------------------------|-------------------|-------------------------------|---------------------------------|------------------------------|-------|---------------------|-----------------------|--------------------|-------|------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|-------------------|-------------------|
|NCT00684515                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2008-05-22                |2014-05-09                  |2008-10-09                      |2018-08-22                |2008-05-22                   |2008-05-26             |Estimate                                                                                |2014-07-28                     |2014-07-29               |Estimate                                                                                |2009-10-21                         |2009-10-22                   |Estimate                                                                                |2018-08-22                   |2018-09-21             |Actual                                                                                |September 21, 2006                                                                                |Actual                                                                                |2006-09-21|August 2018                                                                                |2018-08-31       |November 8, 2007                                                                                |Actual                                                                                |2007-11-08     |November 8, 2007                                                                                |Actual                                                                                |2007-11-08             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Trial to Assess the Safety of Vorapaxar in Japanese Subjects With Cerebral Infarction (P05005; MK-53|Phase II Study of SCH 530348 in Subjects With Cerebral Infarction                                   |Completed                                                                                |                                                                                |Phase 2                                                                                |90         |Actual                                                                                |Merck Sharp & Dohme Corp.                                                                           |                                                                                |3             |                |                                                                                |false              |                               |                                 |                              |true   |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |http://engagezone.msd.com/ds_documentation.php                                                      |Yes                                                                                |https://www.merck.com/clinical-trials/pdf/ProcedureAccessClinicalTrialData.pdf                      |2020-02-26 08:06:42|2020-02-26 08:06:42|
|NCT00684203                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2008-05-22                |2014-05-09                  |2008-10-09                      |2017-03-31                |2008-05-22                   |2008-05-26             |Estimate                                                                                |2014-07-28                     |2014-08-15               |Estimate                                                                                |2009-10-21                         |2009-10-22                   |Estimate                                                                                |2017-03-31                   |2017-05-05             |Actual                                                                                |December 1, 2006                                                                                |Actual                                                                                |2006-12-01|March 2017                                                                                |2017-03-31       |October 1, 2007                                                                                |Actual                                                                                |2007-10-01     |October 1, 2007                                                                                |Actual                                                                                |2007-10-01             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Trial to Assess the Safety and Effects of Vorapaxar in Japanese Subjects With Acute Coronary Syndrom|Phase II Study of SCH 530348 in Subjects With Acute Coronary Syndrome                               |Completed                                                                                |                                                                                |Phase 2                                                                                |120        |Actual                                                                                |Merck Sharp & Dohme Corp.                                                                           |                                                                                |5             |                |                                                                                |false              |                               |                                 |                              |true   |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |2020-02-26 08:06:46|2020-02-26 08:06:46|
|NCT00452426                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2007-03-26                |2010-10-06                  |2008-10-16                      |2010-12-30                |2007-03-26                   |2007-03-27             |Estimate                                                                                |2010-12-30                     |2011-01-25               |Estimate                                                                                |2008-10-22                         |2009-10-02                   |Estimate                                                                                |2010-12-30                   |2011-01-25             |Estimate                                                                                |March 2007                                                                                |                                                                                |2007-03-31|December 2010                                                                                |2010-12-31       |October 2007                                                                                |Actual                                                                                |2007-10-31     |October 2007                                                                                |Actual                                                                                |2007-10-31             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Safety and Effectiveness of a Computer-Assisted Personalized Sedation (CAPS) Device for Propofol Del|Multi-center Pivotal Clinical Trial to Compare the Safety and Effectiveness of Procedural Sedation i|Completed                                                                                |                                                                                |Phase 3                                                                                |1000       |Actual                                                                                |Ethicon Endo-Surgery                                                                                |                                                                                |2             |                |                                                                                |false              |                               |                                 |                              |true   |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |2020-02-26 09:15:02|2020-02-26 09:15:02|
|NCT00318214                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2006-04-24                |                            |2008-12-04                      |2012-05-24                |2006-04-25                   |2006-04-26             |Estimate                                                                                |                               |                         |                                                                                |2009-11-05                         |2009-11-09                   |Estimate                                                                                |2012-05-24                   |2012-06-01             |Estimate                                                                                |June 2006                                                                                |                                                                                |2006-06-30|May 2012                                                                                |2012-05-31       |February 2008                                                                                |Actual                                                                                |2008-02-29     |February 2008                                                                                |Actual                                                                                |2008-02-29             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Safety and Efficacy Study of MRE0094 to Treat Large, Single or Multiple, Chronic, Neuropathic, Diabe|                                                                                |Terminated                                                                                |                                                                                |Phase 2                                                                                |16         |Actual                                                                                |Pfizer                                                                                |                                                                                |2             |                |The study had poor enrollment with only 16 patients randomized across 19 study centers over an¶    1|false              |                               |                                 |                              |false  |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |2020-02-26 09:56:26|2020-02-26 09:56:26|
|NCT00312364                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2006-04-06                |                            |2008-12-04                      |2012-05-24                |2006-04-06                   |2006-04-10             |Estimate                                                                                |                               |                         |                                                                                |2009-11-05                         |2009-11-09                   |Estimate                                                                                |2012-05-24                   |2012-06-01             |Estimate                                                                                |December 2005                                                                                |                                                                                |2005-12-31|May 2012                                                                                |2012-05-31       |December 2007                                                                                |Actual                                                                                |2007-12-31     |December 2007                                                                                |Actual                                                                                |2007-12-31             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Safety and Efficacy Study of MRE0094 to Treat Chronic, Neuropathic, Diabetic Foot Ulcers            |                                                                                |Completed                                                                                |                                                                                |Phase 2                                                                                |322        |Actual                                                                                |Pfizer                                                                                |                                                                                |              |                |                                                                                |                   |                               |                                 |                              |       |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |2020-02-26 09:58:37|2020-02-26 09:58:37|

I suspect disposition in this context is not about the subjects leaving the study or the drug interacting with the patients. If I have to guess: it means the beginning of the study.


text:
How taking up plasmids on heat shock evolutionary advantageous to bacteria?
During the transformation protocol we apply heat shock to bacteria to make them take up plasmids from their environment. It is really useful in the lab.
However, it presents an evolutionary paradox in a bigger context, if bacteria begin to take up free floating plasmids on distress, they will most likely acquire genes from the other bacteria, who perished in the same distress, so those genes most likely will not be useful against their adversity.
I am sure there are other factors here to resolve this paradox. What are they?

The simplest one is they didn't. Not everything an organism does or has is an advantage many are side effects of  other mechanisms or the case of heat shock you are purposely creating highly unlikely conditions to break existing mechanisms. In the case of heat shock, high heat coupled with very high calcium levels break down the normal mechanisms that prevent plasmids from entering the cell, after that normal diffusion takes over.  It is like asking why we evolved to absorb material injected into us, we didn't injection is bypassing the normal defense mechanisms. It is similar to using DMSO to carry molecules across the skin, DMSO is so unbelievably unlikely in nature that there has never been a reason to evolve a defense for it.


text:
What percentage of twins has the same gender
If 30% of all twins are identical twins, what percentage of twins has the same gender? I thought: all identical twins have the same gender so it’s at least 30%. And of the non-identical twins it’s about 50%. So 50+30=80%?? Correct me if I’m wrong..?

I agree that same sex twins account for about two-thirds. Note that this means that the naive hypothesis that the three possible configurations BB, BG and GG have equal probability gives the right answer!

You stated:

30% of twins are identical
50% of non-identical twins have the same gender

Therefore 70% of twins are non-identical and 50% of those will have the same gender. I'll leave the rest of the calculation to you.

So: 35+30= 65% of twins have the same gender?

@Mett123 Based on the information you gave, that would be correct.


text:
New infectious diseases appear mainly as a result of chance mutations in pathogen genomes?
I am reading the book 'Homo Deus: A breief History of Humankid' by Harari. He mentions the following statement highlighted in the picture below (picture provided for context). I would be appreciated if someone could (1) explain the meaning of it (I have very little background in Biology) and (2) the reason behind it.

Welcome to Biology.SE. The issue is that the text is really not rigorous and phrased in slightly vague term. Also, it is a little unclear what exactly your might be misunderstanding from the highlighted part. I don't think we can answer much else than simply giving you an intro course to evolutionary biology. I am therefore voting to close as too broad but maybe you'll be able to explain better what exactly is unclear to you in these few words.

For an very short and very introductory course, you might want to have a look at Evo101 by UC Berkeley

Mutations happen all the time when DNA is replicated. These random mutations are the building blocks for evolution under natural selection. So when a single nucleotide is changed, (or deleted or added), there are three possible outcomes. 1. the mutation is neutral, so nothing happens. 2. The mutation is lethal or mal-adaptive for the organism, in which case natural selection will remove the individuals carrying the mutation from the population, or 3. the mutation results in some change in function that helps the organism compete under natural selection. This 3rd kind is the rarest, but with pathogenic viruses and bacteria, with huge populations, the evolutionary test pool is much larger because there are so many new mutations being put to the test with every generation. So, for example, a mutation in a pathogen adapted to spread through chickens, could change the pathogen to be better adapted for spreading through humans.

I will be a bit picky and awfully pedantic (sorry) but I think a rigorous phrasing is important here. the mutation results in some change in function that helps the organism compete under natural selection. A) associating change of function with beneficial consequence, not not talking about a change in function in other cases is misleading. Change of function can go both ways. B) summarizing "higher fitness" to "helps the organism compete under natural selection" is misleading because 1) fitness differential does not necessarily require competition 2) NS is not a condition under which ...

competition occurs but the concept of fitness differential (+ heritability) itself. Also, it is clear that population size matters but it is not as easy as your answer might make it think. Also expressions like evolutionary test pool are very much undefined. The expression random mutations can also be very misleading (see the post Are mutations random?)

These random mutations are the building blocks for evolution under natural selection. Mutations are the ultimate source of genetic variance. It fuses evolution whether there is a selective pressure or not.

adapted to spread through chickens, could change the pathogen to be better adapted for spreading through humans I understand that this goes along the example of the text given by the OP but, IMHO, I think it would be good to avoid giving the misrepresentation to the OP that evolution for a pathogen is an event that necessarily allows a pathogen to jump from one host to the other and that all other evolutionary events would be of no interest or even would not be part of evolution.

@Remi.b I'd be glad to discuss this with you.


text:
identify this ant queen
can anyone help me identify this ant queen, if it's an ant queen? I only assume it is because I caught another with wings which looks exactly the same. Thanks in advance..

There is only one segment between the thorax and the abdomen and the first segment of the abdomen is not elongated, which indicates this is a Formicinae.
Because the head width is similar to the thorax width from top view, this likely corresponds to a social parasite ant from the genus Lasius.
See ref below:

Seifert, Bernhard. Die Ameisen Mittel-und Nordeuropas. Lutra Verlag-u.
  Vertriebsges., 2007.


text:
Its there a gene or genes for intelligence?
I don't know almost nothing of genetics but I felt a little interested in the subject of genetics and its role in intelligence and i found to reports that talk about certain genes that contribute to intelligence
https://www.nature.com/news/smart-genes-prove-elusive-1.15858 https://www.newsweek.com/how-be-smart-intelligence-linked-500-genes-large-new-study-842454
What I don't understand is if only some people have this 500 genes or all human population has this genes?

Is IQ heritable?

Let me start by saying that there is no commonly agreed upon method to measure IQ (thank you @mdperry). Keeping this in mind...
Yes, studies have shown that IQ is heritable. Or rather, IQ has a heritability that differs from both 0 and 1, meaning that both environment variation and genetic variation plays a role in determining an individual's IQ. Studies show IQ heritability varying between 0.5 (ref) and 0.8 (ref). For more information, please have a look at this post.
To understand the concept of heritability, please have a look at Why is a heritability coefficient not an index of how “genetic” something is?.

What are the genes that contribute to it?

IQ is a polygenic trait, meaning that many loci (locus = position in the genome) are affecting the variation in IQ. For more information about those loci, please have a look at this post.

What I don't understand is if only some people have this 500 genes or all human population has this genes?

Your misunderstanding comes from a misunderstanding about the concepts of gene and allele. You should start by having a look at the definition of the three following terms

gene
allele
locus

Below, I will not comment about the 500 genes claimed in this popular article and will just consider them as valid without considering the complication behind the methodology used for such estimation and about what original articles this popular article is citing.
With the exception of eventual copy number variation, the entire human population share these 500 genes but not everyone has the same allele at these 500 loci.

You say that IQ is polygenic and many genes affect IQ, but theres evidence of certain genes that certain population has but other population dont have? im not talking about alleles

I don't understand your comment. Are you making a claim or asking a question (there is a ? but the sentence is not phrased like a question)? Are you talking about CNV? Are you now talking about among population variance (which was not the subject of your question)?

Oh nevermind im just very bad at formulating scientific questions hahaha, anyway thanks for the initial response and for clarify my doubts.

@Roby If you consider that the answer has answered your question, then you can click the checkmark next to the answer so as to mark the post as answered.

I would be remiss if I did not mention that there is no accepted method to determine the IQ of an individual.


text:
Can enzymes be modeled using classical mechanics?
When enzymes interact with substrates (i.e. a small ADP molecule and the much larger ATP synthase), does quantum mechanics play a significant role? Or can the interactions be relatively accurately be understood using simply classical mechanics principles?
For example, considering a free body diagram when I insert a key into a lock, the interactions between the key and the lock can be accurately modeled using simply classical mechanics (such as friction, normal forces, etc).
However, since the scale of proteins and molecules are much smaller, could the binding of ADP to ATP synthase still be accurately modeled using classical mechanics (i.e. electrostatic forces, physical contact forces, etc.)? Or are quantum principles very significant?

Related.

I think, this paper can help you understand current state of Quantum Biology and related issues.

This question may get more attention on the new Materials Modeling SE


text:
Can mitochondria become cancerous?
Given that mitochondria have their own DNA and can replicate independently, can they ever become cancerous? For example, could a mutation in their DNA cause them to rapidly replicate, ultimately killing the cell it's in?

Interesting question.
As a prelude, I should probably mention that single celled organisms cannot get cancer as we understand and define it. Mitochondria are not, of course, single celled organisms, they are organelles, but this interesting question involves treating them as if they were autonomous. We'll come back to that later. First, single-celled organisms and cancer...
Of all the hallmarks of cancer, unregulated replication is probably the most fundamental, but all the same, cancer is necessarily a disease of multicellular organisms with differentiated tissues. Bacteria do not get cancer. Protozoa do not get cancer. Yeast do not get cancer. I'm spending too much space on my prelude here, but let's pretend like this isn't an issue and just address unregulated replication. Incidentally, the review I linked is an updated version of the classic review of cancer biology. If you're interested in cancer biology, I highly recommend reading it, and perhaps the original 2000 review.
Ok, now to the question. Let's put aside the problem of a single organelle or single celled organism getting cancer, and consider whether mitochondria can develop mutations in their DNA that cause them to replicate in an unregulated fashion.
Yes, mitochondria do have their own DNA, but they are not fully autonomous.  They do "replicate independently", but what is meant by this is that mitochondria replication (via fission) is a process that occurs independent from the replication (via mitosis) of its enclosing cell. The process is regulated by proteins encoded in the nuclear genome (not the mitochondrial genome)
Both fission and fusion are regulated by dynamin related proteins, which you can read about in this, fairly dense review. The mitochondrial genome encodes very few genes, 14 at last count, and while problems with those genes and proteins are implicated in a few diseases, uncontrolled replication is not one of them.

Hmm, thanks for the detailed response. However, that brings me to ask: if the nuclear DNA regulates mitochondrial replication, then if that  DNA is damaged or mutated, could that result in uncontrolled replication of the mitochondria?


text:
When does protein folding begin?
I had always assumed that protein folding is an independent activity that occurs after translation is complete. However, recently, I learned that intermolecular forces begin shaping the peptide bonds as they exit the ribosome, while translation is still occuring.
This leads me to ask: when do the "stages" of protein folding take place? What is a general "timeline" for protein folding? For example, when do secondary and tertiary structures begin forming? Or, when do things like chaperones bind and act?

When does protein folding begin?
With reference to time you have asked, it can be after the translation has occurred (called Translational protein folding) or while translation is still occuring (called Co-Translational protein folding). Here is the link to an article for basic understanding of co-translational protein folding.
There is a lot of debate on the true time. Experimentalists have amassed extensive evidence over the past four decades that proteins appear to fold during production by the ribosome. Protein structure prediction methods, however, do not incorporate this property of folding (reference).
If you are looking at particularly some organisms it is advised to refer to the research articles related to them.The primary mechanism is the interplay between several non-covalent interactions such as hydrophobic effect and hydrogen bonding in a cooperative manner (they also follow basic rules of thermodynamics) which leads to a marginally stable tertiary structure.
When do secondary and tertiary structures begin forming?
Ofcourse, after Primary structure forms.The alpha helices/beta sheets then fold in a cooperative manner to form a tertiary structure.
One point to note is that, slight variations in these cooperative act causes misfoldingng of proteins which may cause certain diseases.

@WYSIWYG Thanks for your comment.I didn't understand where is the contradiction. Let me clarify you that Protein cannot go directly to it's tertiary structure without passing through secondary primary and secondary.On the way of attaining it's tertiary structure these two structure will form.During translation the forming polypeptide itself a primary structure.

Okay. I assumed that you meant the full length polypeptide by primary structure. I'll remove my comment.

Folding starts as soon as the protein starts being translated and actually, the ribosome affects the folding of the protein.
You can read more here.


text:
How do receptors lose their sensitivity?
Recently, I learned that one of the causes of Type II diabetes is that insulin receptors on cell surfaces lose their sensitivity due to long-term high exposure to insulin (which occurs as a result of high blood sugar).
How do receptors (like that for insulin) become more resistant to ligands? Is the receptor itself getting damaged? If so, how, and why don't other frequently activated proteins/receptors (like GPCR's) also get damaged? If not, then how does the cell become more "resistant" to insulin?

There are different mechanisms for different receptors, so this is a very broad question. It's usually a negative feedback from within the cells. For insulin resistance, you can check Figure 1 in this article.

The field of insulin resistance is a very active research area and hundreds of research papers on the topic are published every year. There appear to be many mechanisms involved in the development of insulin resistance and to give a full answer might not be possible at this time.

The major celltypes responsible for getting rid of blood glucose are the liver, adipose tissue (fat cells) and the muscles.
The problem of how muscles becomes insulin resistance was solved by a team of scientist led by Gerald Shulman a few years ago.
The mechanism is that incread levels of diglycerides (note that normal fat in the body is in the form of triglycerides) in the muscle  cells prevents/makes it harder for glucose transporters of the type glut-4 to attach to the cell membrane. Thus causing incread levels of insulin in the blood in order to get the muscle cells to accept the glucose.
This seems to be the major reason for how muscle cells become more "resistant" to insulin. It is mostly not the insulin receptors becoming dysfunctional or fewer but diglycerides stopping the insulin receptors from getting the glucose transporters to the cell membrane imparing the glucose uptake. Listen to Geralds Banting price lecture:
https://www.youtube.com/watch?v=TnvmEUUtoZw


text:
Decision-making in tree limb growth?
Sorry if this is a naive question, but it occurred to me as I was walking across campus today; How does a tree decide which limb is allocated the most resources, and thus grows the largest?
My first thought is the first branch to deviate from the base receives the most energy investment, and so on, but I don't have the time (or will) to actually test that. Does it have more to do with efficacy of the limb for photosynthesis? Or is it largely due to chance/unknown variables?
Thanks in advance, I feel this is something I learned back in botany and just forgot completely.

There is Milton’s Law of resource availability and allocation.
It states that branches act as if they were different individuals, and they grow relative to the availability of their own resources.
The cells that grow are called meristems, there are different kinds of meristems, cambium ones that grow the trink, apical meristems that grow at the top,
Apical dominance is phenomenon where one meristem prevents or inhibits the growth of other meristems. As a result, the plant will have one clearly defined main trunk. For example, in trees, the tip of the main trunk bears the dominant meristem. Therefore, the tip of the trunk grows rapidly and is not shadowed by branches.
If the dominant meristem is cut off, one or more branch tips will assume dominance. The branch will start growing faster and the new growth will be vertical.
Over the years, the branch may begin to look more and more like an extension of the main trunk. Often several branches will exhibit this behaviour after the removal of apical meristem, leading to a bushy growth.
The mechanism of apical dominance is based on the plant hormone auxin. It is produced in the apical meristem and transported towards the roots in the cambium.
If apical dominance is complete, it prevents any branches from forming as long as the apical meristem is active. If the dominance is incomplete, side branches will develop.


text:
How do schistosomes find and attach to human skin?
Schistosomes are parasitic flatworms that have a snail intermediate host and a human definitive host.
After developing in the snail, they (cercariae stage) escape into the water and can attach to the skin of a human. Then, it will penetrate the skin and migrate into areas of the human's body.
I have been unable to find any information on the mechanisms related to attachment to the human host's skin. More specifically, my questions are:

Do they attach to whatever they can find, and can only develop into the next stage if they (by chance) attach to the right host?
If they selectively attach to human host skin, how do they detect the skin? What makes the skin distinguishable to them?

Here is a great picture of the life cycle of these parasites, for reference.

Schistosoma recognize human skin by mechanical, thermal and chemical stimuli from host. Attachment of parasite to skin is  stimulated by L-arginine. Schistosomes specifically bind  to L -argine by chemotaxis. L-arginine guides this parasite towards site of penetration. The lipids on the human skin surface also serve as signal for host invasion.
It is also reported that parasite may use L-arginine to synthesize nitric oxide for blood vessel dilation so that it can easily penetrate into the host. Schistosoma may attach to L-arginine of surrounding tissues to escape the cellular immune response from host.
(Via: https://www.ncbi.nlm.nih.gov/pubmed/11860033)
These parasites enter the host through skin by producing several proteolytic enzymes to degarde the host tissue proteins including elastin, condromucoprotein, keratin, fibronectin, laminin and collagens.
Two distant serine proteases are responsible for digesting host tissue. One is Chymotrypsin-like protease which degrades protein with large hydrophobic side chains. And the second one is Trypsin-like protease which prefers proteins with positively charged side chains.
(Via: http://www.jbc.org/content/275/49/38667.full#ref-2)


text:
How do parasites "reprogram" brains?
Dicrocoelium dendriticum is a parasite that uses ants as a second intermediate host (which means that ants aren't its primary host/target, but are rather a temporary host to help reach their main/definitive host: sheep).
When ants are infected, this parasite causes them to climb onto the top of grass blades, which increases the chance that sheep will devour the ant along with the grass, helping the parasite reach the sheep.
My question is: how do parasites such as (but not limited to) that described above "reprogram" the minds of the hosts? I know that brains are incredibly complex, so I'm fascinated and curious about how a parasite can change the behavior of its hosts - which I'm assuming is only possible by modifying its brain? If so, how do they do this?

Related Q/A:   can-the-dead-be-brought-back-to-life-by-viruses.

Also related: https://biology.stackexchange.com/questions/23297/what-kind-of-fly-is-this/23298#23298

Not much is known about the mechanisms involved, but they do appear to differ significantly from parasite to parasite. I'll discuss a few different examples here, and try to provide as much information as is currently known about how the parasites are doing it.
There are likely to be many more different examples and mechanisms than these, and researchers may well revise the below hypotheses over time. For this reason, I'm thinking about either splitting this answer into multiple separate answers or changing it into a community wiki.
Example 1 - Toxoplasma gondii and rats as an intermediate host
The Toxoplasma gondii parasite infects multiple hosts during its lifecycle. At one stage, it is hosted by a rodent, which must be eaten by a cat if the parasite is to use the feline's gut in the next stage of its life cycle. Somehow, the parasite causes the rodent (I know that rats are affected, but I don't know if mice or other rodent species are) to behave in a less risk-averse way around cats, making it more likely to be eaten by them.
Exactly how Toxoplasma influences its rodent hosts is unclear. An article in Nature ("Parasite makes mice lose fear of cats permanently") mentions that the parasite creates cysts within the rodent's brain cells, increasing their production of dopamine, which may be one of the causes for the change in behaviour. However, the researchers quoted in the article found that the risk-taking behaviour persisted even without the cysts and dopamine.
Link to that research paper: "Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance".
One theory is that the parasite simultaneously infects the ovaries/testes of the rodent, causing increased testosterone levels in the male and thereby causing it to engage in more risk-taking behaviour. A lot of the literature relevant to this theory is behind paywalls, but as far as I can tell studies have shown that:

Male rats with their testes removed are not affected by the behavioural changes, although I do not know if the orchiectomies were performed before or after infection.
Male rats in general are affected.
Female rats are affected by the behavioural changes, whether or not their ovaries have been removed.

This suggests that the parasite has more than one means of inducing the behavioural changes in the rodent, and that the behavioural changes in female rats have a different cause to the same behavioural changes in males. In the case of the male, it is believed that epigenetics play a part. The increased testosterone levels lead to reduced methylation in genes in a certain area of the brain, and this in turn leads to increased production of the chemical "arginine vasopressin" (AVP). I know nothing about AVP, but the increased levels of it are supposed to cause the behavioural changes, according to this theory.
As I mentioned, the presence of paywalls is giving me some difficulty in studying the relevant research for this particular theory, but a link to one paper is provided in the "Sources" list below.
Another theory is that the parasite infects the white blood cells and causes them to produce excess quantities of a chemical that acts as a neurotransmitter, affecting the brain through the increased levels of said chemical. The research paper is "GABAergic Signaling Is Linked to a Hypermigratory Phenotype in Dendritic Cells Infected by Toxoplasma gondii".
There's also a New Scientist article: "Parasite makes mice fearless by hijacking immune cells")
Example 2 - Ophiocordyceps unilateralis (fungus) and carpenter ants
A recent article in Ars Technica ("Zombifying fungus bypasses the brain to make ants its puppets, study finds") described research into another example, the Ophiocordyceps unilateralis fungus that parasitizes carpenter ants. The researchers had found that the fungal cells in the ant's body effectively disconnected its brain and linked up to act as a replacement brain to move the host's limbs.
Link to the research paper: "Three-dimensional visualization and a deep-learning model reveal complex fungal parasite networks in behaviorally manipulated ants"
(If I understand correctly, the brain's disconnection might be due to damage caused to it by chemicals emitted by the fungus. It may be the case that the original brain and fungal network are both able to move the ant's limbs during the early stages of infection, I'm not sure.)
Even then, one piece at least of the host's altered behaviour wasn't in fact due to this, but due to the fungus destroying a protective membrane on the ants' jaw muscles - leading to the famously strong "death grip" as the infected ant bites a high leaf, dies, and is held in place by the grip of its jaws.

The O. unilateralis fungus extending soma stalks and fruting heads from the bodies of dead ants. Image taken from https://en.wikipedia.org/wiki/File:Ophiocordyceps_unilateralis.png. The image was posted under a Creative Commons Attribution 2.5 Generic license and is credited to David P. Hughes and Maj-Britt Pontoppidan.
The research paper for the jaw membrane is, unfortunately, behind a paywall. If you have access: "Zombie ant death grip due to hypercontracted mandibular muscles"
The "cut off and replace the brain" part of this was also covered by a 2017 article in The Atlantic ("How the Zombie Fungus Takes Over Ants’ Bodies to Control Their Minds").
Example 3 - Dicrocoelium dendriticum and ants
For the actual host/parasite pairing that OP was asking about, not as much is known. One fascinating aspect of this infection is that the ant's behaviour is only changed during the evening/nighttime hours. As day approaches, if the ant has not already been eaten, and if the temperature exceeds a certain threshold, the ant climbs back down to ground level. It rejoins the colony (which does not reject it) and continues to function normally until night falls again, whereupon it climbs back up to the top of the blade of grass.
(In some situations, it may climb up a flower stem and attach itself to a petal.)
A team of researchers used micro-CT scanning to examine the brains of infected ants, publishing their results in a 2018 Nature article ("3D virtual histology at the host/parasite interface: visualisation of the master manipulator, Dicrocoelium dendriticum, in the brain of its ant host")
Most of the parasites are situated in a region of the ant's abdomen known as the "gaster". At this stage in their lifecycle, they are known as "metacercariae". At least one of the parasites, however, will enter a region of the ant's nervous system known as the "suboesophageal ganglion" (SOG). In the brains examined by the researchers, one (and only one) of the parasites in that area would attach its "oral sucker" to the brain tissue of the host ant. This would occur in "the ventral-anteriormost region of the SOG".
The parasites in the gaster are contained within cysts. Some or all of the ones in the brain may not be. The parasite that has attached its oral sucker is not. This one is informally nicknamed "the brain worm".
What is so significant about the SOG region? For one thing:

dendrites of the 10–12 motor neurons that stimulate the fast muscle fibres of the mandibular closure muscles in ants share the same neuropil in the ventral-anteriormost region of the SOG24 – the precise location where non-encysted D. dendriticum metacercariae are located. Thus, by targeting this region of the SOG, D. dendriticum has the potential to directly interfere with ... the action of the mandibles.

Thus we see another mechanism used by a parasite to force its ant host to grip something tightly with its mandibles.
The SOG also has some connection to locomotive activity - presumably getting the ant to climb the blade of grass and/or stopping it from climbing down too soon:

Site-selection and development of non-encysted metacercariae within the SOG can provide a direct pathway for the manipulation of locomotory activity.

And even more...

The SOG is a major part of the nervous system-wide network for neuromodulation in insects, evidenced by the many different neuromodulators expressed in neurons that reside in this region of the brain [25,26,27]. The effects of these neuromodulators ... are diverse and far reaching, from flight modulation, visual dishabituation and olfactory learning to mediation of the fight-or-flight response and the control of aggression ... FMRFamide-like peptide is implicated both as a neurotransmitter and a neuromodulator and affects the nervous system as well as skeletal muscle [25]. Thus, any influence exerted by metacercariae on the activity of neuromodulatory neurons in the SOG could have far reaching consequences for the behaviour of infected ants.

The researchers noted that they did not know if the "brain worm" was in contact with the SOG all the time, or just when the temperature was low enough to induce the changed behaviour. Further research was needed.
Sources:

Ingram WM, Goodrich LM, Robey EA, Eisen MB (2013). Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance. PLoS ONE 8(9): e75246. https://doi.org/10.1371/journal.pone.0075246
Abdulai-Saiku, S., Vyas, A. Loss of predator aversion in female rats after Toxoplasma gondii infection is not dependent on
ovarian steroids. Brain Behav. Immun. (2017), http://dx.doi.org/10.1016/j.bbi.2017.04.005
Fuks JM, Arrighi RBG, Weidner JM, Kumar Mendu S, Jin Z, Wallin RPA, et al. (2012). GABAergic Signaling Is Linked to a Hypermigratory Phenotype in Dendritic Cells Infected by Toxoplasma gondii. PLoS Pathog 8(12): e1003051. https://doi.org/10.1371/journal.ppat.1003051
Fredericksen MA, Zhang Y, Hazen ML, Loreto RG, Mangold CA, Chen DZ and Hughes DP. (2017). Three-dimensional visualization and a deep-learning model reveal complex fungal parasite networks in behaviorally manipulated ants. Proceedings of the National Academy of Sciences Nov 2017, 114 (47) 12590-12595; DOI: 10.1073/pnas.1711673114
Mangold CA, Ishler MJ, Loreto RG, Hazen ML and Hughes DP. (2019). Zombie ant death grip due to hypercontracted mandibular muscles. Journal of Experimental Biology 2019 222: jeb200683 doi: 10.1242/jeb.200683
Martín-Vega D, Garbout A, Ahmed F. et al. 3D virtual histology at the host/parasite interface: visualisation of the master manipulator, Dicrocoelium dendriticum, in the brain of its ant host. Sci Rep 8, 8587 (2018) doi:10.1038/s41598-018-26977-2

Welcome to Biology.SE! Nice answer(+1) and a good job on providing supporting references. However, can you please edit to add references to the original research (rather than just popular science articles) and also include the complete reference information since links can break. Search on Google Scholar and click on the ‟ symbol to get reference information for journal articles. This is a good example of how to format references. Thanks!

@tyersome Thanks - I have now added the references.

The answer to OP's question, while complex and not fully understood, varies significantly depending on the parasite/host combination. Due to the large number of different cases with different mechanisms involved, I would like to either (a) make this answer into a community wiki so that more of these can be added over time, or (b) split it up into multiple separate posted answers. Can any of the moderators/most-experienced users advise me on the best choice here - or should I keep it in its current format?

Regarding my above comment - I may want to add more information over time regarding the different mechanisms of parasite-induced behavioural change, so if this were split into separate answers, I may want to post more answers later on.


text:
Reason behind using DNA primer in PCR techcnique while RNA primer use in replication in vivo?
I have went through Lehinger ( biochemistry book) and cooper ( cell Biology) but i didn't find my answer.
plese help me

Your question isn't very clear; could you please elaborate?

The (very) basic answer to your question about in-vitro vs. in-vivo primer usage is:

In-vivo - Although either (DNA or RNA primers) can be used for in-vivo primer extension biochemistry, DNA primers are not available (not made) in living cells. Therefore all natural in-vivo primer chemistries utilize RNA primers.
In-vitro - DNA primers are easily synthesized, inexpensive, functional, and substantially more stable (less likely to be degraded). DNA primers are therefore primarily used for most in-vitro purposes (i.e. PCR and other in-vitro primer extension applications).

Beyond that, all other reasons (complex evolutionary reasons vs. human choices in-vitro); involving subtle differences between RNA and DNA chemistry, structure, and function, similarly can play a role. The links below may be helpful to address some of these differences.
https://en.wikibooks.org/wiki/Structural_Biochemistry/Nucleic_Acid/Difference_between_DNA_and_RNA
https://en.wikipedia.org/wiki/Primer_(molecular_biology)

Generally speaking, initiation of DNA replication in vivo at a defined origin of replication, requires an enzyme with DNA primase activity.  DNA primase is a DNA-dependent RNA polymerase that generates short RNA primers that are used to prime DNA synthesis by the DNA polymerase holoenzyme at a so-called replication fork.
The classical polymerase chain reaction (PCR), on the other hand, is a way for humans to use an in vitro method to amplify relatively large amounts of double-stranded DNA from a specific fragment, using a DNA template target and two artificial, single-stranded DNA oligonucleotide primers (along with dNTP substrates, buffer, Mg++, a thermostable DNA polymerase, and a programmable thermocycler).
So the goals, or outcomes, of the two processes that you are trying to compare seem vastly different to me.  Replicating a chromosome is presumably to keep an organism alive, and reproducing, and dividing, to produce progeny.  Amplifying a desired DNA fragment is a tool to allow some subsequent process or assay to occur.
Your question does not have a clear sense (to me).  There is no stated requirement for biochemical reactions created by human scientists to in any way be limited, or constrained by reactions that occur inside a living cell.