text:
Can life occur from a fertilised egg cell, in which both the egg and sperm possess an extra copy of a chromosome?
Patau, Edward, and Down Syndrome are all the result of either the egg or sperm cell possessing an extra copy of chromosome 13, 18, and 21, respectively. However, what would be the outcome if both cells possessed an extra copy? That is to say, if the fertilised egg cell is left with not three, but four copies of a chromosome?

I'm not qualified to answer this question, but knowing that a chromosome contains a whole lot of genes, that are basically the blueprints for stuff like as an example the hair color or eye color and so on... what if you have 2 chromosomes that contain different blueprints? will the body then destroy itself by trying to follow both blueprints or will one eliminate the other? Interesting question.

There are many ways to answer your question, I'll try a couple.
First, extra chromosomes in humans are commonly deleterious. However, there are known rare forms of tetrasomy that are not lethal, see Wikipedia on tetrasomy. Note that the causes of tetrasomy are rare events, so they are typically occurring in just one of the original gametes, not both; for it to happen in both would require a rare event paired with another rare event - not saying this is impossible, just less likely.
Polyploidy in other organisms, particularly plants, is both common and normal, see Wikipedia on polyploidy.


text:
What determines the amount of data you would get from a sequencing experiment?
When someone performs a sequencing experiment, what determines how much sequencing data you get from the machine (Illumina, PacBio, Nanopore, etc). Or maybe, put differently, how does the machine know that it is done?

On an Illumina machine, the instrument runs as many cycles as you tell it to.  If you tell it to run 150 cycles, you will get 150-mers as output.

Thanks for this, that explains read-length to an extent but what explains sequencing depth?

Having more reads for your sample, which you get by giving your sample a higher % of the space on the flow cell.

source: Stack Exchange

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

sort: votes


text:
Atomic Force Microscopy Imaging of Proteins
I was reading about various imaging techniques, and I came across Atomic Force Microscopy (AFM).  It sounds very interesting, and it also sounds like it is capable of imaging proteins (Page 4)
http://www.cma.fcen.uba.ar/files/prepmuestras.pdf
If that's the case, and since AFM can be done with relatively low expense, why haven't more proteins been imaged?  Apparently around 6500 protein structures have been solved via imaging.
If AFM is a viable technique for protein imaging, what would the consequences of using it on a large scale be?

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


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Has the concept of allostasis been adopted in biology, in place of homeostasis?
Peter Sterling, among others, has been a prominent critic of the concept of homeostasis.  He instead proposes a process called allostasis.
Homeostasis involves having fixed set points for physiological parameters, and when we deviate from those set points, there are mechanisms that restore them.
However, Sterling argues that this process of homeostasis is inefficient and inflexible.  Instead, he posits that the brain is constantly predicting physiological needs based on environmental and bodily demands, such that the "set point" changes depending on the context.  So your mean blood pressure might be X in one context, but Y in another.  And rather than responding after a deviation from the mean, the brain predicts those deviations and adjusts the body accordingly.  This is allostasis.

Allostasis is much more in line with what we know about the brain (e.g., Clark, 2013), but has this idea been adopted much in biology?  Based on my memory from biology class not long ago, it seems like homeostasis is still considered a central feature of living things.
Thanks!

For those that don't have a subscription to that particular journal, can you find or post a copy in some easily and permanently-accessible place? Or, at the very least, highlight his arguments for it and provide links to supporting evidence? Sometimes ideas like this are just too new to have gotten much traction yet, other times they're crackpot hypotheses that don't fit with existing data. Sure, it sounds nice, but where's the evidence?

@MattDMo  Here's a freely available article of his from 2004 and you can download a more recent article from researchgate here.

Thanks. By the way, just to be clear, I have no opinion at all as to whether this is an accepted hypothesis or not, as this isn't my field of study. But I have been involved in other similar questions asking "Why isn't this theory of Professor XYZ more accepted in the community?" and it turns out that XYZ is a crackpot conspiracy theorist who is chief editor and publisher of his own journal and organization that espouses the garbage he writes about, regardless of any possible "merit" or "scientific evidence". I'll try to link you to the question if I can, I don't remember it at the moment.

@MattDMo  I definitely understand the concern.  Although Peter Sterling is a reputable academic, and a prominent physiologist I work with seems to find strong validity in his theory.  But who knows!

Eh, personal views here as a biologist, so I'll keep this in a comment rather than an answer: Everything in biology comes with huge asterisks and exceptions. This is often a point of confusion for novices and non-biologists, but to me it's just a way of thinking when you deal with life. I think it's pretty clear from your diagram that a major component of "allostasis" is indeed homeostasis: it's homeostasis with a little bit of predictive power. Outside of biology, in control theory, this is a pretty basic part of set point regulation: when you want to keep something at a set point, maybe...

...temperature, you don't just think about your current temperature but you look at rate of change, etc, to make some future predictions. So, is homeostasis everything? No of course not. You can maybe get some publicity if you say "Hey everyone! Homeostasis isn't everything!" But of course that's obviously true: organisms grow, they reproduce, they grow old and die. You might start releasing energy stores when you wake up in the morning rather than when you start jogging. Homeostasis is still a pretty powerful descriptor in most cases, a lot like Newtonian physics on Earth.

I don't know Peter Sterling. Maybe he is just trying to get attention. Maybe he just wants to emphasize the exceptions to the rule. From your description it sounds a lot like a physicist who goes around the party telling everyone F=ma is wrong. Everyone knows he is right, but he isn't really convincing them of anything they don't already know, and they think he's annoying anyways.

@BryanKrause  I suppose I'm a bit confused by your last paragraph.  Peter Sterling is a legitimate, well-respected academic.  He's not trying to get attention.  If you read his articles, they're well reasoned and well evidenced.  Did my language somehow paint him as a crackpot?  (Sincere question.)

@BryanKrause  Also, Peter Sterling isn't claiming that "homeostasis isn't everything."  He's saying that such a process isn't functional without prior knowledge and predictions.  This is very, very important in areas like (human and non-human) neuroscience and psychology (where it's routinely ignored and so theory suffers), so I'd imagine it's also very important in biology.

I'm saying that what he calls allostasis doesn't sound any different from what most biologists would understand homeostasis to include. It seems from your description that he is setting up a straw man for homeostasis. The key flags for me in your question were "instead of" and describing him as a "critic" of homeostasis. No experienced biologist would claim that homeostasis means set points can't change - that's silly, hence why it is a straw man argument.

That said there may be nothing wrong with his work, he may just be stressing an issue he feels is overlooked or not treated explicitly by others. Maybe your characterization of his work is a bit exaggerated? Or maybe he exaggerates himself - it's not a bad rhetorical technique, I think you are just taking it to far with the idea that somehow other biologists aren't accepting that set points change or organisms make predictions on future needs.

@BryanKrause   Got it, thanks!   Although, to be fair, if you look at the history of the concept homeostasis, it has a very specific meaning, so I'm not entirely sure it's a straw man.

@mrt I looked at the Wikipedia page for allostasis, a quote: "Allostasis is the process of achieving stability, or homeostasis, through physiological or behavioral change".
I could define a new term myself, "Ezzting: the process of achieving nutritional intake, or eating, by putting food items in your mouth and chewing them." Do you think that term will take the world by storm and replace the clearly inferior verb "to eat"?

I don't think "allostasis" is as much a farce as my example, but it will not replace homeostasis because the definition of "allostasis" is already the definition most biologists would use for "homeostasis" - no one except the people behind "allostasis" seem to be defining homeostasis so narrowly as to need a secondary term. I came to this conclusion independently, but it looks like I am not alone, as the Wikipedia article on allostasis also led me to this paper which seems to share my take.

@BryanKrause  I think if you read the two papers I linked from Sterling, it would clear up a lot of confusion.  Wikipedia isn't really a great source here.  I can't keep defending something if you're not familiar with it.

What exactly is your question?

Allostasis is more than changing set points. The theory of allostasis attempts to unify the theories of stress and homeostasis. And, although Peter Sterling and Joseph Eyer were the first to coin the term "allostasis", the concept is today proposed by a plethora of researchers.
Allostatic responses ensure „stability through change“ in situations of strain and stress. If in allostatic mode a feedback control system is able to change both its set point and its parameters to approach a state vector that is more suitable for survival. An allostatic response involves the activation of actuator variables that is referred to as allostatic state. Although allostasis is basically beneficial for viability it also exposes the organism to some kind of strain, referred to as allostatic load. If ongoing or being excessive, allostatic load may be life-threatening on its own terms. In this situation, it is referred to as allostatic overload.

Figure taken from Chatzitomaris et al. 2017.
The idea of allostasis might have been omitted in your biology class due to didactical reasons. For an introductory course it may be beneficial to begin with the simpler theory of homeostasis.
Today, the concept of allostasis is of increasing importance for psychology and medicine. As of today, a PubMed search for the term "allostasis" results in 730 papers and a search for "allostatic load" delivers 1123 publications (with growing tendency).
The theory of allostasis helped to improve our understanding of a broad range of diseases and non-pathological bio-psycho-social situations. Typical examples include starvation, obesity, exercise, fever, type 2 diabetes, hypertension, thyroid disorders, post-traumatic stress disorder (PTSD) and psychosomatic diseases. Additionally, the recent development of panels for allostatic load facilitates differential diagnosis near the small ridge between health and disease.
References

Sterling P, Eyer J. Biological basis of stress-related mortality. Soc Sci Med E. 1981 Feb;15(1):3-42. PMID 7020084.
Sterling P. Allostasis: a model of predictive regulation. Physiol Behav. 2012 Apr 12;106(1):5-15. doi: 10.1016/j.physbeh.2011.06.004. Epub 2011 Jun 12. PMID 21684297.
Bizik G, Picard M, Nijjar R, Tourjman V, McEwen BS, Lupien SJ, Juster RP. Allostatic load as a tool for monitoring physiological dysregulations and comorbidities in patients with severe mental illnesses. Harv Rev Psychiatry. 2013 Nov-Dec;21(6):296-313. doi: 10.1097/HRP.0000000000000012. PMID 24201821.
Sagner M, McNeil A, Puska P, Auffray C, Price ND, Hood L, Lavie CJ, Han ZG, Chen Z, Brahmachari SK, McEwen BS, Soares MB, Balling R, Epel E, Arena R. The P4 Health Spectrum - A Predictive, Preventive, Personalized and Participatory Continuum for Promoting Healthspan. Prog Cardiovasc Dis. 2017 Mar - Apr;59(5):506-521. doi: 10.1016/j.pcad.2016.08.002. PMID 27546358.
Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood A, Klein HH, Dietrich JW. Thyroid Allostasis-Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming. Front Endocrinol (Lausanne). 2017 Jul 20;8:163. doi: 10.3389/fendo.2017.00163. PMID 28775711.


text:
Is apparent competition a suitable term in situations where one species is not negatively affected?
When two prey (or resource) species share a common predator (consumer), they can be in apparent competition. An increase in one prey species can increase the common predator density, which negatively influences the other prey species.
A textbook (Molles, Seventh edition, ISBN-10: 0077837282) gives an example of apparent competition that confuses me. It gives another definition "one species facilitating populations of a predator or herbivore of the second species." Thus, one of the species does not have to be consumed by the predator/herbivore.
The specific example is that there are two plant species. Species A becomes the habitat for the herbivore (but is not consumed by the herbivore). Species B is consumed by the herbivore. Therefore, an increase in species A will increase the herbivore density and has negative effects on species B. I thought that to form an apparent competition relationship, it has to be mutually negative relationship (-,-).  In this example, there is no mutually negative relationship. Furthermore, the plants do not share the common herbivore.
This is simply a definition question. Different sources have variable definitions, but is the example really considered an apparent competition?

Competition-like interactions where only one species suffers ([0,-]) are usually labelled amensalism, so a suitable term for the situation you describe should be "apparent amensalism". I hadn't actually seen this term in use from before, but a quick Google search reveals that is in fact used. One example is in Jaworski et al. (2015):

Indirect interactions mediated by shared natural enemies are known as apparent competition, if negative interactions are reciprocal, or apparent amensalism, if one prey suffers from the presence of the other prey (Holt 1977; Holt and Lawton 1994).


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How does Genetic drift and selection affect fixation of an allele?
I want to know how does genetic drift, and selection coefficient (s) together affect the fixation of an allele? For example, if there is a neutral allele (s=0), will only genetic drift cause the fixation or loss of an allele? Similarly, if an allele is beneficial which means that s > 0. In that case, how do genetic drift and selection coefficient together determine the fixation and loss of an allele? And what happens when s < 0 that is an allele is deleterious. Lastly, how do genetic drift and selection coefficient gets affected by the population size? I am reading about population genetics, and I am totally confused by this point. I would appreciate if someone can clear this to me.

It would take a lot of writing to fully answer your question. Below I give an answer without spending too much time on the underlying math assuming you are confortable with probability theory and Taylor series. If you really want to understand more of all of that you would just need to consider reading a book in population genetics (see end of the post for recommendation).
Probability of fixation under drift only
In absence of selection, mutation and migration, drift only may yield an allele to eventually reach fixation (or loss). The probability of an allele to get fixed is then just equal to its frequency $P_{fix}=p$. When the neutral mutation has just arisen, this probability is therefore $P_{fix}=p=\frac{1}{2N}$ for a diploid population of size $N$.
See this post for more information.
Drift and population size - Intuition
For some intuition about the effect of population size on drift you might want to have a look at Why is the strength of genetic drift inversely proportional to the population size?.
Drift and population size - Effective population size
To go a little further than the linked post, note that the the strength of genetic drift is defined by what we call the effective population size $Ne$. But before talking about that let's talk about the variance in possible allele frequencies in the next generation (which we'll call $var(p')$).
The number of alleles $A$ in the next generation follows a binomial distribution (if we follow Wright-Fisher model). The variance of this binomial distribution is $2 p N (1-p)$, where $p$ is the frequency of the allele $A$ in the previous generation. Dividing this variance by $(2N)^2$ (the square is caused by the fact that $var(k X) = k^2 var(X)$, where $X$ is a random variable), to get the variance in allele frequency in the next generation
$$var(p') = \frac{p(1-p)}{2N}$$
We define the strength of genetic drift as $var(p')$ and for intuition, we usually refers to it as the value of $N$ that corresponds and to avoid confusion with the actual population size we call this new measure $Ne$. Therefore,
$$var(p') = \frac{p(1-p)}{2Ne}$$
Solving for $Ne$ yields to
$$Ne = \frac{p(1-p)}{2var(p')}$$
and this effective population size $Ne$ is what we use to talk about strength of genetic drift.
Probability of not reproducing
As I will refer to this statistic later, I will introduce it here. What is the probability of a given individual to not reproduce? Let's call this quantity $P(k=0)$ as the probability that the number of offspring $k$ is $0$.
Imagine you sample $2N$ haplotypes (with replacement) to form the next generation and each of them has a probability $1-\frac{1}{2N}$ to be chosen, the the probability of not reproducing is $p(k=0) = \left(1-\frac{1}{2N}\right)^{2N}$. Taking the Taylor series of this expression for large values of $N$ yield to the approximation $p(k=0) = \left(1-\frac{1}{2N}\right)^{2N} ≈ e^{-1} ≈ 0.37$. So, any individual has a probability greater than a third to leave any offspring in the following generation.
Probability of fixation under both drift and selection
If an allele if beneficial, then its probability of fixation is greater than its frequency $p$ (and vice-versa if deleterious).
Approximation
There are a number of ways to derive such probability and they all end up with some complicated form. An easy approximation (which I am not going to make any demonstration) for this probability is
$$P_{fix}≈\frac{1-e^{-4Ns} }{1-e^{-4Nsp}}$$
Just to give you some intuition about the form of the above approximation (but without doing a full demonstration that would be quite long), consider that the number of offspring an individual have follows a Poisson distribution with fitness as the rate. The fitness of the mutant individual is $1+s$, and therefore the probability of this individual of having $k$ offspring is
$$P(k) = \frac{(1+s)^k e^{-1-s}}{k!}$$
Think of the generation where the mutation just arised and only one individual has this mutation. The probability of this mutation to disappear immediately is therefore
$$P(0) = e^{-1-s}$$
, which for reasonable values of $s$ is not very different from the probability of not reproducing when $s=0$ and the probability become $e^{-1}$ (as already shown above via an other mean).
A less accurate approximation (but with a very easy form) for the probability of fixation is
$$P_{fix} = 2Ns$$
Some more calculations about the interplay of drift and selection can be found in this post.
Source of information
The post Book recommendation on population/evolutionary genetics? will give you great sources of information to learn more on the subject. It will also re-explain what I just said with a lower pace. I particularly recommend Population Genetics: A Concise Guide


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What is Tandem repeat?
After reading -

(wikipedia) Tandem repeats occur in DNA when a pattern of one or more nucleotides is repeated and the repetitions are directly adjacent to each other.
( a paper) A tandem repeat in DNA is two or more contiguous, approximate copies of a pattern of nucleotides.

I deduced that the portion of oriC containing all four 9mer-s
was to be called a tandem repeat and it together with all three 13 mer-s, two tandem repeats.
But again while reading Principles of genetics by Simmons I stumbled upon the following-

The single ori in E.coli has been characterised in considerable detail. It is 245 nucleotide pair long and contains two repeated sequences. One 13-bp is present in three tandem repeats. The three repeats are rich in ...

So here it says that each 9-mer in the series is a tandem repeat actually.
Which meaning is more accepted?

I don't know much about Simmons, but the definition by wikipedia is seemingly more accepted.

The DNA sequence "TATATATA" contains 4 repeats of the 2-mer "TA" and because these repeats are adjacent to each other, they are tandem repeats. The pattern of  nucleotides is repeated and the repetitions are next to each other.
This is what both the Wikipedia and the Simmons definitions are trying to communicate.  The statement you quote from Benson'a paper can be taken to mean the same thing (except for "approximate"), but might also be construed as saying the collection of all contiguous repeats is one tandem repeat, but that is not what was intended.
So, the oriC sequence has 4 tandem repeats of one kind (9-mers) and 3 tandem repeats of another pattern (13-mers).


text:
Why do we urinate more often in winter compaired to summer?
I have been thinking of this question for a long time, but I do not seem to find an answer yet. Is there a hormonal change in our body during winter due to which we have to run to toilet often?

Is this really the case and not just observation bias? It is possibly that it is connected to more sweating in the summer - the body produces higher concentrated urine then to save water.

Is this a well-known phenomenon that and general to others? As in, is there evidence for this pattern?

I posted my answer @user28194. Hope you find it useful :)

Who exactly is 'we' here?  I don't, at least to any noticable degree, though I admit to not keeping detailed records of frequency/volume.

Istead of counting your volume why dont you answer the Q. I had asked the Q.because it is generally seen in many people. You may be an exception case but a lot of people are having this probem.

It's a problem? Seems like a solution.

@user28194 If "a lot of people are having this probem [sic]", then surely you can find a scientific citation for this phenomenon? Saying that "it is generally seen in many people" is not proof, it is anecdotal evidence at best. Also, you would do well to stop insulting people and demanding answers. You don't have a right to have your question answered. We are all volunteers here, and answer if and when we feel like it.

There is no 100 % sure answer for this as, obviously, nobody is that much interested in studying about urination. But there are some theories, of which the most popular and accepted one is cold diuresis.

Cold-induced diuresis, or cold diuresis, is a phenomenon that occurs in humans after exposure to a hypothermic environment, usually during mild to moderate hypothermia.

According to this theory, what exactly happens is this (I'll explain in steps for better understanding):

When your body senses cold or low temperature of environment, it constricts the blood vessels near your skin and external organs and restricts your blood to the inner core of your body to maintain its temperature.
Thus, it causes the blood pressure to increase as there is same amount of blood in lesser volume.
This induces negative feedback on ADH (a vasoconstrictor) i.e. its secretion is reduced.
Now when blood vessels in kidney get proper amount of blood (as blood vessels aren't constricted now), they sense high blood pressure and try to reduce it as soon as possible.
So they transfer more amount of water from blood to bladder which fills the bladder more quickly and causes an urge to urinate.
Thus, we urinate more in colder climate.

There are some more theories related to it too, but they aren't as popular. According to another theory, when we are exposed to cold weather, aquaporins are inhibited around the body, making it impossible for water to be taken in by cells, leaving a lot more of it in the blood. Again, the body will try to balance that pressure, pulling water from the blood and storing it in the bladder. You can get a more frank and interactive explanation here.

So i am not wrong completely...ADH is responsible.

Yeah it is responsible, but not how you thought it to be ;)

ADH is not secreted by the kidneys, it acts on kidneys. It's secreted by the neurohypophysis.

@GerardoFurtado yeah right, but I said so as its secretion is induced from kidneys. I'll correct that, thx.

I think that due to cold temperature the hormone ADH cannot function well. As in low temperature the enzymes becomes less active. So as the ADH hormone is not working well the suger concentration will increase in our blood due to which more amount of water will transfer from our cell to the blood stream. And this excess water will be removed by the kidney and result in polyurea.

First: What is ADH? Then: Although enzymes do have a lower productivity when it is colder, this plays no role here. The outside temperature does not influence your body temperature (at least mostly) so this does not play a role.

ADH is the antideuratichormone or anti diabetic hormone.

It would be good to edit your answer, so people who are not familiar with the topic can understand this.

Well its anti-diuretic hormone (i.e. unrelated to sugar control) if that wasn't a typo error. The reason is actually different, I'll post an answer soon.

Ok..i am looking forword to you answer.@another'Homo sapien'


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What is Pseudopalindrome?
I stumbled upon this word in a webpage by bio.libretexts.org:

The dam-methylase of E. coli recognizes the tetranucleotide GATC in DNA and transfers a methyl group (from S‑adenosyl methionine) to the amino group at position 6 of the adenine in that sequence. Note that GATC is a pseudopalindrome, so both strands read the same for these four nucletides in DNA.

What does it mean? How is it different from palindromic sequence?
I've searched google,ncbi and google.books but couldn't find anything.

Please rephrase the title of your query, so that it actually reads and appears like a question.

'True' palindromes read the same from 5' to 3' as 3' to 5' on the same strand. Pseudopalindromes read the same as their reverse complements.

@Galen What is reverse complement?

@SanjuktaGhosh 1. Reverse order of characters (GATC ->CTAG); 2. Find complement strand (CTAG -> GATC). Note for this particular (pseudopalindrome) sequence, the steps invert each other.

Try this app to get a feel for what is happening in reverse complementation: http://www.bugaco.com/calculators/dna_reverse_complement.php

If you have Shell or Shell-like terminal, try playing around with: (tr ACGT TGCA | rev) <<< 'input_seq'

I believe a main problem here is that the quoted text is not using the term 'pseudopalindrome' in a biological-jargon sense. Unfortunately, molecular biology does not use 'palindrome' in the normal sense, but in a sense that directly contradicts the normal sense. A normal palindrome formed from GA would be GAAG, but a bio palindrome formed from GA would be GATC.

In DNA there are four nucleotides or "bases", each of which can be matched with a complementary base on the partner chain in the double helix. Thus:
Adenine (A) and Thymine (T) are complementary and Cytosine (C) and  Guanine (G) are complementary.
So, a nucleotide sequence is said to be a palindrome if it has an even number of base pairs and is equal to the reverse of its complementary sequence.
For example, in a single strand of DNA the sequence of bases CCATTAATGG is palindromic because the sequence of bases in the complementary strand is GGTAATTACC, its reverse.
A pseudopalindrome is a DNA sequence with an odd number of base pairs yielding a symmetrical complement except at the central base-pair. For example, the DNA sequence ACCTGGT is pseudopalindromic, because its complement on the other strand is TGGACCA, which is its reverse except for the central element.
[There may be some confusion in the literature. The example cited in the question, GATC, is a palindrome, having CTAG as its complement, not a pseudopalindrome.]

Some of the papers I found also portrayed in your direction. Could you provide a link that I can check out?


text:
where to buy DNA sample kit? why isn't it easy to find online?
I guess you can say that it's a hobby of mine to research my ancestry and gather as much information from my family's history as I can. Being a student I can't afford to pay for mtDNA or Y DNA test of my relatives. For the first time I'll be doing it for myself fortunately :)
Now I came up with the idea of storing saliva samples of my oldest relatives just in case they pass away. I'm afraid that can happen at any time since they are getting very old. I guess it's a good plan for now. It still depends on how much a DNA sample kit costs. I'm not going to say any brand names here, but it'd be very nice if someone pointed me out where I can buy self-collecting saliva sample kits on the internet. I've found producers, but no online store.... I also wonder why this is the case.

yurihbss, you might get more of a genealogy perspective if you asked this on Genealogy & Family History SE

Most people using these tools for research and diagnosis have long-established connections and providers of industry standard tools. Most companies that provide these tools need a steady, reliable source of income, and historically demand for those tools comes from facilities such as hospitals and labs, not DIY biotechnologists (who typically can not afford the tools), so they focus on getting their products to the population demanding them most. There is budding interest in providing research and development tools to the general public such as this startup's stated goal:
http://www.the-odin.com/about-us/
But generally you have to go to a company's website, select the product you desire, and request a quote based on how many kits you'd like to order. The process isn't as easy or accessible for DIYers simply because the demand has not been great enough until recent technological advances such as CRISPR and DNA sequencing technologies made it cheap enough to run these tests on home equipment. It's similar to how not every computer geek could afford a CPU of a certain speed 20 years ago, but now CPU's of that speed are wide spread.
Salimetrics has some swab kits available for under 100 USD here
http://store.salimetrics.com/saliva-collection-methods/
Oragene offers saliva collection kits and this link details some storage options.
http://blog.dnagenotek.com/blogdnagenotekcom/bid/40944/Best-Practices-for-Long-term-Storage-of-Oragene-DNA-Samples
A list containing price per sample of oragene sample kits can be found here:
http://genomics.pitt.edu/pricing/price/HSCRF%20Genomics%20Research%20Core%20Price%20List.pdf
Some issues with collecting a saliva sample for DNA testing are neutralizing the enzymes and materials present that will degrade the DNA, and then isolating, storing, and testing the DNA. These techniques are usually used by trained professionals, once again highlighting the reason companies do not focus on selling to individuals, but to professional organizations.
An overview of the process of saliva collection and links to a few providers of the tools required to acquire your sample can be found here:
http://www.the-scientist.com/?articles.view/articleNo/43347/title/Tools-for-Drools/
This is a handbook detailing some tips on techniques used for collection and storage:
https://www.salimetrics.com/assets/documents/Saliva_Collection_Handbook.pdf
I am not affiliated with any of the companies mentioned above but if linking them is a no-no here on Stack Exchange the links will be removed and I will mention the companies only as examples. Hope this helps!


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Is there a simple test that can differentiate menstrual blood " period blood" from spotting blood?
I have a simple question: If I give two samples of blood; one from a the menstrual period and one from spotting, is there a simple way to know which one is from the period and which one is from spotting " normal, non uterus " blood?
Thanks

Spotting is "normal, non uterus"? Where does spotting come from if not the uterus?

agree with above comment - menstrual blood and blood from "spotting" are likely both uterine (except in the case of trauma, vaginal laceration, etc)

@VanceLAlbaugh - in which case(s), it would not be "normal".

@anongoodnurse exactly

The blood during the period is from the enlarged lining of the uterus caused by estrogen. spotting may be from the uterus but not related to period

My instinct is that it depends on where it's coming from. Menstrual product, either from menstruation or an endometrial condition would probably show evidence of decidualized glands. Blood from something like a leiomyoma or a tubal rupture (from, say ectopic pregnancy) would probably not show as many glands and would look more like a regular peripheral smear. That's my guess, but I don't have sources, so comment and not an answer.


text:
Why do some people have cold hands and some have warm?
I've known people who have warm hands even in the most chilling weather and also those having cold hands in a relatively hot climate. Why does this happen?

Although there is certainly something to this phenomenon regarding circulation and other factors, I think it's important to note that this is very relative: the people with cold hands are people with colder hands than you and the people with warm hands are people with warmer hands than you in either circumstance.

@SanjuktaGhosh Homoeopathy "medicine" is not in any way empirically more effective than a placebo. I used quotations because sugar pills are as effective, and sometimes more so than homoeopathic treatment. If hot hands are used as a diagnostic tool in homoeopathy, it doesn't mean that symptom has any biological or medical underpinning.

@James I won't argue, it being more effective or not as compared to placebo. I have been taking them since time unknown(before I could have any expectations). I often wonder how it works actually (I believe it does). Well, it was a comment, just trying to add an information which can be considered not constructive,the science behind it is unknown( with a bit of research I have done). Hence I delete.

@SanjuktaGhosh A meta-study in 2002 found that there was no consistent evidence that homoeopathy is effective above placebo level. The controversial journal of homeopathy remains in dispute. No article I know of outside this journal has found evidence in support of homoeopathy. As for understanding homoeopathy, it is extremely diluted medicine. There is no mechanism by which it works without fundamentally misunderstanding physics.

@James I won't blame either you or @ SanjuktaGhosh for this...homoeopathy is still the first choice for many in (at least) India. And people (don't know why) don't like homoeopathy being called as pseudoscience... :/

@another'Homosapien' Probably because the only way that homeopathy has any chance of working (and the only way for homeopathy peddlers to get anyone to buy their goods) is via a placebo effect; the more people understand that it is pseudoscience, the less effective the placebo effect will be.

Though I haven't heard of people having warm hands in cold temperatures (unless your using a hot pack or something), there are biological explanations for cold hands.

Having cold hands even when you're not in a cold environment is
  common. Often, having cold hands is a part of your body's natural
  response to regulate your body temperature and shouldn't be cause for
  concern.
But if you have persistently cold hands, particularly if accompanied
  by color changes, it could be a warning sign. For example, having cold
  hands could mean you have a problem with the nerves or blood
  circulation or a problem with tissue damage in your hands or fingers.
  If you are outside in extreme cold weather and you have cold hands,
  you should watch for warning signs of frostbite.
  - MayoClinic

Other than frostbite, there are also reports of the Reynaud's disease.
Sources:
Clinic
CNN

Hi, GH05T, and welcome. A mostly copy/paste text doesn't make for a high quality answer on SE sites. Paraphrases of relevant information with quotes as necessary, plus references are much more in keeping with the SE model. Just letting you know, not trying to offend. Thanks, and again, welcome.


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Questions in Regards to Isolating Promotor Region for Recombinant DNA Techniques
For a while now I have been trying to isolate the promotor region of this Protein.
Using sticky end PCR, I need to isolate this promotor region so it has paticular sticky ends for the purpose of placing it into a plasmid. However, I have a couple of questions on how to do this:
A. For inserting it into a plasmid, how precise does the sequence have to be? It is nearly impossible to find a restriction enzyme which lines up exactly to the start codon. How far can I deviate away, while still allowing the protein to be transcribed properly (on the plasmid)?
Thanks.

If you are performing sticky end PCR you do not need any restriction enzymes at all.
Design primers for your acceptor plasmid to 'linearize' it at the ATG and add a unique 4 nucleotide on the full length forward and another unique on on the full reverse primer. Design your promoter fragment primers to have compatible overhangs to that of the vector. And to answer your question: you will have very very poor yields if both are not perfectly complementary.
You will need to phosphorylate the full length primers for the promoter because primers are usually not phosphorylated at the 5' end. Do your PCR, anneal and ligation as per normal.
But if I were you I would switch over to Golden Gate cloning, our lab did a year ago and I have not regretted it one moment.
Edit:
I have added a diagram below. There was one thing which I overlooked in my original answer: You can get a direct repeat of the overhangs when the two longest products of each annealing reaction combine in a blunt end ligation but that should not affect your expression too much. However I still think that sticky end PCR is not the best way out of this. Blunt end ligation, gibson or my favourite: Golden Gate are all much more powerful techniques

Sorry, I may not completly understand how these primers work: This is how I currently think they work:

Sorry, I may not completly understand how these primers work: This is how I currently think they work: Lets say you have a 5' to 3' fragment GGATTCGATCGAAG. And I have I want to make it have sticky ends GGA. I design a primer that binds to TTC, and another that binds onto the 3' end. When the PCR cycle goes though, I will obtain the stick ends?

Or can I design my primers to contain the sticky ends, so I do not need to worry about finding the correct overhang regions


text:
What is significance of opsonization?
Wikipedia says

Antibody opsonization is the process by which a pathogen is marked for ingestion and eliminated by a phagocyte. Opsonization involves the binding of an opsonin, e.g., antibody, to an epitope on an antigen. After opsonin binds to the membrane, phagocytes are attracted to the pathogen.

But why is it necessary for pathogen to bind with opsonin? Can't phagocytes attracted towards pathogen without opsonization? Simply I want to know what is significance of opsonization?

In this process a number of pathogens are already inactivated due to the antibody (the most common opsonin) binding. This is highly important for substances which occur only in very small amounts, but still have a great effect as the tetanus toxin. Here the protective effect of the vaccination comes from highly specific antibodies. The toxin in an infection acts not as a immunogen, since its concentration is too low for that - but enough for the toxic effect.


text:
Are there organisms which have compartments of different body temperature?
I was wondering if there are organisms which have compartments(inside the body) with different body temperatures. To clarify are there organisms which have tissue/organs which are surrounded by something (other cells, tissues) which have an other temperature.I'm not talking about fluctuation in body temperature, such as in ectotherm organisms. I have never heard about something like this and nor I could find information or articles about this (the reason why this question doesn't provide much background research). However I'm still wondering if there are organisms like this (or at least come close to this)?

Ps. please edit this question or comment if you can provide more background information regarding this topic

How broad is your definition of "compartment"? For example, in animals with external, scrotal testes, that compartment is a few degrees colder than core body temperature.

I was more looking for compartments inside the organism, I will clarify that in my question thankyou!! @kmm

By compartments, are you referring to the term cavum or cavity? example, thoracic cavity, abdominal cavity

I'm not specifically refering to something just in general so yes it could be a cavum/cavity for example @Hallur

A number of predatory fish - swordfish, for instance - keep their brains & eyes warmer than the rest of their body: https://www.newscientist.com/article/dn6861-swordfish-heat-their-eyes-for-the-hunt/

For most of the multicellular organism; different part of body would exist in  different temperature; however there are more extreme/ drastic examples too.
Bombardier beetles; a group of beetles; that have a specialized reaction chamber in the body; where they can produce a hot and noxious reaction-mixture. They project it towards the enemy; and can throw by bending their pygidial region to wide range of directions. They do it as a defense mechanism.

Wikipedia image of bombardier beetle. They are some members from the tribes  Brachinini, Paussini, Ozaenini, Metriini of family Carabidae.
The reaction mixture can attain a temperature up to 100°C , more than enough to cause thermal death of normal protoplasm. But the reaction take place in a specialized compartment inside their body... and nothing else happen to the life of the beetle.
Here are some image of the anatomy of bombardier beetles (from here)

pygidial glands within a Bombardier Beetle; highly diagrammatic.
 more detailed diagram of the gland, however, diagrammatic.
 this is a more realistic diagram of the gland in bombardier-type carabid beetles; whole diagram showing forms of this glands in other-type carabid beetles  is available in the main website.
This paper includes a simplified diagram of chemical reaction in the chamber. reaction summary.
Here is an image from BBC showing bombardier beetle in action.

Reference: Wikipedia

As @kmm suggested, the scrotum is a common "compartment" that is commonly a few degrees lower than the core temperature.
A key concept is the core temperature. That's only in the core.
I'm not sure if I understand your use of "compartments". Can an arm or a leg be a compartment? By definition, it is. A compartment is a section. A body part fits that definition.
Decades ago, I realized something fascinating about body parts and body temperature.
I had rescued a pregnant Siamese cat. In the litter she birthed, every kitten was a light ivory color everywhere. Over the next few weeks, the limbs, ears, tail, and face of each kitten darkened. At the time, my field was Molecular Biology, and my theory was simple: coloration in this breed was due to a temperature-sensitive enzyme. The kittens had come from an environment that had a constant (the core) temperature throughout: the uterus. Therefore a lower-temperature-sensitive enzyme would be inactive. After birth, their extremities were cooler, allowing the enzyme to produce melanin in the newly growing hair.
While I couldn't prove it in my cats, after some searching I found that someone else had already proven it in similarly colored rabbits.
So, yes, different sections (or compartments) of the body can have different temperatures.
 See Tyrosinase mutations associated with Siamese and Burmese patterns in the domestic cat (Felis catus), Lyons LA, et al. Anim Genet. 2005.

I don't understand your kitten example because if all kittens were completely Ivory then this wouldn't suggest a different body temperature at different compartments (if only half of the kitten was black and the other half is Ivory I would understand this example)? The fading is more likely a transition from "cold" to "warmer" instead of compartilization

@RickBeeloo - I've added an explanation. Does it make more sense now?


text:
Bacteria and semi-permeable membranes
"The knowledge about semi-permeable membranes is applied for various purposes. We know that semi-permeable membrane is capable of separating substances when a driving force is applied across it. Artificially synthesized semi-permeable membranes are used for separation of bacteria from viruses, because bacteria cannot cross a semi-permeable membrane."
My Question is Why Bacteria cannot cross a semi-permeable membrane? Reason?

In my opinion, it should work by size exclusion. Bacteria are on the size of few microns, whereas the pores in semi-permeable membranes are on the size of nanometers. Therefore, bacteria will not pass through the membrane.
Viruses are usually smaller than bacteria, and so maybe more likely to pass through such a membrane. However, you have not included the pore size of the semipermeable membrane in question, and so I am unable to give a more specific answer at this point. If the pores of the membrane are very small, even viruses will not be able to pass through it.

Please add some references.

A semipermeable membrane is like a sieve. It has pores on the surfaces and tunnels that connect them. Molecules may pass through depending on their size. The pores in semipermeable membranes may be highly elliptical and the shape of molecules branched and complex rather than spherical.
However, the pore size (for example in the Polyflux 210H commonly used in hemodialysis) is 34 and 45 nm. There are spherical bacteria but often not and their size is usually greater than 0.5 micro meters. That is more than 10 times the size of pore in a Polyflux 210H semipermeable membrane.
Some viruses however are 20nm and may pass through though typically viruses are in the 100nm range.
Here is a paper on the morphology of the 210H with SEM images.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3502870/

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


text:
Small, brownish bird with reddish spot around eyes

This bird was seen in the Bourgoyen-Ossemeersen nature park, Ghent (Belgium) on December 3rd 2016. It is about the size of a common chaffinch.
We couldn't get a very good picture of it, unfortunately. What is the species of this bird?

From the the tree ("aulne" in French, with very typical fruits), I would have bet on this bird: https://fr.wikipedia.org/wiki/Tarin_des_aulnes, but is is true that the individual on the left looks much more like /Fringilla coelebs/.

It's a Chaffinch (Fringilla coelebs). From the first picture you see the
greyish head and orangish chick. From the second picture the typical whitish/greenish
wing bars. From the third pic the bricky belly.


text:
Will I hyperventilate if I breath twice as fast at an altitude with half as much oxygen as I am used to?
Will I hyperventilate if I breath twice as fast at an altitude with half as much oxygen as I am used to? If not twice as fast, should I breath any amount faster on average than usual when at high altitudes?

Possibly better suited to Health S.E.

Maybe I gave of the wrong impression in my question. This is purely theoretical, and I don't care about the health effects of hyperventilation. I'm interested in the biological basis for hyperventilation and whether hyperventilation occurs due to increased respiration alone, or some combination or respiration and oxygen levels.

Understood. But I think it would have worked on that site as well. I don't believe it will be closed or anything here though. :)

you also breath 2x as much other gases when breathing faster

probably this article (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495772/) will answer some of your questions

By definition, hyperventilation is a state of increased breathing where the exhaled $CO_2$ is greater than what is produced by the body.
Except in artificial condition or in disease process, breathing faster than the autonomously-dictated rate is going to cause hyperventilation. You have a fine-tuned control of respiration that will work out the correct breating rate for you.
Oxygen is actually irrelevant for this phenomenon, first because of the definition of hyperventilation, but also because oxygen is mostly transported through haemoglobin (98+%). This means there is a fixed quantity of oxygen that can be transported by unit volume of blood (and by breath, for a given cardiac output), and the maximum is already reached at normal breathing rate. Breathing faster does not allow for better oxygenation of the blood. (even at an higher altitude)
On the other hand, $CO_2$ is transported by the plasma, dissolved (7%), but also in the form of bicarbonate (93%) through the following equilibrium :
$$ H_2O + CO_2 \rightleftharpoons \underbrace{H_2CO_3}_\text{Carbonic acid}  \rightleftharpoons \underbrace{HCO_3^-}_\text{Bicarbonate} + H^+  $$
In the alveoli, a quantity of $CO_2$  will diffuse to the alveolar air, and be breathed out, the target being eliminating the quantity produced by the body. However, in opposition to oxygen transport, it is possible to overshoot by breathing faster, because removing $CO_2$ drives the equilibrium in direction of $H_2O + CO_2 \leftarrow  HCO_3^- + H^+ $ that is, eliminating additional $CO_2$ through the removal of bicarbonate from the blood.
This is hyperventilation, and leads to hypocapnia, causing that particular sensation of dizzyness. It is also leads to respiratory alkalosis, because, as seen in the reaction equation, this incurs the loss of protons ($H^+$).


text:
What kind of spider is in this pic I took?
What kind of spider is this?
It has a weird black and white backpack looking thing. Found a couple of them in Auburn, Alabama. Any help is greatly appreciated.

It's a Spiny Orb Weaver, aka Spiny-backed Orb Weaver. Orb Weavers are a very large genus of spiders; this one is a Gasteracantha cancriformis. The spikes can be black or red; there are many colors as well.

Pictures uploaded for you :) Feel free to change them

@Remi.b - Oh, thank you!!! I only have a phone now, and I couldn't figure out how to do it! And you included the creepiest one, too, ha!


text:
Using egg whites as DNA destruction test possible?
My current theory to test for the destruction of any DNA that may be used as forensic evidence is to use an egg white. I would like to test various myths and methods for destroying DNA evidence and need a sure-fire method of testing whether or not the DNA is destroyed. The reasoning behind the egg white is because when you cook one or expose it to strong acids or bases, it turns white. Indicating the denaturing of the proteins within the whites. Would this work to test for the denaturing of DNA molecules to? Several experiments would be conducted with each method, using egg whites to determine whether or not the DNA would be destroyed. Would egg whites, with great accuracy, determine whether or not the sample can be identified. If not, could you please suggest another alternative?

just a side note: do you want to destroy DNA (e.g. remove traces of DNA presence) or damage it so that investigator won't be able to assign given DNA to particular person?

@aaaaaa First I'd try damaging DNA and then move on to removing any trace of it.

what is the end goal of this project? BTW this community does not support illegal activities

@aaaaaa Mabye create a youtube series and destroy the myltiple biohazardous samples ive collected from myself over the past month.

This isn't a valid test as egg white contains a lot of proteins and DNA is chemically completely different. For example you can heat DNA several times to 95°C and you will not damage it (in fact it renaturates when cooled down slow enough), but this is not possible with proteins. "Biohazard samples" (whatever this means in your case) are deactivated either by autoclaving or by incubating the cells/tubes/whatever with chlorine bleach. Both methods work well and are approved in labs.

Egg white would not destroy DNA. Egg white is composed primarily of proteins. How does denaturation of proteins upon heating in any way link with the proteins being able to destroy DNA? Since your hypothesis is not correct, the question is unclear.

@WYSIWYG I am not stating that the egg whites will be used to destroy DNA, instead I'm asking whether egg whites can be subjected to the same treatment and indicate if such treatment would have destroyed DNA. That is if I had enough DNA material and replaced the egg whites with DNA. I am trying to find a cheap solution to test whether or not the DNA would have been destroyed because I do not have the equipment to do so. Mabye try a bit more to comprehend the question next time.

@Chris Thank you. This should have been used as an answer, exactly what I was looking for. And the samples are mainly blood. Though I dont have an autoclave, I will use a NaOH and NaClO solution.

@TommyWoldt This was more a quick comment - but I can make it an answer later if you like.

@Chris I dont think that the question is going to be "unholded".

Cooking DNA will absolutely not destroy it. Few things will actually destroy DNA. Bleach is one of the only common substances that will do it.
To test for DNA quantity you need to perform qPCR. The equipment is $20,000+.


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Relationship between fatty acid chain and saponification number
Why do long chain fatty acids have low saponification number? What is the relation of fatty acid chain( R)  with saponification number?

The saponification number, or saponification value, can be described as...

the measure of the amount of alkali required to saponify a definite weight of fat. It is expressed in milligrams of potassium hydroxide required to saponify 1g of fat.

(source: Food Analysis: Theory and Practice. Y. Pomeranz and C. E. Meloan)
Notice that, in the definition, we're talking about grams and milligrams, not mols.
Now comes the important information: in the saponification, the base reacts with the ester group, and any triglyceride, regardless its chain length, has exactly three ester groups.
Let's see this is an oversimplified example:
Suppose we have two triglycerides, A and B. A has a chain twice as long as B. So, suppose that a given number of mols of A weights around two times the weight of the same number of mols of B.
However, they have the same number of esters, and they will require the same amount of potassium hydroxide. As A has a greater weight (which is in the denominator on our equation), it will have a lower saponification number compared to B.

You might add some citations too.

@another'Homosapien' I just did, but some times it's absolutely useless. Have a look at this answer: http://biology.stackexchange.com/a/48341/24284 I explained that flowers are modified leaves. I provided half-dozen books, and I quoted even "Nature"! But the first comment is from a person saying "It would be too far-fetched saying what you're saying"... and 2 downvotes. Apparently, "Nature" is not enough for this site.

Well I can't tell about that kind of "person"s but its like a rule to put citations, so I just reminded you about that :)


text:
How long do fishes survive in a milk environment?
Suppose you placed a fish, a goldfish for example, into milk instead of water. How long could you expect the fish to survive?
Would it die due to lack of oxygen? Is there any other factor that could cause the death?

Why not a trout?

I am voting to close this thread because no previous research attempt is shown. You can't just come, ask a three line long question as if you were on the net. This goes against this forum's strict rules

@Algae — Unfortunately, in practice, you can't vote to close until you have more points (aka reputation). But I did it on your (and my own) behalf. However it's an old question, and, like the goldfish, dead by now.

I can't support this answer with scholarly articles. But it's an interesting question if you think of milk as highly polluted water.
Water from a tap (which is what goldfish usually live in) is 'fairly pure', with the naturally occurring minerals sodium, calcium, magnesium and potassium respectively in highest concentrations (varies by location.)
Milk, on the other hand, has not only a much higher mineral content, but also has fat, protein, carbohydrates, and white blood cells as 'pollutants'. In fact, whole cow's milk is only ~87.8% water.
Looking at calcium alone, the concentration of Ca in water is about  3 mg per 100cc, or .003%. Milk has .13% Ca, or 130 mg per 100cc. Since Ca is a major player in nerve and muscle function (in humans, a very relatively mild increase in serum Ca causes tetanic contraction of muscle), my guess is that the poor little fish would not be able to maintain normal serum Ca levels for long. It would die of inability to move fluid over its gills, that is, it would suffocate even in the presence of dissolved oxygen. Not to mention that the gills would also be coated to some extent by fat (3.5%), protein (3.8%) and other 'gunk'.
How long would it last? Probably not more than a few minutes.

Thanks for the answer. Now I can do some more reading about the effects that the presence of these minerals have on fish.


text:
Quantity of hemoglobin in the cells
According to my book- red blood cells have the ability to concentrate hemoglobin in the cell fluid upto about 34g in each 100 ml of cells.The concentration does not rise above this value because this is the metabolic limit of cell's hemoglobin-forming mechanism.
Furthermore, In normal people,the percentage of hemoglobin is almost always near the maximum In each cell.
The next statement says- the quantity of hemoglobin in each respective cell contains an average of 15g of hemoglobin per 100ml.
So what is the actual concentration of hemoglobin in 100 ml of blood?

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

The reference range for hemoglobin Hb content in whole blood is 13 - 17 g/100ml for adult men, and 12 - 16 g/100ml for adult women.
There are other related metrics : the mean corpuscular hemoglobin concentration MCHC, that is the concentration in a red blood cell (reference range : 31 - 36 g/100mL), and mean corpuscular hemoglobin MCH, which is mass in one cell (reference range : 29 - 35 pg)
So I think that book is refering to different values :  the concentration in the red blood cell itself (MCHC = 34g/100ml), and the resulting concentration in the whole blood (Hb = 15g/100ml).
By the way, there is a value relating Hb and MCHC, the hematocrit Ht, the proportion of volume of whole blood occupied by red blood cells. Reference range 40% - 50% for adult men, 35% - 47% for adult women.


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Is it possible to establish a newer animal model completely based on Bioinformatics studies?
I wanted to know, if it is possible to prove a new organism as an animal model for any human disease by only Bioinformatics methods like NGS and Structural bioinformatics.
For Example, let's say Drosophila is an animal model for Disease X as it have some 60-70% similarity in the gene and protein structure. Can we prove, a newer organism is a better model for X, if it shows a higher similarity, let's say 80-85%, to gene and protein structure of human?
UPDATE
(First I posted it as comment! But I think, this is suited here best!)
@David: Thanks for your answer! Actually, I did looked into it, Large animal models of rare genetic disorders: sheep as phenotypically relevant models of human genetic disease. I am more interested in listing down the problems if we do start this kind of project in our lab. Do NGS is a solution or what part of biology we need to focus so, that we can be more accurate.

The general problem of predicting the effects [of variation] of sequence on phenotype is far from being solved, so i'd say no. But still, that could be an encouraging signal to pursue experimentation on the new organism.

It is naïve to think that the extent of protein similarity is sufficient to determine what is the best animal model for a human disease. The physiology of the animal and the question of compensatory genes are all factors that contribute.
Indeed, if the protein is functionally similar, it may be irrelevant if it has diverged in other regions. And, of course, there are ethical and cost considerations — the animals closest to humans are the apes!
I suggest you search for literature on the subject. It’s not my field, but Googling brought up this paper discussing models for kidney disease, and no doubt you could find much more yourself.


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Why is compensatory negative supercoiling generated in a positively supercoiling ccDNA?
I was reading DNA replication in E.coli in Lehninger Principles of Biochemistry 6th Ed. and stumbled upon the following --

The tight right handed wrapping of DNA around DnaA oligomeric complex induces an effective positive supercoil. The associated strain in the nearby DNA leads to denaturation of AT rich DUE region.

Edit:
Yet again I have come across the following in  in Indian Molecular Biology books which certainly contradict Lehninger.
Binding of DnaA protein to oriC initiates unwinding of the DUE by introduction of negative superhelical turns.
I've done a little more research and found this paper, which clarifies the problem I previously had:

As a right-handed ATP-DnaA spiral would be expected to
  wrap DNA into a positive supercoil, adjacent DNA regions would be
  subjected to compensatory negative writhe (Fig. 6d, left). Although
  any superhelical strain generated by DnaA-mediated wrapping would
  be expected to spread throughout the topological domain that con-
  tains the origin, it may preferentially affect the nearby DUE, which is
  unstable and prone to spontaneous unwinding (Fig. 6d, top arrow).

Changed question: Why is this negative supercoiling generated in a positively supercoiling ccDNA?

Not my area of expertise, but can you further explain the inconsistency/contradiction? I'm not seeing it.

@BryanKrause Expecting that you are aware of DNA replication and supercoiling in general I put the issue in my words,one book says that DnaA protein forms an oligomeric complex and the DNA wraps around it in right handed fashion creating positive supercoils that denatures the weak A=T rich regions and that's where the rep. bubble is formed. The other book says that the DNA wraps around in left handed fashion underwinding the DUE(region rich in AT), not breaking them(remember) by producing negative supercoils.

Again, not my area of expertise, but I think what is happening is that DNA is wrapping "more tightly than normal" around the oligomeric complex - this causes it to be wrapped "less tightly than normal" at the DUE region. The two books are describing the same process from two perspectives - one is the perspective of the protein, the other is the perspective of the DNA where transcription is taking place.

For a piece of topologically constrained DNA, Lk is constant. Since Lk = Wr + Tw, if you increase Wr in one area, it can be compensated by decreased Wr or Tw in an adjacent area. You may ask why the unwinding is concentrated in the adjacent region and not spread throughout. This is explained in the paper you link to:

Although any superhelical strain generated by DnaA-mediated wrapping would be expected to spread throughout the topological domain that contains the origin, it may preferentially affect the nearby DUE, which is unstable and prone to spontaneous unwinding.

The DNA unwinding element (DUE) is unstable because it is AT rich:

…the opening of individual AT/TA base pairs in the three DUEs investigated differs from that of GC/CG base pairs in at least two respects. First, the opening of AT/TA base pairs is significantly more favorable, kinetically and energetically, than that of GC/CG base pairs. Second, the opening of AT/TA base pairs is affected by long range effects of the DNA base sequences, whereas the opening of GC/CG is insensitive to the base sequence beyond that of nearest neighbors. The first difference confirms the earlier proposal that the high content of AT and TA base pairs is necessary to lower the stability and enhance the dynamics of the three DUE sites. The second difference suggests that the sequences of these AT and TA base pairs have been selected by evolution as a means to modulate the energetic stability of the three DUE sites according to their location and function in the origin of DNA replication.


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What are fish seeds?
I stumbled upon this term in a section called Induced breeding of Carps in an Applied Zoogy book.

Traditional practice is to collect seed from the natural riverine habitatwhich also contain uneconomic,unwanted and predator fish species.

What are seeds? Does it mean zygote ?

I can't tell from the quoted text, but could this refer to milt/sperm? 'Seed' (not seeds) is used in this context.

Hmm. This FAO document seems to imply that it is a collective term for all the young life stages of fish from hatchling to fingerling.

Interesting - looks like this is used fairly widely in fish farming but not actually defined anywhere I can see. From the context, another possible definition is 'juvenile life stages used to start a fish farm, usually but not always collected from the wild'.

Fertilized fish eggs are known as Fish seeds. In simple words, they are the baby fishes used for seeding new Ponds in fisheries.
They can be used in 4 stages:

Hatchling : Larvae stage where it have yolk sac hanging below from where it draws its nutrition for 2–3 days. It can't eat from outside as mouth is not formed yet!

Spawn: Stage where mouth is formed.

Fry: About ~2 cm long, now, it can eat small size zooplanktons!

Fingerling: About ~15 cm long. It is now becomes easier to transport these kinds of fishes to Ponds.

Source (Picture Credits) :
Pic 1. https://www.ucdavis.edu (https://www.ucdavis.edu/sites/default/files/images/article/trout_lg.jpg)
Pic 2. Wikimedia (https://upload.wikimedia.org/wikipedia/commons/f/fe/Anemone_Fish_protecting_it's_spawn.jpg)
Pic 3. Fishbio (http://fishbio.com/wp-content/uploads/2011/03/Oncorhynchus-mykiss-fry.jpg)
Pic 4. Deveron (http://www.deveron.org/wb/media/images/parr.jpg)

''Fertilized fish eggs are known as Fish seeds. In simple words, they are the baby fishes used for seeding new Ponds in fisheries.'' -can you support your claim with citations?

A fish 'seed' is a juvenile fish to be used for fish farming.
'Seed' appears to be an industrial/technical term in fish farming used to refer either collectively to the juvenile life stages of fish (hatchling, spawn, fry and fingerling), or specifically to fry (the stage after the yolk sac disappears and before scales form).
It is used in contrast to broodstock or broodfish - essentially, it is what you collect from broodfish, or from the wild, to start a new farming 'batch' (fish farming is a batch process). It sounds like it can be used as a mass noun.
It is surprisingly difficult to find anywhere this definition is stated straightforwardly, although it is used in multiple places in the fish farming literature. However, the definition can be inferred from the context. For example, it is used as a collective heading for the columns "Feeding fry", "Dhani" (a Bengali term for post-larvae) and "Fingerling" in Table 3 (Section 2.1.2, "Broodfish requirement") of the FAO manual on seed production of carps. However, in the FAO document "Seed production: an overview" and this presentation on Slideshare it appears to be used interchangeably with 'fry'. It is clearly differentiated from eggs; for example in the Slideshare presentation above it is mentioned that seed is produced by hatcheries (so consists of hatched fish).


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Reason behind selection of sites of administration of pituitary extracts?
There are two ways by which pituitary extracts are administered in a fish's body during induced breeding of fish.

Intramuscular injection is the most common practice in India and it is less risky in comparison with the other methods.The extract is injected into the muscle near the tail above the lateral line.
Intra-peritoneal injections are given through the soft regions of the body, generally at the base of the pelvic fin or sometimes at the base of the pectoral fin.

Why are these sites chosen? What physiological effects arise as a result of administration that these sites got chosen ?

maybe to avoid injecting nerves as it may cause paralysis due to damaged nerves.

Intramuscular injections are usually preferred because they result in a more constant delivery of hormone and there is less chance of injuring the fish. The preferred site for an intramuscular injection is into the thick muscle of the back. This is because it is mostly used for fish movement and therefore has the most intensive blood circulation. Thus, injected hormone will be transferred thought the body quickly. Additionally, as this muscle is big, there is smaller chance to injure internal organs by the needle.

Source: assignmentexpert.com

Melatonin is an evolutionary highly conserved molecule that plays an important role in conveying the clock and calendar information to all living organisms, including man. The hormone is synthesized mainly by the pineal gland, and, to a lesser extent, by extrapineal tissues--such as the retina, Harderian gland, and gastrointestinal tract.
It is a standard slow acting hormone injection. Once the injection is in the animal, it just propagates throughout the animal's physiology and takes the normal melatonin chemical and physiological pathways that it does in vertebrates, it prompts the pituitary gland to produce a lot of different hormones including sex and serotonin.
It doesn't act instantaneously if you overdose (humans have tried), OD negative effects occur after 1-2 days and thereafter. It doesn't react as violently as some other hormones such as Adrenaline, which is absorbed fast and dissipates fast and can give you a heart attack. Melatonin has a physiological effect that is more extended, for example steroids for inflammation.
The aim of intramuscular injection of the fish is that it is effective and safe, If you read the guides, they are concerned with the safety of the fish, it's nerves and vital organs... The tail is mostly muscle and the injection is IM. Once the hormone is injected, its absorbed by the animal over an extended period. There have been many experiments of pineal injection in rodents so refer to them to know the time frame of absorption.

For your kind information the question is about injection of pituitary extract and not pineal extract.        P.S. I didn't read the entire answer but up till the second paragraph.


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Where are epitopes located on HLA molecules?
Normally HLA molecules present cellular and extra cellular proteins to the immune system; presumably the proteins in this case are where antibody /t-cells etc bind.
But when an organ is transplanted to a HLA incompatible recipient, are they binding to the HLA molecule itself? If antibody response was reliant on the proteome expressed in and around the cell HLA incompatibility wouldn't be such a problem.
What about auto immune diseases?

Your question is both unclear and quite broad. "presumably the proteins in this case are where antibody /t-cells etc bind." Please expand on this, I really don't know what you mean. "But when an organ is transplanted to a HLA incompatible recipient, are they binding to the HLA molecule itself?" What do you mean by they? "If antibody response was reliant on the proteome expressed in and around the cell HLA incompatibility wouldn't be such a problem." Why do you think that? "What about auto immune diseases?" What about them? Please [edit] your question to make it clearer.

@MattDMo the question is pretty clear, he's using correct terminology for the topic

@iayork I'm an immunologist, and I don't really think it's clear at all. In the first sentence, the OP is mixing antibody and HLA/TCR epitopes, and it's not clear which is being discussed where. "are they binding..." is definitely unclear, I don't know what "they" is. I don't understand the reasoning behind the 2nd sentence in the 2nd paragraph. Finally, the last sentence is completely apropos of nothing - what about autoimmunity? The whole thing is unclear and far too broad.

Seems clear to me (also an immunologist).  He's asking how transplant non-self MHC is recognized (peptide dependent or not) and how autoimmune MHC is recognized (peptide dependent or not).  Good questions, if rather basic, and worth addressing.

@mattdmo you rightly picked up on my confusion. I work with hla antibody, but am a mathematician by background. Most of the material I can find doesn't seem to make clear where the epitopes are located. I am not sure if hla antibody bind to the same epitopes as the t cells or to others entirety. So if you want more clarity, I am interested in the locations of the binding sites of either.

@Abijah HLA antibody, meaning antibody that binds HLA? Mostly it binds in regions other than where the peptide epitope is, but there are a handful that bind to the combination of peptide epitope plus HLA, and therefore recognize only the specific combination of HLA plus peptide epitope

Thanks so much- I think that finally makes sense! Thanks for all your help

T cells in a graft see both non-self peptides associated with the non-self HLA molecules, and can also see the non-self HLA molecules regardless of peptide. (MHC is a broader term than HLA, and I will use MHC here.)

Surface expression of CD4 or CD8 is commonly used to identify T-cell subsets that recognize antigen presented by class II MHC or class I MHC, respectively. This holds true for T cells that respond to allogeneic MHC molecules that are directly recognized as foreign, as well as peptides from allogeneic MHC molecules that are indirectly presented by self MHC molecules.

--Contrasting Alloreactive CD4+ and CD8+ T Cells: There's More to It Than MHC Restriction
Recall that as T cells mature in the thymus, they undergo negative selection such that those T cells that spontaneously recognize self MHC molecules are deleted, but there's also positive selection that ensures the T cells can recognize MHC features in general. That leaves many T cells that could spontaneously recognize slightly different MHC molecules (i.e. non-self) that are not deleted. That means that in a transplant, there are a large number of T cells that can recognize the non-self MHC in a non-peptide-dependent manner.  There's also a much smaller number that can interact with the non-self-MHC but only in a peptide-dependent manner; this is just by chance, in that that particular T cell receptor happened to have the shape that sees that non-self-MHC and the peptide.
As for autoimmunity, that's all peptide-dependent, as far as we know, barring some of the really horrendous infant-onset autoimmunities that result from improper T cell maturation in the thymus.


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Why can’t plants prepare their own water?
Water is needed by every living object. If plants have developed that property of theirs to prepare their own food from simple molecules, why can't they also prepare water?  Oxygen are present in the atmosphere in bulk!
Or more generally, why isn't any living system capable of generating water and using it for itself?
Is it because, the plant does not want to make something that is already available to it in excess? Or is it because water is needed by the plant in excess but food is needed by it in a relatively small amount, so it is just built up in such a way that it does not prepare those things which are needed to it in excess?

Hydrogen is not present in the atmosphere in bulk; if it were, when you lit a match the air around you would explode in flame. Most of the hydrogen in air is in the form of water vapor.

@BryanKrause, Thanks for the comment but I disagree with you.  The air doesn't explode because of Nitrogen. You see, P, Mg, Na etc are present in much much smaller amounts than H but then also, they are used very effectively!

Right, because the atmosphere is mostly nitrogen and oxygen, just about everything else is present in trace amounts only. You said hydrogen is present in the air in bulk: citation please? I would also like to know what gaseous forms of phosphorus, magnesium, and sodium you have around you.

@BryanKrause, on some research i found out that I was wrong. Hydrogen is not present in bulk but in quite small quantities which can be compared to Mg,Na etc. But, Oxygen is present in bulk! Why can't the plant take advantage of that?

Water is H2O - you can't make water with only oxygen. There is way way more water vapor in a typical atmosphere than there is free hydrogen.

Exactly @BryanKrause . Okay, i got an idea. So, a plant does not prepare it's own water because water is itself present in excess in the atmosphere , just like it is useless for the son of Bill Gates to go to a job to earn some money?

Somewhat. It is just extremely more practical to get water from the ground, or in some rare cases, from the atmosphere. (Maybe this goes with your Bill Gates analogy) But there is also no practical way for a plant to synthesize water from the atmosphere - plants need to use a LOT of water, way more than things like nitrogen, potassium, etc, and the ingredients just aren't there.

So @BryanKrause , are plants built in such a way that they prepare things which are needed by them in small amounts but they just don't want to prepare those things which are needed by them in excess?

Water is also quite abundant. Life evolved in water

Assume you are any living thing. You have the option of drinking water from a river, or painstakingly extracting and purifying trace elements from the upper reaches of the atmosphere. What would you pick?

Hydrogen is not present in the atmosphere in bulk (the original question stated it was); if it were, when you lit a match the air around you would explode in flame. Most of the hydrogen in air is in the form of water vapor. Water is H2O - you can't make water with only oxygen. There is way way more water vapor in a typical atmosphere than there is free hydrogen.
It is just extremely more practical to get water from the ground, or in some rare cases, from the atmosphere. But there is also no practical way for a plant to synthesize water from the atmosphere - plants need to use a LOT of water, way more than things like nitrogen, potassium, etc, and the ingredients just aren't there.
To clarify a bit though, there are reactions in plants that produce water: plants use cellular respiration just like animals do, but the source of this water is oxygen from the atmosphere plus sugars synthesized by the plant - those sugars originally required intake of water, so there is no net production of water for the plant.
It isn't an issue of plants "wanting" to do anything. The big thing that plants make for themselves (that animals do not) is by their ability to turn atmospheric carbon into sugars and carbohydrates via photosynthesis. Everything else is either A) not particularly distinct from other organisms, or B) depends on the plant species. Even nitrogen fixation isn't really done by plants, but by microorganisms, some of which have symbiotic relationships with some plants.
The general rule is that organisms have roughly 3 ways to get the things they use from the environment, in order of efficiency: diffusion of things that are in high supply in the outside environment (depends on the particular environment but might include oxygen from the air, salts in the ocean, water in some contexts), using pumps to transfer desirable things into the organism directly or indirectly by utilizing established concentration or electrical gradients, including osmosis - note that these processes occur in digestion as well, and finally, synthesis. Synthesis can be expensive, depends on the development of very specific enzymes, and requires component parts to be available, so when the other options are available there is not much selection pressure to develop synthetic machinery. Water is incredibly abundant on Earth, and even where it is rare, it is present in the environment in more accessible ways than are the ingredients.
There are some organisms that produce enough water through metabolism that they do not need to drink; plants would not be included in this category because they need to use water to produce the products that the metabolic water would come from. However, the source of water in these reactions is not gaseous hydrogen and oxygen, but produced from cellular respiration.

Please answer my edited question, sir.

@AaryanDewan You should not edit a question to make previous answers to the question invalid - edits should only be for clarification or spelling/grammar issues. That said, I believe this answer still addresses your edited question. Please let me know what your specific issue with this answer is: which part of your question is left unanswered?

The last paragraph. Is this a general rule which is visible in most living organisms? ( humans and other animals excluded )

@AaryanDewan See my edits.


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How can bobcats feel the mice under the snow?
I've just seen the Planet Earth II's second episode "Mountains" where they shock us with these North American bobcats that can feel mice from the distance of several meters, sneak to them and kill them with a single jump. What is their biggest source of information about them? The smell? Feeling of the quiet rumbling of the earth? Hearing it? Any of it seems almost impossible to me, with regard to the conditions of the polar regions.

You can smell roughly where your pan is cooking, but you can hear it with more precision, in order to pin point something you would tend to use your ears, especially if it is under snow.
Cats use all their senses and experience to hunt. The mice have tunnels under the snow to get around and they mark their territory randomly, so the smell doesn't provide a very precise coordinates for tracking: it propagates via wind, through snow, and takes a lot longer than sound to be sensed by the cat. Smell can travel further amd mouse piss smells strong, and freezes. Freezing temps prevent aromatics from diffusing outwards and from reacting with other chemicals. Snow is a very good thermal and therefore airflow insulator. Wind doesnt go through snow very fast, and aromatics take a while to get through (aromatic molecules can even travel through steel and glass)
Cats can hear higher-pitched sounds than either dogs or humans, detecting frequencies from 55 Hz up to 79 kHz (a range of 10.5 octaves) and dogs hear from 67 Hz to 45 kHz, a range of about 9 octaves.
To compare the hearing of a cat to that of a bat, the most sensitive range of bat hearing is 15 kHz to 90 kHz. A human adult hears up to 16-18khz and a child up to 20-22khz.
Sound arrives at the cat nearly instantaneously and provides a direct triangulated reference to the mouse position... One sound arrives slightly later than the other depending on the position of the sound source, and the entire sound spectrum is used in the brain to construct a clear image of the mouse position... shuffling sounds and percussive grey noise generated by animal movement tends to have peaks of energy distributed over a wide range. If the mouse is out of it's den in the middle of winter, it means that it's mostly searching for food, forageing, actually quite noisy activities.
Snow dampens the propagation of sound, so in winter you may notice that ambient sound is different in snowy conditions. That cats can pin point a mouse under snow is not that suprising, given the ambient silence of mid winter, the foraging of rodents, and the olfactory and auditory faculties of felines. it's a good quesiton because you wonder what cats do near mole hills, they are probably sensing a lot of activity there that we don't think about.
https://upload.wikimedia.org/wikipedia/commons/thumb/5/5d/Animal_hearing_frequency_range.svg/512px-Animal_hearing_frequency_range.svg.png

And from personal experience, even humans can sometimes hear mice/voles/similar critters under the snow in favorable conditions.

The bobcats have a very sensitive nose, and also a keen sense of sight. They use their senses to view the environment around them.

and their keen eyesight and hearing are always on the alert for possible danger. Very capable predators, bobcats hunt by stalking their prey.
  from National Trapers Association

Nice answer but needs to be supported by a reference


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Is Near-infrared focused light safe for your eyes?
I found a new product, but I'm afraid it's not safe. Can you help me understand what the safety limits are when it comes to near-infrared light focused on your eyes is?
I'm assuming the wavelength of the light is important, but probably more important is the amount of focus. (For instance, visible light isn't very dangerous unless it's focused in a laser).
Product: http://theeyetribe.com/
Here is their quote about safety on the FAQ:

Yes, The Eye Tribe Tracker complies with the essential health and
  safety requirements set by the FCC and CE directives. The Eye Tribe
  Tracker is using near-infrared illumination, it conforms with the EN
  62471 standard and we have obtained an EU declaration of conformity.
  Our hardware has been tested and approved by a certified lab according
  to said standard, and is therefore safe to use.

Related question:
Is it safe to look at infrared LEDs?

Unfortunately, personal medical questions and health advice are off-topic on Biology. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice.

I understand. In that case: http://health.stackexchange.com/questions/10396/is-near-infrared-focused-light-safe-for-your-eyes


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Questions about scientific method in neuroscience
In what ways does intuition from subjective experience guide topic choice in neuroscience? How important is it to frame research questions quantitatively? Can our own beliefs about how we think bias what topics are studied in neuroscience?

Beliefs can always bias a study. Questions and Studies should have some numerical base to be considered scientific, in that sense they use measurements and statistics, using standards statistics methods and a numerical deviation in the certainty of the results, i.e. to within 5 percent. The first question is vague. Topic choice is vague, for students, researchers, reading materials. For students it's course based and for researchers it's interest/finance/other based.

Can you please specify why your question is specific to neuroscience? I think this is a question of philosophy of knowledge and the nature of human bias in the scientific methodology. Such question (especially if refined) would be on topic on Philosophy.SE but not here. I am voting to close.

Belief will always bias topic choice in science. Because, if we would know everything about it already we don't need to study it. If we don't know everything, there is just the belief that there is more interesting stuff to be known. It's not like I ask a computer to randomly generate letters until it spells out a possible research topic.

Of course.  Our beliefs govern what topics we study, we look for the proof of existing hypothesis and tend to blindly blunder toward what we "know to be true" ignoring all indications to the contrary.  We set out to prove what we believe, it's all very artificial.  However, ironically this could be correct because there is a psychological argument to suggest that what we believe governs what becomes anyway.


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What is the length of tunnels puffins dig in the Farne Islands?
I was watching this video and the host said that the puffins dig over 80km of tunnels in the Farne Islands. Is that true? I couldn't find a source to confirm that number.

If that's the current number of tunnels at any one time, it can be right, it depends if they dig a new nest every year.
Farne islands has mostly horned puffins with rainbow beaks as opposed to tufted puffins which have an different beak, the former makes nest around 1 meter and the latter up to 2.75 meters,
Puffins lay one egg per year, there are 30-50,000 pairs of them on Farne islands, that's about 40km of new tunnels every year.
Every five years the trust carries out a larger audit, the last being in 2013, when puffin numbers on the islands were strong, at just under 40,000 pairs.
That was an increase on the 2008 figure when a stormy summer hit numbers hard from a high of more than 50,000 down to 36,000 breeding pairs.


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How are fluorochromes conjugated to proteins such as antibody?
How are fluorochromes like FITC conjugated to antibodies? Are they covalently bonded? If they are covalently bonded, will low temperature (-20 Celsius or lower) break the covalent bonds and detach the fluorochrome label from the protein?

Fluorochromes are covalently bound to the antibodies to form stably labelled molecules. This paper describes it in great detail, from the abstract:

Fluorochromes can be covalently conjugated to antibodies through
  reactions with thiol or amine groups. Typically, fluorochromes
  containing isothiocyanate, succinimidyl ester, or sulfonyl chloride
  reactive groups are conjugated to amines on the antibody molecules.

These covalent bonds are stable at room temperature and are also at -20°C. It's more likely that repeated freeze-thaw cycles damage the antibody.

most of the direct-conjugated antibodies for cytometric analysis I've purchased usually specifically point out "Do not freeze". I am recently staining FITC labeled peanut agglutinin for B220+ B cells. The labeled PNA was stored in 4C but when I took it out, it was in frozen form. I've tried dilutions to 1:1000 but there doesn't seem to have enough negative population compared to negative control. Almost all stained populations displayed fluorescent intensity over 10^2. I was worried if the freezing caused the fluorochrome to detach from the PNA protein.

@AlexB I think it is more the repeated freeze-thaw cycles which are problematic for the antibody. The labelling is pretty stable as far as I know.

@AlexB is the FITC-PNA in DMSO or aqueous solution? If it's DMSO, it'll freeze at 4°.


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How to prevent HL-60 cell contamination?
I have thawed Hl-60 cells from liquid nitrogen chamber two times in RPMI 1640 media (containing 10% FBS, L glutamin, penicillin/streptomycin). In the first day the cells remain okay. But when subcultured from the first flask to new flasks (cell solution : media= 1:3) all the flasks became contaminated on the 2nd day of culture. Cloud was found in both time. It can be mentioned that I used sterile one-time usable pipettes and uncoated flask for growth. All the transfers to other flasks and media addition were done very carefully and done inside clean bench. Before using clean bench, it was sprayed by 70% EtOH.
Has anyone experienced like this problem?  Please share and if have, please give some valuable suggestions or references.
Thanks

The single most likely reason for the contamination is that your frozen stock is contaminated. Assuming you've been properly trained in cell culture, you're working in a correctly-maintained biosafety cabinet, your reagents are all sterile (has your media been sterile-filtered after adding FBS, etc.?), and the incubator is clean (water bath pan has been autoclaved, sterile water with biocide/fungicide added to it, entire incubator wiped down and all removable parts autoclaved periodically, etc.), then stock contamination is the most reasonable answer. Try thawing earlier passages than you have been working with, or order a new vial or two from ATCC or whoever your cell vendor is. Make sure your pipetors are clean, and you're using sterile filtered pipet tips.

Avoid passing your hands through the openings of the flasks/tubes since skin originated bacteria are the major source of contamination. It's safe to briefly burn the caps and the opening of the tubes before opening or capping. If you maintained good aseptic techniques through thawing and subcultures, it's possible that the frozen cells were contaminated previously.
Try thawing a new vial of frozen cells and see if there's improvement.

There is a simple reason for this "cloudy" cultures. HL-60 is a suspension cell line (see ATCC on this), so most of the cells stay in the liquid phase and do not adhere to the plastic surface of the culture flask. Some may, but usually they don't adhere very good and come off when moving the flask or gently tapping it.
Suspension cultures look different from bacterial contamination, they are less dense and you can see the cells (which are much bigger than bacteria) in the microscope when you look at the culture. Bacterial cultures often of build up deposits of bacteria at the border of the medium. And the media of bacterial contaminated cultures are almost always yellow, as the metabolism products make the media acidic. An image would be helpful here.

Under inverted microscope cluster of very tiny colony were observed along with the cells. It was clearly distinguished between the unwelcoming materials and cells. The color of the media was not so changed, it was the same like normal media.  @Chris

Ok, then please post some images of the culture. And if possible microscopic as well.

Sorry to say, they were discarded, and thinking to thaw new vial of HL-60 again. That is why searching for suggestion or advice.


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Why do Indian Major Carps spawn in running water?
I think running water serves as a cue necessary for hypothalamus to release GnRH into hypophyseal portal system which initiates a cascade of hormone actions ultimately leading to release of gametes.
I have looked up in Internet with no results. I guess no work has actually been done to discover the reason. But as it's an assumption I would like to here from anybody more specialised.

Some fish spawn in running water for a simple reason: There eggs need oxygen and survival rate will be low under hypoxic conditions. Running water has a much lower change of becoming hypoxic than standing water, so that is why many fish spawn in running water. Some fish of standing water, like sticklebacks, wave fresh water over the eggs to achieve the same.
How they sense oxygen level is another matter. In fish, the neuroepithelial cells (NEC) have been implicated as the major oxygen sensing cells. See wikipedia above and specifically this if.you want to know more.