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Can bioluminescence be used for cancer or tumor detection?
What diagnostic applications, if any, are there in using bioluminescence to detect cancer or tumors (in vivo)?

Could you elaborate on your intenstions? E.g. are you talking in vivo labeling (patients) or in vitro (cell cultures).

A list of all possible applications would make a very long textbook. If you could narrow that down to just diagnostic applications for example, that would help greatly.

Not in human but you can use this technique with genetically modified model organisms as described here.
The procedure is quite simple, you express the luciferase enzyme under the control of a specific promoter (specific for your cell type, like cancer) and provide luciferin via intravascular or intraperitoneal injection. The targeted cell type (for example cancer) will light up.
If you want to use that as a diagnostic tool in human you can't as the organism must express an enzyme catalyzing a bioluminescent reaction. Actually with the advance of genome engineering tools you might be able to do that even in humans (e.g. using CRISP/Cas9).
What is the advantage of bioluminescence over fluorescence? I might be wrong but I don't think there are any. I would rather express a fluorophore rather than an enzyme that requires a substrat.

What would a cancer specific promoter be? You could target a particular cell type, but how would you distinguish between tumorous and healthy? They have the same promoters. You could, perhaps, use promoters that are only active in proliferating cells but that limits the usefulness of the approach. More importantly, how would you detect the bioluminescence in, say, the liver?

@terdon several exist. See this list for example. I agree you can't detect bioluminescence of internal organs but strictly speaking you can use bioluminescence to detect (some type of) cancer cells which was the question (can it be used?). I also don't think bioluminescence is a great detection tool but this would be my opinion and not actual facts.

Huh, I stand corrected, thanks. I didn't know there were tumor-specific promoters.

@terdon, well you are not completely wrong :) Some promoters are more/less express (which give them the "specific" tag) in tumors than normal cells but there are, as far as I know, no promoters totally OFF in normal cell and totally ON in tumor cell or vice-versa. Still that should be sufficient to apply that technique.

Ah OK, that makes more sense. I was having trouble imagining how a promoter could be completely specific to tumor cells.

@terdon. biology has a special usage of the term "specific"...

I don't think CRISPR would be appropriate to insert an entire luciferase gene. The luciferase gene is just too large, and if you could get the luciferase template DNA into the cell, why not just deliver the whole working plasmid instead of relying on CRISPR to correctly insert it?

As far as using mice goes, you can get expression of luciferase/GFP through something like lentiviral transfection to a subconfluent tumor cell culture. Non-invasive imaging equipment like IVIS 200 can then be used to view luminescence in vivo. We're generally detecting grafted tumor cells, however, so i don't believe the process exists to simply detect new tumors, especially in humans.

@Kendall Agree. I am also quite certain it does not exist in human. My answer is tailored to the question which is "using bioluminescence to detect cancer or tumors (in vivo)?". Does not speak about any organisms or about native, induced or graphed tumors so I just went as general as the question is.

@user137 I just mentioned that as an eventuality to apply that to humans one day. For model organisms I agree any ways of delivering the construct should do. This goes way beyond the question but CRIPSR/Cas9 actually might be required as if you want to do genome engineering in humans you need to insert the gene in a very specific location in the genome as you probably cannot directly target only tumors cells but likely just some closely-related cell types. In a more general view, to be one day applied, genome engineering will have to be very specific in the genome modifications provoked.

@Kendall This paper shows that existing tumors in mice can be transfected with mRNA. It's not high level expression yet, but you could use something like this to make cancer cells express luciferase, or a suicide gene.

In vivo, none.
Bioluminescence is cool, but it's not a powerful light source. Even if you could tag a cancer cell (all of them), unless it were on your skin or in your eye, you wouldn't be able to see it, even with some kind of scope.

Wrong you actually can.

@cagliari2005 Can you then elaborate your comment?

@chris writing an answer right now

Bioluminescence could not be used but it is possible to 'tag' with fluorescence to better view pathways within the body. Tagging is often used in research, a simple google search should produce a plethora of results.


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Why are pilots under the illusion of gaining altitude without doing so?
We had a lecture about the balancing systems of the body (mainly the otolith organ / semilunar canals) in which a case was described where a pilot crashed into a ship. He was supposed to keep his altitude and had not been looking at his instruments, but was guiding the plane by feeling.
However, he was under the illusion that the plane was gaining altitude when it wasn't and so steered it downwards, dropping and eventually crashing into a ship which happened to be at that particular spot that moment.
Since the otolith organs detect de- and acceleration in all directions (that just comes from how the mechanism works), if the pilot was flying at steady altitude, why would they signal that he is rising?
(Will add an article later if I find one.)

See this link. It provides a great overview. The answer you want is in the otolith section. To paraphrase, it states that our otolith organs are designed to help us lean forward while running to maintain our center of gravity when in motion; however, in a plane this reflex can backfire by causing a pilot to believe he is going straight when in actuality he may be going downward.

source: Stack Exchange

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sort: votes


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Why is Botulinum toxin the most potent poison known?
Botulinum toxin (trade name Botox) inhibits acetylcholine release in neurons and causes botulism, an acute paralytic disease which leads to nerve degeneration and takes a long time to recover. I've read the statement that Botox is the most potent poison we know a few times now and was wondering why exactly it is. All sources I've found only claim that it is, without explanation.

do you want to know the mechanism? Or numbers for comparison?

A quick search for a list of LD50 (median lethal dose; half of the people will die with that dosage) gave me 1 ng/kg for Botulinum toxin. This is pretty darn small amount, and in fact the smallest amount within that table.

True. Also look at the potency page on Wikipedia

This doesn't seem to answer the why, it doesn't explain the reason for the high toxicity.

@MadScientist I didn't know if OP wanted to know "why it is known for the most potent poision" or mechanism of Botox. I asked OP via comment, but with no answer so far.

Thanks for this answer, LD50 is a good criterion for a statement like this and I expect many of the sources where I've read it are probably referring to this. Though the question remains what exactly gives BT such a low LD50 - it's not the only neurotoxin out there, and some members of the BT family have much higher LD50's despite a very similar mechanism of action. I'm afraid that might be a question yet unanswered by science though.

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Intracellular lipid transport
I know that lipids are carried around the body in the blood either as micelles or by lipid-binding proteins which allow them to be solved.
Lipids can't always be integrated in a membrane though, the phospholipids used in membranes have to be synthesised somewhere from a precursor which will also by hydrophobic.
Consequently, at some point there will have to be transport of lipids within the cell where the lipids will need to be in solution. How is this facilitated?

Like in the blood, intracellular lipid trafficking is facilitated by vesicular transport and lipid carriers like fatty acid binding proteins. In addition, intracellular membranes are densely packed and they can exchange lipids by collision and transient hemifusion. If you have access to Cell, a good review is from Prinz W. 2010 Lipid Trafficking sans vesicles, Where, Why, How?

I have got access to Cell when I'm on my uni's VPN but it appears I can download the PDF even without access that way. Thanks, very interesting!


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How does the immune system distinguish own and foreign antibodies?
Therapeutic antibodies, for example Rituximab which recognises CD20 on B lymphoma cells, can cause adverse effects (e.g. http://www.ncbi.nlm.nih.gov/pubmed/19399690)
One reason behind these adverse effects could of course be an over-response of immune cells stimulated by the Fc region of antibodies attached to lymphona cells.
However, it could also be thinkable that the immune system launches a response against the antibody itself, recognising it as foreign. Does this occur? If so, what part of the injected antibody acts as the epitope recognised by immune cells as foreign?

The short answer is that antibodies are proteins like any other, and if an antibody from a foreign source is injected it can result in an immune response. This is, of course, exploited in the production of secondary antibodies for use in research (e.g. goat anti-rabbit IgG is a goat  antibody that recognises rabbit IgG).
Because of this, therapeutic antibodies are "humanised" and this is the case with Rituximab which is derived from a mouse monoclonal IgG:

Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids

Presumably it would be possible for the remaining mouse-derived variable regions to be recognised as foreign by the human immune system, and this possibility is hinted at in the abstract of an early paper on rituximab (McLaughlin et al. (1998) Rituximab chimeric anti-CD20 monoclonal antibody therapy for relapsed indolent lymphoma: half of patients respond to a four-dose treatment program. J Clin Oncol.16:2825-33.) My emphasis...

A chimeric monoclonal antibody more effectively mediates host effector functions and is itself less immunogenic than are murine antibodies.

However, I'm not aware of any evidence that simple immune responses to Rituximab actually occur.

You are correct that it is possible for the human immune system to detect remaining traces of "mouse-ness" in the variable regions of this particular monoclonal, as the humanization process was rather unsophisticated. Nowadays it is possible to take sequences from the mouse CDRs that are actually responsible for antigen binding and put them in a more human variable domain scaffold that is less likely to be antigenic to the host.

In this case the real question would be, do foreign antibodies trigger an innate or a specific immune response, or both? If innate, what sort of pathogen pattern do they match? If specific, how are B and T lymphocytes specific to own Abs removed during negative selection (especially seeing as their specific sites could be specific to parts of an Ab antigen binding site)?

It is unlikely that an antibody would bind another antibody within just the human species. Human antibodies which bind to the human Fc portion cannot exist as they would be filtered by self tolerance mechanisms (as these B cells would be chronically activated or would the T cells that would be required for costimulatory help allowing the B cells to class switch and make the antibodies). Antibodies that bind to other portions are possible but unlikely because they wouldn't be pathogenic thus wouldn't cause an inflammatory response so wouldn't be presented with the relevant danger signals to instruct T cells and B cells to respond. If they were CD8 T cells would rapidly destroy these B cells by binding to these B cells so again, no B cell antibodies recognising self antibodies.
There must be mechanisms to prevent this as if there weren't as B cell survival is dependent on its cognate antigen, if its cognate antigen were itself or other antibodies we would be in for deep trouble: namely a lymphoproliferative disorder is assume. But all this is off the top of my head, so guys correct me if I'm wrong.
I don't say there aren't B cells that can recognise antibodies, I just say they'll be deleted.


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Two different sized colonies from the same species of bacteria. What does it mean?
I have got two different sized colonies in a plate of Salmonella Paratyphi, identified by biochemical methods. What does two different sized colonies mean? What kind of question can I investigate in this regard?
Protocol followed:
Positivity of serum sample was checked in BacT/Alert blood culture system. Bacteria was subcultured from the positive result giving culture bottle from the BacT/Alert system and incubated overnight at 35 degree celsius. Two different sized colonies were found and they were subjected to biochemical and antisera tests and both identified as Salmonella Paratyphi.

Could you please add details about the protocol you followed ?

@MauroM Some details added

Do you happen to have an image of your plate?

Thanks @AhmedAbdullah ! Unfortunately i'm not expert enough to solve your doubts; the only thing that i can think is that the founders of the two colonies reacted to the culture environment differently e.g. the founder of the bigger colony was more rapid to adapt and divided more rapidly compared to the other... I would try to made another culture (exactly same conditions) to see if the size difference persists and then investigate the genomes of the two colonies even if i'm not sure wich technique to use since i'm not a microbiology expert.

@Chris Sorry I am away from lab for couple of days. When I return I'll try to manage a picture.

@MauroM thanks for you suggestion. I'll try along this line.

You're welcome @AhmedAbdullah !

It could be thousands of things, but only a few of them will persist if you keep subculturing both colonies. Happily those are the interesting things, so if you subculture both colonies and they're the same size it was probably something as boring as 'two bacteria stuck together, giving one colony an edge'. If they're still different sizes, report back! Something interesting has happened.

How different are the colonies in size? This could also be a result of human error while plating. You should repeat these experiments and measure the statistics and if the trend is consistent then consider looking for a reason.


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Is there a difference between sleeping late and waking up late vs sleeping early and waking up early?
For example, if I sleep at 1 AM and wake up at 10 AM, will it negatively affect my health opposed to sleeping at 10 PM and waking up at 7 AM?

To add onto Louis' answer briefly, there are a lot of factors at play in this question. The way your own circadian rhythm has been set will play a role - any change away from your normal routine will be met with stress. Also, other factors like eating times and light cues that normally affect waking time will play a role in determining whether either of those schedules will impact your health. Hopefully someone more knowledgeable than me can provide a more complete answer.

There is a popular theory that each person has a certain "chronotype" [Ref 1]. Based on your genetics, you could be naturally an early person ("Lark") or a late person ("Owl") [Ref. 2].  What will negatively affect your health is actually fighting what you naturally are.  You probably know which chronotype you are, and if not you can go by what time you naturally sleep/wake when you don't have school/job scheduling such as at the weekend.
[Ref. 1]:Chronotype Review
[Ref. 2]:Social jetlag paper

Welcome to Biology SE! Could you please add references to your claims? Answers without references maybe challenged or deleted. For more information please have a look at our how to answer guide.

Note there is also evidence chronotype can change with age. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5479630/


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Is cell wall and cytoplasm an organelle?
So cell wall is an organelle?
Whereas, it is not a membrane-closed organelle?
Cytoplasm is an organelle?
Whereas, it is not a membrane-closed organelle?

@AlwaysConfused This is a semantic question without any real value in biology. I'm going to vote to close since this ultimately comes down to a matter of opinion without more information or a detailed scientific question. i.e cell biologists may care about the organization of all sub-cellular components, so the cytoplasm is important, whereas biophysicists may count it as exceptional since luminal spaces are more akin to extra-cellular spaces than the cytoplasm, so it's a very different cellular structure to them.

The cell wall isn't an organelle (according to VCE biology textbook) and the cytoplasm is not.
My guess is that the wall regulates movement (ie, active function), whereas cytoplasm is just a fluid in which the other cells are surrounded (ie, passive).
http://www.edu.pe.ca/gray/class_pages/rcfleming/cells/notes.htm
Note that the terms active and passive are not being used in any scientific term, but are rather referring to if the mentioned item is actively carrying out (a) process(es)

Please add some reference(s)!

Cytoplasm is not reduced to cytosol!

I was not saying it was. It is water, salts and proteins.

whereas cytoplasm is just a fluid in which the other cells are surrounded (ie, passive). Just a passive fluid, is it? It's the bedrock of all life as we know it! "Passive" indeed... :P

Cytoplasm is not an organelle. This is simply a generic term that describes everything within the plasma membrane and outside the nucleus.
We typically think of organelles as being within cells. The cell wall surrounds the cell, lying just outside the plasma membrane, usually considered the boundry of a cell. On the other hand it provides vital function for the cells having them and could be considered an organelle in this context. While it offers some regulation of passage of substance between cells, its principal function is support. I would have accepted either yes or no from my high school students.
(I'm about to depart to a 6th grade class to lead them in an activity demonstrating the support function of cell walls! Balloons. i.e. cells, inside heavy paper bags, i.e. cell walls.)

Wikipedia gives quite clear and sourced answers in this case:

an organelle is a specialized subunit within a cell that has a specific function. Individual organelles are usually separately enclosed within their own lipid bilayers.
Under the more restricted definition of membrane-bound structures,
some parts of the cell do not qualify as organelles. Nevertheless, the
use of organelle to refer to non-membrane bound structures such as
ribosomes is common.[11] This has led some texts to delineate between
membrane-bound and non-membrane bound organelles.[12] The non-membrane
bound organelles, also called large biomolecular complexes, are large
assemblies of macromolecules that carry out particular and specialized
functions, but they lack membrane boundaries.

To answer our question, the cell wall can be considered an organelle as it is a subunit with a defined (set of related) function(s).
The cytoplasm in itself is difficult to consider as an organelle, but the cytoskeleton can be considered one.

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Relationship between action potentials and EEG recordings
It is possible that I am overthinking this but I have difficulties relating the neural activation to the amplitude and frequency of EEG recordings.
For example; if at the EEG location P3/P4 we observe alpha waves at 10Herts, what will that tell us about the action potentials and membrane polarisation within the population of neurons generating the wave at this frequency?
Also, high amplitude within alpha frequency may indicate attention deficits, but how is the high amplitude related to or explained in terms of electrochemical activity within a neuron?
Informed replies are very much appreciated!
Many thanks

Most of the EEG waves are not directly generated by action potential, because it is too short and has a high frequency. They are generated by synaptic activity (overall propagation potential of axons).
The amplitude of this propagation potential depends on the impedance of the brain. Higher impedance means higher amplitude. Impedance is higher for low frequency signals.
The amplitude is also affected by the direction of the EEG vector so parallel axons which go in the same direction should produce a higher wave in amplitude.

Reference: Rudell AP, Fox SE. The propagation potential. An axonal response with implications for scalp-recorded EEG. Biophys. J. 1991 Sep;60(3):556-67. doi: 10.1016/S0006-3495(91)82085-9. PubMed PMID: 1932547.

Hi Cornelius, Your answer is really helpful, and thanks for the link.


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What are some examples of coupled reactions in the cell?
Except DNA Synthesis that requires ATP hydrolysis, which other reactions require activated carriers?

All the anabolic reaction inside our body require energy. The majority of those reactions use the hydrolysis of ATP as source of energy.
To cite a few reaction that require ATP:

Gluconeogenesis where 4 ATP, 2 GTP and 2 NADH2 are consume to produce glucose from pyruvate.
Formation of peptide bond between two amino acids.  Here the amino acid have to be first activate by binding to the tRNAc consuming ATP, as explain here (from wikipedia)

Polymerization of amino acids is what creates proteins. This condensation reaction yields the newly formed peptide bond and a molecule of water. In cells, this reaction does not occur directly; instead, the amino acid is first activated by attachment to a transfer RNA molecule through an ester bond. This aminoacyl-tRNA is produced in an ATP-dependent reaction carried out by an aminoacyl tRNA synthetase

Ubiquitin ligase, that require ATP to activate ubiquitin for conjugaison and it transfer to an E2 enzyme. This pathway is mediate by the E1 enzyme, as suggested here

There is one major E1 enzyme, shared by all ubiquitin ligases, that uses ATP to activate ubiquitin for conjugation and transfers it to an E2 enzyme. The E2 enzyme interacts with a specific E3 partner and transfers the ubiquitin to the target protein.

Hope that it helps.


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

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

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

Source: flowersofindia.net


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What is the difference between Single Nucleotide Polymorphism (SNP), Mutation and Structural Variation(SV)?
This is a question which plagues many people and today I was wondering it myself while writing a grant. Indeed, I've seen many people use the terms interchangeably, but they are all very different from each other.
So What is the difference between SNPs, Mutations and Structural Variations?

it is always good idea to start with googling and present some results in the question. then move to asking for clarifications,m instead of asking for definitions.

Lets state what a Mutation is first.
Mutation: A mutation is any change in an organism's genetic sequence which varies from that of the wild-type reference sequence (hg19/GrCH37 from 2009 or hg38/GrCH38 from 2013, which are the most current genome assembly).
Single Nucleotide Polymorphisms (SNPs): These are any single nucleotide base mutations which have been validated to be present in more than 1% of the population with the help of Genome-wide Association Studies.
Structural Variations: These are any mutations which cause a change in the organism's chromosome structure, such as Insertions, deletions, copy number variations, duplications, inversions and translocation.
For more please read Wiki Link here.

Thanks to WYSIWYG for his interesting question regarding SNPs.
This piqued my interest a bit, and to my surprise I found that the same actually applies to all other species for example chickens; This paper from way back in 2002 describes how EST mining was sometimes used to generate potential SNPs but also notes the possible false positives due to the possibility of RNA-Editing.
This paper describes the usage of SNPs to allocate bovine individuals to their source population. As does this paper which highlights the economic importance that SNPs may hold for identifying pure breeds and crossbreeds.
Apparently there are also SNP chips available for other animals as highlighted by this particular paper

Is this definition applicable to all species (esp regarding SNP. Can you add some info with references on that) ?

I hope the new edits answer your question

Yes, these terms are well established terms for describing mutations in genetic data. SNV is the more general term for SNP (without restriction of > 1% in popn). You will also hear the terms indel (insertion + deletion) and mnp (multi nucleotide polymorphisms). It should be noted that SNP is often used synonymously with SNV. All these things (SV, SNP, SNV, indel, MNP) are types of genetic mutations.

Nice. Just a minor comment, you don't need to do an association study to establish that an allele frequency is > 1%. Just genotyping.


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How fast do hummingbirds fly?
Hhhmz! A hummingbirds flew past me while I was in the garden and yet, it still managed to halt perfectly in front of a blooming flower nearest to me. Just as soon I began to wonder, how fast do hummingbirds fly and in which way do they achieve their flight in addition to their distinctive hum.

"distinctive humming sound"??  Are you sure you are talking about mockingbirds?

Thanks mgkrebbs, I meant to write hummingbird although I wrote mockingbird.

Have youo tried to google your question? Are you talking of the flapping frequency or the distance they can travel per unit of time?

You also need to differentiate between the speed they can achieve for a short distance, and their average speed in migrations.  Answers are easily found with a search engine: about 30 mph in level flight, up to 60 mph in dives, and the rufous hummingbird can migrate between southern Mexico to Canada & Alaska in a couple of months.

Hummingbirds can give the impression by their small body size that they are very fast and of course they are. The Anna-Hummingbird, about ten centimeters in size, reach speeds of 385 body lengths per second (27. 3 m/s or 98 km/h).
So they can get acceleration values of about ten times the acceleration due to gravity.
To the comparison: Peregrine falcons come on speeds of up to 200 body lengths per second in the nosedive and fighter jets, like e. g. the MiG-25 (a Mach 3 fast interceptor), reach only the approximately by 40 times of its total length by one second.
They got this enormous achievement mostly by their biological construction.
For example: the heart of the hummingbird is very large in relation to the body and beats 400 to 500 times per minute, its respiratory rate is up to 250 strokes per minute, so  lots of oxygen gets into their wings and they can perform so strong. During sleep, many hummingbirds reduce their heart rate to save energy.

Thanks for answering Mr. Amstrand, are you able to expand on hummingbird's biological construction?

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What are the classical adaptations of amphibians?
My question is about amphibians in humid or underwater environments. What biological adaptations can found in them, further what purposes do they serve?

"Amphibian" literally means "living both in water and on land" (see here)

Imagine asking "Why do fish prefer water over land?" Well... because they are adapted to water life but not land life. What kind of answer are you looking for exactly for amphibians? Do you want us to list adaptations of amphibians such as the eyes that are positionned to poke out of the water, the ears that don't let any water gets in, the skin who is thin and allow direct gazeous and water exchange or the webbed paws to move into water. Note that you will find many of these classical adaptations by just googling "amphibian adaptation".

@Remi.b: Indeed, if I were to try to answer this question from anything more than general knowledge, I'd simply copy parts of the Wikipedia page: https://en.wikipedia.org/wiki/Amphibian

@jamesqf Indeed. The OP changed the post without me noticing. I think the current post can basically be answered by my second comment. I'll post it as an answer.

"Amphibian" means "living both in water and on land" (see here). Here is a small list of classic adaptations in amphibians:

Eyes and nostril are positioned to poke out of the water while the rest of the body is immersed
Ears don't let any water gets in
Skin is very thin and allow direct gazeous and water exchange
Paws are webbed to move into water
Larvae of most amphibian species start their life in the water


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Almost philosophical question about controlling a pest/plague
Once in a math congress someone presented a paper on a mathematical model used to predict the impact of certain measures that could be taken in order to control some pest/plague. A guy in the audience interrupted the speaker and asked why not to "kill them all"(referring to the specimens of the pest/plague) and put a stop to the problem. The speaker observed that we were thinking that kind of things because almost all of us were mathematicians and so we were not aware that it would be a big problem to do that.
From my point of view, he was suggesting that "the right way to control a plague is not to kill them all" is a standard, uncontroversial fact that all biologists would agree. My question is about this last point.
Is that a scientific thesis or an ideological one? I mean, do biologists have theories that allow them to know that the "right" way to control a plague is not to kill every specimen of the species?
Why is it the case that we can assure that exterminating a species is necessarily going to affect, directly or not, humankind?
Is it a matter of chance and, as we are not completely certain of what may happen after exterminating the species, then we don't want to take a risk?
Thanks! And feel free to edit tags :)

There are multiple things to consider. Eradicating a specific pest which we could have controlled might make it possible for another pest to take over the old ones ecological nice. Maybe that one than is not so easy to control or kill. But that is just one idea.

This is outside of my field of molecular biology, but I have a few musings. Just because humans consider something a pest doesn't mean that it doesn't play a role in maintaining ecological equilibrium. The effect of pest control on an ecosystem can often be predicted, as the speaker was apparently doing, and/or modelled on previous experiences. When the effects are unknown, the prudent course is certainly restraint.

What do you mean by "kill them all". All infected persons or all transmitters?

Just to clarify; you are referring to a pest species in a general sense right (e.g. an agricultural pest species), not plague as in the disease?

You might consider the old (probably apocryphal) story about how persecuting witches led to epidemics of the black plague: Witches keep cats, therefore cats are evil, so kill all the cats (and witches) you can. But cats kill rats, so without the cats the rats have a population explosion.  Rats carry fleas, and fleas are the vector for the plague...

Biologists are certainly not afraid to exterminate pests and plagues in the wild. See: smallpox and polio. However, such exterminations are nearly impossible and very expensive. See: smallpox and polio. In both cases extinction is through  extensive vaccination, preventing the disease from having any hosts to live in. To achieve this you need to vaccinate a huge fraction of the human population for quite some time.
Practically, how would you go about exterminating an agricultural pest? A beetle, for example? Perhaps an army of men, forming a cordon the width of the united states, turning over every rock and every tree from the west coast to the east coast. With a high net or something to prevent beetles from flying over the cordon. And some method for dealing with cities and roads and tunnels and things, because if you miss only five or six they'll be back soon, depending on life cycle and offspring numbers. Or if you forget Canada.
And to use a biological solution to a biological problem, consider myxomatosis and the Australian rabbit problem. Rabbits were(and are) a pest, myxomatosis is a rabbit plague that has a 99.99% fatality rate and is fiercely infectious. Sure enough, myxomatosis wiped out the rabbit population. A few years later the rabbits were back but now the survivors were resistant to myxomatosis.
I would argue that it's a scientific thesis based on hard lessons biologists have learned about doing 100% of anything. There are many biologists with moral precepts against the extinction of pest species. It's a bit of a moot point, however. The only reliable method of extinction is habitat destruction. Whether that's immunizing all the humans or cutting down the rainforests, it does work. It's just usually impractical.

First, lets define a pest as a species that lives in places we don't want it to live.
To explain why exterminating a species is counterproductive without using moral arguments I need to explain what will happen when you exterminate a species.
To explain that, I will need to explain how a species 'decides' where to exist.
Every species lives in their niche. A niche is the n-dimensional hypervolume where a species could live. (Wikipedia is a good starting point for this subject https://en.wikipedia.org/wiki/Ecological_niche#Hutchinsonian_niche )
Their niche is a subset of their adaptive zone. Species could, and would, live in their entire adaptive zone, if only those pesky other species would stop interfering. This means that the limits of almost all species are mostly determined by the presence or absence of other species.
We are getting closer to an answer.
If you change one of the N dimensions that make the place the pest lives a good niche, then they will live there in lower numbers. Lower numbers means they don't bother us and that means they are no longer a pest according to the definition at the top. Problem solved!
Practically, this could mean something like keeping the humidity low to keep mold from taking over your bathroom ceiling.
On the other hand, if you use some kind of one-time intervention to destroy the species, the niche will still be there. And you can be absolutely sure that the niche is part of another species' adaptive zone. So after all the effort and poisoned pets (You have no chance of killing a species without serious side effects), all you will have done is exchange one pest for another.
This is a best case scenario, all other scenarios include extinction cascades or severe ecological destruction.
For further reading, here is a very hopeful paper exploring ways to reduce the impact of cascade effects. https://www.nature.com/articles/ncomms1163
It requires killing more species.


text:
Lack of A/B-antigen equivalent to Rhesus disease
Rhesus disease occurs when an Rh- mother is exposed to Rh antigens (often due to blood contact with an Rh+ child during delivery) and mounts an immune response which eventually results in the production of IgG Rh antibodies. In subsequent pregnancies, these antibodies cross the placenta. When the foetus is Rh+, these antibodies can bind to the corresponding antigens on the foetal erythrocytes and cause haemolysis, which can result in anaemia or even, in serious cases, stillbirth.
Given all of this, why does the same principle not apply to A and B antibodies? In other words, what is special about Rhesus antigens or antibodies that does not apply to other erythrocytic antigens or their corresponding antibodies?
I'm specifically wondering about Rhesus disease and its effects on the foetus, and why similar effects do not occur on the foetus in the case of an ABO type mismatch between mother and foetus.

It does happen. That's why you need to know a patient's blood type before giving a transfusion - AB is the universal acceptor, and O is the universal donor.

This question is specifically about the effect on the foetus in pregnancy, not normal blood agglutination. Sorry for the confusion; I'll edit the question to clarify.

So it turns out it can occur. It's called Hemolytic Disease of the Newborn (ABO), and according to the article (the relevant citations are a book and some journals to which I do not have access), it is very rare, and severe cases are even more rare. Apparently anti-A and anti-B antibodies are typically of the IgM isotype, which cannot cross the placental barrier. However, occasionally IgG is produced, which can cross.
This is what causes the hemolysis in the fetus - if the mother is type O, and the baby is either A or B, the mother is exposed to unknown antigen and produces antibodies. If they happen to class-switch to IgG, they can cross the placenta and, if in large enough quantities, cause the opsonization and lysis of red blood cells.

It occurs much less commonly for a reason. Many/most people who produce natural antibodies against the A and B antigens they do not possess. (Type Os against both A/B, As against B, etc). These antibodies are typically IgM produced by a specialized class of B cell (B-1 B cells) independent of a T-cell response. The coating of fetal RBCs with these IgM antibodies in the maternal blood stream facilitates their removal while dampening the generation of a T cell response against these antigens. B-1 B cells may also be resistant to IgG class switching.

One more point is that the ABO antibodies are cold antibodies. They react when the temperature is less than the body temperature generally.

@OneFace do you have citations for that? I honestly don't believe a word of it. Why would the human body make antibodies that bind optimally below 37°C? It's not doing Western blots...

http://www.webmd.com/a-to-z-guides/cold-agglutinins MattDMo, it is good practice to check if something is wrong before accusing!


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Why do frogs and toads only appear when it is dark outside?
I noticed outdoors how frogs and toads only appear when it is dark or cloudy. Such as only after it rains or during night time. Why is this?

The premise is false.  Frogs and toads don't only appear when it's cloudy (personal observation, easily repeated in most rural areas).  Most amphibians prefer cool, humid environments, as their moist skin serves as a secondary respiratory organ: https://en.wikipedia.org/wiki/Amphibian#Skin

I understand.. Do you think I should I reword my question?

I think it needs to be almost a completely different question, something like "why do amphibians prefer humid environments?".  Because at least in temperate areas, any small pond is likely to have frogs &c active during the day.  For instance, there's a medium-sized pond near me where during the season when tadpoles become frogs, you can hardly walk along the edge without stepping on small ones - and this is on the edge of the semi-desert Great Basin.

I see them,( or their ripples after they jump into the water ) during the day; I have 2 small ponds in the yard. I see tree frogs in my patio plants during the day but they are sleeping. The frogs/toads certainly make more noise when it rains ,has rained, or is going to rain. even during the day. They are certainly more active at night . I expect more bugs around then . I only see the geckos at night ,near the lights.

This sounds nice . maybe they need to conserve their energy during the day . maybe they are attracted to the water in your ponds!

Yes, the pond are a big draw. The neighborhood is very quiet at night , except within a hundred yards of the ponds. People on the phone have asked my wife the noise in the background. My son made the frog noise the ring tone for his phone.


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What kind of bird is this and what does it eat?

My father found this little guy in one of the tractors of where he works (in the fields) i’m not sure what species of bird it is and what it eats. It just keeps chirping not stop and I have no clue what so ever to what it eats. If anyone knows please tell me, I don’t want to see him starve to death.

Hi Maria, if you can give a general location it’ll help us give you more accurate information. Are you in the US?

when in doubt finely ground meat can work temporarily there are very few (non-mammalian) vertebrates that cannot digest meat. not a long term solution but can buy time.

Could you provide a photo showing the little guy from the side so that one can see the pattern of the wings? Would be very helpful. Frm this view I'd say that this is some sort of sparrrow

Based on the photo, it looks like you have a fledgling American Goldfinch (Spinus tristis). Here's a photo of an adult female feeding a young goldfinch. This link has dietary information.

I would suggest contacting your local Wildlife Rehabilitation Centre or leaving the young guy where he was found. He could of jumped the nest a bit early, but typically the parents are always nearby.


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Are free-nuclear division and endomitosis the same?
As far as I understood it, both are cases of karyokinesis, not followed by cytokinesis.

No. If you google the terms you'll get a lot of sites with definitions. For example:

Nuclear division
Definition
noun
The process by which a nucleus divides, resulting in the segregation of the genome to opposite poles of a dividing cell.

source: http://www.biology-online.org/dictionary/Nuclear_division
Edit:
or

free nuclear division    mitotic division of nuclei without accompanying cytokinesis, i.e. nuclei divide in a common cytoplasm, the cells walls only forming around each later

source: http://ecflora.cavehill.uwi.edu/bio_courses/bl14apl/Gloss.htm
versus

endomitosis
mitosis taking place without dissolution of the nuclear membrane, and not followed by cytoplasmic division, resulting in doubling of the number of chromosomes within the nucleus.

source: http://medical-dictionary.thefreedictionary.com/endomitosis
or a bit more revealing:

Duplicated chromosomes produced by endomitosis exist as discrete units
in a single polyploid nucleus or may be packaged into separate nuclei,
depending on the phase at which mitosis is aborted

source: http://en.wikipedia.org/wiki/Endoreduplication
So as you see by definition nuclear division is part of a bigger process (cell division), and accoriding to the first source karyokinesis is a synonim for nuclear division (karyo = nucleus kinesis = moving, both come form greek language).
Edit:
If you check the definition above, you can see that free-nuclear division is a mitosis without cytokinesis, thus chromosome separation still occurs.
In endomitosis the can end up with a polyploid nucleus, in contrast to the other two aforementioned mechanism where no polyploidy occurs.

I was talking about free nuclear divisions, not just nuclear division - which is just karyokinesis. Free nuclear divisions happen for instance during formation of the female gametophyte from the megaspore in angiosperms - the nucleus divides but separate cells don't form.

Oh I see, I missed that part sorry. I will look into that

I have a doubt though: in case when endomitosis is aborted in between anaphase (i.e. centromere splits but chromatids are not segregated) then in that case I thought nuclear membrane has disappeared in prophase, and now reforms to enclose 4n chromosomes. But one of these definitions says the nuclear membrane does not disintegrate - so how can spindle fibres attach to the chromosomes? Then again, since chromatids don't separate, spindle fibre formation isn't needed and may not occur.

Errors / failures / abortions in during mitosis results (most of the time) in pausing the process to try to fix the problem and if its not possible than the cell undergoes apoptosis to avoid having cells with abnormal genome. If somehow the cell still gets through (cell) division, then you get abnormal cells with chromosome trisomies, missing chromosomets etc.

In the cases of pollen grains free nuclear division occurs. entering into the s phase the chromosome no remains as 46 but the DNA doubles ie 4n condition occurs. During the anaphase the sister chromatids separate and reaches both ends. And when telo phase occurs nuclear membrane is surrounded around 2 genetic material. But cytokinesis is blocked there. But when again this cell enters s phase there again the genetic material replicated ie 2 nucleus having 4n condition is formed.this is free nuclear mitosis. These chromosomes doesn't separate in anaphase due to failure in attachment of spindle fibres. So karyokinesis also get stopped resulting cell to 8n condition or polyploidy. This is endomitosis

Welcome - can you add your sources here so people can background read on your answer?


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Operators and Enhancers/Silencers
Wikipedia has two images, of a eukaryotic gene and of a prokaryotic gene.
They show the difference that the prokaryotic gene also has an operator while the eukaryotic gene does not. Both also have enhancers and silencers separately. I thought enhancers and silencers were types of operators. Is this wrong?

Operators were classically defined by cis-Dominant mutations, located upstream of the protein-coding region of a gene, that rendered the gene's expression constitutive, or un-regulated.  This was before the promoter was defined as a separate control element.

Enhancers and silencers are binding sequences for transcriptional activators or repressors, in which case the sequence is often located some distance upstream or downstream of the gene it regulates. See regulation of transcription for information about how these interact with their target genes (through DNA bending, mediator, etc.). A note about enhancers and silencers, though, they're not necessarily required for transcription: they help the gene attain robust up- or down-regulation of transcription.
The operator, on the other hand, influences whether the promoter will do something, or nothing. If we're talking about inducible systems, the repressor is bound to the operator, blocking action to/from the promoter (an inducer will bind the repressor and keep the operator from blocking the promoter). If we're talking about a repressible system, the repressor will need a corepressor to bind the operator to abrogate transcription by blocking action to/from the promoter.


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Overcoming Inbreeding Depression
When inbreeding depression occurs, a genetically unrelated individual is mated with the animal to introduce genetic variability and remove homozygosity. In this case either outbreeding or crossbreeding may be carried out. Is there any preference for either technique over the other?
Out-breeding here refers to mating between two individuals in the same breed, but no recent common ancestors.
Cross-breeding refers to mating between two individuals of different breeds entirely.

can you clarify language? Is it that outcrossing is mating between different populations, whereas crossbreeding is mating between members of inbred populations? E.g. mating between european and asian peasants versus mating between members of european and asian royal families.

this article mentions both outcrossing and crossbreeding. Language seems confusing to me

I don't think there is any accepted clear definitions of outbreeding vs crossbreeding. Therefore, definitions should be provided in the post.

@Remi.b my point exactly. Although, broadly, if you cross inbre(a)d species, you get less variation than crossing more wild-typish (forgive me) animals


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Safe parameters for external nerve stimulation using electrical impulses
Introduction
I've recently stumbled upon David Eagleman's TED talk on the concept of sensory substitution and addition. Being the most inspiring thing I've seen on the internet for the last few months I've decided to give it a try and mix it with some of my coding/electronics projects.
I've settled on using electrical impulses over electrode pads to feed sensory data onto a patch of skin, instead of vibro-motors as it is more energy efficient. That being said, when planning on running electrical current through me 24/7, safety obviously comes first.
[edit]
I am targeting the lower back or the side of the hips as these parts have the least contact with the environment and won't make you look goofy. In the long run this would probably have to run on dry skin to avoid the "wrinkling effect", caused when staying in water for too long.
Questions
Main unknowns I want to sort out are:

What is the range of perceivable voltage and current that can be safely  fed through the skin without causing any damage to the nerves or any other part of the body?
Is there a risk of permanent damage or reduction of sensitivity of nerves when exposed to an electrical current for a prolonged time? Any way to circumvent this problem?
What "resolution" or input density can I hope to achieve, before signal becomes "blurry" because of cross-talk?

Welcome to Bio.SE! Interesting question. Are you planning on using the electrode grid on dry skin, on the skin using an electrolytic solution/gel or are you targeting the tongue (aka BrainPort). Your questions hinge on impedance, that's why I ask. As of now the question is too broad to my opinion.

Thanks for the support! Added some additional info in the description.

Nice question(s). I will go through them in sequence.

Safe current limits. With regard to electrical stimuli it is current density that determines safety limits. Therefore, in medical devices, it is not a matter of what is a safe maximum current level, but what is the maximum safe current level given the surface of the electrode? And in terms of skin stimulation, it is not the safety limit that is the bottle neck, but the maximum tolerable current density, which is around 0.5 mA/cm2 (Prausnitz, 1996). Higher stimuli result in pain sensations. This is one of the reasons why the BrainPort device is used on the tongue; the moist surface reduces impedance and hence the currrent needed to elicit a tactile response.
Permanent damage. As said, the tolerable sensation limit is more of an issue (a must-read in this regard is Kaczmareck et al., 1991).
Acuity. The best-possible tactile "resolution" is generally expressed in terms of tactile acuity. Tactile acuity varies across body sites, and unfortunately it is about the worst on the thigh (45 mm) and the back (40 mm). A much cited picture on tactile acuities is the following from Weinstein (1968):

These acuities represent the distance in which 2 simultaneously presented, static pressure points need to be spaced to be just noticeable (the so called two-point discrimination threshold). Although your proposed electric stimuli are different from pressure stimuli, these reported values in the figure (40 - 45 mm) give an impression on the inter-electrode distance needed. From my own work I can confirm the ~40 mm using vibratory stimuli. The unfavorable acuity of the back and external bodily skin in general was also one of the rasons to put the electrode grid of the BrainPort on the tongue, which has excellent tactile acuity.
References
 - Kaczmareck et al. IEEE Trans Biomed Eng 1991;38:1-16
 - Prausnitz, Adv Drug Delivery Rev 1996;18:395-425
 - Weinstein S. 1968. In: Kenshalo. The Skin Senses:195-222. Springfield, IL: Thomas

Thanks for the answers and references. The chart is especially eye-opening and would help placing the "display" somewhere more appropriate. I am approaching this whole matter with the hope that the brain can (learn to) subconsciously recognize information more finely than the perceived tactile acuity, which can then be a measure for base precision to be built upon.

While, for practical reasons, the tongue might not be suited for sensory addition, I am now considering other mucous membranes such as the inner part of the cheeks as viable surfaces which are more sensitive and require less power to stimulate.


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How can I use this data to make a function?
I'm currently in high school biology (final year) and am currently working on an assignment. I need to create some sort of interactive model, so I've decided to make a simulation-type program.
I've looked a bunch at lots of papers and journals and I was wondering how I could take the data and make a function out of it.
Here is one example (Pleasants & Oberhauser, 2012):

In particular, I want to know how to make sense of the values F_1,11; r^2; and P. I am finding a lot of these values in the papers I'm looking at so it would be awesome if one of you guys could point me in the right direction.
Thanks!

This is not really related to biology more like mathematics. The values you're interested in come from statistical tests, in your case linear regression that is indicated in the last line under the image. You should check math and statistical books for these.

Thanks for the advice. I thought posting under biology would be better than math because the function could be specific to biology? Clearly, my knowledge in this is pretty thin so thanks for pointing me in the right direction.

@poka.nandor yes this question is about statistics but those measures are so often used in biology that I consider them "part of the job".

Clearly, this question is about statistics and is off-topic here. cagliari2005 answered the question though. The answer might be a bit complicated though. You may want to follow an introductory course in statistics. You can find here an excellent introductory class of statistics. Good luck.

I'm voting to close this question as off-topic because it is about statistics. CrossValidated.SE would be a better fit.

@Remi.b. Agree might be a bit complicated. On the other hand I couldn't really explain it more simply as some fundamental bases in statistics are needed to understand p and r-squared.

I think it will likely get shut down on cross validated because it's about basics - open an introductory statistics book/ Web page/ Youtube video and you'll be able to get an answer, then if you're stuck ask about specifics on cross validated

I will not go too deep into the details but here some information to facilitate your understanding of these ubiquitous statistics in biology.
The F, $r^2$ and p-value are all equivalent statistics to measures the goodness-of-fit of a model against the data.
The F is the ratio of the $unexplained~variance~/~explained~variance$. I let you look out what the variance is. The F (originating from a F-test) allows, using the proper F-distribution cumulative density function (cdf) for the number of observation you have, to compute a p-value.
The p-value gives you the probability of obtaining the observed fit with your model (here a linear one) by random chance only. For example in your case a p-value=0.01 means that you have a 1% chance to observe this correlation just by chance. Usually the p-value threshold used to claim statistical significance is 0.05 (i.e. 5% chances to observe that fitting by random chance). In linear regression, the lowest the p-value the closest the distance (called variance) of the observed data point to the line.
The $r^2$ is the coefficient of determination (or the square of the correlation coefficient). This measure is very interesting as it give you an estimate of the "proportion of the data" explained by your model. For example a $r^2$=1 means that 100% of the variance of the data is explained by your model, in other terms your model perfectly fits the data. A $r^2$=0 in the other hand means that your model does not at all explain the data (no fits between your model and the data).
The $r^2$ and the p-value can be computed for any type of fitting, like trying to fit an exponential curve instead of a linear one. What you usually look for when modeling data is the highest $r^2$ possible. As all of this statistics are linked a higher $r^2$ means a lower p-value for an identical number of observations.

p.values are by themselves not probabilities, and nor do they refer to the probability of observing the fit by random chance only. P.values are the frequencies at which you would expect to see an effect size (be it difference in means, or a goodness of fit) as large as your observed one if the null hypothesis were true. Eg, a null hypothesis for a two sample t.test is that the means of the samples are equal).
probabilities are degrees of belief, p.values don't give you the probability of the null hypothesis being true.

@AnkurChakravarthy Frequencies are the exact equivalent of probabilities in this case. Having a frequency of FDR of 0.01 is exactly the same as saying you have 1% chance to observe this fit by random chance (or more precisely to reject the null hypothesis by random chance). I used probabilities as it makes p-values much more understandable (and useful) in my opinion.


text:
Cellular Immunity Response
What response of cellular immunity would appear after complementary protein activation to keep pathogenic bacteria away from our body?
Notes: I do appreciate your explanation. Though I am facing multiple choices:
(a) wrapping the bacteria cell (b) immobilize the bacteria cell (c)    destroying the bacteria cell by enzyme (d) creating pores on the bacteria cell
The key answer is (c) but then I do not know what enzymes make this happens. Any Idea?

Your first sentence is not really a question. You want to know which mechanism of the complement is respsonsible for this protection? If so, can you please re-phrase it?

Does that has anything to do with your topic? http://en.wikipedia.org/wiki/Complement_system Then, maybe, you are looking for this mechanism: http://en.wikipedia.org/wiki/Complement_membrane_attack_complex

@aandreev so.. option (d) is actually correct then, am I getting this wrong?

that is for you to decide

The complement does d.)

As you can simply find on Wikipedia, the cellular immunity, or Cell-mediated immunity,

is an immune response that does not involve antibodies, but rather
  involves the activation of phagocytes, antigen-specific cytotoxic
  T-lymphocytes, and the release of various cytokines in response to an
  antigen.

The answer (c) (destroying the bacteria cell by enzyme) refers to the phagocytes, cells that contain many enzymes, like lysozymes. Those funny enzyme can destroy the bacteria cell's wall.
Actually, I think that the answer (d) could be right, but it's not complete. In fact not every enzymes works on the cell's wall!

After opsonization the antigen goes through phagocytosis or the complement system destroys it. The complement is a cascade of reactions, which at the end creates a hole (many holes) on the membrane of bacteria which causes lysis. http://en.wikipedia.org/wiki/Complement_membrane_attack_complex
So the right answer is d.) in your case.


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Why *morning walk*?
My PT teachers professes working-out/training in early morning hours is the best time to do so. A quick search on benefits of morning walk (or similar phrases) reveals a lot of information which seem to be backed by sound scientific evidence. In fact it is common wisdom around the world, across all cultures.
Okay - accepted. But why is it beneficial in first place? Because there is plenty of oxygen in the morning; or is it?
After long hours of darkness (plants respirating at night) when first light comes plants would have just started photosynthesis, that too at a pretty slower rate (owing to lower intensity of light at dawn). In fact I remember having read something about compensation point

The (light) compensation point is the amount of light intensity on the light curve where the rate of photosynthesis exactly matches the rate of respiration. At this point, the uptake of CO2 through photosynthetic pathways is exactly matched to the respiratory release of carbon dioxide, and the uptake of O2 by respiration is exactly matched to the photosynthetic release of oxygen. SRC

So now, obviously, we can establish the fact that concentration of oxygen should be/is much lower than carbon-dioxide in early morning hours.

So why morning walk or early morning exercises?
If oxygen content is important why not exercise in early evening hours because not all people would like an endurance drill at theoretically perfect time of noon :)?
Is there some other mechanism makes oxygen content more than carbon-dioxide content in the morning?

Personally - I do feel more fresh in the morning hours but maybe that is because of my internal biology, correct me if I am wrong.

P.S. I am not a biology student, so pardon my ignorance.

Personally, I would argue with the premise that it's more beneficial.  Of course I have no data to support this, because (bar a long-ago stretch in the military) morning exercise is just not something I'm going to do.

1: The only benefit I've heard of scientifically is to do with the circadian rhythm. I heard a talk that basically said a dose of bright light in the morning can help set hormonal levels to a daily rhythm. This seems to suggest the same.
2 and 3: I think the overall oxygen levels would not be significantly different at different times of day, but pollution levels might be, this might be relevant.
edit: didn't realise this was such an old thread...

I am going to play the devil's advocate here.
I don't know if working out within the first three hours of waking is necessarily the best time to do so. In the morning, we have what is called cortisol awakening response which is where the body releases cortisol. Cortisol is a by product of the sympathetic nervous nervous system. Dr.s James E. Muller, Geoffrey H. Tofler, and Richard L. Verrier in their article Sympathetic Activity as the Cause of the Morning Increase in Cardiac Events said that early morning activity is a likely culprit but only circumstantial in sudden cardiac infarction [1]. However, Dr.s Douglas P. Zipes and Hein J. J. Wellens in their article Clinical Cardiology: New Frontiers Sudden Cardiac Death found that:

Time of day is also important, with more sudden cardiac deaths, strokes, and myocardial infarctions occurring in the morning on arising from bed, perhaps related to increased sympathetic discharge in response to venous pooling that then triggers increased blood viscosity and platelet aggregation [2].

In Exercise and Acute Cardiovascular Events in Collaboration With the American College of Sports Medicine and Dr.s Paul D. Thompson, FAHA, Co-Chair; Barry A. Franklin, FAHA, Co-Chair; Gary J. Balady, FAHA, Steven N. Blair, PED, FAHA; Domenico Corrado, N.A. Mark Estes III, FAHA; Janet E. Fulton, Neil F. Gordon, William L. Haskell, FAHA, Mark S. Link, Barry J. Maron, Murray A. Mittleman, FAHA, Antonio Pelliccia, Nanette K. Wenger, FAHA, Stefan N. Willich, FAHA, and Fernando Costa, FAHA, felt they that didn't have enough data on claiming early morning exercises and sudden cardiac death (SCD); however, early morning SCD occurred in adults whereas for teens it SCD occurred in the afternoon [3] but "vigorous exercise, however, transiently increases the risk of acute myocardial infarction (AMI) and SCD, even in exercise-conditioned individuals, and several strategies are recommended to potentially reduce this risk"

Active individuals should know the nature of cardiac prodromal symptoms and seek prompt medical care if such symptoms develop.

That is, I wouldn't claim victory for working out as soon as you rise the best choice. However, I am not suggesting that you don't work out in the morning either but just be carefully about it. The best time to workout is the time that will allow you to be consistent, get in at least 30mins, and keep you motivated. If that time is the morning, just be aware of what is going on in the body.
Additional article found in support of afternoon/evening training
Serendipitously, I stumbled across an article on swim performance and time. The article found that the best performance was afternoon to evening and not in the morning [4]. This was published in 2007 in the Journal of Applied Physiology.

I would offer the counter point that this has to do with energy availability. (I'm on my phone so I can't put in references just yet). But there was just a great recent study published in Science (I'll go find it), in which a group looked at plaque deposition as a proxy of overall cardiovascular health of groups of mice exercised before and after food intake. They find that exercise under fasting conditions, which would be akin to morning running, appears to be significantly more protective against cadiovascular disease than exercise after feeding. This is also consistent with some human data suggestive of fasting exercise benefits as well. In a separate experiment the mice were fed the same number of calories per day, but those that were exercises after sleep and before eating were significantly leaner and had less plaque deposition in their vasculature.
In part the idea is that after a period of fasting exercise will promote scavenging of residual cholesterols in the vasculature as well as cellular autophagy (which promotes "fixing" of current cells rather than just replacing them). To the layman, Resveratrol from red wine is probably the most commonly known way in which autophagy might be promoted. But in general think of periodic fasting and feasting as protective because it can help maintain metabolic homeostasis and prevent unnecessary cell turnover.
Hopeful that helps lead you in the right direction. Metabolics and aging is a huge and exciting field and this question could be answered with a small textbook. But you should at least understand that this field is far from being well understood. And that your PT teachers may end up being right, but this field still quite primitive, and this is not accepted yet or really understood by the scientific community.

Did you forget to look up the links? I am rather interested in looking up this study that you have cited.

You know, I've looked and I can't seem to find it. Unfortunately, not being my field of concentration I never saved the reference. I'll keep looking but I can't seem to find it in science, so it may have been in nature or cell, though I looked and can't seem to locate the study. Sorry.

If walking in the morning is truly more beneficial than walking at a different, it certainly wouldn't be related to atmospheric oxygen content. The oxygen content of the atmosphere fluctuates on the timescale of years, not hours. And keep in mind that when it's morning where you are currently, it's going to be noon somewhere else, and dusk somewhere else.

W.r.t. keep in mind that when it's morning where you are currently, it's going to be noon somewhere else, and dusk somewhere else - But the distance between morning & noon would be several longitudes, oxygen, under the effect of diffusion or even torrential winds, wouldn't normalize its concentraion so quickly.

Morning walks are preferred because the sunlight that falls on the earth in the morning is good for your skin for producing Vitamin D.
and also it is said that morning walks are good for:

Strengthening Bones and Joints
Weight control

and also independent of the time of the day, due to exercise and walking you keep moving your joints an this improves your Blood circulation.
And also as you keep moving your muscles too which improves Muscle Strength .
this was from my knowledge.If you want to know more :
Click Here(link 1) ||
and here(link 2)
Share your thoughts with comments,
Any suggestions and questions welcomed,
Anurag .

This is nothing I would attribute only to a morning walk. Vitamin D will be produced as well in all other parts of the day during sun exposure, the training effect as well.

Ditto, there is no difference in the sunlight hitting the earth at different times of day. edit, other than intensity.


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Oscillatory electrical system using a chain of neurons
Many daily activities that we perform are result of inbuilt oscillatory circuits in our body. For example walking, breathing, heart beat, blinking, etc. The coding and decoding of stored memory also happen via controlled oscillations. The link http://en.wikipedia.org/wiki/Neural_oscillation contains information about neural oscillations. It says in here that a single neuron, an ensemble of neurons and activity of brain may exhibit synchronised oscillations. It is also said that these oscillatory circuits can control all the parameters of oscillations i.e. frequency, phase and amplitude.While above are true for neurons as a part of bigger systems, my question is related to study of isolated neurons.
There are many instances of studies of artificial neural circuitary created on a customized substrate(Micro Electrode Array) by masking techniques. Also there are loads of ongoing research to study the simple neural circuits in temporal and spatial domain by electrical interfacing of semiconductor and nerve cells using Field Effect Transistor(FET).
I want to know if these kind of oscillations are unique to some special kinds of neuron? Is the control of oscillation parameter possible in every neurons and isolated neurons? Can a neuron or any other cell exhibit change in action potential independently? Do other cells except neuron and pacemaker cells exhibit oscillation? Can a single neuron exhibit memory?
Can a simple circuit like below generate oscillations?
Suppose I culture the neurons on a substrate in a controlled way such that one neuron is connected to only one other neuron in a linear fashion and the last neuron is connected to first. Assuming we supply the ions if there is loss, can a clock pulse of varying frequencies be generated, where the frequency is the function of the no. of intermediate neurons and their length.
It would be a great help if somebody can provide information about softwares to simulate simple neural circuits (If available).

What is your analysis on this? Theoretically you can build a continuously oscillating system but there will always be some loss. If the neuron never runs out of energy then it would keep firing. The period of the oscillation and the nature of the steady states depend on system parameters. Your question is broad and you have not made any effort to find an answer to the question. Therefore I am voting to close this.

Agreed with @WYSIWYG - No neuron ever evolved to live like a bacterium. This is too theoretical and probably more suitable for another more theoretical SE site.

I'm voting to close this question as off-topic because it is too theoretical for Biology.SE

ps - I ran a few searches on Scholar and there is really nothing to be found (search terms autostimulation&neuron, self-wired neuron and the likes).

@AliceD FHN model is continuously oscillating system.

@WYSIWYG - yes, but it is a model not applicable to a biological system. That is my issue with this question.

@AliceD yeah.. This case has to be specifically modelled.

I wanted to know about generating clock pulse using neurons by giving its own signal as feedback

Suppose for example I culture the neurons on a substrate in a controlled way such that one neuron is connected to only one other neuron in a linear fashion and the last neuron is connected to first. Assuming we supply the ions if there is loss, can a clock pulse of varying frequencies can be generated, where the frequency depends on the no. of intermediate neurons

Interesting add @DivyaPrakash, I retracted my close vote.

single neurons can act as oscillators without the need for feedback, simply by the interplay between various channels.

@AliceD please, can you explain more? If possible give the answer to my question too.

I vote to re-open this (edited) question. At least there are some theoretical studies on such systems, and also relation to how such constructions can't explain the scalar property.

Original poster (question author) did not provide any evidence of even basic research, using google, or pubmed, or google scholar. Hence, it should be closed

I'm voting to close this question as off-topic because OP did not provide any work on answering question. This might be asked in chat room, rather than Bio@SE. Although, I might be wrong

Short answer
A single pacemaker neuron can generate oscillatory behavior.
Background
Given our exchange in the comments, I will focus on single neurons with intrinsic oscillatory behavior. For example, thalamocortical relay neurons and inferior olive neurons have intrinsic oscillatory properties, mainly through the interaction of a hyperpolarization-activated cation current (Ih) and a low-threshold activated Ca2+ current (IT) (McCormick & Huguenard, 1992, and Fig. 1).

Fig. 1 Model for an oscillatory inferior olive neuron. Source: Bal & McCormick (1997)
Rhythmic burst firing is created through generation of a low-threshold Ca2+ current (IT), which activates fast action potentials mediated by Na+, K+, and Ca2+ currents (INa, IK, and ICa, respectively). Entry of Ca2+ in the cell during fast action-potential firing and low-threshold Ca2+ spiking result in after-hyperpolarization through activation of a Ca2+-activated K+ current. This afterhyperpolarization activates Ih. Combined activation of Ih and decrease of a Ca2+ activated K+ current (IK,Ca) results in depolarization of neuron, which activates another low-threshold Ca2+ spike. In this manner, Ih modulates frequency of oscillation. In addition, tonic activation of Ih also contributes to average membrane potential, and therefore to presence, strength, and frequency of oscillation
in these neurons.
Regarding the series of sub-questions - these are quite varied. Perhaps it is better to generate another one or two focused, well-formulated questions on this. For now, I will answer them curtly below. Further, the papers I linked contain a wealth of information, and the McCormick & Huguenard (1992) paper is a detailed modeling study. Both papers are awesome and the authors are three of my all-time favorites so far.
I want to know if these kind of oscillations are unique to some special kinds of neuron?
Answer: Yes quite unique, because Ih channels are quite unique (they have been called "funny currents") and they are not present in every cell.
Is the control of oscillation parameter possible in every neurons and isolated neurons?
Answer: No, as the molecular machinery such as Ih channels may be lacking in most other cells.
Can a neuron or any other cell exhibit change in action potential independently?
Answer: That depends whether the cells are coupled through synapses or other means.
Do other cells except neuron and pacemaker cells exhibit oscillation?
Answer: Yes, some cells start to oscillate, for example in the degenerated retina (modeling work only) and there are non-neural cells that when cultured spontaneously start to oscillate.
Can a single neuron exhibit memory?
Answer: Yes, through long-term potentiation or depression.
References
- Bal & McCormick, J Neurophysiol (1997); 77:3145-56
- McCormick & Huguenard, J Neurophysiol (1992), 68(4): 1384-1400


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Needle-like crystals observed in wild-grape wine under microscope. Potentially harmful?
I recently crushed and strained about thirty pounds of wild grapes to ferment into wine. About a month in, I did a visual inspection of the wine under microscope to try and identify some yeast and bacteria species. However I was more taken by the sight of many sharp, needle-shaped crystals in the wine (along with microbes). Pictures are below:

My best guess is that they are raphides (crystals of calcium oxalate/carbonate), a supposed defense mechanism of some plants. These seem to be complicit in causing acridity in certain plants, and indeed the grapes (and resultant wine) were extremely tart. I've not, however, heard of any wild grape species having known toxicity.
My question is, then: are any wild grape species known to produce such crystals and, if so, are they known to be harmful in any way? Is there another explanation?

They certainly do look like calcium oxalate crystals!

You just reproduced some of Louis Pasteur's work. https://en.wikipedia.org/wiki/Louis_Pasteur#Molecular_asymmetry

Try here. https://www.awri.com.au/industry_support/winemaking_resources/wine_instabilities/hazes_and_deposits/crystalline_deposits/#calciumoxalate

If they are really oxalate crystals, the harm depends on the concentration. Some ppl are on oxalate diet, because they would develop gallstones or kidney stones otherwise. It is not considered toxic, you can drink it.

you are correct that these grapes have raphides. After doing some research, I found out that the grape raphides are twinned crystals. Raphides can cause much irritation for many herbivores (therefore, it is a protection mechanism) but less so for humans. In grapes, however, the irritation is much less than other raphide-containing species. This probably has to do eith the fact that it has a twinned structure (this is what I think, but I haven't found any research on this).
As a side note, what you have done is known as a whole mount, in which is entire organism specimen is placed on the slide, usually after crushing. It is a geeat way to examine the contents of the cell vacuole, which is where this raphides are commonly found.
References:

http://www.ncbi.nlm.nih.gov/pubmed/10648203
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091341

You should add some references. :-)

@inf3rno I have added references


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How does food intake affect medicine? Why pill instructions recommends taking them before (after) meal?
Even simple vitamins seem to have this in the instruction. Why is is so? Is there some simple model of how do pills interact with food? Does it depend on the food type? (What about drinks?)
Should not eating at all on some day be considered "before food" or "after food"?

This question is asking for medical advice, which is off-topic on all Stack Exchange sites, including Biology. Please consult with your physician if you have questions about any medications you may be taken, and when/why they should be taken. We cannot safely give you advice without knowing your full health situation.

@closevoters This can be taken as something that deals with pharmacokinetics.

@MattDMo I don't have any doctor around; the question is not about me and my pills, but about pills in general. Inconvenient "before meal" is just stated in the instruction, but not explained.

@anonymous If you remove your last question (sentence) about higher dosage, I think people will vote to reopen this question. As such the people here do not want to be responsible for something bad happening because of health related answers from SE

I'll vote to reopen if this is changed into a purely pharmacokinetic question.

I can tell you why you should take iron with food. Because you need something with it to "buffer" it so that you don't get a stomach ache!

From the Merck website :

Drug absorption is the movement of a drug into the bloodstream after administration.
Absorption affects bioavailability—how quickly and how much of a drug reaches its >intended target (site) of action. Factors that affect absorption (and therefore >bioavailability) include
1.The way a drug product is designed and manufactured
2.Its physical and chemical properties
3.Other ingredients it contains
4.The physiologic characteristics of the person taking the drug
5.How the drug is stored
If a tablet releases the drug too quickly, the blood level of the drug may become too high, causing an excessive response. If the tablet does not release the drug quickly enough, much of the drug may be eliminated in the feces without being absorbed, and blood levels may be too low. Drug manufacturers formulate the tablet to release the drug at the desired speed.

Essentially, most drug's absorption rates are slowed down by food in the digestive tract, which is beneficial for various reasons depending on the drug.
Some pills are irritants to the stomach, in which case they usually have a coating that may need an acidic environment to break down. Food would assist in this, as well as serving as a sort of diluting agent and even a physical barrier for the stomach.
Conversely, some nutrients (and certain pharmaceuticals) are absorbed by the stomach lining and small intestine much more efficiently when the body is actively digesting food, which is why vitamins and other supplements have the food recommendation.
I think that 'before or after' food should be read as 'shortly before or after', i.e., so food and pill are digested simultaneously. Otherwise, I believe they just don't mention it. Of course, this is a simplistic rendering of pharmacological absorption vis a vis food (there are some very specific interactions; grapefruit and various blood pressure medications come to mind), but this is the general answer to your general question, I believe.


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Stable transfection
I need to achieve stable transfection of a pCI-Neo plasmid into the genome of a mouse embryo. The most common way to achieve stable transfection is through positive selection, however positive selection would not work with embryos. How can I ensure stable transfection of this plasmid in a mouse embryo without damaging the embryo? Would this plasmid integrate itself when the cell divided? I plan to use effectene as the transfection agent.
Thank you.

I'm not familiar with that specific plasmid, but if you need integration, I think you need some sort of transposon or to take advantage of homologous recombination.

You can use lentiviral transfection.

don't people use ES cells in culture first and transplant positive cells into blastocyst? and in ES cells, since it is culture, you can rely on very low efficient homologous recombination, but still select your cells by Neo resistance

Thank you all very much for your suggestions, I am looking into integrating my gene into a lentivirus (I can't believe I didn't think of that). I'm very glad I came here for suggestions. =) Thanks again.


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Do sulfate reducing bacteria help during the formation of the mineral dolomite in low temperature environments?
Do sulfate reducing bacteria help during the formation of the mineral dolomite in low temperature environments?
Wikipedia says

The actual role of bacteria in the low-temperature formation of
  dolomite remains to be demonstrated. The specific mechanism of
  dolomitization, involving sulfate-reducing bacteria, has not yet been
  demonstrated.

I wonder if someone has any updates on this. The reference given in the Wikipedia article is from 2000, from a source titled suspiciously "Journal of Conference Abstracts". Now it's 2013 and maybe someone else has found out something new.

The appropriate answer seems to be that bacteria help somewhat sometimes, maybe.
The evidence for this appears to be mixed, and appears to have been historically controversial.
One old-ish paper claims that bacteria (and more importantly, Archaea) are necessary at least under some conditions. Another somewhat later paper including some of the same authors claims to have found conditions for abiotic dolomite synthesis in the laboratory.
It appears that in terms of mechanisms, the relevant process may involve the proper state of magnesium ions, to which apparently microbes contribute via extracellular polysaccharides:

Literature values for carboxyl group density are not available for all bacteria involved in dolomite formation, however Braissant et al. (2007) demonstrated disordered dolomite phases forming in the presence of the EPS of sulfate reducing bacteria with a carboxyl group density of ~10-3 moles g-1, similar to our values. We suggest that these carboxyl groups promote desolvation of the Mg ion, known to be a kinetic inhibitor in dolomite precipitation (Wright and Wacey, 2004), but are needed in a high density for nucleation to commence.

However, what process exactly is generating geological dolomites appears to be still a matter of debate, and also here, with some suggestive evidence in favor of microbes affecting that process.


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What is the benefit for cells having the ATP production regulated in mitochondria compared to being from the nucleus?
Mitochondria have their own DNA and appear to be loosely connected to the nucleus and it role.
Why are the functions of mitochondria not in the nucleus? Why doesn't the nucleus control the mitochondria's functions as it controls regulation for other chemical reactions?
Are there evolutionary/competitive benefits for this separation?

For starters, see this thread.
My understanding is that the ancient predecessors of mitochondria were free-living unicellular organisms. Supposedly at one point, these mitochondria-like cells developed an endosymbiotic relationship with a larger cell. This relationship was advantageous for both cells: the smaller cell could focus on energy production, leaving tasks like homeostasis, nutrient collection, etc, to the larger cell. Over evolutionary time, this endosymbiosis caused the smaller cell to lose all functions unrelated to energy production, while the larger cell (as we now know it) came to rely heavily on the mitochondria for energy production.
So it's possible that at one time the nucleus encoded machinery for ATP production, but apparently the modularity and separation of function provided by this ancient symbiosis turned out to be successful.

wouldn't some examples of a mononucleotic system emerged to compete if it was slightly as efficient? Why does this arrangement dominate?

it is a matter of opinion if it dominates. Louis Pasteur would have said: Ce sont les microbes qui ont le dernier mot (the microbes have the last word)


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What is the speed of neurotransmitter release and receptor binding in a neuronal synapse?
Obviously neural signals travel at extremely high speeds, but I'm wondering how much that speed is affected by the release and binding time of neurotransmitters.
If my sources are correct, a well myelinated axon generates an action potential with a speed of roughly 119.807 m/s. How much does the speed of neurotransmitter release by the presynaptic neuron and binding to the postsynaptic neuron's receptors impact that speed? In other words, I am wondering how much the total speed of a neural signal from one neuron to another is affected by the time it takes for the first neuron to release neurotransmitters and the second neuron to receive the neurotransmitters and propagate an action potential within its own cell.
I assume it takes at least some time, but exactly how much does it slow the signal down?
Thank you for your answers.

It seems to depend on the size of the neurotransmitter. The bigger the neurotransmitter is the longer the neuron has to be stimulated to actually release the neurotransmitter. But in the case of Acetylcholine it seems to need only about 2ms after a presynaptic stimulus to generate a postsynaptic membrane potential and after about 5ms all the Acetylcholine in the synaptic gap is cleaved allowing the postsynaptic cell to repolarize. The example get described here.

What do you mean by "cleaved"?


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Leaves growing on a leaf of a Begonia
I've a Begonia species. Somehow it started to grow new leaves on top and right in the center of an existing leaf which you can see in the center of the image. Why is it doing this? Apparently it is not a disease because the Begonia itself is growing fast. Will the new leaves eventually become a new Begonia which can survive on its own?

The phenomenon you are observing is probably Adventitious buds. The plantlets can develop on intact leaves or on injured one.
Back to Begonia, this phenomenon usually occurs on injured leaves, so, probably, the plant was injured during movement/by insect or by other means and because of this started to create plantlets.

Will these plantlets eventually be able to survive on their own?

@wie5Ooma I think yes, definitely...

 African Violet plantlet growing from another african violet leaf that I'm growing. This one is growing at the stem and leaf junction. I also have another leaf that has three plants starting to grow along the bottom edge of a leaf. If I remember from my high school days in horticulture class,(when I was in school with Moses), this probably occured when I cut and potted the leaf and scratched or rubbed the leaf thereby stimulating the cells and causing growth. The article before mine gives you the scientific version of this phenomenon.

Hi James. Welcome to [biology.se]. I want to point out that this post does not really answer the question; it is more like "I have this problem too". If at all it does answer the question to some extent, it is based on anecdotal evidences. Can you please cite a relevant source (perhaps a horticulture manual, book or a research article) to support your claim?


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how to quantify toxicity
When going through this link, Table 1, what are the numbers mentioned there? How is one quantifying toxicity?

Usually, toxicity is given in the units of mass of the substance per unit mass of body mass of the organism that will kill 50% of the organisms in a species if those organisms ingest the toxin at that dose (e.g. mg/kg, ng/kg). This measurement is called the median lethal dose, and is often abbreviated as LD50.
In your table, they only provide the mass of the (average) dose of the substance needed to kill the organism listed, as can be seen by the (mg) after the words "Toxic dose". They likely multiplied the LD50 of the toxin by the average mass of the organism to obtain those numbers. Based on Google's estimation that a mouse has an average weight of 0.68 oz (0.019 kg), and on this table of murine LD50 measurements, I calculated that for tetanus toxin, the lethal dose in the average mouse is 3.8x10$^{-8}$ mg, which is basically what your table provides, which supports my guess on how they obtained their numbers.
The other values listed under "Lethal toxicity compared with" appear to be ratios, given by the formula [lethal dose of toxin above]/[lethal dose of toxin on left]. Using Wikipedia's LD50 for Strychnine in mice (2 mg/kg) and the tetanus toxin LD50 from my previous source, I obtain the exact ratio that they do (1x10$^6$). The lack of units makes sense, as ratios are unitless.
Source on LD50

"needed to kill 50% of the organisms of a species tested", what does this mean?

It means that when they were testing the drug on animals, 50% of the animals tested died when given the dose. So, if the LD50 of X is 1 mg/kg in mice when ingested orally, then 50% of mice can be expected to die if they consume 1 mg of X orally for every 1 kg of their own mass.

no  my question is whichever value is the correct value, how can one get that correct value. How is the quantity of the toxin related to the functionality of the host?

@Rishika I am not sure I quite understand your question. If you want to know how LD50 is calculated, the LD50 value is obtained experimentally. If you want to familiarize yourself with the methods used to calculate LD50 values, I would read some articles that report research doing that. Here is an article I found with a quick pubmed search where the LD50 of several compounds was calculated in silkworms: https://www.jstage.jst.go.jp/article/ddt/10/1/10_2016.01025/_pdf. If this does not answer your question, I would encourage you to post it as a new question on stack exchange.

A small note: There are some other measures too such as Maximum Tolerated Dose, Minimum Lethal Dose, therapeutic index etc.

@Rishika How is toxicity experimentally measured is a different question. Your comments are not actually asking for clarifications but asking new questions. Either edit your question to add these aspects or ask another question. Moreover, try reading about LD50/Lethal dose on wikipedia or other online resources instead of simply asking a user to explain it.


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Are human chromosomes connected or separate molecules?
Do the 46 human chromosomes form a single unbroken DNA helix?  Or is it rather that a human's genome consists of 46 disconnected helices?
If it is the former, does the common numbering scheme for the chromosomes have any correlation to their actual ordering in the one large strand?
If is the latter, is there a convention on how the chromosomes are ordered in genomic datasets?  Also, is there a clear understanding of how sister chromosomes "find" each other in Meiosis I?
Generally, during periods when Mitosis/Meiosis are not occurring,  what's a good physical picture for how the chromosomes are physically arranged (e.g. a bowl of 46 spaghetti noodles, or maybe the sister chromosomes always stay close together, etc)
thanks!

Each chromosome is a pair of distinct, separate DNA molecules.  A chromosome of an eukaryotic cell nucleus is a (long) helix of two linear molecules and so has two ends, which are called telomeres.  DNA naturally forms a double helix with its complementary DNA molecule, and the double helix can further curl in what are called supercoils.
In humans, the chromosomes occur in 23 pairs (totaling 46). Except for the sex chromosome pair, each member of the pair is identical in appearance in a karyotype (picture) and each such pair has a number assigned from 1 to 22; the numbering generally follows the size of the chromosome, with chromosome 1 being the longest.  In mammals, the sex chromosomes in a male are quite different in size and are labelled X and Y; a female has two identical X chromosomes.

Technically each chromosome consists of two DNA molecules.

@canadianer Well... it depends on whether you consider hydrogen bonding being strong enough to consider the whole thing as a single molecule.

@Remi.b I don't ;) Not that it means anything, but I've also never heard anyone use hydrogen bonding in the definition of a molecule. Is a glass of water a single molecule?

@canadianer My chemistry teacher in high school used to say that $H_20$ should rather be called $H_{12}0_6$ or something like that. :) And the two DNA strands literally stick to each other and are really not moving independently. But I agree with you. I'd rather consider one chromosome as being made of two molecules.

@canadianer, Remi.b,: edited to reflect what you pointed out.


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Effects of antibiotics on bacterial growth
I will do an experiment on effects of antibiotics on antibacterial growth and I will use three antibiotics: ampicilin, chloramphenicol and streptomycin. To make a hypothesis I must have a guess on which antibiotic will have the most severe effect on bacteria. So, do you know any source to find this information out or I would appreciate if you explain the reasoning behind a comparison of how severe these antibiotics.
Edit: Bacteria that will be used is E.coli.

This is impossible to answer without specifying what bacteria, and even so most antibiotics will not be effective against all bacteria of the same species (due to resistance). All these antibiotics are broad-spectrum and will have a "severe effect" on some types of bacteria.

Sorry, I edited the question.

I mean, theoritically which one is the most harmful?

The dose makes the poison.

@MarchHo - Not necessarily.

There is no previous research i guess

@BobSacamano there is research on this. Look for minimum inhibitory concentration (MIC) and LD50 values for these antibiotics. I hope your E.coli strain is not naturally resistant to either of these. Is it a lab strain such as K-12 or DH5a?

What would you recommend