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Why is alcohol purged from the body more slowly when we sleep?
It is a popular belief that when you get asleep after drinking alcohol, in the morning you have higher level in your blood than if you stayed awake the whole night.

Is this true?
If so, why? Is it because the liver works more slowly while sleeping, or because the intestines work more slowly and there is still more alcohol in the morning to be processed by the liver?

I never heard of that. That'd be great if you could provide a link to prove that it is a noticeable claim? Note that your question would also be on-topic on Skeptics.SE.

@HonzaZidek agree with comment above - this is a flawed question - alcohol is not purged more slowly when you sleep and you don't wake up with more alcohol in the morning - check out zero order kinetics if you want to learn more about alcohol metabolism

You are right, Culprit is Ethanol in Alcohol. It contains 2 carbon atoms, 6 Hydrogen atoms and 1 Oxygen atom.

Ethanol is readily soluble in water, so it easily dissolves in the
bloodstream and gets carried to various parts of the body. The most
affected areas of the body include the liver and the brain. In the
brain, ethanol adversely affects Glutamate receptors, which causes
slurred speech, memory loss, slow reaction to stimuli, and other
common side effects of being a bit too tipsy.
Not only this, ethanol molecules bind with GABA (gamma-aminobutyric acid) receptors, which is able to slow down the
activity of brain. Unlike glutamate receptors, ethanol actually makes
GABA receptors more receptive, causing the brain to slow down even
further. However, alcohol doesn’t just act to slow everything down in
the body. It also stimulates the production of dopamine and
endorphins, chemicals that produce feelings of pleasure. This is the
reason why people choose to get that alcohol “high”, despite knowing
the negative consequences that it may lead to.

So basically when you are physically working body needs more oxygen while Ethanol only has one oxygen atom, and Since Liver starts to work on regular pace, Which plays a central role in all metabolic processes in the body.
Everyone's oxygen levels in the blood are lower during sleep , in fact while sleeping or in meditation body needs very less oxygen to survive.

Why would I need to wear oxygen while sleeping?
Everyone's oxygen levels in the blood are lower during sleep, due to a
mildly reduced level of breathing. Also, some alveoli drop out of use
during sleep.
If your waking oxygen saturation is greater than about 94 percent on
room air, it is unlikely that your saturation during sleep will fall
below 88 percent. However, your doctor can order an overnight oximetry
test if there is a question about your oxygen saturation levels while
you are sleeping.

In general, metabolic rate is higher when you are awake, because then you tend to be moving about doing stuff.

Welcome to Biology. This answer just touches the question. Further, sources are lacking and this is mandatory when quoting stretches of text

@AliceD Thanks, I will get better if you give me a few more chances.


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What is the H+ gradient in mitochondria?
I would like to understand what the term H+ Gradient means. I googled this question and found terms such as chemiosmosis and ion gradient being tossed around. I am very new to biology and I do not know any advanced terms or anything of the like. What I do understand is that the mitochondria produces ATP and has something called a proton pump.
Thank you in advance.

A gradient is defined as the difference in concentration of a solutant between two places. For example a sodium gradient along a cellular membrane is the concentration difference between the inside of the cell and the outside space. A H+ gradient (also called proton gradient) is therefore the concentration difference between the inner mitochondrial membrane and the outer mitochondrial membrane. Does this help you? I can expand this later today in a proper answer.

This is really helpful, thank you! Why is it called proton, though? Shouldn't it be ion? And why is this necessary to maintain? I know that lysosomes break down cells that cannot maintain their H+ Gradient, what does ion concentration have to do with the organisms need to break it down? Sorry to ask so many questions. Thank you very much for the help!

@Sciiiiience An H+ ion is a proton

Oh I see! Sorry, I didn't think that through. I forgot hydrogen is just proton-electron. Thanks

Lets start with a general definition: A gradient is the difference in the concentration of a substance (this can be a solutant in liquids, a gas or whatever) between two places. The image below shows the general definition. If nothing else happens what keeps the gradient stable, over time diffusion will cause an equilibrium between both places. The flow of substance always goes from the high concentration to the low (indicated by the arrows).

In biological systems the two parts of the gradient are usually divided by a membrane and are more stable. Gradients can be generated by active transport which requires the input of energy to work against the gradient. Examples would be the concentration gradient along a membrane like protons (positively charged hydrogen-ions), as this can be seen in the mitochondria. Here three complexes of the respiratory chain (I, III and IV) pump protons from the matrix in the intermembrane space, which requires energy. The fourth complex (V) pumps the protons back and uses the released energy from this process to make ATP. See the figure below which shows this process schematically (from here):

source: Stack Exchange

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Why are there more stomatal openings on the lower surface of a dicot leaf?
This causes more transpiration to occur from lower leaf surface. What's the exact reason for why are there more stomatal openings on the lower surface of a dicot leaf?

I believe water conservation is the main reason. I'll try to write up a proper answer when I have time

@CactusWoman Could you please post an answer if you have time now? :)

Firstly, it is not necessary that all dicots have stomata on their lower surface of their leaves. The lotus Nelumbo nucifera has its stomata on its upper surface, due to the lower surface of its leaves being in contact with water, and therefore unable to transpire effectively.
The reason that stomata are usually on the lower surface has been analysed in this paper, which rejects the commonly held hypothesis that stomata appear on the lower surface of leaves (hypostomatous) as a response to dryness, by citing that hypostomatous leaves are relatively less common in dry environments.

The paper then analyses the correlation observed between parameters of leaves and their stomatal locations.

By using a number of computational models (which conclude that given the set of assumptions in the paper, leaves should not generally be hypostomatous), the paper addresses the faults of the model and concludes that there is no one single reason why leaves are usually hypostomatous, and then brings up a couple other possibilities that may help in explaining the majority of plants being hypostomatous.

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border zone of the infarcted heart
I did myocardial infarction experiments on mice and I am a newbie in this area. I need to isolate RNA and protein from the remote and the border zone. Where should I cut the heart so i can separate the infarct zone, border, and the remote zone? Can anybody help me with this?

I'm no expert but does this help? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1888481/


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Antigenic and non antigenic
Can any foreign molecule be non- antigenic ? Can any foreign peptide be non-antigenic ? What is the difference between an antigenic and a non-antigenic peptide ?

Molecules are antigenic if they are able to elicit an immune response. Let's incorrectly equate "antigenic" with "elicits antibody response". It's conceivable that a molecule might elicit an immune response, but not generate antibodies - this nuance is not particularly helpful for answering the question.
Antibodies are proteins which recognize antigens. Exactly which antigen they will recognize depends on the exact sequence of the antibody. This sequence is generated by chance, but it is generated by recombining an array of pre-existing sequences: This means that not every conceivable antibody sequence can be generated by the immune system. Moreover, it is also possible that no antibody at all can be generated for a given substance. So, no, it is not guaranteed that you will be able to generate antibodies for every possible substance. In fact, companies which sell monoclonal antibodies for Western blots often find the occasional substance which will not generate antibodies from their animals (rabbits, mice, goats, and so on).
A second complication is that many molecules are very weakly immunogenic and rely on adjuvants.
Lastly, there is a simple counter example to your question: There are many foreign molecules, both LPS and peptide, produced by bacteria which do not trigger the immune system at all. This applies to all the species that make up our gut flora, since it would counter productive for the body to attack its own symbiotes.
Of course, the immune cells at some stage learn which molecules are "own" molecules, so that they do not attack their own body. If the "foreign" molecule is presented to them at that learning stage, they will not recognize it as an antigen in the future.

Something is antigenic because it acts as an antigen - it binds to an antigen receptor in the immune system (antibody, B-cell receptor, T-cell receptor, etc.). While the concept of "foreign" in immunology is often (incorrectly) equated with antigen, that is not the case. For example, there are many chemicals one could think of that are foreign (non-self), but don't usually raise immune responses - nylon, for example.
The difference between an antigenic and non-antigenic peptide is that the antigenic peptide, when presented in the correct circumstances, can raise an immune response. This means that, theoretically, the exact same peptide sequence can be both antigenic and non-antigenic depending on the environment - whether it's being presented in an immune-suppressed environment, for example. However, it's more common to classify antigenic potential based on whether it's possible for the substance to raise a response in an otherwise "normal" immune environment.

What exactly makes a substance antigenic/non antigenic ? I want to know the molecular basis for this/

In principle every molecule above a certain size (single amino acids for example can not) can be immunogenic. A very important function of the immune system is to differentiate between molecules, which are foreign and which should raise an immune response and those, which are not and which therefore have to be tolerated. If this differentiation doesn't work, this lead to autoimmunic diseases.
There are two processes which are important here: self-tolerance and tolerance against foreign (or peripheral) antigens. Basically said for self-tolerance autoreactive lymphocites (B- and T-cells) are eliminated from the pool of developing cells, before they can fully differentiate. Only 1-2% of the cells which start developing go get through this selection process. Peripheral antigens (for example from food) are usually tolerated when there is not other immunologic process in the peripheral lymphoid tissues.
The process looks in principle like this (image taken from the second review listed below):

I will not write the whole process here, but the Wikipedia article on this topic is a good start. What I can also recommend is the Immunology book written by Janeway and colleagues (if you can get it via a library) and you can have a look on this two reviews:

Immunological Tolerance: Mechanisms
Primer: mechanisms of immunologic tolerance.

If you have problems accessing the articles, let me know.


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Calibration curve for single radial immunodiffusion
When we draw a calibration curve for single radial immunodiffusion, the curve does not pass through origin. Instead, there is a y intercept. Why does that happen ? Shouldn't zero antigen give zero ring diameter ?

When the radial immunodiffusion method is used to measure antigen concentrations in samples, a plate or slide is set up using agarose containing an antibody or antiserum. Holes are punched out of the agarose to form wells into which antigen is dispensed. The antigen diffuses out into the agarose and when the antigen/antibody ratio is favourable an immunoprecipitate will form as a ring (immunoprecipitin ring). The final diameter of the ring is proportional to the initial concentration of antigen.
Addressing the question: isn't this simply explained because the values on the Y axis are squares of the diameters of the rings, and this includes the well into which the antigen is dispensed?

Thanks ! I thought the diameters were taken from edge of the ring.


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Functioning of BRCA2
I know that BRCA2 interacts with RAD51 to repair DNA damage.
But how exactly does it function ? What are the other proteins that interact with it ?

I'm just skimming through it now, but this 2011 review in Nature Reviews Cancer looks like it has everything you could possibly want to know about the BRCA1/BRCA2 pathway. If you don't have access to the journal, the first page of this Google search should have a PDF link to Researchgate down near the bottom, or you can try this direct link.
I apologize for the "link-only" answer, but there is a ton of info in the paper, and it would be rather difficult to summarize it in just a few paragraphs. This is a rather broad question, so perhaps you could read through the review and references, and if you still have specific questions about the pathways or interactions you can ask another question.

I agree with you, this paper offers a very good overview.

Here is an image of BRCA2 and RAD51 oriented.( I produced this using PyMOL!)
The chocolate coloured part is some BRCA repeats. You can see how BRCA repeats and RAD51 are oriented. Here, the association is shown only for one of the 7 subunits of RAD51
The exact mechanism in brief :
.

BRCA2 binds to RAD51 subunits within the ring via BRC repeat mimicry of the RAD51 polymerization motif.

2.BRC repeats disassembles the ring.
3.The RAD51:BRCA2 comple is recruited to a DNA double strand break.
4.BRCA2 helps displace a protective protein, Replication protein A- RPA, and binds the primary ssDNA substrate by its B folds.
5.It loads RAD51 onto DNA. The handoff reaction might be facilitated by attraction of DNA by the positively charged BRC repeat helical arches.The BRCA2 helix-turn-helix domain(red) at the end of the tower may bind dsDNA in cis at the ssDNA/dsDNA intra-DNA junction (3) or in trans to the dsDNA that later serves as the homologous DNA template (6) and the positively charged arch may also help to attract the dsDNA template.
Source : Yang etal. 2002 , Shin et al 2003
Thanks to Nicholas Provert for teaching me basics of PyMOL on Coursera.


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Conserved proteins are non immunogenic
I read that proteins that have been highly conserved are non-immunogenic.
Why is it so ? What is the special thing that makes it non immunogenic(antibodies against them are hard to make) ?

Immunogenicity has nothing to do with how conserved a protein is. As nico already pointed out, it is a mechanism to prevent autoimmunity. But this is only valid for proteins which are similar to human proteins.
If you design a vaccine, you try to choose proteins as vaccine candidates, which are as conserved as possible. This makes the vaccine more universal (since conserved proteins are shared between different strains of a bacterium or a virus) and also prevents it from getting ineffective when the target protein mutates. An example would be the flu virus where you need to predict the strains which will be in circulation to formulate a vaccine. If it would be possible to find a conserved protein, which is shared between all viruses (and of course has no similarities to human proteins) than you would have a universal flu vaccine.
Antibodies can (and are) be designed artificially, this is for example done for capsulated bacteria like Menningococcus B, where so far no vaccine was available. These vaccines are either relatively short peptides or single proteins from the from the pathogen. The proteins for the vaccine are then usually made in a biotechnological way, purified and can be used as a vaccine. This approach is called reverse vaccinology.

Hi! Please see my comment to nico's answer.

@biogirl I expanded my answer. Does this answer your question?

Immunogenicity is

the ability of a particular substance, such as an antigen or epitope, to provoke an immune response in the body of a human or animal. In other words, immunogenecity is the ability to induce a humoral or/and cell mediated immune response.

If a protein is highly conserved between species it means that its epitopes will be recognised as self by most species, hence the organism will avoid producing antibodies against them to prevent autoimmunity.
You may want to read about central tolerance to see how T cells and B cells are rendered non-reactive to self.

Hi! thank u . I read this not in relation to living organism but artificially trying to make antibodies. Do artificially made antibodies also always involve living organism ? Can we make antibody(just like we make some chemicals) that can not be induced to be made in a living organism ?

@biogirl: most commercial antibodies are generated by injecting the antigen into an animal. Most used speciars are rabbits, sheep, goats, chicken, guinea pigs, rats and mice. You can get antibodies synthesized in bacteria as Chris pointed out, but I would say that is not the most common way nowadays.


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Identification of unknown bagworm (Singapore)
This bagworm was found in Singapore (near McRitchie Reservoir) some time in June 2012.
This is the plant from which the bagworms were obtained:

A few examples of the bagworms:

The bagworm when dissected out of its bag:

Is the plant Banana (looks similar)? If so, the bagworm (Psychidae) Kophene cuprea could be a possibility, since it is considered a pest on banana (Mosich & Larsen, 1978). The larval case is also supposed to be conical, but I cannot find an online picture for comparison.


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Flower identification (England, late May)
I took this photo near Stratford upon Avon by the side of a road. Can anyone identify this flower?

Do you have a closeup of the petals?

@dd3 Unfortunately not, sorry.

MY guess would be Centranthus ruber coccineus, also known as red valerian. See this picture (from here):

Could be pink allium, considering the thickness of the stem?

Allium is an onion; they're monocots (would have blade-like leaves from base, not stem.)


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Banana cultivar identification
I found a cultivar of banana that I haven't seen before (and that was significantly different from the standard Cavendish cultivar) in a market in Hong Kong today, due to the language barrier (Mandarin Chinese vs Cantonese), I was unable to ask the store owner about the name of the banana.
This is a picture of the banana, pictured next to a pack of standard AA batteries, as well as the peeled banana and a transverse section of the banana.
Can anyone identify the specific cultivar of this banana?

I found the same cultivar of banana being sold in a market while on a recent trip to Sulawesi, Indonesia. I was told by the owner that this cultivar is locally known as the pisang kepok, or alternatively the Saba banana. This cultivar is thought to originate from the Philippines.


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What is the probe that absorbs at 450nm in the presence of NADH in this assay?
The colorimetric assays by Biovision and Sigma Aldrich seem to utilise a probe that binds to or reacts with NADH in order to cause absorbance at 450nm which can then be quantified by a spectrophotometer.
What is the chemical basis of this reaction?

I don't think they would reveal it but perhaps the substrate is this molecule.

@WYSIWYG Thanks! You should convert that to an answer.

I am not sure if that is the same compound.

They will most likely not reveal which substance they are using. Most likely it is something which is oxidized by NADH and then gives a blue color.

@Chris it absorbs 450nm it may emit a longer wavelength.

@MarchHo the substrate can also be Dansyl aminoacetaldehyde (See here). But Sigma does not mention a fluorimetric assay and DAAA absorbs at a lower wavelength; so can't really comment on what that substrate can be.

This is not an answer, but you don't need the mysterious probe to measure NADH production. NADH absorbs at 340nm (while NAD+ is flat at 340nm) and A340 is measured in many well-documented colorimetric (coupled) kinase assays before any kinase assay kit was in the market.

@SYK Thanks for the note, but I am aware of it (and am actually using it in some of my experiments). I was just curious on the chemical nature of this assay.


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Textbook/lab manual for mammalian cell culture
For general techniques involving molecular biology, I know of Sambrook and Maniatis Molecular Cloning which covers many of the standard cloning techniques.
However, mammalian cell culture has many significant differences from bacterial cell culture, some of which include the many different variants of cell culture media as well as the relatively complex systems which cannot be provided using standardised media such as LB or TB in E. coli culture.
Are there any similar textbooks/lab manuals for cell culture? Alternatively, good review papers covering the different kinds of media used in mammalian cell culture and their relative benefits would also be a good answer to this question.

Culture of Animal Cells: A Manual of Basic Technique and Specialized Applications by Ian Freshney is the most popular book on the topic of animal cell culture.
You can also refer to ATCC animal cell culture guide which also has information about media formulations.


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Is there an organism which has a common English name which overlaps with another organism's scientific name (or vice versa?)
Many organisms have their common names identical to their scientific names. For example, there exist apes of the genus Gorilla known commonly as gorillas, and plants of the genus Delphinium known as delphiniums.
However, are there any examples of the common name of an organism overlapping with the scientific name of another organism, therefore causing ambiguity when the organism's name is spoken aloud? If written with correct formatting, this should not cause a problem in any case, due to the formatting specifically describing a genus/species.

For extra points, "boa constrictor" is both the common English name and the scientific genus+species name. Whereas "gorilla" is the genus and also the species, but they're not commonly referred to as "gorilla gorillas" ;-)

One great example I know of is the duck-billed platypus (Ornithorhynchus anatinus),  often simply called a platypus, which shares its name with the Platypus genus of ambrosia beetle.
Wikipedia gives a brief history of the taxonomy of the duck-billed platypus:

The common name "platypus" is the latinisation of the Greek word πλατύπους (platupous), "flat-footed", from πλατύς (platus), "broad, wide, flat" and πούς (pous), "foot". Shaw assigned it as a Linnaean genus name when he initially described it, but the term was quickly discovered to belong already to the wood-boring ambrosia beetle genus Platypus. It was independently described as Ornithorhynchus paradoxus by Johann Blumenbach in 1800 (from a specimen given to him by Sir Joseph Banks) and following the rules of priority of nomenclature, it was later officially recognised as Ornithorhynchus anatinus. The scientific name Ornithorhynchus anatinus is derived from ορνιθόρυνχος (ornithorhynkhos), which literally means "bird snout" in Greek; and anatinus, which means "duck-like" in Latin.

Plants known commonly as geraniums belong to the genus Pelargonium.
Similarly, plants known commonly as cranesbills belong to the genus Geranium.

"Armadillidium" is the name of a genus of isopods (woodlice, also called armadillo bug). The armadillo familiar to residents of the southwestern US is a mammal belong to the genus Dasypus.There are related genera going all the way through South America.

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Telomeres in cloning experiments
In whole animal cloning ( eg. Dolly ) the nucleus is taken from a somatic cell. So isn't shortening of telomeres a problem ?

Yes, it is. Dolly died of cancer in early years. Length of the telomeres depends on the donor tissue: "In Dolly's study, the animal produced from fetal tissue appeared to have telomere lengths non-distinguishable from normal controls, while the other two, including Dolly, which originated from adult cells, were found to have shorter telomeres." (Xu & Yang, 2003) This statement doesn't mean that embryonic cells are the only cells able to maintain telomere length.
This also doesn't mean, that offspring of animals cloned from nuclei with shorter telomeres, inherits this shortedness: Miyashita et al, 2011
The Xu & Yang, 2003 review is pretty old, you can find newer articles on the topic.

After cloning, the recipient cell is converted into embryonic stem cell. When it is a stem cell, it can produce enzyme telomerase itself which a naturally occurring enzyme that maintains telomeres and prevents them from shortening during cell division in cells. So i think there are no problem on shortening of telomeres.

@Duc Could you give a source for this ?

@biogirl yes, you can search about telomerase activity in embryonic stem cell, and you will see a lot of source document : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360127/ . "Thus, telomerase activity and telomere maintenance are associated with the immortality of cancer cells, germ-line cells, and embryonic stem (ES) cells."


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Is ability to easily pollinate desirable?
In Mendel's crosses was it desirable for the plants to be able to cross-pollinate and self pollinate easily ?

Yes, the fact that pea plants were easy to pollinate was desirable and helpful in understanding the effects of Mendelian factors (genes) but for the proper study of the factors expressed CROSS POLLINATION of homozygous plants having different phenotype and genotype ( e.g. cross between RR and rr) was preffered rather than self pollination.


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Order of events in hibernation

Arrange this in sequence :
i. Heat loss exceeds heat production.
ii.As body temperature falls, heat loss decreases.
iii.Body temperature equals environmental temperature.
iv.Metabolic activities fall to the basal level.

I am confused between i,iii,ii,iv and iv,i,ii,iii.

@satwik you have answered my question. Just for the sake of our question to answer ratio why don't you " answer " it ?

I think the order i,ii,iii should be correct, since the fall in temperature occurs after the heat loss exceeds production and will continue only till the temperature equals the ambient temperature. iv is the reason for i. Hence iv,i,ii,iii sounds pretty convincing to me.
With i,iii,ii,iv , the main problem is that there can not be any appreciable fall in temperature ii after the temperature equals the environmental temperature iii. And iv seems more probably to be the reason for i rather than the reverse


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Mesosome - does it exist?
This wikipedia page says that mesosomes are artifacts produced by chemical fixing techniques. Most of my textbooks still show a mesosome and describes it as having functions like - respiration, helping in DNA replication, etc.
Has the idea that it is an artifact been widely accepted by the scientific community ?

when are the textbooks from?

@GriffinEvo I read that, in 1970s this was recognized as an artifact but all my textbooks are written well after 1970 and also if u google mesosomes u will get most of the results showing the "old" answer.

I've always wondered about mesosomes. They were controversial 35 years ago when I was working in a related field. I decided to check the current status of the term.
I checked for research activity in this area using a Web of Science search "mesosome" in Title: this gave just 54 hits. I list the most recent here (unless otherwise indicated, these are single hits per year).
2010; 2008; 2004 (human cell mesosome??); 1994; 1988 (geology); 1983; 1982 (2); 1980
So it doesn't seem to be a very active area of research. The 2008 and 2010 papers are from the same group. The earlier paper is:

Li, X et al. (2008) Mesosome formation is accompanied by hydrogen peroxide accumulation in bacteria during the rifampicin effect. MOLECULAR AND CELLULAR BIOCHEMISTRY 311: 241-247   DOI: 10.1007/s11010-007-9690-4
Abstract: Ultrastructural alteration and hydrogen peroxide localization were examined in Xanthomonas campestris pv. phaseoli during rifampicin effect using transmission electron microscopy. Bacterial cells were treated with rifampicin and then were examined by electron microscopy to observe the changes of ultrastructure or hydrogen peroxide accumulation in living cells that took place before lysis. Intriguingly, rifampicin treatment led to presence of an additional location of hydrogen peroxide accumulation within the cells. There was an association between the frequency and size of the additional location of hydrogen peroxide accumulation and the concentration of rifampicin. Furthermore, an additional ultrastructure, mesosomes, was also present in cells during rifampicin effect. The frequency and size of mesosome increased with the increasing concentration of rifampicin. Result of multiple linear regression showed that the size of mesosome plays as a key factor in the quantity of excess hydrogen peroxide accumulation in cells during rifampicin effect. Linear correlation was confirmed between quantity of excess hydrogen peroxide accumulation and the size of mesosome in cells during rifampicin effect. This finding intensely indicated that mesosomes are just the additional location of hydrogen peroxide accumulation in cells under cellular injury caused by rifampicin treatment. The mesosome formation is always accompanied by excess hydrogen peroxide accumulation in X. campestris pv. phaseoli during rifampicin effect.

This paper has been cited 7 times. One of those citations is from:

Saier, MH. & Bogdanov, V. (2013)  Membranous Organelles in Bacteria. JOURNAL OF MOLECULAR MICROBIOLOGY AND BIOTECHNOLOGY 23: 5-12   DOI: 10.1159/000346496

Free full text here.
The language used in this review seems to support the existence of mesosomes as some sort of intermediate in the formation of intracellular membranes in prokaryotes. This review is a polemic in favour of the idea that prokaryotes do indeed contain intracellular membrane-bounded compartments. It has no abstract, but the first paragraph gives a flavour of its stance:

The traditional view of life on Earth divides the living world into two major groups, prokaryotes and eukaryotes. These two groups were originally suggested to differ in very basic respects. While eukaryotes had complex cell structures including a cytoskeleton and intracellular membrane-bounded organelles, prokaryotes were believed to lack them. In fact, numerous textbooks and current sources still note this distinction and hold it to be true. For example, in Campbell’s Biology [Campbell, 1993, p. 515] it is stated without equivocation: ‘Prokaryotic cells lack membrane-enclosed organelles.’ In ‘Functional Anatomy of Prokaryotic and Eukaryotic Cells’ [Tortora et al., 2009, chapt. 4] it is similarly claimed that ‘Prokaryotes lack membrane-enclosed organelles, specialized structures that carry on various activities’. In the current Wikipedia, under ‘Prokaryote’ the following statement can be found: ‘The prokaryotes are a group of organisms whose cells lack a cell nucleus (karyon) or any other membrane-bounded organelles’. In the same online compendium under ‘Organelle’, one can read: ‘whilst prokaryotes do not possess organelles per se, some do contain protein-based microcompartments’. Proteinceous microcompartments will be the subject of a forthcoming Journal of Molecular Microbiology and Biotechnology written symposium, but this one will show that these generalizations, suggesting a lack of subcellular compartmentalization in prokaryotes, are blatantly in error [Murat et al., 2010a].


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Colchicine addition to cells

When is colchicine added to dividing cells for karyotype studies?

I know that colchicine inhibits polymerization of microtubules.
2 So, why should it stop the cell cycle at metaphase when microtubules have already assembled and the next step(anaphase) requires depolymerization rather than polymerization ?

colchicine is used to synchronize the cells.. so whenever you add it, the cells will eventually be arrested at metaphase.

Colchicine inhibits the formation of the microtubules by binding to tubilin and rendering it unavailable for the polymerization. Thats why the cells get arrested in the metaphase and can not go on further in the cell cycle and divide. For chromosome studies this is very useful since this is the phase where the chromatin is most condensed and can be viewed best. It inhibits the positive side producing the microtubules to prevent it from moving to the negative side, in cell division.

I would like to point out that copying from wikipedia without mentioning it as a source is not allowed here.

Sorry, but I haven't looked up this in Wikipedia. Since I have done this stuff myself in the lab I know the background. But I can remove the answer.

In fact I should say sorry because I thought that I had read that exact lines on wikipedia. I looked it up and you say the same thing but not in the same exact words. I really am sorry , I should not have written the comment without confirming.

Fine for me, such things happen.

Thanks. I have one question : I still do not understand why binding tubulin would lead to arrest at metaphase. By metaphase, the whole spindle is complete so why will anything that does not allow polymerization to occur affect this ? Doesn't only depolymerization happen after metaphase ?

@biogirl When the cells are in the metaphase they have their spindles and can divide. But in cells, which are not, the spindle apparatus can not be build (because the tubulin is not available for it) and the cells get stuck in what I would call early metaphase (there is no further differentiation for this step, so its all called metaphase). The cells get ready for dividing (chromatin gets condensed and so on) but the cells can't go on.

let us continue this discussion in chat

@biogirl there is a cell cycle checkpoint for the full formation of the mitotic spindle, and a cell poisoned by colchicine will never pass this checkpoint, hence it will never progress to anaphase.

@chris When exactly is colchicine added for chromosomal studies ?

There is no exact timepoint, since the cells are not synchronized in respect to their growth phase. You simply add it to the proliferating cell culture (meaning the cells are still in the growth phase). You can find a protocol here.


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How is it decided that one drug is better than others by X times?
I read in Tortora and Derrickson that :

Enkephelins are 200 times powerful than morphine in their analgesic effects.

I wonder how exactly researchers arrive at a number (like 200 here). I also want to know what exactly is meant by "powerful".

I don't know if it is applicable for the drugs under discussion, but many a times, quantifiable effects are used to compare, for example, the amount of medicine required to block gastric proton pumps to such an extent that a predetermined acidity is maintained in stomach is used. Now different drugs will require different amounts and hence can be quantitatively compared.

In general, there is no universal way to quantify the effect of a drug; the quantification procedure depends crucially on what effect the drug is supposed to have. For example, if the drug is supposed to decrease blood thickness, then a measure of the drug's efficacy is a measurement of change in blood thickness upon application of a given concentration of drug. So I'll focus on the case of analgesics, since that's the context of your original question.
While I can't say for sure how this particular quantity was measured, it appears that the effect of analgesics like morphine or enkephalins is measured by direct measurements of pain under different administered concentrations of drug. This can be done in animal or human studies. In animal studies, varying concentrations of a drug are administered, and then the response of the animal to different pain stimuli is recorded. One common example of a pain measurement is a hot plate, where the animal's foot is placed on a hot plate and the time until it tries to remove its foot is measured.
These studies can also be done in humans. In this study (1), the effect of a particular drug was measured by different tests, including

electrical shocks of increasing intensity; maximum intensity of pain subject wanted to endure was measured.
pressure applied to the finger: maximum pressure subject wanted to endure was measured.
heat applied to the forearm (maximum tolerable temperature measured)
dominant hand immersed in ice water for up to 2 minutes. Subjects continually reported level of pain on a 0-10 scale, sum of all pain levels over course of experiment was used as measurement of total pain endured.
Tourniquet applied to cut off blood supply for up to 2 minutes, pain measured in same way as above.

If these pain measurements are recorded when the patient has different levels of the drug in their system, then comparing drug effects amounts to identifying the concentration of drug at which a particular pain response is achieved. In other words

Drug A is X times more powerful than drug B if drug A causes the same effect on pain response (measured in some way like the ones measured before) as drug B at X times lower concentration.

As a side note, the initial thought I had was that this might be measured by quantifying the receptor-ligand affinity of the various drugs for the pain receptors (opioid receptors) in the nervous system. In that situation, saying that drug A was 200 times more powerful than drug B would amount to saying that A's affinity (or Kd) for a particular receptor was 200 times greater than B. Or something along those lines (see the Wikipedia article on receptor-ligand interactions). That would be a 'universal' way to measure drug efficacies, since a large number of drugs work by blocking certain receptors in the brain. But biology is too complicated to permit a straightforward relationship between binding affinity and perceived drug effect. At least, not yet!
References and Further Reading
(1): Luginbuhl M et al (2001). Comparison of Five Experimental Pain Tests to Measure Analgesic Effects of Alfentanil. Anesthesiology 95:22-29
(2): Jackson H. (1952) The effect of analgesic drugs on the sensation of thermal pain in man. Br. J. Pharmacol Chemother. 7(2): 204–214.
(3):Estrup Olesen A et al. (2012). Pharmacological Reviews 64(3):722-779 Extensive review of this subject.


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Identification of a bird on the beach of a small lake
Last December in France (lake of Divonne, Ain) I took a picture of this bird looking for some food on the beach of the lake.

It looks like a specimen of the genus Anthus (Family Motacillidae) but as these specimen are quite difficult to identify (especially winter time), I would like to have some confirmation.
By the picture I found on different Internet sites, my potentials guess are (by order of confidence):

Water pipit (Anthus spinoletta)
Meadow Pipit (Anthus pratensis)
Buff-bellied Pipit (Anthus rubescens)
Eurasian rock pipit (Anthus petrosus)

The Eurasian rock pipit could be present in the region while migrating but this is the less probable in my opinion.

Anthus spinoletta seems to be the way to go. It's feather patterns and beak shape are so identical to the one that you have posted. Considering that this was taken in December in France, it definitely matches with the  seasonal locations of Anthus spinoletta.

I agree with @Twisted Genes it's a water pipit no doubt.

if someone would post an answer, i will accept it.

Water pipit
https://en.wikipedia.org/wiki/Water_pipit
I agree with what was discussed in the comments and don't like open questions.

i understand that the quality of the answer is not high. but when you down vote please let me know why. the question is still open and needs to be answered. (in this community seems to be stricter rules than I'm used to from other stack exchange communities)


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Plant disease identification
I’ve noticed recently strange formations on the leaves of my flower.
No idea what could it be.
Could anyone help with the identification?

The white things look like scale insects, you can scrape them (and their waxy fluffy coats) off the leaves.
If you can identify the plant, that would also help.
The gardening SE is also a good place for these questions.

For the limited amount you have it will be much more effective to scrape them off than try to poison them.

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


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Is this statement in agreement with Darwin's theory of evolution?
Is the following statement in agreement with Darwin's theory of evolution?

The number of offspring is not related to fitness.

If so, why? This is not a homework assignment, I just want to justify the reason for which this statment is in agreement (which I really hope it is).

could you explain what makes you think it is inline with Darwin's theory of evolution?

@GriffinEvo Not necessarily inline, but in agreement with. Darwin's idea of natural selection consisted of differential reproduction, which portrayed his concept of fitness. Fitness, is a measure of an organism's ability to survive and reproduce. Nevertheless, it solely stated reproduce and it did not pertain to the exact amount. For this reason, I think that it is inline, (or in agreement), with Darwin's theory of evolution.

what's your source, I'm not convinced the statement makes sense in isolation

@GriffinEvo It seems this quote is an answer to an evolution jeopardy. Google the phrase in "" and see for the outcome.

@chris what is an Evolution Jeopardy game? I was quizzing the OP because the statement made me think it was a creationist trying to start a debate

It's a stupid statement. I'm not sure how it's supposed to help review evolutionary concepts(It's on flashcards?), because as is the statement is just vague to the point of meaninglessness. Fit creatures have offspring. Creatures with offspring are not necessarily fit(see: mules, seedless watermelons). A convincing argument could be set up that they are related, because adding more offspring often increases fitness. But: there are counterexamples that imply a better statement might be "the fitness, and not number, of offspring is related to parent fitness". It's a trick question.

Short Answer
The statement "The number of offspring is not related to fitness." is wrong! In other words, The number of offspring is related to fitness.
Various definitions of fitness exist depending on the model you want to use but whatever is the model you want to use the number of offspring is always related to fitness. For the purpose of a beginner in evolutionary biology, it is probably enough to assume that the number of offsprings that managed to survive to some adult age and fitness are actually the exact same thing.
Long Answer
Darwin's theory of evolution?
What do you call Darwin's theory of evolution? Do you mean the theory of evolution as it was formulated by Charles Darwin at its time or do you mean the current theory of evolution? Charles Darwin never used the word fitness (if I am not mistaken), so I will talk about the modern theory of evolution only.
Generalities
For most of the purpose it is enough to consider fitness as being the expected number of offsprings that manage to survive to some adult age of an individual given its environment and its genotype. The word "expected" used above refers to the first statistical moment (mean) of the random variable which is the number of offspring of an individual given its genotype and its environment. In other words, the number of offsprings is "related" to fitness.
Absolute versus Relative fitness
In general, we talk about absolute and relative fitness, where the absolute fitness of an individual is its number of offsprings and the relative fitness of an individual is its absolute fitness divided by either the mean fitness of the population or more often divided by the absolute fitness of the fittest individual in the population.
Fitness is a function of fecundity and survival
To be a bit more accurate, fitness is a function of both age-specific survival and age-specific fecundity. A very good measure of fitness is given be the elements of leading eigenvalue of the Leslie matrix $L$ in $\overrightarrow n_{t+1} = L \overrightarrow n_t $ where $\overrightarrow n_t$ is a vector that gives the number of individuals of a given genotype of each age living at time $t$. $\overrightarrow n_t = (n_{1t}, n_{2t}, …, n_{nt})^T$, where $T$ indicates transpose and $n_{xt}$ is the number of individuals of age classe $x$ at time $t$.
Definitions of fitness slightly varies depending on the model you want to use
One may want to use an even more complex definitions of fitness, typically when using models that apply to species that have an alternation of generation. Or when considering, genotypes that have different norms of reactions and considering a changing environment through time.
Anyway, whatever is the model you want to apply, fitness is always related to the expected number of offsprings. It would be wrong though to reduce fitness to the expected number of offsprings only, because a more complex definition might be necessary in some special cases. In any case, fitness is always an index of how much will a variant spread in a population and is therefore closely linked to the number of offsprings.

It is definitely in line with Darwin's theory.  You can look at living things as having two sorts of reproduction strategies (for the sake of this question - of course there are many diverse strategies, but this is just one dimension of it).  r and K strategies.
K-selective strategies try to select the best mates and produce the strongest offspring, which they invest a lot of resources in so a to maximize their chances of reproducing.  Human beings are a classic example of K-selective evolution.  A human child will take a decade or even two before it is independent.  Birds might give their offspring a few weeks.  That is why as a person you might tend to think that all animals succeed by investing in offspring.
r- selective strategies do not value their offspring at all.  They produce hundreds or thousands of offspring and don't invest in any of them at all.  A common example of this is cockaroaches or guppies, which are as likely to eat their offspring as acknowledge it, having thousands or hundreds of eggs in one clutch respectively.
For these animals, life is cheap, the fit and the unfit all come out together, but those who survive are the strongest.


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What is the evolutionary cause for various finger lengths?
Why are the lengths the way they are with middle finger the longest?

I'm no expert but the relative length of fingers perhaps represents functional significance. It's always helpful in the question to mention what you have found on the topic so far so people can have a constructive input/answer.

When you bend your fingers, they all arrive at the same height. I would tend to think that their lengths differ when you keep them straight because they need to have similar length when you bend them. And I guess that there is some optimal length (when bended) for fingers to grasp things.
It is nothing but a quick hypothesis. But it sounds quite plausible to me.
As @JordiZambrino commented, it is possible also that middle fingers evolved to be longer in reaction for the need for throwing things.

Very interesting angle. Never thought of this. Thank you for your answer.

with the middle finger, I read somewhere that hominid lineage began when a group of  apes began to throw rocks at  their antagonists/rivals, and that this behaviour provided procreative advantages for  a long time, and thus driving natural selection for improved throwing. Also, I think that the hand grip  was/is vital and that a longer central finger is biophysically helpful.

This is interesting. I'll add your comment to the answer. Would be great if you could find the reference.

@Remi.b I'll try to find the reference.

@Remi.b I'm leaving a citation notice on this 5 year old post due to it getting new traffic from this post. If you can, please update with a bit more referenced substance if you've learned or explored this topic further since posting your answer. Thanks!


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Biologically, does life and death matter?
(Sorry that I'm on mobile, so I can't make a good formated question (no links). I will add them later. Just can't resist the urge to ask)
In the recent hot question about whether mitochondrial is alive or dead (it's technically dead), the top answers don't only explain whether it is dead or not, but also further explain why it doesn't matter: they just do what they need to do. This provokes me a question:
Q: Biologically, do life and death matter? Is the functionality of something the only thing that life cares?
We human are scare of death. Because of that, we tend to apply that idea into everything we can observe, even if it's meaningless. But why is death scary? Isn't it because when you die, you stop function anymore? So ultimately, isn't what we really mean when discussing whether something is dead or not the functionality of that?
Not only that, "there is no consensus regarding the answer to the question as to when does life begin". If we approach this in a different way: the time when an individual function begins to work, will there be a consensus? I mean, just don't think if an organism is alive or not, just think that how much functions of it have started to work.
If we are the combination of the numerous of selfish genes, would "humanity" be a collection of functions?

" Isn't it because when you die, you stop function anymore? "       Your body still has use after you die, Bacteria and fungi can decompose you and recycle your elements like Nitrogen to put it back into the Cycles that exist. Like the Nitrogen Cycle. I also feel like your question is still vague, since you haven't really set a definition to use for "life" or "death". A "function" is a bit vague too, since as I stated before, there can be the concept of recycling to allow for various functions, whether the source is living or dead.

The "death" definition is taken from the discussed question which I haven't linked to this. A "function", well yeah, it isn't defined well. But I would define it like a mathematic function: output = f(inputs). (Thinking a while). Ahh, what I mean is the metabolism.

I feel like your question answers itself almost. I mean I feel this topic is becoming more philosphy than biology, but could there be something biologicaly existing without a function? If not then I suppose functionality would be important. And I personaly can not think of some object(s) that are biological and that lack a function. Maybe that is just my lack of imagination though.

Then we have to define what is "biologically existing", or specifically, "biological". I think we will lead to the point that there is no such thing "biological". Anyway, why the downvote?

Well there is a limit to defintions, which is why I think the topic is better suited to philispohy. If I was vague though, I guess I meant " something that's living or dead ".

On a very different note, I feel that this particular question has hardly any relevance in biology. This question is a philosophical which is not really the same as science.  Many will argue that biology is the study of life itself, I strongly disagree, biology is a field in science aimed towards the study of aspects which can lead to better human wellbeing/welfare/health. The study of science itself is ofcourse the sating of one's curiosity. Philosophy has no place in science.

@KoustavPal would this be on topic on Philosophy? (Though I think it would be a dup there)

I feel so, and I think the mods will agree with me on this. I went over there and searched once or twice, they have certainly many questions discussing different philosophical aspects of death. So certainly you will get a much better answer to your question which discusses; if the question of what is life or death is even worth discussing, over there than here.

Man fear death because he does not know what happens after that. No one knows if we really cease to exist or if there is a life after death as many claim. Biologically the concept of life after death can't be researched as of now, I mean with our current level of technology. It is mostly a fear of unknown.

We human are scare of death. Because of that, we tend to apply that idea into everything we can observe, even if it's meaningless. But why is death scary? Isn't it because when you die, you stop function anymore?

Fear of death is hard-wired into our nervous systems. A thirsty wildebeest will approach crocodile-infested water very, very reluctantly. The wildebeest isn't thinking about the selfish gene or the loss of his function in the world; he's hardwired to be afraid of the situation. The same is true for any prey animal: fawn, rabbit, gazelle, mouse. The difference (maybe; simplifying for convenience) is that we are rational, and like all of our primitive fears (e.g., of the dark, when there really were sharp-toothed predators with better night vision than ourselves), we try to rationalize them. We also rationalize our existence.

Is the functionality of something the only thing that life cares?

Nature is red in tooth and claw. If you want to anthropomorphize Nature, then sure, we matter (we're destroying the earth at unprecedented speeds). If you believe in a spirit, we matter. But if you believe in none of it, the only purpose we serve is to propagate ourselves, and when the last of our species is gone, Nature will not care a whit. Just as it doesn't care that dinosaurs, wooly mammoths, passenger pigeons, tasmanian tigers or baiji river dolphin are gone.
It can be argued that in the grand scheme of things (and here I'm speaking of the entire Universe), biological life doesn't matter at all.

Then the sun, the earth and everything else don't matter at all. Sorry, I think my question is not clear. "Is the functionality of something the only thing that life cares?" should be read as "Is the functionality of something the only thing that we should care at all?". I don't intend to anthropomorphize nature.

@Ooker - That's a very different question! The answer to that, I think, is very, very different. I can't answer that because of the words "functionality" (who gets to define that?) and "should". Should, to me, implies a moral perspective. I believe we "should" treat life in and of itself as precious. If everyone agreed with my moral perspective, there would be no starving people in the world, livestock would be raised much more humanely, etc. etc. Clearly, everyone does not.

Nice comment! @anongoodnurse


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Definition of "essentially diploid"
While researching the F12 cell culture medium (Ham, 1965), I came across the term "essentially diploid Chinese hamster ovary cells". The terms "subdiploid" and "near diploid" were also used to refer to the same cells.

Attempts at searching Google Scholar and regular Google failed to turn up a definition of the phrase.
What exactly is meant by "essentially diploid", and how is it different from regular diploid cells?

Secondary cell lines often show aneuploidy. I think it is a reference to that.

I think that the rest of the paragraph that you left out of your quotation helps to clarify. The CHO have 21 chromosomes, while the somatic lung cells have 23.
Neither case is exact for Chinese Hamsters, 2n = 22. So they have almost the complement of chromosomes that a diploid Chinese hamster somatic cell would have but they are missing one or have one extra. For the most part they will behave like normal somatic cells in culture, but it is an important fact to note as you can have cases where dosage dependence of a missing chromosome in a pair or an additional chromosome (trisomy) can affect the outcomes of research.
In the back of your mind you always need to be thinking how does the missing/extra chromosome affect the data I am collecting.
This Nature article may also be of interest.

@MarchHo, if you are not a native English speaker, then one thing that you need to remember about the English language is that it is contextual, and definition can often be defined from the context of usage. Here "essentially diploid," combined with the knowledge that 2n=22 and that the cell lineages are 21 and 23 chromosomes, means that while they are almost the same as somatic cells, they are not exact, which as I stated above has implications. If the CHO cells are missing an X-chromosome, then maybe it doesn't matter, as we now know about X-chromosome inactivations...

... while a different chromosome might be problematic. They are "essentially diploid" but one should keep in the back of their mind that there could be effects to the missing/extra chromosome in these lines that could have implications to the research results and the conclusions drawn from the data.

"Essentially diploid" means that a normal (most common normal) state is diploid, while any other state will be considered rare (can be normal yet) or abnormal or unusual.
The "essentially diploid" is in some way a tautologic, since we can say "human somatic cell is essentially diploid" as well as "human somatic cell is diploid" omitting "essentially". But the goal of "essentially" is to clarify other states:
If some essentially diploic organism has one chromosome set it will be called "monoploid", while cell/organism etc which normally has one set will be called "haploid".
Sub-Diploid and Near diploid means there are incomplete (aka less than normal) sets of genetic material.

Do you have any references for your answer?

@MarchHo Please, look at this one - http://www.ncbi.nlm.nih.gov/books/NBK21229/  You can easuly find additional supporting refs if you need them.


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How is excess semen removed if ejaculation does not occur?
There are some attempts to answer the question that I found via cursory Google search, but none of them were appropriately sourced.
This site claims that they are "recycled like blood cells", but the blood cells are recycled using the spleen, and I don't think spermatozoa normally enter the blood stream at any point in time.
This other site contradicts the first site, and claims that they are removed from the body by "dripping" them, therefore expelling them in the normal urine stream.
What is the actual process through which semen is removed if ejaculation does not occur?

Well as far as my knowledge goes in this aspect..
If sperms are not ejaculated then they are simply reabsorbed by the epididymis and recycled.
I would say the first website you have linked up there is what is a more appropriate explanation.


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What is this bee-like insect flying above the swallow in Singapore?
Photo was taken within the past week in the Singapore Botanical Garden. The bird is the Pacific swallow Hirundo tahitica, but there is also an unidentified insect flying above the bird, which is sizing up the insect. The insect wandered into the frame of view while attempting to photograph the bird, which was the reason that it is out of focus.
The insect appears to be about 1cm long, and has the black and yellow colouration as well as wing shape of a bee, but the mouthpiece doesn't appear to resemble any species of bee or wasp that I am aware of. What could this insect be?

I think that's some sort of nectar feeding moth. Search for ones that mimic bee or wasps.


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Does myopia tend to decrease the risk for later hyperopia?
It seems like being nearsighted for much of your life due to elongated eyes would make it easier in general to focus on near objects rather than far since the lens would not have to change much. Since in old age we lose the ability to focus close images due to a hardening of the lens over time, wouldn't having eyes shaped more for near images be helpful in maintaining the ability to see close up, and thus nearsighted, or myopic people, would be less likely to develop farsightedness, or hyperopia, with age? It seems then that nearsightedness is more of an adaptation that occurs at a young age, so that these people can work up close for longer periods of time both in the the short term(studying) and long term(age). I'd love to hear if any research has been done on this subject, and any other input you have.

It is generally understood that we tend to become hyperopic as we age (reference). As to whether this aids in decreasing myopia is stated as marginal in papers. One paper titled "Is there a hyperopic shift in myopic eyes during the presbyopic years?" states that

it was found that almost all hyperopic and emmetropic eyes showed an
  age-related hyperopic shift; but only a small proportion of myopic
  eyes shifted toward hyperopia, with others remaining relatively stable
  and still others increasing in myopia.

In a second study titled "Age-Related Decreases in the Prevalence of Myopia: Longitudinal Change or Cohort Effect?", it was found that there is a decline in the prevalence of myopia in older adults.
Some people in personal experiences have stated that their myopia has decreased (reference) while others found themselves wearing bifocals (reference). In closing, I would say that this is something that your Ophthalmologist may be able to predict better but it is not a given that your myopia would decrease. It may or may not be so with many factors like your eye shape coming into play.

Let me see whether I can explain this quickly. The eye size is tightly regulated genetically. Babies don't have big eyes, they have exactly the same sized eyes like adults, only their head is smaller. Myopic eyes are larger than normal and hyperopic eyes are smaller than normal, even though the difference is only 1 to a few millimeters. When you focus to the far point, the light focusses to the nearest point possible in the back of your eye. When you come closer to an object, the focus point inside the eye moves further out. Thus, the farsighted person with the small eye can only see when the object is away. Moving closer moves the focal point inside the eye to behind the retina. The opposite is true for myopic people with too large eyes. When a person gets old, the lens gets stiff and cannot adjust the focal point inside the eye to the distance of the retina. Thus, the lens remains stiff in the most relaxed state (extended), or - in other words - at the most distant focal point the person had when it was young. A normal-sighted person has his old-age focal point at the horizon and since his lens is stiff, can only see sharp from the horizon to a few meters in front of him (depending on the intensity and wavelength of the light - blue light better than red). A short-sighted person is of disadvantage when old, since his far point remains to be at short distance. He gains a little sharpness over the normal sighted person in the short distance, but loses it in the distance like he always did. You can calculate this nicely, actually. All physics.


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Why do Mangoes have a single large seed, and not multiple small ones?
I was just thinking about this, wouldn't it make more sense for a mango to have multiple seeds, as it would allow more seed propagation?

It is an interesting question and it applies to other fruits with big seeds as the avocado as well. It is very likely that these fruits evolved to be spread by large animals (like big birds or large mamals) which existed for a relatively long time, but are extinct today. These animals swallowed whole fruits and excreted the seeds afterwards (most of these seeds are slighty laxative) together with dung to support the growth.
They are called "evolutionary anachronisms" and there is a very interesting book about them, called "The ghosts of evolution: nonsensical fruit, missing partners, and other ecological anachronisms." (which can be found as a PDF online)
Two interesting articles about this phenomenon can be found here:

The Trees That Miss The Mammoths
Anachronistic Fruits and the Ghosts Who Haunt Them


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Does a non-extinct gliding species of bird exist?
According to wikipedia was Archaeopteryx rather glider than capable of active flight. As a hunting strategy it crawl up to a tree (or other high positioned place) and glide from it to a prey.
Most of the modern birds are capable of active flight. Does anybody know if a (purely) gliding species of bird exist in present?

That's really not how Archaeopteryx hunted, maniraptorans have really abysmal climbing ability, and Archaeopteryx shows no improvement on that. The current consensus is that Archaeopteryx was an active flier, albeit a poor one.

There is a classification of birds called Soaring birds.
Soaring Birds

In definition, some land birds, such as vultures and certain hawks,
sustain flight for long periods without flapping their wings. They
take advantage of updrafts produced when the wind blows over hills and
mountain ridges or make use of rising columns of warm air called
"thermals."
Vultures stay within thermals by flying slowly in tight circles. They
have short, broad wings and a low wing loading (ratio of bird weight
to wing area) that allows them to remain aloft and to be highly
maneuverable at slow speeds. [1]

List of soaring birds

Birds of Prey

Buzzards
Condors
Eagles
Falcons
Harriers
Hawks
Kites
Osprey
Secretary Bird
Vultures

Passerine

Chough

Cranes

Sandhill

Sea birds

Albatrosses
Frigatebirds
Gulls
Herons
Pelicans
Petrels
Shearwaters
Storks
Terns

Extinct

Argentavis

Buzzard

Chough

Sandhill

Albatrosses

(source: scienceviews.com)
Argentavis[Extinct]

(source: mnn.com)
Update:
Most similar morphology to Archaeopteryx is found in Hoatzin (Opisthocomus hoazin) like claws as hands as they hold the branch when they are small.

(source: pbworks.com)
Source:
[1] Soaring Birds by Paul R. Ehrlich, David S. Dobkin, and Darryl Wheye.

Hi @Devashishish Das!. Thank you for your answer, howerver I can not accept it. I am looking for "pure" gliding species (WITHOUT ability of active flight).

@LadislavNado: Are you sure? Soaring Birds Are gliding birds. Moreover, flight pattern of  Archaeopteryx is still under research.

Thank you @Devashish Das for updating your answer! Opisthocomus hoazin is a great example!!! If you in future find another similar species, please add it. Many thanks again, I will use Opisthocomus hoazin for my popular science lecture where I wil make acknowledges to you ;)

I think this might be a better approximation of the most current consensus for the comparative size of Argentavis to humans than the one you've used?


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Could habitat selection pattern be deformed in environment with low variability?
It is possible that strong (clearly visible) pattern of selection towards particular parameter is detectable only in environment with high variability (difference between used (red) and non-used (grey) space will be significant) whereas in sub-optimal environment used and non-used space do not differ due to low variability.
And if this is possible, is there any relevant study which focuses on such issue?

P.S. It seems to be very basic idea, however I could not find any relevant sources on this topic.

What is an environment with high and low variability? Does "variability" mean spatial heterogeneity?

Hi @Remi.b! For example: Parameter = tree height. High variability environment will be primeval forest, whereas low variability environment will be even aged monoculture (extensively managed forest). If we hypothesize that squirrel will prefer high positioned places for roosting, we could detect such selection only in "green" area. I need an article on this topic. Animal species is irrelevant.

I am sorry if picture above is not clear. In circles are histograms of tree heights. In first, we have "normal" distribution from which the squirrels are selecting trees with higher than average height. The second histogram is probaly close to uniform distribution. In such sub-optimal conditions is selection not detectable due to absence of height difference between used and available trees.

If I understand your question correctly, I've seen this idea in many papers, sometimes stated clearly and sometimes in more implicit terms. After a quick look I found a paper which should be relevant as a starting point for you: Mayor et al. 2007. Spectrum of selection: new approaches to detecting the scale-dependent response to habitat. Ecology 88(7).
In my mind, there are two questions here. First, to what extent will low population size in sub-optimal environments (leading to a smaller sample to work with) lead to more uncertain inferences of preferred habitat/substrate; basically saying that noise might swamp signal in sub-optimal environments. Second, to detect selection for a particular habitat/substrate, you must sample a wide enough range of environments so that you capture both preferred and unpreferred habitats and transitions between them. In the paper I linked to this issue is touched upon in the discussion:

Second, evidence of habitat selection depends on the scale of analysis. To understand scale dependence, investigations must encompass a spatial scope sufficiently wide to uncover scale domains of selection and the thresholds or transitions between them. In both cases, spatial scale is the empowering principle, and scaling continua are the means of application.

I've seen similar ideas as this show up in papers on habitat choice in birds living in agricultural landscapes as well, where some species are often found in rather poor environments (because these environments are common). Looking at habitat preferences only in these environments might then give a misleading view, since individual choices are constrained. Also relevant, even if not mentioned in your question, is the concept of maladaptive habitat selection (sometimes called ecological traps), where you can have situations where species use environmental cues that used to indicate high fitness habitats, but might now result in maladaptive choices, see e.g. Pärt el al. (2007). However, in this case you will still have a clear preference/selection (as in your high variability environment), the problem being that the organism is selecting suboptimal habitats from a fitness perspective.

Perfect @fileunderwater. This finding is exactly what I need....[this study] is the first to quantify [recognize] habitat selection explicitly as a response [function] to habitat heterogeneity...


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Is it dangerous to rub closed eyes?
Phosphene from rubbing the closed eyes where first described at least since Ancient Greece, but I caught myself thinking that I wouldn't want to try it out. So I wonder, how safe it is to actually rub closed eyes or put pressure on the human eye in general? Can frequent but small, or rare but sharp, application of pressure cause myopia or other eye disorders? What is the maximum pressure before the eye is damaged? What happens with the eye if you accidentally hit it?
I remember several times during my childhood accidentally poking myself in the eye with a finger—the experience was very uncomfortable, I couldn't even open the eye for several minutes, but I don't think anything happened to my eyes since then, and my myopia was probably caused by any other factor than pressure damage.

According to scientific articles I read, myopia can be caused by light pollution at night, or not enough light during the day.
(In my case I had a small amount of black mold on my window, and its toxin caused a lot of health problems, e.g. diplopia, and probably myopia was a side effect as well. Now 2 days after the removal of the mold I don't need glasses anymore. I guess the complete recovery will take a few months, we will see.)

The answer is both yes and no, depending on how often and how hard one rubs his or her own eyes.
Occasional light rubbing is not a problem-- it stimulates tear production and relieves stress by lowering heart rate via the oculocardiac reflex.
Frequent hard rubbing is a problem-- it can worsen eyesight in people who already have progressive myopia, and worst-case-scenario lead to retinal detachment. For those with glaucoma, can interrupt blood flow and even cause nerve damage. It can (but rarely) scratch, tear, or deform the cornea leading to pain and distorted vision. It can lead to damage of small delicate vessels, causing a subconjunctival hemorrhage, which is benign despite its worrisome appearance.
It is generally recommended to just avoiding rubbing the eyes altogether!
References:

www.abc.net.au/health/talkinghealth/factbuster/stories/2012/09/18/3592456.htm
http://www.visioneyeinstitute.com.au/dangers-rubbing-eyes/


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IPTG and lac operator with e coli for foreign gene question
We did an experiment were we have e coli with a plasmid with a gene from another bacteria in it, and we put in IPTG in for induction. Will after looking up more about IPTG online I see it's related to the lac operator, which from what I've found just deals with lactose. Is there some other function that has? How can this be related to or effect the thing we put in and what we're doing? I'm missing the connection here.

The lac operon contains genes which are important for the metabolization of lactose as an energy source - normally glucose is used for this purpose. Usually the operon is tighly regulated and as long as there is another source of energy it is kept in an inhibited state.
The presence of lactose removes the lac repressor from the lac operon and allows the expression of the genes and thus allowing the metabolization of lactose. The mechanism can be turned on and off depending on the presence of lactose.
IPTG is a substance which mimicks the presence of allolactose (a metabolite of lactose) and it can activate transcription from the lac operon. As IPTG (in contrast to allolactose) cannot be hydrolyzed by β-galactosidase, it's concentration in the cell stays the same. Using the lac operon and IPTG enables you to switch on the expression of the gene on your plasmid and to start the overexpression.

So does the lac operon effect other things then lactose to that could have any affect on our protein? Or would there be something in the plasmid to let it be controlled by the lac operator? Is the presence or lack of the repressor having some effect? I mean what we're doing isn't related to lactose so I just don't get how messing with the lac repressor as an effect on what we put in the cell.

@windy401 In your plasmid (an artificial construct), the gene of interest will be under the control of the lac operator. Lac repressor can be expressed constitutively from another gene on the plasmid.

Finally found this, and after reading it and the rest of the pages(http://www.mfa.od.ua/page274.htm), I get it now.
"The essential element involved in lac-mediated protein expression is not the lac genes, but rather the lac regulatory apparatus. Generally, a gene selected for over-expression is cloned into a plasmid vector behind the lac promoter. Expression of this gene is then under lac control, either as an independent gene or fused to a fragment of lacZ or other genes."
I just wasn't seeing how/why our gene was being controlled by something that just controlled lactose stuff.

You only use the promoter of the lac operon, sorry for being unclear here. This allows the control of the expression of your target gene. I will edit the answer later.


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Why is water a polar molecule?
Also, what is the definition of polar in this case? (9th Grade)
Does it have to do with the bonds it makes?

I recommend posting this on Chemistry. Here on Biology it is just a bit out of place and that's why we put it on hold. It's an interesting question for sure. Good luck! And a pretty darn smart question for a 14-year-old. At your age, I was pondering other questions - like, what star wars figurine to buy next and stuff :)

Thank you for your advice! Haha, and of course a 14 yr old wouldn't be a 14 yr old without games right? I'm a gamer lol.

Polar means there's a higher density of electron on the oxygen and a lower density of electrons on the hydrogens. This has to do with the electronegativity of the elements in question. Hydrogen is in group 1 which likes to lose it's electron and oxygen in group 16 which likes to get two electrons (in this case one from each hydrogen) in order to complete the octet in it's valence shell.
Also it has to do with the shape, water molecules are not linear, but rather bent in a 'v' shape. the two sides are positively charged and the middle is negatively charged. if it were linear then the middle wouldn't matter, but because it is bent, on side has a negative charge and the other side has positive charge. It's not an negative/positive change the way it is in an ion, just a slight negative/positive charge.

Basically this means it has a hydogen bond?

hydrogen bonds are intermolecular, as in they occur between different water molecules that are interacting. the bond between hydrogen and oxygen is covalent.

not all molecules that are polar and have dipoles are examples of hydrogen bonds... hydrogen bonds are a special case... hydrogen bond is when Hydrogen is covalently bonded to nitrogen, oxygen or fluorine, and this slightly positively charged hydrogen comes in contact with a negative dipole on some adjacent (neighboring) molecule...

@JasandPruski A molecule is polar when there is a net non-zero dipole moment. So asymmetric charge density though a factor, is not sufficient. You have alluded to this point when you mention linear molecule but note that canceling of dipole moments doesn't require the molecule to be linear; for e.g. CCl₄. DM is a vector and it follows the principles of vector addition.

yes of coarse, I merely narrowed it down to linearity on the case of the water molecule, because the molecular formula could indicate linearity if you didn't know the actual shape of the water molecule...

Polar simply means the electron density is not distributed evenly across a molecule. In water this is caused by the comparatively higher electronegativity of the Oxygen (you can think of this like Oxygen wants the electrons it shares in the covalent bond a lot more than the Hydrogen does so it keeps them closer but this is an oversimplification). This translates to the Oxygen having a partial negative charge (higher electron density) and the Hydrogen being slightly positive (lower electron density). The individual water molecules will form Hydrogen bonds between each other, with the positive Hydrogen of one molecule forming a weak bond with the negative Oxygen of another molecule. A molecule being polar has an effect on many of physical and chemical properties of the molecule.
http://en.wikipedia.org/wiki/Electronegativity
http://en.wikipedia.org/wiki/Hydrogen_bond

Polar simply means the electron density is not distributed evenly across a molecule... Not completely correct. Polar means when there is a net non-zero dipole moment.


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Why is ATP the main nucleoside triphosphate used to exchange energy?
Out of all of the nucleoside triphosphates what makes ATP the most used? Is it its structure? The amount of energy it contains? Why is GTP not used as much? What is the deal with the other nucleoside triphosphates (dATP, dGTP, dTTP, dCTP, UTP, CTP)? Are there any artificial NTPs that can substitute for ATP? (like something that could cure Cyanide poisoning or a disease/illness that somehow de-functionalizes the Electron Transport Chain)

This was a question I too asked, during intro biochem. I still don't know the answer. I'm not sure if there's a satisfactory one beyond "evolutionary contingency".

I know GTP is often involved in signaling pathways such as in G Proteins.

@tel do you think there is a way to find this out? an expirement or something?

Apparently some GTP is involved in energy transfer. Following those references might be helpful.

@user137 Yes, so maybe the best version of the question is "Why ATP and not GTP?", since the two molecules are so similar in terms of their chemistry and biological role.

In terms of experiments, you could find an organism (probably some extremophile archaea or something) that produces mostly GTP during glycolysis in place of ATP. Alternatively, you could synthetically alter one of the ATP producing enzymes so that they instead produce GTP. Either one would provide strong evidence that the preference for using ATP in metabolism is mostly a matter of coincidence.

I think that it would be more questionable if every nucleotide was used equally.

It would require multiple and/or multispecific enzymes.

I believe the purines are more reactive, and ATP has a number of factors that make it's hydrolysis much quicker than GTP. Lots of GTP-mediated mechanisms seem to be time-dependent. The hydrolysis energies should be equal.

Cyanide poisoning is because of inhibition of Cyt-c oxidase. Nothing to actually do with ATP. Other complexes are not affected.

@tel that's a great idea. I am only a high school student, and I do not know much about running my own experiments. So, any suggestions on where to get materials for it? and by the way what equipment do I need? I need to know, because the high school doesn't have a lot of equipment

@WYSIWYG I thought cyanide disabled the electron transport chain. Am I wrong?

@Kendall Where did you find out this piece of information? can you point me in a direction that would allow me to learn more?

@AlexStacks it does; but at a particular step. There are some electron transport chains that are insensitive to cyanide


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What makes living beings alive?
To clarify, I'm not asking about the common properties of living organisms, such as reproducing and having a metabolism, etc. What I'm curious about is, what is the difference between organic molecules and actual living beings?
For example, if a person's heart stops beating, they are technically dead, but all the chemical compounds and molecules are still there.. I guess another approach to this question would be "If we bring together all the atoms of a living being in the same exact arrangement, would that new thing be alive?"

organic compounds are carbon based molecules. Living being contains several properties, some of which you have named!

I don't think you can ignore the common properties of living organisms (or the definition of organism) if you want to talk about life. Someone whose heart has stopped is no longer alive because they can't deliver oxygen to their cells any longer for metabolism to occur.

@anongoodnurse I understand that, but what separates what was alive just a minute ago from the dead state of it? I just can't wrap my head around how these seemingly ordinary chemical compounds get together and do things with a purpose (which is to not die and to reproduce I guess).

The minute a critical component stops functioning, the organism dies. That's why the definition of organism counts. For a highly complex organism, it has to be that organism, not all the cells which make it up. This can go on and on. If the cell membrane integrity of a single celled organism is lost, it dies. But what if enzymatic processes are still going on before cell lysis? Is that protein alive? No, it's not. Similarly, a person's death is not negated by how long it takes for all of his cells to stop metabolizing.

@anongoodnurse That's a pretty good explanation. Thanks a lot


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Can Galactose be synthesized with photosynthesis?
I know that galactose can be found in sugar beets and some gums so I thought plants could synthesize galactose but in my book the answer to the question "Which of these can be synthesized with photosynthesis in plants" was only fructose and glucose. Is that correct?

i suspect that this is only true if you expect the galactose to be made directly by carbon fixation from photosynthesis.  galactose and other sugars are often made by enzymes that convert from one type of sugar to another...

Yes, that makes sense, but the question was asking direct synthesis by photosynthesis, so I think the question (or rather the answer to the question) is incorrect. Thanks for your answer

you ask, you learn...


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Why does K+ have more concentration inside of the cell compared to outside of the cell? Why is Na+ and Cl- the opposite?
Can someone tell me the fundamental reason why K+ has low concentration outside of the cell and more inside of the cell?

Is this a homework question?

By "why" are you looking for the purpose (physiological/evolutionary) or are you looking for the mechanism (membrane transporters/ion channels)?

Just why. Why is it not Sodium that is dominant on the outside of the cell?

@ProjectBacklog it is sodium that is dominant on the outside of the cell.

I maintain that there is no "just why?" here. It's either "for what purpose?" or "how is this accomplished?" To try to cover both seems too broad to me.

Why nature has done it this way around is difficult to explain. What is certain, however, is that the membrane potential which results from the imbalance of these ions across the membrane is used for a variety of purposes, such as transport of other ions and molecules, action potential generation in neurons among many other things.
How it is accomplished is mainly through the Na+,K+-Atpase pump and secondarily through Cl- channels that exchange Na+ for Cl- to lift the amount of Cl- outside the cell.

The question is kind of broad and once narrowed down I am happy to include citations if and where needed.

Your question isn't all that precise but I think looking at individual ionic equilibrium potentials begins to give us some understanding.
Looking at the equilibrium potentials(EK for potassium and ENA for sodium) for these two ions and their channels you have that EK = -90mV and ENA = +60mV in a typical neuron. This means that at these voltages you will have no NET flow of that ion across the membrane. Inside a cell you will have a certain amount of negatively charged ions called anions which will not diffuse, or move across the membrane regardless of the concentration gradient. To compensate for this (because the inside and outside of the cells like to have equal charges when there are not action potentials) you need a certain amount of a positively charged ion on the inside. NOW, there is no NET flow of EK at a negative voltage, this is around the same voltage of the entire membrane resting potential (this varies). If you look at the numbers and consider the voltage at which an action potential occurs, then you cannot have sodium be the cation inside the membrane since ENA = +60 since an action potential propagates when the membrane is driven towards a positive voltage.

A few remarks here (1) "..you will have no NET flow of that ion across the membrane" - There is a leak current yes, but when the channels are closed you can assume there is no flow. (2) "called anions which are impermeable" - ions are never (im)permeable, the membrane is (not). (3) "they cannot and will not move across the membrane regardless of the concentration gradient" - you just claimed there is a net flow of both ions? (4) By calculating the Nernst potential, you already use the pre-existing concentration gradients, so of course you cannot swap the ions to meet the Nernst equation.

@ChrisStronks When I say there is no net flow of ions I mean this for sodium and potassium. At resting membrane potential the exchange of these ions across the membrane is essentially equal, sodium and potassium are cations. The anion I'm talking about which will not move across the membrane unless you break the membrane and remove them are proteins and other molecules essential to the cell. Also, equilibrium potential for a specific ion is different from the resting membrane potential. The resting membrane potential will however tend towards the potassium equilibrium potential.

If anyone wants a reference, specifically, chapter 6 in "From Neuron to Brain" fifth edition by Nicholls and others. However to get a overall picture of what I'm talking about I suggest going over chapters 4 through 6 in that book.

agreed, but your answer still does not address the question I think, as the question deals with any type of cell, while you focus on action potentials.

yes, because action potentials don't just occur in neuronal cells. My answer may not be the "fundamental reason" but it does provide a reason for the difference in distribution of potassium and sodium in a variety of cells termed excitable cells(those which produce action potentials). Aside from this all cells, not just excitable cells have the static - electric properties of resting membrane potential, ionic potentials and concentration gradients. Differences in distribution here can be blamed on pumps and leak channels.


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Whats the difference between voltage gated and ligand gated neurons?
How are they similar and how are they different?

Is this a homework question? If so, please read our homework policy. Essentially, we require that you attempt to answer your own question as much as possible, explaining your thinking on the matter and where you are stuck. We will not answer homework question without any effort on the questioner's part.

no... ... ... .

There is no such thing as voltage gated or ligand gated NEURONS. I believe what you are refering to are what is known as voltage gated and ligand gated ion CHANNELS. Each neuron has both types of channels in their cell membrane.
Voltage gated ion channels open in response to voltage (i.e. when the cell gets depolarized) where as ligand gated channels open in response to a ligand (some chemical signal) binding to them.
Both types of channels are critical for proper activation of the post synaptic neuron. The pre synaptic neuron releases neurotransmitters into the synaptic cleft, these neurotransmitters then bind to the ligand gated channels, thus activating them. The ligand gated channels open up and allow the influx of sodium, which depolarizes the cell. This depolarization activates nearby voltage gated ion channels, which open up and let in even more sodium. Voltage gated sodium channels open up one region at a time, the previous region providing enough depolarization to activate the next regions voltage gated channels. This effectively allows the action potential to propagate through the cell.


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Why can't NMR be used on large RNA molecules?
While reading my Molecular Bio textbook, I came across a sentence that stated that NMR cannot be used on large RNA molecules to determine their structure. Why is this? Is it because RNA is single stranded?

RNA usually has pretty complex structures. What causes the problem with NMR however is that large RNAs, such as mRNAs, don't have 1 structure, they have a population of possible secondary structures, and even if small parts of the RNA always have the same local structure, the overall molecule will occupy a variety of forms. The NMR will see a population of structures and won't be able to get good signal. DNA and RNA seem like tempting targets for NMR because the phosphorus in the backbone is NMR active, potentially allowing for backbone structure determination, but this only works on short pieces of RNA that adopts a single conformation.
Unfortunately I don't have sources to cite, only a couple semesters of NMR courses and a year of in vitro transcription of mRNA.


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Molecular Cloning- Blunt end restriction endonucleases
I work in a microbiology lab where we do a lot of cloning. I have always used restriction endonucleases to cleave the DNA to have sticky ends and not blunt ends. I currently am working on a project that suggests using a blunt end restriction enzyme, such as EvoRV, and then to perform a T-tailing of the plasmid, pl4440. My question is why do I not treat my pcr'd insert with a restriction digest just like I would the plasmid as the protocol suggests? How do I know the insert has ends that are able to ligate into the plasmid if I don't design the restriction sites into the primers?

If i understand the question correctly, your are asked to make a single EcoRV cut in your backbone plasmid and make blunt ended inserts?

Well, the plasmid has a single cut in the back bone but I'm not sure how the insert will ligate correctly if I do not treat the insert to make blunt ends.

if then you can only use EcoRV and nothing else then you have to use blunt ended inserts but you will have problems with insert orientation and multiple ligations of insert!

I think you can turn sticky ends into blunt ends with klenow enzyme. Been too long to be sure.

@user137, yes thats correct! the OP can use DNA polymerase I, large (Klenow) fragment (from NEB) to blunt end the insert. or alternatively an EcoRV site can be designed into the primers so long as it is not present elsewhere in the insert.

Just remember that in blunt end ligation the insert can go in either direction, so you need some way to differentiate direction, such as sequencing, and that half of your clones that look right on gel will be backwards.

To know if the ends are compatible see compatible cohesive ends (isoschizomers) from NEB website.
If you are unsure then do a blunt end ligation. For blunting a sticky end (From the comments):
Use Klenow or Pfu polymerase (or any proofreading/high fidelity polymerase).
You can use Taq if you intend to to a TA cloning.


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Molting in arthropods
Do all the arthropods molt ? Which ones do not molt ? Why don't they need to molt ?
I tried googling this - but did not get satisfactory answers.

in my opinion all arthropods molt. In fact arthropods are a part of clade called ecdysozoa, the members of which undergo ecdysis (molting).
Molting is necessary because arthropods have an exoskeleton which has to be removed if the organism has to grow.


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Identifying internal structures of dissected fish
Note : Images displayed below might be disturbing to some people.
I have dissected a fish for the first time ! I have some idea of what some of the structures might be but I am not sure and so would like your help.
1.Here is the fish I dissected. Are the white structures (towards the dorsal surface) muscles ? They are beautifully arranged.

2.I want to know what the yellow coloured structure (towards the ventral side) is. I guess it's the intestine. It looks "noodly". Here is a close up.

3.I have pointed at two different parts in the following images. I want to know whether they are part of the same structure - ie swim bladder or whether they are two different structures altogether. When I poked one of the parts the other part increased in size ,so I guess it's one structure but I just wanna make sure.

Since I can't actually look at and handle the yellow structures, it is difficult for me to provide any information on them.

As far as the white structures you mention on the first picture, I believe those are most likely muscles.
As for your third question. That does appear to be all one structure; and yes, going on that assumption, the entire structure would be the swim bladder.

Thanks! You can see the white structure very well in the second picture. I am pretty sure the yellow stuff isn't fat. I am actually confused between calling it intestine or pyloric seca.

A swim bladder in two parts is a common thing. At least I remember having seen at least in some of the few fish dissection I've made.


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Properties of Satellite Chromosomes
I have some questions regarding Satellite chromsomes which could not be resolved by a google search.

Does the satellite consist of telomeric sequences ?
If not, What is the function of a satellite ? And where will the telomeric sequences be present - in the main body ? On the secondary constriction ?
Satellite chromosomes are also known as SAT chromosome which stands for Sino Acid Thymidine. I read in some sources that SAT means without thymidine. But how is that possible, if there is A then obviously there has to be T ? ( in dsDNA)

I'm no expert but as far as I understand it, satellite sequences such as micro satellites are just repeating sequences of DNA (http://en.wikipedia.org/wiki/Satellite_DNA), which seems to satisfy telomere sequence repeats (http://en.wikipedia.org/wiki/Telomere). Satellite DNA is the main component of functional centromeres, and form the main structural constituent of heterochromatin (ref above). SAT chromosomes and presumably their sequences play a vital role in the formation of the nucleolus after cell division is completed (http://en.wikipedia.org/wiki/Satellite_chromosome). Not sure about 3

If by "satellite chromosomes" you mean "satellite repeats", then:

Not always. There many types of satellites, such as telomeric, centromeric (like gamma, alpha, beta satellites), simple repeats (CT)n.
It is still an open question. Some say they are important for chromosome structure (e.g., centromeres). Sometimes satellites get transcribed as might act as lncRNAs. And of course, most of them are just junk DNA.
If there is T then there is A too.

Edit

Satellites contain telomeric repeats at their ends as all chromosomes do. But they are more about NOR repeats.
They are important for the nucleolus functioning. But shorts arms of acrocentric chromosomes are not crucial, take Robertsonian translocation as an example.

satellite chromesome and satellite dna are different. I mean satellite chromosome

I edited my answer.