Will omega 7 make it harder to produce high quality meat? I heard from a medical show that Omega 7 makes it harder to gain weight, and was wondering if I would be be able to put on muscle better if I have sheep and pigs getting omega 7 through sea berry branches.

No. The only sure thing about omega-7 is that the suppliers are making money.

There's no evidence that it's doing anything more than just being an unsaturated fat in humans. This make it extremely unlikely that it would do anything after you put it through a pig.


Why the C6 intermediate molecule in the Calvin cycle is so unstable During the Calvin cycle, it is speculated that after Ribulose bisphosphate carboxylase/oxidase carboxylate ribulose bisphosphate, a 6C molecule is created and decomposed instantaneously into two phosphoglycerates because it is extremely unstable so:

Can anyone clarify why this molecule is so unstable? and...

how we know this molecule exists?.

I did not find anything useful while researching this, perhaps I'm not looking properly or there is no debate about it.

The question of why the molecule is unstable belongs to the realm of chemistry, which is not the subject of this list. Presumably the reaction for its hydration is thermodynamically favourable and there is a reaction mechanism which allows the reaction to proceed with a low activation energy.

The question of the existence of 2-carboxy-3-keto-D-arabinitol 1,5-bisphosphate and its role as an intermediate in the RuBisCO reaction was solved in 1986 and is no longer the subject of speculation. Its synthesis was described in a paper in Phil. Trans. R. Soc. Lond. B, which is behind a pay wall, but can be found in a post on ResearchGate.

In brief, they trapped this C6 compound in a more stable form with acid, and so could characterize it chemically. Its enzymic hydrolysis could then be studied at a slower rate.

The subsequent solution of the crystal structure of RuBisCO provided further confirmation of the reaction mechanism and molecular information on the role of the enzymic groups and magnesium ion cofactor. See, for example, the review by Gutteridge and Gettenby in Cell.

So the era of speculation would appear to be long past, and the account in standard biochemical texts such as Berg et al. — shown below — would appear to be reliable.


Why do some insects constantly move their abdomens? Why do some insects, such as wasps, constantly move their abdomens?

Insect respiration is passive, with sclerotized tracheal tubes taking oxygen directly to the tissues, and moving carbon dioxide out. By pulsating the abdomen, the movement of gases through this system is accelerated. Wasps, as in your example, are relatively active metabolically, so it is not a surprise that they tend to use this strategy.


Where can I find an at least Semi-Comprehensive list of what biochemical reactions Acetyl-CoA participates in? Acetyl-CoA has a number of biochemical roles in the body and I'm curious as to whether anybody knows where I can find at least a semi-comprehensive list (i.e. comprising all the major roles in the human body it serves) of the biochemical reactions in which acetyl-CoA partakes in the human body.

I may be missing some fantastic resource, but my first thought is to send you to KEGG.  Is that crazy?  Maybe, but a simple search for Acetyl-CoA in humans can give you tons of useful information, including GO terms, enzymes, genes, and, yes, biochemical reactions; just use the KEGG Pathways tool and specify humans (hsa).  You can click on each individual pathway for more information, such as the cholinergic synapse.


What is this - nest, eggs, fungus? Anyone know what these are? I found them in our local park today attached to a wooden earth-retaining wall.I was thinking some kind of insect nest/egg sac (spider?) They're about the size of a medium egg (hen's egg!)

Updated Answer:

Why it's not the egg sac of Argiope aurantia:

Upon knowing your location to UK, we can rule out quite a few spiders, especially the Argiope aurantia since it is endemic to Northern and Central America.  The spider's egg sacs are also noticeably smaller than "a hen's egg" as this post describes.

Why it's not a gall:

We can rule this out since it appears to be located on a wooden fence post.  Galls require living plant matter to grow.

Why it's not a wasp nest:

There are not wasps that produce threadlike materials. Wasp nests are made from fibers of dead wood and plant stems mixed with saliva of the wasps, and no webbing or threadlike material.  In the picture, we can clearly see some white 'webbing' between the gap of the fence posts directly underneath the mass.

So I really think it is an...

Aethalium of a slime mold:

Given the location, described area, spreading pattern in the picture, and apparent spongy texture of the mass, this looks to be the aethalium (or fruiting body) of a slime mold.  My guess would be in the genus Reticularia or Enteridium, which are typically seen in its reproductive phase as a white 'swelling' on standing dead trees in the spring, or on large pieces of fallen wood.  For example, Enteridium lycoperdon are common throughout the UK and are commonly associated with pine trees, the most common wood used to make fences in the UK.

*This post was edited from my original response.  Please refer to the edit history concerning the previous answer.


Can jellyfish improve the Black Sea ecosystem? According to this study, cited by many popular science magazines, jellyfish and other, smaller animals can contribute to the vertical ocean stir as much as currents do.

Black Sea chemistry and biodiversity is highly coupled with the lack of vertical currents, present in oceans or bigger seas. Some of the effects are low salinity in the top layers - many ocean fish species cannot tolerate the Black Sea salinity, and limited space for life (below 50 meters there is no oxygen)

Can the jellyfish population (which is exploding now) change the stratification of water layers enough that the highly saline waters from bottom go up, and oxygen goes to the deeper layers, allowing a completely new ecosystem here?

If yes, what are the outcomes of such prospects? Besides the potentially catastrophic release of hydrogen sulphide form the bottom, can it be an improvement for the biodiversity here?

To quote the PI from the BBC article:

But, Dr Dabiri explained, the jellyfish were unlikely to be the "primary ocean mixers".  "Crustaceans - like copepods and krill - are likely the primary biogenic mixers, because there are so many of them," he explained.
"But much of the open ocean is like desert," he added, "and the density of these animals is unlikely to be sufficient (to cause mixing)."

My guess therefore is no, jellyfish would not be sufficient to dramatically change the current structure of ocean layers.  Animals in general, as the paper and its references suggest, do contribute significantly, on-par with tides and wind.


Which virus capsids consist of only one type of capsid protein? The Tobacco Mosaic Virus (TMV) capsid consists of many copies of one protein (http://www.rcsb.org/pdb/101/motm.do?momID=109).

Which other viral capsids consist of only one kind of coat protein?

Does each copy of the protein in these also have the same tertiary structure?

Interestingly, the fact that viruses might be made up of repeating subunits was a hypothesis by the famous Watson and Crick in 1956.

A useful resource for this is the Viral Zone website maintained at by the ExPASy bioinformatics system. It contains an easily browsable and human interpretable list of viral families and their characteristics. In particular, you can "browse by virion" which will show you different structural classifications of viruses; make sure to look at all the different genetic classes of viruses (single-strand RNA, double-strand RNA, DNA, etc).

From my preliminary investigation, it appears that many capsids are composed of only a single subunit; in addition to TMV, some other examples I found are the totiviridae family of viruses which infect single-celled eukaryotes such as Giardia lamblia, the human-infecting astroviridae and calciviridae families, and (as far as I can tell) the Heptatitis B virus. It also appears that Dengue virus has a single capsid protein.

As for the tertiary structure of capsid subunits, you might find this review of interest. Basically, due to symmetries in the shape of icosahedra (or helices or other geometric shapes adopted by capsids), you can argue that the structure of subunits in certain symmetrical parts of the capsid has to be the same (because they are copies of the same protein and, by positional symmetry, they have to be experiencing the same forces). When there are asymmetries in the structure of the icosahedron, then it is often hypothesized that there exists a state of "quasi-equivalence;" that is, the deviation from symmetry is small enough that the tertiary structure of each subunit is not affected very much. The review goes into these points in much greater detail.


Why didn't Mendel ever see the recombination? I saw a video on youtube of a professor saying it's because of the quantity of peas. So Mendel would never have published his work if by any chance he had found a pea with recombination.

Someone can explain to me in a dummie way the reason?

I'm not sure what you mean by "recombination".  Peas have 7 chromosomes.  Mendel's seven published traits are each on a different chromosome.  Mendel's second law states that all genes assort independently.  This is wrong, but it is correct for genes located on different chromosomes, which Mendel's were.


Help identifying winged, moth-like creature I noticed this moth (?) on my sofa yesterday. It matched the color of the sofa, so it was pretty hard to see. It's about an inch long, with a yellow body and light brown wings. I think it's a T. bisselliella. I'm from Kerala, South India.

The wings:

I'm quite certain that this is an owlet moth that belongs to the species Asota caricae. It has the nickname "Tiger Moth", and is commonly found in the tropics of India.

I would like to note though that your first picture is somewhat misleading, just from where the flash washes the color so much. Because of this, I decided to more heavily rely on the second image than the first, which exhibits orange instead of yellow.


Can botulinum toxin be grown or kept from denaturing in an UNWRAPPED 50 pound hay bale? Botulinum toxin is the neurotoxin protein created when botulism spores grow. The requirements for growth and/or for keeping the toxin from denaturing would seem to be very difficult to create in bale of hay.

There are well documented incidents of botulism in horses who are eating hay, all the references I found were centered around hay in large plastic wrapped bales.

I have been involved in an event where the presumed DX is botulism secondary to ingestion from hay from last year.  In this case the hay is second cutting timothy hay (making it 6 plus months old), in rectangular 50 pound (22 kg) bales that are not wrapped, have been barn kept, and when purchased from the vendor where stacked in rows 4 feet wide, by 6 feet (2 meters) high. The bale then spent more then a week on an shelf (chrome platted heavy wire) with good air circulation.

Three pet house rabbits appear to have been effected. with 2 dead and one recovering from a case of descending paralysis.  Several tests are underway, but my understanding is that it may be difficult to conclusively show either the botulism in the rabbits, or significant presence of 'botulinum toxin' or 'clostridium botulinum' in the hay (samples from the mangers of effected animals are being tested).

Is it possible to logically conclude that Botulinum toxin could, or could not, be created and/or survive in a bale of hay meeting the above criteria?

Note

If there is an awareness of a plant based neurotoxin that would cause similar symptoms that may be growing in the hay field please offer that in an answer at Gardnening.

Clostridium botulinum toxin is present ubiquitously in soil. As such it is more than plausible that hay bails, which come into contact with soil can and I should expect almost probably will be infected with these bacteria. However it is not the mere presence of the bacteria itself which causes poisoning, it is the toxins they produce when the appropriate conditions are met. These toxins are produced as a consequence of spore formation.

Traditionally in human cases, the presence of toxins has been linked to home canned foods, where there is an anaerobic environment with a ph < 4.5 (http://cid.oxfordjournals.org/content/41/8/1167.full). It is conceivable that such an anaerobic environment exists within a hay bail (even if not wrapped). The following site from the ontario minestry agriculture and food (http://www.omafra.gov.on.ca/english/livestock/horses/facts/info_haylage.htm) suggest that the pH certain methods of hay bailing have pH < 5. This would seemingly confirm hay as potential source for botulinum toxins.

With regards to testing the hay for C. botulinum I would expect there to be a very high chance of finding this, due to soil contamination, however this does not imply this was a definite source for poisoning. A more conclusive test would be for the toxin. So in summary it is logical to suggest that hay could be the toxin source, but this does not mean it was the source.


Calculating number of amino acids in mRNA Assuming there were 20 different amino acids and less than 40 types of different tRNAs found in this alien organism. How many amino acids would be found in the translational product of a 600-nucleotide mRNA?

I am very confused over how I should solve this question.

If we assume 1 codon = 1 nucleotide,

20 amino acids require 20 different codons = 20 different nucleotides < 40 different tRNAs.

If we assume 1 codon = 2 nucleotides,

20 amino acids require 20 different codons = 5 x 5 combination of nucleotides? (considering A, T, C, G, U)?

5 x 5 = 25 < 40 different tRNAs.

The correct answer is to consider 1 codon = 2 nucleotides.

My question,

Since both 1 codon = 1 nucleotide and 1 codon = 2 nucleotides fit the requirement of this question, why is 1 codon = 2 nucleotides the correct answer?

I think I have this figured out. Had to do some math. With our 4 nucleotide system, the number of possible codons is 43 = 64. That is number of nucleotides to the codon length power. The question asks us to determine codon length while giving us the number of amino acids and an upper limit on tRNAs. Using the same formula,  #Nucleotides(Codon-Length) = #Codons, we must find a combination of nucleotide number and codon length that gives between 20 and 40 codons.

                               Codon Length
Nucleotides    1         2        3        4        5
     2         2         4        8        16       32
     3         3         9        27       81       243
     4         4         16       64       256      1024
     5         5         25       125      625      3125
     6         6         36       216      1296     7776
     7         7         49       343      2401     16807

So using this table we see that a few different combinations of Nucleotide number and codon length will fit in that range. A 2-nucleotide system could work if each codon was 5 bases long. A 3-nucleotide system could work with 3 base long codons. A 4-base system cannot work, it goes from less than 20 to more than 40. A 5-base system can work with 2 base codons. A 6-base system can also work with 2-base codons. 7 or more bases fails because even a 2-base codon will make more than 40 codons.

A codon length of 1 nucleotide would require at least 20 nucleotides, so it would not be a good answer.

5 is probably the correct answer because it works with the shortest codon length, though I don't know how you'd get base pairing with an odd number of bases. Perhaps the 5th base pairs with itself. A 6 base system can also work with the same codon length and wouldn't need a self pairing base. However that table shows several combinations could work, so this question might have been to see how you defend your answer.


What species is this worm? I was at the park lying on the grass and its the third time I have seen them, I used to think they were parasites when I was like 7. It is the very small brown worm on the green leaf. It moves by squiggling. It comes in different colors but same size.

http://postimg.org/image/ea3x2nw95/
http://postimg.org/image/zfawh9pr1/

Is this what you mean?

It's pretty hard to tell from this photo, and I'm no entemologist, but to me, it looks like it may be a wireworm, a larvae of a click beetle. This is a diverse group, so I think it would be pretty difficult to give a specific identification. (More images)


I photographed a couple of butterflies and birds in Argentina but can't identify them. What are my options? I photographed a couple of birds and butterflies in Argentina and tried to identify them. I tried online species identification tools, looked in books, and just tried to find pictures on Google with similar animals. This worked for some of the pictures, but for others I couldn't find the correct species. So as a layman, what options do I have?
Here are the ones that I couldn't identify so far
1 (There seems to be a bird and a beetle in this picture. The bird could be a Thraupis Episcopus)

2 (A hummingbird but which one?)

3 (Seems to be the same hummingbird)

4 (No idea)

5 (No idea)

6 (No idea)

7 (No idea)

8 (No idea)

First, I think it is more useful to post separate questions, at least for each taxonomic group (birds, butterflies etc). To make a question a dumping ground for all sorts of species determination pictures is a bad idea.

That said, the butterflies seem to belong to the families Nymphalidae,  (nr 5) and Papilionidae (Swallowtails) (nr 7), judged by overall apperance. I'm not directly familiar with South American butterflies, but two likely species are:

Doxocopa agathina (Nr 5), or related species in the Doxocopa genus.

(from wikipedia commons)

Papilio thoas (Nr 7)
This is the King Swallowtail, your specimen probably of the subspecies P. t. brasiliensis which is found in Argentina. Sometimes the name Heraclides thoas is used. Pictures of subspecies can be found here: Butterflycorner.net. Your speciemen have lost the tail appendages (could be due to wear-and-tear or bird attacks). A related similar species is Papilio astyalus, which is also found in Argentina (pictures), but it usually has a broader yellow band.

(from wikipedia commons)

The bird in nr. 6 looks like a Black vulture (Coragyps atratus).


What is the difference between a viral strain and a viral isolate? Both are characterized, their genes are usually described and published, they are kept safe, they could be used as inoculum or to produce vaccine... Would it be correct to say a strain would be somehow a successful isolate ?

An isolate is a sample. It's this particular virus in this fridge, that was isolated from this, e.g., sputum sample, and cultured. A strain is more abstract -- it is a distinguishable, stable genetic variant of a species. An isolate may be identified as a particular strain of a particular species. That's how I and my colleagues use these terms, in any case, and how they're generally used in the literature. You can read more about this here and here
From the first reference (since it's behind a paywall)
Isolate

An isolate may be defined as “a sample of biological material, especially a microorganism, that has been cultured for study” which is clear, perfectly acceptable and useable by virologists.

Strain

Although there is no official definition of a strain, the strain concept is widely used and a de facto definition states “strains are viruses that belong to the same species and differ in having stable and heritable biological, serological, and/or molecular characters”.


Where can I find a diagram of cortex connections? Has anyone come across a diagram (2D, 3D, maybe even interactive) of the connectiontions between cortex regions? Especially, the diagram should display the strength and direction of those connections (but not every single axon). I am interested in information like "Brodmann area 7 receives heavy connections from area 1,2,3 and 17,18", displayed in a neatly arranged way.

If there is no diagram that fulfills my need, is there another source of information, like a table, where I can find that sort of information?

Edit: After some more research I found this paper which contains some interesting diagrams in its appendix. However, this paper does not describe the human brain.

The Human Connectome Project looks at imaging the functional pathways in the brain and might include some answers to your question:

http://www.humanconnectomeproject.org

Here is an article in Nature about the project:

https://www.nature.com/articles/mp201792


How does one find the corresponding SNPs in the pair of chromonosmes in a FASTA file? You might say I'm an amateur bioinformatician, or trying to become one.  I have a BAM file, from which I have succeeded, using UGENE , in extracting consensus data in FASTA format.  I now see a single series of nucleotides, and their complements, for each chromosome.  What I don't see is two corresponding sequences.  SNP data (e.g., SNPedia ) cites (if I understand it correctly) the SNP at the same site on each chromosome in the pair.  I don't know how to determine my variation, since I see only one nucleotide at any given site, not the pair.

Pretty sure I'm missing something fundamental here.  Thanks for any help navigating this jungle!

If you are looking for simple one off queries it might be better to load the BAM file and a relevant reference genome into a browser like IGV and simply navigate to that specific position.

For some data I had lying around a heterozygous SNP would look like the picture below, there has been an A to G SNP and a C to T:

For longer lists of queries I would take a look at BEDtools: https://bedtools.readthedocs.org/en/latest/content/bedtools-suite.html

If this does not help you, I recommend you ask your question on https://www.biostars.org/ There you will find help from true bioinformaticians.


What is the title of Darwin's paper on cellular structure? I read somewhere that Darwin wrote a paper that dealt with cellular structure, but I've been unable to find the title or contents of the paper because Darwin wrote such a volume of material. What is the title of this paper or papers?

A google search does not turn up any helpful results, and a similar search in google scholar yields equally ambiguous results (at least to me, since I do not have a background in biology).

Darwin had written lots of papers which dealt with fertilization (which involves single cells), as he primarily dealt with the reproduction, continuation and thus evolution of a species, but these did not deal with cell biology specifically.

After a closer look at the complete list of all his publications, I found that he did have two cell-related publishings, specifically about the size of cells, one entitled Bees in Jamaica increase the size and substance of their cells, and the other, Bee-cells in Jamaica not larger than in England, in which he retracts the statement he had made in the previous article.

Ultimately, to answer your question, it seems as though none of his works dealt with cellular structures.

References

Charles Darwin. "Bees in Jamaica increase the size and substance of their cells". Journal of Horticulture (15 July): 305.
Charles Darwin. "Bee-cells in Jamaica not larger than in England." Journal of Horticulture (22 July): 323.


Viruses: Adaptation to a new host through repeated host jumps A friend told me, during a 3 minute discussion, that viruses that are endemic in host $A$ and make repeated jumps to host $B$ but can't be transmitted between individuals of species $B$, may slowly adapt (through these repeated jumps) to be able to be transmitted between individuals of host $B$ and become epidemic.

I don't know much about epidemiology. I don't understand how a virus population that is endemic to host $A$ may adapt to host $B$ with repeated jumps while the viruses that jump to host $B$ are dead end because they cannot be transmitted further more. Or Are these viruses able to jump back to host $A$ to bring back their newly acquired adaptations to host $B$?

Also, I might misunderstand the meaning of "repeated host jumps transmission". I first thought it meant repeated jumps from a reservoir population in host $A$ to host $B$, but it is also possible that it describes the dynamic of a virus population that is adapted to jump from species to species and they actually gain this ability by keeping jumping and jumping. But then, how could a virus species get adapted to jump from species to species? I'm a bit confused…. Can you give me some hints about this process of cross-species transmission through repeated jumps?

A friend told me, during a 3 minute discussion, that viruses that are
  endemic in host A and make repeated jumps to host B but can't be
  transmitted between individuals of species B, may slowly adapt
  (through these repeated jumps) to be able to be transmitted between
  individuals of host B and become epidemic.

This is...mostly true. A good example is avian influenza - there are a number of human infections linked to contact with infected poultry, but the virus is not particularly good at sustaining long chains of human-to-human transmission, likely due to differences in the respiratory tract between humans and birds.

  I don't know much about epidemiology. I don't understand how a virus
  population that is endemic to host A may adapt to host B with repeated
  jumps while the viruses that jump to host B are dead end because they
  cannot be transmitted further more. Or Are these viruses able to jump
  back to host A to bring back their newly acquired adaptations to host
  B?

What they mean by repeated jumps, or what they should mean, is not a virus hopping back and forth, but a virus going from A to B many times. This is my problem with your friend's statement, it's not so much a "slow adaptation" as, well, random chance.

Imagine that there's a mutation in Virus A, which lives in chickens, that will make it well adapted to live in human beings. It's an extremely rare mutation, so the dominant strain of Virus A is maladapted for human to human transmission. That means most Virus A infections in humans will be the non-productive kind, that will infect a person, but not go on to infect other people. But, with enough rolls of the dice, a human might get the human-favored Virus A, and since there's now intense selective pressure for that strain of the virus within its new human host, it might establish itself and take off.


Is there evidence to suggest that sharks from prehistoric times live in the deep of the oceans? I've had friends see the boat and giant teeth of a giant shark attack of a boat in Japan. (Teeth larger than a great white). [I can't find anything about this on the Internet].
In addition, this report from Pakistan seems to suggest that there are large sharks in the deep of the Oceans.

15-TON PREHISTORIC SHARK CAPTURED OFF COAST OF PAKISTAN

Karachi | A giant prehistoric shark previously thought to be extinct for more than 20 million years has been captured by local fishermen off the coast of Pakistan, reports the Islamabad Herald this morning.
The giant creature first thought to be a great white shark was rapidly declared by experts to be an unknown species of shark as it’s great weight and size were unheard of. Analysis of the teeth suggest the shark to be a parent of the Megalodon, an extinct species of shark that lived approximately 28 to 1.5 million years ago, during the Cenozoic Era.
The sea creature that measures an incredible 10.4 meters and weighs an astounding 15.6 tons is the largest living shark ever caught to date, great white sharks reaching an impressive 7 tons at full growth, a size that is no match for this giant prehistoric shark that can reach an imposing 20 meters in length and possibly weight up to 30 tons, depending on estimates.

My question is: Is there evidence to suggest that sharks from prehistoric times live in the deep of the oceans?

No.

The article linked to is a hoax, and was debunked by Snopes.

The website is known for its hoaxes and satirical articles, and it states itself that its articles are faked.

  WNDR assumes however all responsibility for the satirical nature of its articles and for the fictional nature of their content. All characters appearing in the articles in this website – even those based on real people –  are entirely fictional and any resemblance between them and any persons, living, dead, or undead is purely a miracle.

The image of the shark was taken from a 2009 photograph of a great white shark caught in South Africa. The shark was reportedly 4.3m long, a normal length for a great white shark.

The large apparent size of the shark as compared to the fisherman is due to a trick of perspective. This article shows the shark in perspective in a second image, which clearly shows that it is not as large as it apparently is in the first image.


Genomic DNA resuspension after ethanol precipitation I am having trouble resuspending purified human genomic DNA.
The genomic DNA is purified using phenol:chlorofom from ~ 1 mL of blood. After ethanol precipitation, I normally see a large pellet which is then resuspended in 150 uL of TE (10 mM Tris pH 8.0, 1 mM EDTA).

But the resulting DNA solution is extremely sticky.
There are the options I have tried:

1) Incubation at 37C for 1 hr to overnight

2) Incubation at 50C for 1 hr to overnight

3) Incubation at 65C for 1 hr to overnight

The 65C incubations for up to 3 hours do make the DNA solution less sticky, but in the mean times, cause increasing DNA smearing when running on agarose gel. After overnight incubation at 65C, the DNA solution is no longer sticky but shows extensive smearing on gel, indicating DNA degredation/fragmentation at high temperature.

I have also tried resuspending the DNA in 8 mM NaOH, then neutralise it with Hepes, but this doesn't help either.

I am thinking to try silica/glassmilk beads based methodology. Will genomic DNA captured in silica beads be easier to elute and resuspended without the "sticky" issue.

Just a thought, have you tried eluting the DNA in Molecular Grade Water instead of TE?

For DNA which are supposed to be used in downstream applications like sequencing or transformation, elution with Water instead of TE buffer is frequently done.
I agree longer genomic DNA can be sticky upon elution, but if by chance the DNA is not entirely dissolved when you add the eluant (you see some very small clumps of flakes instead of a homogeneous clear solution) , that may be because of the presence of low amounts of alcohol (organic solvent). That's why it is recommended that after aspirating the alcohol, you should leave the tube opened for ~10 minutes for the trace amounts of alcohol to dry out before you add the eluant.

Sorry if you have done these things already, just wanted to be sure.

Hope this helps!


human gene PCR primers database I wonder if there is a place on the internet to get PCR primers for a specific gene.
For instance, exon 15 in CFTR gene. I don't want to design myself because I am sure sombody else already did it.

Answer is, obviously, yes.

Primerbank

Here. You can search primers using accession number or Gene-ID


Most human-like teratoma ever recorded? I'm curious to learn about the 'most human' teratoma ever recorded. By that I mean a teratoma which most resembles the form of a human being.

I suppose there are several factors which would contribute to this criteria:
-Most organs, and components found in a human (e.g. brain, teeth, organs, etc.)
-Most closely organized structurally like a developing human.

Also I was wondering. Given the right conditions could a teratoma grow into a living being? Could they theoretically develop the necessary organs to be excised from their host and sustain the functions necessary for survival.

Basically I am curious to learn about the possibility of teratoma maturing into a bonafide organism.

There's a 2003 paper published in the Journal of Korean Medical Science describing a case of a 'homunculus' within a teratoma: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055135/

It contained some hair, brain tissues, cranial and other bones, but no internal organs.


Do bees make honey from fallen fruit? I know bees make honey from nectar, and I know they drink the juice of fallen fruit, but do they actually make honey from fruit, or do they only eat from it for themselves?

The substances that bees consume do end up in honey. There was a high-profile case in Brooklyn in 2010 (The Mystery of the Red Bees of Red Hook) where bees from several hives began producing red honey after feeding on dyed maraschino cherry juice from a local factory.

A follow-up article from 2015 (How Bees Revealed a Pot Farm Beneath the Maraschino Cherries) claims that the substance they began producing was not honey but “red gunk”; however, that may have been editorial license.


Has medical progress stopped human evolution? We can cure many diseases nowadays, and thus the natural selection is very limited.
Plus, mankind spent the whole beginning of its existence in almost the same hostile environment, and that's where he evolved the most, whereas our environment is changing very quickly. So, can we say that mankind froze, if not stopped, its own evolution ?

Not at all.

Mutations accumulate independent of medical progress. In fact harmful mutations which would otherwise cause an individual to die can now be "cured" thus if anything increasing the gene pool.
Typically medical progress extends our lives when we are much older, thus we have already passed mutations on to our children before a bottleneck in evolution could occur
We are getting taller, less hairy and women are getting more attractive which is another form of evolution
As new diseases develop the selective pressures on humans are ever changing. HIV which was never as widespread is now pushing certain immunogenetic traits to be favourable, the same is true for malaria (HLA 5701) and many others

In conclusion, whilst there are fewer and fewer strong selective pressures forcing extreme evolution, our bodies are designed to evolve slowly unlike viruses like HIV. Our mutation rates are around 1 in 10^9, allowing us to always slowly evolve as there will always be traits which are slightly more advantageous.


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 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.


Who are Ursprungliche Eukaryoten? The school textbook of my daughter (the textbook is written in German) describes the five kingdoms of life: prokaryota, plants, fungi, animals and "Ursprungliche Eukaryoten". These are defined as "single cell organisms with real nucleus and other specialized organoids, both autotrophs and heterotrophs". No Latin name is given.

I am somewhat confused, as I know that there are both multi and single cell varieties between algae, and these used to belong to even particular taxon within algae (a single cell Rhodella, for instance, not just belongs to plants but also specifically belongs to red algae). Also, there are unicellular fungi like yeast that used to be fungi (and, OK, protists used to be a separate group that probably also belongs to "Ursprungliche Eukaryoten"). Are they all pulled out of they groups into this new kingdom in this system?

The summary of the proposed classification schemes over history can be found at https://en.wikipedia.org/wiki/Kingdom_(biology)#Summary . Which scheme, if any does this taxon correspond? Is something missing in that table?

The textbook is Training Gymnasium - Biologie Mittelstufe Band 1, Harald Steinhofer (2013), ISBN 978-3-86668-709-7, seen here. The description in question is on the page 16.

It is natural to be confused because the consensus has changed over the years and is still not settled.  In part this is because knowledge has been gained but remains incomplete, and in part it is a matter of opinion and aesthetics about what is best for usefulness at various levels of detail and understanding.

The system put forth in the textbook seems to best match the system Whittaker put forward in 1969.  His Monera is the text's Prokaryota, and his Protista corresponds to the text's Ursprungliche Eukaryoten.  Essentially Protista/Ursprungliche Eukaryoten is a catch-all for all Eukaryotes not included among the Plants, Animals, and Fungi.  There may be some variations in which of the eukaryotic algae are included among the Plants versus the Protista/Ursprungliche Eukaryoten.

It should be noted that in most or all systems of "Kingdoms", at least some of the kingdom groups are not monophyletic, that is, do not include all descendants of a common ancestor, and so do not exactly reflect a true tree of descent.  The Wikipedia Kingdom article notes:

  Some recent classifications based on modern cladistics have explicitly abandoned the term "kingdom", noting that the traditional kingdoms are not monophyletic, i.e., do not consist of all the descendants of a common ancestor.


What happens when seeds are refrigerated before planting? My son is doing a science research project at school, and he's chosen to research what happens when seeds are refrigerated before planting.

I cannot provide any information in regards to background research (I couldn't find any), but I want to know if refrigerating seeds before planting them will have any effect at all on the seed (so that my son's experiment can be interesting).

Thanks.

That might be a good experiment.

I know that before planting bulbs you want to put them in the refrigerator or even the freezer sometimes.

In fact this process of cold treating seeds has a name: Stratification.

To paraphrase: some seeds become inactivated at higher temperatures like lettuce and delphinium.  You can place the seeds in medium and put them in the fridge or freezer for a day or two.

You can see how this makes sense.  The seeds have adapted to start growing when they are freezing because the timing results in the plants breaking ground as early as possible when the temperature is warm enough in the spring.

A quick search doesn't seem to imply that silverbeet needs to be stratified before planting.  The result might be negative, but there is definitely some good expectation that it makes a difference to some plants.


Is it correct to use the terms multinucleate and syncitia interchangeably? If you see the skeletal muscle,it is having several nuclei and is said to be "multinucleate".Similarly the cardiac muscle is also having several nuclei yet it is specifically termed"syncitial".So my question is: Is there any reason behind this or are the terms interchangeable?
I am listing the sources from which the question came up in my mind:
[Source1]

Individual muscle fibers are formed during development from the fusion of several undifferentiated immature cells known as myoblasts into long, cylindrical, multi-nucleated cells. Differentiation into this state is primarily completed before birth.[Source2]
The cardiac syncytium is a network of cardiomyocytes connected to each other by intercalated discs that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium.[Source3]

No, the terms multinucleate and syncytium are not synonymous in this context.  Most cardiomyocytes are not multinuclear. To be clear, syncytium is used to refer to multinuclear cells that originate from fusion of uninuclear cells, including the skeletal muscle, but that isn't what is referred to in the context of cardiac muscle.

The Wikipedia page on syncytium summarizes this nicely:

  Cardiac tissue is therefore described as a functional syncytium, as opposed to the true syncytium of skeletal muscle.

The "intercalated disks" of cardiac muscle are filled with gap junctions and desmosomes. The desmosomes hold the cells together physically, while gap junctions allow ions (and small molecules) to pass directly between cells, forming "electrical synapses". This allows electrical signals to propagate between the myocytes to coordinate contraction.

Gap junctions are formed by proteins, rather than fusions of the plasma membrane, so they are relatively small. This means that not everything in the cytoplasm can pass through them, mostly just ions and some small molecules. Proteins, for example, would not pass through gap junctions. Therefore, cells that are connected via gap junctions, like cardiomyocytes, are still somewhat independent, unlike fully multinuclear cells.

There are also types of neurons, including some in the CNS, that also form gap junctions and act at least somewhat in concert in this way.


What is the fate of the typical tree? Walking through the local established broadleaf forests dominated by oak and tulip poplar (Eastern U.S.), it is common to find patches of young tree saplings, say 10-20 oak or tulip poplar saplings growing in close proximity. The obvious restriction on living space means that probably at most one of these trees will make it to maturity. In fact, judging by the apparent lack of mid-aged trees of these types in the woods, it seems very possible that none of these trees will last much longer. I'm curious: at what point and how would these trees die? The answer might also help me take better care of trees I've planted in my yard.
I can easily speculate about some causes:

Competition for water/nutrients in the soil
Not enough sunlight
Animal predators
Pathogens

But these suggestions don't answer the how or the when. And it's not clear which accounts the biggest impact. Clearly, the above factors didn't prevent the trees from growing in the first place. And the first suggestion (competition for nutrients) puts a limit on their growth but doesn't say per se why a plant would die.

This is a great question.
Without going into too much detail, there is a series of studies done in northeastern US temperate forests (specifically at Great Mountain Forest in Connecticut, USA) on the growth, survival, and dispersal of canopy trees. In this particular community, light appears to be the primary limiting factor. Seedlings and saplings in low-light environments (i.e. stuck under the canopies of mature trees) grow slowly and have poor carbon balance, which makes them susceptible to mortality (probably from pathogens, although the proximal cause of death of seedlings and saplings is rarely known). Early successional tree species (in GMF, white ash/red maple/red and white oak) grow especially slowly, and hence are more likely to die, in low-light conditions; late successional (hemlock and beech) grow slowly even in high light, but are tolerant of slow growth, so are likely to survive until the adult tree above them dies and falls down.
The exact answer to "at what point do these trees die" is a little tricky, but here's a figure from Kobe et al. showing estimated survival probability for different species as a function of light availability (the assumption is of independent mortality probabilities, given light availability, at each time step, so there is no particular stage at which individuals die in the model).

Kobe, Richard K., Stephen W. Pacala, John A. Silander Jr, and Charles D. Canham. “Juvenile Tree Survivorship as a Component of Shade Tolerance.” Ecological Applications 5, no. 2 (1995): 517–532.
Pacala, Stephen W., Charles D. Canham, John Saponara, John A. Silander Jr, Richard K. Kobe, and Eric Ribbens. “Forest Models Defined by Field Measurements: Estimation, Error Analysis and Dynamics.” Ecological Monographs 66, no. 1 (1996): 1–43.
Pacala, Stephen W., Charles D. Canham, and John A. Silander Jr. “Forest Models Defined by Field Measurements: I. The Design of a Northeastern Forest Simulator.” Canadian Journal of Forest Research 23, no. 10 (1993): 1980–1988.
Pacala, Stephen W., Charles D. Canham, John A. Silander Jr, and Richard K. Kobe. “Sapling Growth as a Function of Resources in a North Temperate Forest.” Canadian Journal of Forest Research 24, no. 11 (1994): 2172–2183.


What types of plants are Gibberellin used on? On what type of plant (monocot/ eudicot? family? species?) is Gibberellin used on?

I searched through many sources but could not find whether Gibberellin works for all plants or just a specific type or family. I read that it works well for biennials, but what are some of the other plant families that it is useful for?

I don't know what you mean with 'used on' but gibberellins are plant hormones in ferns, monocots and dicots. All of these plants will react to the application of gibberellin but the effect will depend on the dose, type of molecule and tissue where it is applied. All plant hormones have multiple effects but the classic one for gibberellic acid is stem elongation.

Too much of this can kill the plant though as is the case with Bakanae fungus infection which forces the plant to overproduce gibberellic acid which kills it (reference).

One common agricultural use is boosting the growth of seedless grapes as the seed is an important site of gibberellin production for maturing fruits.

This pdf gives you a reasonable overview of what gibberellins do


Why is cyanide poisonous? I know cyanide inhibits complex IV in the electron transport chain, but I don't understand why this makes it so toxic. If cyanide is bound to the complex, can't the electrons just bypass it   and reduce oxygen directly? That way fewer protons would be pumped out of the matrix, but most still would, and aerobic respiration would just be less efficient, rather than stopping entirely.

Essentially what I'm asking is what causes the electrons to get "stuck"?

Cyanide binds cytochrome oxidase so as to prevent the binding of oxygen. Electron transport is reduced to zero, and none of the oxygen breathed in can be used. Cytochrome oxidase is one of a superfamily of proteins which act as the terminal enzymes of respiratory chains, so if the cyanide is binding to the cytochrome then it inhibits the process and making it dangerous. Another example I would give rotenone which binds competitively.


Could an animal with an open circulatory system survive in a near-zero gravity environment? An animal such as a crayfish relies on gravity to keep its circulatory system running. If it is turned upside down, the gravity works against the system, suffocating the animal. Now if, instead of placing the animal on it's back, we were to take take it to a space station, gravity would not be working against it, and random blood flow plus capillary action should get some blood flowing. Would the animal survive this?

I believe that fruit flies have been taken aboard the Space Shuttle for experiments. They survived and the adults have an open circulatory system.


reason for "not for diagnostic use" advice in protocols I read "not for diagnostic use" in every protocol i saw. why is it so?
which differences have the kits and material that are used for diagnostic purposes?

the FDA has to approve diagnostics - a rigorous and expensive process.  Its a legal distinction, but also one which conveys a significant level of usefulness and reliability.


Do there exist enzymes that can take up multiple cofactors to do different reactions? I was thinking about enzyme catalysis, and it seems like enzymes can only catalyse one kind of forward/reverse reaction (please correct me if I am wrong). Does there exist an enzyme that can catalyse multiple reactions with different cofactors? For example, an oxidoreductase that has $Fe(III)$ as a cofactor for one reaction and $H_2O_2$ as a cofactor for another reaction.

It sounds like you are asking about what are commonly referred to as "multifunctional enzymes".

For a reasonably recent article covering this subject — see:
Cheng, X. Y., Huang, W. J., Hu, S. C., Zhang, H. L., Wang, H., Zhang, J. X., ... & Ji, Z. L. (2012). A global characterization and identification of multifunctional enzymes. PloS one, 7(6), e38979.

A specific example of such an enzyme is the fatty-acyl-CoA synthase from yeast — this enzyme catalyzes multiple reaction steps that use both NADP and Coenzyme A and also uses a third cofactor, FMN.

  The enzyme from yeasts (Ascomycota and Basidiomycota) is a multi-functional protein complex composed of two subunits. One subunit catalyses the reactions EC 1.1.1.100, 3-oxoacyl-[acyl-carrier-protein] reductase and EC 2.3.1.41, 3-oxoacyl-[acyl-carrier-protein] synthase, while the other subunit catalyses the reactions of EC 2.3.1.38, [acyl-carrier-protein] S-acetyltransferase, EC 2.3.1.39, [acyl-carrier-protein] S-malonyltransferase, EC 4.2.1.59, 3-hydroxypalmitoyl-[acyl-carrier-protein] dehydratase, EC 1.3.1.10, enoyl-[acyl-carrier-protein] reductase (NADPH, Si-specific) and EC 1.1.1.279, (R)-3-hydroxyacid ester dehydrogenase. The enzyme differs from the animal enzyme (EC 2.3.1.85) in that the enoyl reductase domain requires FMN as a cofactor, and the ultimate product is an acyl-CoA (usually palmitoyl-CoA) instead of a free fatty acid.

Source: https://www.ebi.ac.uk/intenz/query?cmd=SearchEC&ec=2.3.1.86


Was the evolution of humans inevitable? Suppose we wind time back to the instance when life emerged on Earth and let evolution start over again, will human beings or any other kind of self-conscious animals evolve ultimately, inevitably?

Or do these sorts of animals just evolve as a result of some randomness processes in evolution, if so, what's the probability? Is it great or small?

If randomness does exist, then to what degree will it affect our ability to depict evolution? Will we still be able to describe the general trends of evolution, for example, the trend of more and more complicated animals evolving?

Evolution is largely random, because most of the processes that drive evolution are random. A few ideas you should understand to realize why it is so random.

Most people are only aware of natural selection when it comes to evolution, and think that natural selection has a goal of creating new, increasingly sophisticated forms of life. None of this, of course, is true. Evolution is not only natural selection, there's also genetic drift, gene flow, and mutation, which are random. Natural selection is not technically random, but it's not the biggest player. Secondly, natural selection does not have any goals and does not move forward, create more complex life, invent adaptations, or does anything of this sort. Natural selection is not designed to produce perfection, it just acts upon whatever variation is present in population, and favours individuals that are more successful in reproduction. Case study: 98% of our DNA doesn't code for any proteins, and presumably most of this DNA is junk. Does it sound like perfection to you, like we are the ultimate species?

The reason I tell you all this is because, in my opinion, when asking this question of "inevitability", you assume that there's some guiding hand that leads evolution towards some end-point, a climax. But there is no such guiding hand, and it takes a number of incredibly unlikely events to occur in a specific order for: Earth to be created with such conditions, life to start on Earth, collective learning to evolve in some form of live, agricultural revolution to occur so this form of life can thrive, etc. If at any stage something went different, everything would be different.

Final thoughts, why are you so sure that humans won't go extinct just like 99.9% of all the species that ever existed on Earth? A typical species goes extinct in about 10 million years, and we've been around for only 200,000 years. If you accept this possibility (which is real, in my opinion), suddenly, it doesn't seem that intelligent life, and we as its representatives, is some inevitable end-point in evolution, does it?

Edited: As to your last (new) question, "if randomness in evolution exists, are we still able to describe the general trends in evolution?". Firstly, of course randomness exists in evolution! Mutations are caused by errors in the process of DNA replication, genetic drift is caused by random sampling by definition. Secondly, there is no universal trend to more complicated organisms being evolved, as I mentioned above. Some organisms do get more complex, but some organisms haven't changed much over very long time, some are "living-fossils". Once again, evolution has no goal to create more complex life -- if, say, nautiluses or horseshoe crabs are capable of surviving and reproducing in the niches they occupy -- there's nothing else needed for their existence. Furthermore, fitness is linked to the environment, which is dynamic -- many complex species went extinct during global changes in the environment, whereas what you might call as "primitive" species of unicellular bacteria survived.


Is there a difference between NADH and NADH2? I've been reading a lot about the oxidative dissimilation etc, and often I see different sources use NADH and NADH2 in the same reactions. One source uses NADH and another uses NADH2 in the exact same way. Is there a difference or is it just a different name for the same substance?

They are often used interchangeably to indicate the reduced form of $\ce{NAD+}$.  The overall reaction when oxidizing some molecule $\ce{RH2}$ is: $\ce{RH2 + NAD+ -> NADH + H+ + R}$.  The proper reduced $\ce{NAD+}$ is $\ce{NADH}$ (it accepts two electrons and one proton), but sometimes $\ce{NADH2}$ is used to account for that second hydrogen that gets removed from the substrate being oxidized.  The notation $\ce{NADH2}$ doesn't really take into account the fact that the second hydrogen is charged, and not bound to the $\ce{NAD}$ in the same way that the first hydrogen is, so it is confusing.  The notation: "$\ce{NADH + H+}$" is more correct and is also sometimes used.


Creating a Phylogenetic tree using DNA sequences I was wondering given DNA samples, how can we create a phylogenetic tree? I mean I don't even want to have actual DNA sequence. Can I generate small samples, like reads of a length 100 or 1000 of nucleotide chains and figure out how they are related.

Suppose we have two reads of DNA samples, for brevity let's have them really small like: AAAGGTCTTGA and ATAAAGTGTA. I can run the sequence alignment algorithm on the strings and I will get {"A", {"", "T"}, "AA", {"G", "A"}, "GT", {"C", "G"}, "T", {"TG",""}, "A"} So basically what alighns then where you have indels or substitutions. I can easily now write up a function that calculates how close are these two strings by giving positive weights for matches strong negative weights for indels, etc. Now I want to know if these two guys with really short DNA are related or no. What is the mathematical measure of relatedness? And after I do Multiple Sequence Alignments and get similar results how do I build a tree from it.

There is no single mathematical measure of relatedness.

In the context of phylogeny, you need a model of evolution in order to be able to evaluate some relatedness between your strings of nucleotides. Then you would have various option for how to build a tree so that it reflects this relatedness. See for instance the wikipedia page about computational phylogenetics: https://en.wikipedia.org/wiki/Computational_phylogenetics.

Through what kind of historical process were your sequences generated ?
If there is no historical process underlying the generation of your sequences, then it is not meaningful to build a phylogeny with them. You can still define distances between them and use clustering techniques to build a tree, but that tree will not be a phylogeny.


Retrieve all predicted cds from NCBI Please apologies if this has been answered somewhere else, but I couldn't find an answer to this problem.

I would like to retrieve all the predicted coding sequences on the NCBI ftp for a given species. Let's say my interest species today is Stegastes partitus and that I go here. I know how to get all the predicted mRNAs (./RNA/Gnomon_mRNA.fsa) or all the predicted proteins (./protein/protein.fa) but I cannot find how to get the CDS... if ever it's possible? This can be done on the Ensembl FTP.

Thanks for any insight!

EDIT: The output would ideally be a multifasta file like this:

>Stegastes_partitus_gene1_cds
ATG(.................................)TAA
>Stegastes_partitus_gene2_cds
ATG(.............................)TGA
>Stegastes_partitus_gene3_cds
...

The GNOMON and GFF folder contains the files you want, the GNOMON if you check the README relates to the GNOMON gene predictor and the GFF I think links back to the same file. I think the file you want is ref_Stegastes_partitus-1.0.2_scaffolds.gff3.gz which contains the coordinates on the scaffolds.

And as you stated you are on linux, so the best and geeky way to go is awk.

awk '!/#/{if($3=="CDS")print}' ref_Stegastes_partitus-1.0.2_scaffolds.gff3 > SomeFile.gff3

UPDATE

This part is from python. With reference to the previous user's answer if you fetch the GBK file, rna.gbk, this should allow you to fetch CDS using biopython

You should also check out Peter cook's tutorial on handling genbank files in python

from Bio import SeqIO
from __future__ import print_function

Genome = SeqIO.parse("Examples/rna.gbk","genbank")
handle = open("Examples/rna.faa","w")
for genes in Genome:
    i=1
    for Feature in genes.features:
        if Feature.type=="CDS":
            FASTA=Feature.extract(genes.seq)
            print(">"+genes.id+"_CDS_"+str(i),file=handle)
            print(FASTA,file=handle)
            i += 1

I would recommend that you install anaconda, it is a package management software, which when installed installs its own python version and alongside it installs some 400 different packages. Instructions are available on the link. So these packages should come with the link.

After you have installed anaconda, put all that code from up there into a Myfile.py and execute on the command line with python Myfile.py.


Is it plausible that strict lockdowns made it more likely for the new variant of COVID to have emerged? My idea is that strict lockdowns put greater evolutionary pressure on the coronavirus by restricting oppurtunities to be transmitted, meaning that a faster-spreading variant had much less competition.
Is this at all plausible? Was it just as likely for a faster-spreading variant to become the predominant one without lockdowns?

While I get your intuition, the hypothesis seems implausible

Emerge of new CoV variants should be considered proportional to the
current spread of the virus. Each virus has a certain mutation rate that surely does not depend on lock-downs.
It seems implausible to interpret
lock-downs as physical limitations to viral spread, that could potentially be
overcome by any mutation.
Even if CoV magically learned to
teleport to different households, such an ability would always represent immense advantages; an advantage that does not need lock-downs to be effective
Lastly, the differential viral competition is neglectable so far; we are at 6 of 100 thousand infected persons. So basically a 0% chance that a virus would infect a person who has acquired an immunity due to a previous CoV infection. In your model this person, who is immune, further would need to NOT be immune because quarantine prevented the (previous) infection.


What is this fungus that is growing on my plant, and is it dangerous? This fungus is growing on a plant in my front yard and I do not know if it is dangerous for my health or for the plants health. Can you please identify it? I live in Dominican Republic, a tropical island in the Caribbean Sea.

Here are some photos from my yard:

My answer won't apply if your plant isn't a cycad (a species from the genus Cycas) as only cycads are affected. Cycad aren't native to the Dominican Republic but have been planted as ornamentals in many parts of the world. If your plant's a cycad, I'm convinced that what your plant has is NOT a fungal but insect infection - something far more serious for your plant but not harmful for you or other people.

Please compare photos provided to make sure of identification. Even enlarging your top photo,  it's not quite focused or clear enough to be sure. It appears that your white 'fungus' is actually Aulacaspis yasumatsui or the Asian cycad scale insect. Athough native to southeast Asia, it's been spreading to many places where cycad are found. Whether it's reached the Dominican Republic yet, I don't know but its been in Florida since the mid-1990s and is found in a number of Caribbean countries. It's now a very serious pest of cycad worldwide, resulting in the death of many.

Here are some photos for you to compare. I did my best to find photos that show greater detail for you to check. If the photos fit what you have, you need to treat your plant to prevent it dying and for the infestation spreading to other cycad on the island. I've no experience with this but the information on how to deal with this pest comes from Central Florida Palm & Cycad Society so they should know the best way to treat this.

Treatment of Asian Scale

 Image from Forestry Images courtesy of Jeffrey W. Lotz

 Image from Central Florida Palm & Cycad Society


Can the spinal cord contain an "epileptic focus"? I was wondering, is there a possibility of an something similar to an epileptic focus to exist within the spinal cord?

Note I am using the terminology "epileptic" loosely here, principally for the lack of a better name for it. When I say epileptic focus I mean an excitable area capable of sustaining a pathological rhythmic electrical activity which may or may not extend to other areas of the central nervous system.

I believe it is due to the connection types that occur within the spinal chord (closed loops that exist there are resistant to this) and as such this might be true for other CNS areas (epileptogenic susceptible tissue might be specific of cortex areas). But I did some research on the topic and couldn't find any data on this.

If it isn't possible to have this problem on the spinal chord then, why is that?

Short answer
Epilepsy is a disorder confined to the brain.

Background
Terminology is crucial in this question. The International League Against Epilepsy (ILAE) defines epilepsy as a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiologic, cognitive, psychological, and social consequences of this condition. ILAE defines an epileptic seizure as a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain (Fisher et al., 2005).

Hence, by definition, epilepsy is a disorder of the brain. Note that the ILAE is an authorative organ and their definition overrides whatever your medical textbook on internal medicine says.

An epileptic focus is a commonly used term, but as far as I know not well-defined. It's often used in relation to EEG and other methods such as MRI and PET that attempt to define the hot spot of seizure activity. More strictly defined terms in this regard are eloquent cortex and epileptogenic zone. The eloquent cortex refers to any cortical area in which injury produces symptomatic cognitive or motor deficit. The epileptogenic zone refers to the region of cerebral cortex that is both necessary and sufficient to generate epileptic seizures. Its entire removal can be used as a treatment for intractable epilepsy (Richardson, 2003).

With regard to your question, I expect you are referring to the epileptogenic zone. By definition, this refers to a region in the brain.

References
- Fisher et al, Epilepsia (2005); 46(4): 470-2
- Richardson, Brit Med Bull (2003); 65: 179–92

Note
I expect this answer may not be entirely satisfactory. If you are looking to the  physiological basis of the occurrence of seizures and why they occur in the brain and not in the spinal cord, it may be wise to formulate a more specific separate question. Preferably do not grossly edit this question given it received three answers. vervet's answer on focal epilepsy clearly shows the confusing terminology in epilepsy world. Focal epilepsy is not the same as an epileptic focus. However, epileptic focus is a term often used for focal epilepsy. Long story short, specific answers need specific questions, preferably with the definitions embedded to prevent deleted answers and under-appreciated answers like vervet's.


If an insect becomes upside down, do they have mechanisms to turn themselves right side up? This question is mainly applicable to beetle's and cockroaches. If I flip them so their legs point upward, they usually squirm around and wiggle trying to come back upright. Sometimes they succeed, and turn right side up again; sometimes they don't. Do insects have any built in mechanisms to unflip themselves.

I was unable to find any sources, but I believe they should, since insects climb stuff, and they may land inverted if they fall, so a mechanism might've been evolved to unflip themselves.

Well, many insects have developed ways to right themselves when they get turned over.

One of the more interesting families are the Elateridae, or click beetles: so named because they press their prosternum and mesosternum against each other which causes pressure. That pressure is eventually released causing a "clicking" sound and springing the insect upward (or away from predators).

You can see an additional video of a click beetle doing so here.


What is the difference between options protein and replication in the NCBI database? After checking the NCBI help page, I am still unclear about the difference between protein and replication interactions for HIV.

http://www.ncbi.nlm.nih.gov/genome/viruses/retroviruses/hiv-1/interactions/

Interactions denote protein-protein interactions, which means physical association between proteins. By nature, these networks/graphs are undirected.

Replication interactions (actually a not very good term) denote gene regulatory interactions that affect HIV replication. These sets also include the regulatory effects of HIV genes on host genes (and hence the terminology is unsuitable). These networks are directed as well as signed (positive or negative interactions i.e. activation or inhibition respectively).

You can see for yourself, from the dropdown boxes and the interaction lists in this page.


Why does a stomach come before the gizzard in birds? Since the gizzard is for mechanical digestion, shouldn't that happen before the stomach digests the food with acids? (to make the morsels smaller)

The gizzard appears to be a structure that bird inherited from a distant ancestor, as the structure is found in dinosaurs (which birds are derived from) and crocodilians.  https://en.wikipedia.org/wiki/Gastrolith

As to why, the bird gizzard is not in a better position, (like say the grasshopper gizzard which is located in front of its stomach), the best reply I think off is evolution is blind.  The innovations that appear, are random and further constrained by the features that the animal already has.

It is probably the same reason why rabbit eat their own poop to better digest their food, even though cows have evolved a four chamber stomach to handle the same problem of digesting grass. Or why no animal has evolved a second set limbs to fly even though it would be super useful to keep arms to catch prey and not sacrifice said arms to be made into wings.

In a sense these questions of why didn't evolution design it better is evidence that the concept of intelligent design is rubbish. Designs in animals (and bacteria) can be really really dumb.


How does natural selection explain how organisms that are poisonous evolved? Natural selection makes perfect sense when describing the evolution of say camouflage. For example 2 bugs of the same species live on a tree. One is mutated to look slightly more like a tree, so the bird misses it and eats the one that sticks out more.

This logic seems to fail for poisonous animals though. For example, two bugs are equally visible but one has developed a mutation to be poisonous. Since they are both easy to spot they both get eaten. Now the poisonous mutation has died out. How does natural selection explain the poison mutation overcoming the initial hurdle?

There is a lot to say on this question. I will try to keep it short, to the risk of oversimplifying the problem. I can think of three main reasons:

1. Predation does not necessarily means death of the prey

Most of predation does not directly kill the prey. Typically herbivory, will often damage the prey but a single individual won't kill the prey entirely. In such systems, being poisonous may eventually either directly stop the predator (because the predator quickly sense it is poisonous or because the predator immediately dies) or will ensure that the predator remembers not to attack this same individual.

2. Kin selection

kin selection (aka. Group selection although there are a few authors who do not equate them), is selection above the level of the population of individuals (see also unit of selection; see this recent answer for some book recommendation on the subject).

In very short, under kin selection, an individual who dies of predation but can either cause suffering to the predator or just kill it, will protect its close relatives that live nearby from the same predator (who is iether dead or who may have learned to avoid these particular plants). As close relatives share of lot of DNA in common, a gene for toxicity - even if it fails to protect the individual being preyed upon - can protect the copies of itself present in the siblings of this individual.

3. Side effect

Let's not make the mistake of assuming that a trait has necessarily come to high frequency because it was selected for the specific purpose we associate this trait with. A plant may happen to become toxic for reasons that are unrelated to predation. While toxicity is often costly to the plant, it may sometimes eventually just be a by-product. Unfortunately, I would not be able to cite an example where toxicity is simply a side effect.


How fast do stomata respond to environmental changes? How fast does stomatal resistance respond to environmental changes? Correct me if I'm wrong, but I assume that atmospheric humidity would be the fastest changing factor (e.g. rain storm on a dry day, or a warm change coming through). If the relative humidity changes from say 50% to 100%, how quickly will stomata open? And how fast in the opposite direction?

Stomatal speed varies depending on a lot of factors, especially anatomy even within species, but especially between species.

  Evidence from several studies has also suggested that smaller stomata respond faster than larger stomata

The paper I just cited from (first link below) includes is a long review of the what is currently known and also original research into the process. It includes a really detailed, lengthy chapter on the stomatal speed, but which is mostly lacking in easily citable numbers except for closing times:

  Stomatal aperture responds more slowly, typically with half-times of 10 to 20 min, reaching a new stable, (near) closed state after 45 to 60 min

A few more clear numbers come from the second paper I link to below, however this is in response to changes in light, not humidity.

It includes a table (table 1) on mean stomatal closing and opening time delays in four plant groups and plants adapted to two climate conditions. In most groups, closing happens slower, taking about 50 percent longer, with mean times varying between 6 and 18 minutes. Opening is faster in every group but one and takes between 4 and 30 minutes. In plants adapted to dry climate conditions stomata respond faster.

Sources:

Stomatal Size, Speed, and Responsiveness Impact on Photosynthesis and Water Use Efficiency

Effects of stomatal delays on the economics of leaf gas exchange under intermittent light regimes


At what total rate is water used in metabolic processes over the entire biosphere? A recent column on "The Straight Dope" website discussed the idea that water molecules are largely cycled around through the water cycle, and that therefore the water molecules that come out of your tap could have been drunk (and excreted) by the dinosaurs.  Cecil Adams (the author) points out a few flaws with this argument, namely that we've been burning fossil fuels for a couple of centuries and releasing water into the atmosphere, and that liquid water is constantly dissociating and reforming;  so it's not strictly true to say that every water molecule on Earth has been around since the time of the dinosaurs.

One thing that occurred to me in reading this article is that biological processes have also been consuming and producing water for many millions of years now;  this would be another mechanism by which water molecules can be "reshuffled".  Is is possible to estimate how much water participates in these processes (per annum)?  I know that there are estimates out there about how much carbon dioxide is produced/consumed by the biosphere, for example, but I'm not sure whether one can straightforwardly extrapolate from "carbon consumed" to "water consumed," and I don't know if there are other significant metabolic processes that consume/produce water molecules.

The lifetime of a water molecule is less than 1 millisecond, in the sense that two particular protons will not remain bonded to same oxygen ion for longer than that order of time.  Also, the protons of water are constantly exchanging with protons of other molecules and ions, such as alcohols, amines, carboxylic acids, bicarbonate, and countless acids.   So it would only make sense to discuss the rate at which the oxygen atoms of water become atoms of another substance (beyond just hydroxide or hydronium) such as dioxygen or sugar.

For photosynthesis, one molecule of water is consumed for each molecule of carbon dioxide.  The link says that about 110 billion tons of carbon undergoes photosynthesis per year and since a water molecule is 1.5 times the mass of a carbon atom, this means 160 billion tons of water consumed in photosynthesis.

So at a minimum, biological processes destroy and create 160 billion tons of water per year (on the basis of whether an oxygen atom is or isn't part of a water molecule).


If a dead snake reflexively attacks itself, why does it not always attack itself? Recently there has been this video going around of a snake that had been decapitated.  Its body swung around to the decapitated head and the head attacked the body on "reflex".  Now we know that most reflex arcs bypass the brain.  So if it is the case that this strike attack is reflex then how is that suppressed when the snake is alive? Why aren't snakes always reflexively attacking themselves?

Here is the video.

Is this some other phenomenon than reflexive attack?

It seems that National Geographic were just as curious, in their interview in this article with James Murphy, he states the answer to your final question - that even though the snake is dead, it can still reflexively 'attack' the nearest object - in this case, the remains of its own body - as it is not attached, it is a 'foreign object' and the reflexes result in an 'attack'.


Production of plant derivatives using genetic engineered micro-organisms I saw a Thought Emporium video where spider silk was produced by genetically modifying yeast. I have also read about companies making vanillin (vanilla flavour) using this technique.
I am curious to know if plant derivatives like saffron (or its flavour), rubber, or even substances like quinine, tetrahydrocannabinol and cocaine, can also be produced by this same technique. From the information I have found, it seems that some plant derivatives are being manufactured in genetic engineered micro-organisms, but most are not.
Some of these derivatives are very expensive, so I would imagine such techniques could be used to mass-produce them more cheaply. If so, what is stopping industry from doing it? If not, what is the problem?

In principle, any biological product should be able to be developed through microbial synthesis, with the appropriate choice of chassis. Indeed, this was the goal of the DARPA "1000 Molecules" program, which did indeed demonstrate it was possible to rapidly engineer new pathways for production of new biomolecules.
In practice, however, some products are far more difficult to achieve than others.
A (very) rough sorting from easiest to hardest:

Small-molecule chemicals that are "near" to an existing metabolite already being produced by the organism, requiring only small number of modifications to the organism.
Proteins, polymers, and small molecules requiring more extensive or difficult synthesis
Materials with a homogeneous structure
Materials with a highly heterogeneous structure

Basically, the more you have to manipulate the cells, the harder it is, and if you need the cells to coordinate with each other to make a material it gets much harder yet. Even some simple everyday materials, such as cotton, are actually fantastically complex and would be extremely difficult to synthetically generate, since even a single cotton fiber has a carefully controlled multilayer structure far larger than any microbe.
Finally, just because something can be produced doesn't mean it will be produced efficiently. Getting from a proof-of-principle to something that operated effectively at industrial scale is a massive challenge, and while this is likely to become easier in the future we just aren't there yet.
Something to keep an eye on, however, is BioMADE, a major government funded venture just kicking off with the aim of making such production much more feasible.
In short: in the near term, expect to see mostly high-value products with relatively simple routes to synthesis, but over the long term a much broader range of materials can in principle be produced.


How long can a human neuron live outside the body in a controlled environment? Have there been any experiments that have kept neurons alive (stationary), without preserving methods such as freezing? If yes, then how long were the cells kept alive for?

According to this paper from 2001, they've got the survival time up to about a year on average. The trick is sealing the neuron inside a permeable membrane so you don't actually risk contamination when feeding. This paper lays out experiments that take many weeks to perform, so as far as I can tell the science of keeping neurons alive has advanced to 'as long as I keep feeding them and nothing bad happens'.


Can an infectious diseases come from a plant? Coronavirus, HIV, 1918 Flu, etc. They all come from animals. Do any infectious diseases (in humans) come from plants? More specifically, are there viruses that infect plants that can mutate to infect humans?

This is a great biological question! I'm glad we encourage such questions from curious people who want to learn more about modern biology.
Much as other animals can be vectors for diseases that infect humans, plants can be vectors for pathogenic infectious agents.
You may occasionally read news stories of disease-causing strains of Escherichia coli which contaminate vegetables and force product recalls. There is currently a CDC advisory to not eat clover sprouts, as an example, because of contamination with E. coli O103, a strain which can cause a variety of health problems (including kidney damage, in severe cases).
This kind of contamination is becoming more common, largely as a consequence of how we produce food:

Fresh fruits and vegetables once were thought to be relatively free of disease-producing pathogens. In recent years, however, outbreaks of foodborne illness linked to fruits and vegetables have become more common. These outbreaks come from produce grown both in the United States and in other countries. Outbreaks have been linked to Escherichia coli O157:H7 and Salmonella on apples, lettuce, cantaloupe and sprouts; Listeria monocytogenes on cabbage and cantaloupe; Shigella on parsley and lettuce; and Cyclospora on imported raspberries.
Changes in microorganisms have undoubtedly contributed to this increase, as have changes in growing, harvesting, distribution, processing and consumption practices. Listeria monocytogenes, Clostridium botulinum and Bacillus cereus are naturally present in some soils. Their presence on fresh produce is not uncommon. Salmonella, E. coli O157:H7, Campylobacter jejuni, Vibrio cholerae, parasites and viruses can contaminate produce through raw or improperly composted manure, irrigation water containing untreated sewage or manure, and contaminated wash water. Contact with mammals, reptiles, fowl, insects and unpasteurized animal products are other sources of contamination.

Wash your fruits and veggies!


Basic Amino Acid Residue Binding Mechanism to DNA I understand that many protein DNA binding domains bind to DNA via basic residues such as Arginine and Lysine. But what is the mechanism used to bind to DNA and where on the DNA would these residues bind?

This question has no particular answer.  There are several families of DNA binding proteins, some of them bind specifically (e.g. restriction enzymes like EcoRI which binds to and cuts GAATTC or transcription factors like lac repressor which binds a particular point of the e coli genome about 25 base pairs long) and some of them bind semi-specifically (e.g. zinc fingers which bind GC rich regions), others non specifically (e.g. the sliding DNA clamp).

For all of these proteins, they will have a tendency to have positively charged amino acids facing the DNA because the DNA's phosphate backbone is negatively charged.  There are lots of protein motifs (like the helix turn helix motif) that fits into the major or minor groove of the DNA.  The lysine and argenine are important because they are the positively charged amino acids.  Histidine is also positively charged, but it is not as long and flexible, and doesn't seem to fit as often or as well.

http://en.wikipedia.org/wiki/DNA-binding_protein


Why does dissociation of carbonic acid cause a decrease in pH? When a molecule of carbonic acid (H2CO3) dissociates, the two products are a bicarbonate ion (HCO3-) and a hydrogen ion/proton (H+). Because of the addition of a hydrogen ion, this process causes a decrease in the pH of the blood, and if someone breathes too slowly and doesn't quickly remove CO2 from their body, respiratory acidosis will take place.

However, why is it the case that the addition of this hydrogen ion lowers pH? While this might sound like a stupid question, it's also the case that the dissociation of carbonic acid produces a bicarbonate ion, which is a weak base. Therefore, the dissociation produces both an acid and a base in a 1:1 ratio. Therefore, the concentration of hydrogen ions relative to bicarbonate ions doesn't actually change. Given this fact, wouldn't there be no change in pH at all?

I read a paper on carbon dioxide transport which addressed some of my other questions but didn't touch on this precise point.

Any acid that releases a proton when it dissociates in water will also produce a conjugate base. We can conceptualize this as $\ce{HA <=> H+ + A-} $. In this particular example, $\ce{HCO3-}$ is $\ce{A-}$.  The strength of the acid is determined by the extent to which the acid, $\ce{HA}$, dissociates. This can be expressed using the equilibrium constant for this reaction, which has a particular name, $\ce{K_a = \frac{[H^+][A^-]}{[HA]}}$, (where $\ce{[X]}$ is the concentration of $\ce{X}$ at equilibrium). The larger $\ce{K_a}$ is, the further the reaction moves to the right (or, as it is often expressed, the smaller the $\ce{pK_a}$, which is $\mathrm{-log_{10}}$  $\ce{K_a}$).

Here, the addition of any $\ce{HA}$ will produce $\ce{H^+}$ and $\ce{A^-}$ in an aqueous solution (the blood), and decrease the $\ce{pH}$. $\ce{A^-}$ is only a base insomuch as it can form $\ce{HA}$ by combining with $\ce{H^+}$. This can occur if you add (or, as occurs in the kidney, reabsorb) $\ce{A^-}$ with some counter ion other than a proton. Then you can drive the equilibrium to to the left, towards $\ce{HA}$, decreasing $\ce{[H^+]}$. Otherwise, $\ce{A^-}$ derived from $\ce{HA}$ will not drive the equilibrium one way or the other. $\ce{H^+}$ will still dissociate as determined by the $\ce{K_a}$.


Specialist evaluation for people aged under 40 years with stage 1 hypertension Reading the NICE clinical guideline for Hypertension it says...

For people aged under 40 years with stage 1 hypertension and no evidence of target organ damage, cardiovascular disease, renal disease or diabetes, consider seeking specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage.

However it is not clear in the guidelines exactly what "specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage" would entail.
I understand that it is typical to carry out blood tests to look at kidney function, thyroid function, cholesterol and glucose levels; and that further tests such as a 12-lead ECG, echocardiography and renal ultrasound scan may be ordered if necessary to test for organ damage.
My question is what further tests would be performed by a specialist on a patient aged under 40 years with stage 1 hypertension and no evidence of target organ damage, cardiovascular disease, renal disease or diabetes? I have done several searches on Google but most of the papers I've read relate to patients who already have signs of organ damage or existing disease.

Alongside full guidance released by NICE they also produce treatment pathways which give further advice - here is the treatment pathway for hypertension.  You've listed most of the investigations that would be considered in your original question.

Investigations that may be considered as appropriate include:

Urine dipping for proteinuria or haematuria indicative of renal damage
Measuring of plasma urea and electrolytes and estimation of glomerular filtration rate, again as an indicator of renal damage
Measuring of plasma glucose, total cholesterol and LDL/HDL cholesterol to rule out additional risk factors as part of cardiovascular risk assessment - e.g. diabetes, hypercholestrolaemia
Fundoscopy to examine the retina for damage resulting from hypertension
12 lead ECG to show any changes compatible with left ventricular hypertrophy
Scanning for the presence of a phaeochromocytoma if clinically suspected

You may also find the professional reference page on hypertension from patient.co.uk useful.


How Circumcision could reduce the chance for a HIV infection? Circumcision removes the foreskin of the penis which mainly acts as a cover to the penis. Normally removing the foreskin makes more vulnerable to any STD, so how could circumcision reduce the risk of a HIV infection?

This is an interesting question, which has not been answered yet. It is also questionable, if this protective effect is present at all. There are around 40 studies on the topic available which have subsequently undergone meta-analysis. In a meta-analysis all data from recent studies which meet certain quality criteria are analysed together. This gives a much bigger dataset and stronger statistical data. It also helps eliminating the effects of too small test groups.

One of these meta-analysis identified circumcision to have a positive effect on the prevention of HIV infections (reference 1). The authors recommended considering it as a preventive measure.

Two other meta-analysis were more cautious on the topic and either found only a weak link (reference 2) or that only "randomized control studies" (reference 3) would provide clear data. The problem with all these studies is, that they are observational studies, where unknown other effects can play a bigger role than the supposed main effect. It is ethically very difficult to make controlled trials on the transmission of deadly diseases in humans. This is also the reason why all trials on this have been stopped.

There is a hypothesis on how circumcision may help preventing the infection with HIV (when you not get infected in the operation itself due to improper hygienic standards). The skin in the penis contains a large number of immune cells (dendritic cells, CD4/CD8-T-cells) which are the target cells of the HIV virus. It is thought that the virus can more easily penetrate the relatively thin skin of the foreskin. It is also possible, that the surface size is important here, as there are reports which show that men with a larger foreskin also have a larger risk of getting infected. See reference 4.

Another hypothesis has to do with the with the bacteria which live under the foreskin. The number of different strains present is much lower in circumcised men, which led to the conclusion that the dendritic cells, which present these to the immune system have an easier job in the circumcised men and are more likely to prevent the infection with HIV.
See reference 5 and 6 for more information.

References:

Male circumcision and risk of HIV infection in sub-Saharan Africa: a
systematic review and meta-analysis
Male circumcision for prevention of heterosexual acquisition of HIV
in men
HIV and male circumcision--a systematic review with assessment of
the quality of studies.
Male circumcision for HIV prevention: current research and
programmatic issues.
Why Circumcision Lowers Risk of HIV
Male Circumcision Significantly Reduces Prevalence and Load of
Genital Anaerobic Bacteria


Giving a sign to Pressure Potential, Osmotic Potential And Other Similar Quantities When these quantities are mentioned with what reference do we give signs to them?
Why is Osmotic Pressure positive, but Osmotic Potential, negative?
What about Turgor Pressure (Pressure exerted by the protoplasmic fluid on the cell wall) and the Wall Pressure (Pressure exerted by the Wall as a reaction to the Turgor Pressure), what signs do we assign to them?
What I understand is that it's based on the tendency of water to enter or exit the system being studied, but I lack clarity on how signs are being assigned to these different quantities. When we talk about soil having a low, does low mean more negative or does it mean a lower magnitude osmotic potential, for example?

I think you already know the sign convention in calculating the water potential: the addition of solutes lowers the potential (negative vector), while an increase in pressure increases the potential (positive vector).(Another way of saying the same would be more solute = more negative.) {1} This is the same everywhere.

Pressure potential: The pressure potential in a plant cell is usually positive. In plasmolysed cells, pressure potential is almost zero. Negative pressure potentials occur when water is pulled through an open system such as a plant xylem vessel.{1} This means that it is negative during a "suction" action, otherwise, it is positive.

Osmotic potential (solute potential): The relationship of solute concentration (in molarity) to solute potential is given by the Van't Hoff equation:
Ψπ=−MiRTΨπ=−MiRT

(The formula, note, has a -ve sign.)
For example, when a solute is dissolved in water, water molecules are less likely to diffuse away via osmosis than when there is no solute. A solution will have a lower and hence more negative water potential than that of pure water. Furthermore, the more solute molecules present, the more negative the solute potential is.

Turgor pressure and wall pressure: I recommend reading this for a clearer understanding.

...This actual pressure which develops within such a cell is called turgor
pressure. This term can be applied with equal appropriateness to the actual
pressures developing in purely physical osmotic systems such, for example, as a
sucrose solution enclosed within a collodion or cellophane membrane and immersed
in water. As will become clear in the following discussion, TPs in osmotic systems
can sometimes be negative in value.

When the TP
is negative, that is, when the cell sap is under tension (see later), the WP is
likewise negative, the wall being subjected to a centripetal pull because of its
adhesion to the protoplasmic layer and cell sap mass within the cell.

On the basis of fundamental physical principles it is generally considered
that the WP and TP of a cell are equal in magnitude and oppositely directed.
This situation is not difficult to visualize for a cell in an equilibrium condition.
For dynamic states in which water is being gained or lost by a cell, however,
the validity of this assumption has been questioned.

{1}-https://en.wikipedia.org/wiki/Water_potential


What is exactly a phosphoester bond? I've spent some hours trying to understand what exactly is a phosphoester bond, but I'm still confused and at this point I just want to throw myself out of the window. I've already read that post which treats the question but it doesn't really help me since, according to the link given by WYSIWYG♦:

  A phosphoester bond is a bond between the phosphorous atom of a phosphate group and an oxygen atom.

But considering the answer of electronpusher:

  Each nucleotide contains one phosphoester bond (between a phosphate O and sugar 5'-C).

It doesn't really make sense to me, since such a bond (in a nucleotide) is not exactly a bond between the phosphorous atom of the phosphate group and an oxygen atom (that is, it's a O-C bond, not a P-O bond).

So, what is exactly a phosphoester bond? Is it a O-glycosidic bond between the sugar (ribose or 2'-deoxyribose, in a nucleotide) and the phosphate group? Or is it the bond that there is between the phosphorous atom of a phosphate group and an oxygen atom of the same phosphate group?

I'm really confused and desperate by all this, so any help would be greatly appreciated. Thanks in advance!

A phosphoester bond is in fact a bond between the phosphorus atom of a phosphate group and an oxygen atom. Your confusion comes from the fact that electronpusher's statement is inaccurate.

Instead, electronpusher should have said:

  Each nucleotide contains one phosphodiester bond (between a phosphate O & a 5'-C on one sugar belonging to one nucleotide, and then another bond between a phosphate O & a 3'-C on another sugar belonging to another nucleotide).

More elegantly put, "a phosphodiester bond occurs when two of the hydroxyl groups in phosphoric acid react with hydroxyl groups on other molecules to form two ester bonds" (source).

The resulting bond is between O-C because the hydroxyl groups react with each other and transesterification occurs. The OH from the phosphate interacts with the OH (attached to the carbon) from the sugar, transesterification occurs, thus leaving only 1 oxygen, of which is the oxygen in the P-O-C bond sequence, exhibited in the following image.

The next image is a simplification of the reaction mechanism. Dehydration does not actually occur (transesterification does, as mentioned), but instead, this image is provided as to more easily identify which entities are involved in the reaction, as to more directly address the concerns expressed by the OP. The true reaction mechanism can be found here.


SEREX serological analysis of cDNA expression library What is Serological Analysis of cDNA expression library? I went through this article:http://cancerimmunity.org/serex/introduction/ but could not really make out. Can someone please explain this to me in a simpler manner?(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

With this method you want to identify proteins on cancer cells which are immunogenic so you can use them to boost an immune response against the cancer cells.

To do so, you extract the complete mRNA from a cancer. These mRNAs represent all the genes which this cancers expresses (which then also contains the immunogenic proteins). These mRNAs are cloned into bacteriophages (viruses that only infect bacteria) and are then used to infect bacteria. During this infection the virus expresses the protein which has been cloned into his sequence and which originates from the cancer cell. The infection of the bacteria leads to the formation of plaques (wholes) in the bacteria which grow on the surface of a culture plate.

You then use the serum of cancer patients on these expressed proteins to see, if there are antibodies which can recognize these cancer antigens (and could be used to detect and mark them). If there are proteins which only react to the sera of cancer patients but not to controls (to exclude) unspecific reactions, then these proteins are identified and can be used to generate antibodies against this specific cancer type. It works like in the figure below (from this paper):


Difference between PCR for linear template and a plasmid? I believe PCR can be conducted both on a linear template and a plasmid, and I was wondering how these procedures differ in what enzymes are used, how the enzymes work on the template, primers used etc.

There's not much difference between them. The same enzyme and condition can be used whether the template is circular or linear.

You can amplify plasmids, but PCR intrinsically generates linear DNA fragments even if you use circular DNAs.


Is life in the open ocean homogenously spread? Obviously around land masses or in shallow water where reefs and coral may grow, life is diverse and numerous. But how spread out is sea life in the open ocean (for example, half-way between Hawaii and California) where there is no land mass or shallow depths for hundreds or thousands of miles?
Does life exist in clusters with large swaths of oceanic desert in between or is it relatively homogenously spread?

This is sort of a partial answer, but here is a map using chloryphyl density to map the global distribution of marine life. As you would expect, most is clustered around costal regions, but you can also see some pretty distinct zones in open ocean, with more primary production apparently in the northern and southern latitudes. Not sure how much this map projection distorts apparent distances, but it should help give you an idea.

Here's where I found this map.
And here's one of the links they references, which looks to have some more resources to explore.