Is a single cell "irreducibly complex"? (sorry if the title seems like flame-bait - but it's a real question).
I'm trying to understand what could have come before the first cell (What are the "minimum requirements" for a single cell?)

From what I've seen, the presented chemical evolution (aka abiogenesis) process centers around self-replicating RNA that gets trapped inside a lipid-based protocell and then somehow turns into a functioning cell.  But it seems like a giant leap to go from that situation to the most basic cell we know about.

Instead of starting from basic molecule and trying to get more complex, what if we take a simple cell (which is actually really complicated) and try to get more simple - try to take out some of the pieces. Work our way backwards. The problem is, I don't know what pieces you can take out. It seems there are several molecular systems that need to be functioning for cell to be viable.  Once you start to imagine a cell without them, it seems the cell will not be able to survive or replicate.

My question is, what would the step just before a "minimum cell" look like?  Are there pieces we can take away and it would still be able to survive and replicate?

** Edit **

Based on some of the discussions in the comments, I wanted to clarify what I'm asking. This is a bit long - but hopefully it will help.

Evolution is a process in which replicating systems transfer beneficial permutations to 'offspring'.  Usually the term is applied to "biological evolution) (meaning something living - from a cell to more complex organism) but I've also heard people refer to "chemical evolution" which is the process in which atoms combine to make molecules and amino acids and the amino acids combine to make RNA which can replicate.  Or fatty molecules combine to make a lipid membrane, etc.

In this process to get to something more complex, you have to have gone through a simpler stage.  To arrive at RNA, you had to have a system that would first produce nucleic acids.  If the first life was in the oceans, you needed something that could survive in and out of water before you now have creatures on dry land.  Each stage has to have a predecessor.

Generally question of the origin of life start at the raw materials and work their way towards the more complicated.  Most of the discussion I've seen basically end with RNA in lipid cells + billions of years = a prokaryote.  The difference between RNA in a protocell and a working basic cell is vast and I haven't seen an explanation on how to bridge that gap.

I'm approaching the question from the opposite direction.  If we take the most basic, simple prokaryote cell - what came before it? Even such a simple cell is in actually very very complicated (semi-permeable membrane, nucleoid, ribosomes, cytoplasm, etc..) There are so many interconnected pieces that it seems are only valuable when working as a whole. Eg, could I have had a cell without ribosomes and then some how it mutated to have ribosomes?  It seem not, because a cell without ribosomes would never have survived/replicated.  The same with other components.. if I have some precursors without that piece, it would never have survived long enough to mutate to now have that component.

So my question is what could the predecessor to a basic cell have been, considering its complexity and the seeming interdependence on the pieces for the cells survival?

I hope that helps explain the question better - thanks for any insight you can provide!

There is no straightforward answer as to whether a "single cell" is irreducibly complex. Which cell are we talking about? Human mitochondria do not survive without their genome, but those of Cryptosporidium do persist without it. The Minimal Genome Project, led by biotechnologist Craig Venter, concluded with the creation of Mycoplasma laboratorium, the result of removing non-essential genes from Mycoplasma genitalium. This minimum cell had 382 genes.

Are 382 genes the minimum number of genes required for life then? No. That number refers to the total number of genes necessary for a particular organism, which happened to be Mycoplasma. Iterative trials of removing genes will reveal different numbers of essential genes for different organisms. Primates will require a high number of essential genes, whilst archaea could survive with fewer genes.

Regarding the transition from RNA-only to RNA-protein world, peptides function as cofactors for some ribozymes. Amino acids and peptides are known to have existed in the prebiotic environment and have been found in space (glycine has been found in comets, along with other 70 amino acids).

Regarding the formation of nucleotides, from Scientific American.

  A New Route
  In the presence of phosphate, the raw materials for nucleobases and ribose first form 2-aminooxazole, a molecule that contains part of a sugar and part of a C or U nucleobase. Further reactions yield a full ribose-base block and then a
  full nucleotide. The reactions also produce “wrong” combinations of the original molecules, but after exposure to ultraviolet rays, only the “right” versions—the nucleotides—survive.

This answer is not complete, I will add more information and provide citations in the future.


Why do sea mammals die on land, and drown on sea? It's quite confusing to me, why do sea mammals die on land, but also die from drowning if they couldn't reach the sea surface to breath?

Excuse my ignorance but I am really confused!

Mammals use lungs as their respiratory system. These animals in the process of evolution left land and started to live in the water, they developed organs that are used to swim. The shape of body also changed to reduce the resistance of water. In spite of all this they didn't developed gills.

Lungs can help in respiration only in air. So the mammals have to come above water in order to take air. You correctly have noticed that these animals die if they can't reach air, i.e. they die of drowning.

But one thing I want to mention is that they don't need to reach land in order to take breath. They just need to swim up to the surface of water for this purpose.

Anyway, I think you got the point. Feel free to ask if you have further confusion on this topic. I shall explain more if needed.


Why antipyretics do not bring the body-temperature below normal? Antipyretics like paracetamol are used to decrease the body-temperature in fever patients.

But some of them are also used as pain-killers in sprain or other injuries (where there's no fever). In that case they changes the body temperature very little (if any).

Why? Is there any molecular mechanism responsible for  this?

Antipyretics doesn't work by reducing the body temperature but blocking pathways that make it higher.

For paracetamol/acetaminophen the mechanisms implied are not currently completely clear (as reported on Wikipedia or on Katzung's "Basic & Clinical Pharmacology").

For the most common NSAIDs (aspirin, ibuprofen, naproxen, ...) the mechanisms instead are more clear as they block some enzymes that are involved in production on inflammatory molecules (enzymes COX1 and COX2 that are implied in the arachidonic acid pathway as said on this article).

When these inflammatory molecules rise concentration in blood they can get to the hypothalamus so it will set the body temperature at an higher level; when these signals stop coming (inflammation stops or no more molecules are produced because of drug's block) the hypothalamus sets the temperature to the normal range.

More infos about hypothalamic temperature set point.


Why is cholera toxin added to certain culture media? I was reading an article [1] where they cultured SEB-1 human sebocytes in DMEM F12 + FBS + EGF + adenine + hydrocortisone + insuline as well as cholera toxin. Why is cholera toxin added to the media? Will the toxin not initiate some kind of unwanted immune response?

https://www.ncbi.nlm.nih.gov/pubmed/25647437/

Empirically, it can improve growth of cell cultures (https://www.atcc.org/Global/FAQs/C/C/Cholera%20toxin-541.aspx).

It furthermore has the potential to make cell populations more homogeneous by selectively binding to gm1 containing cells that can arise from spatial inhomogeneities among cultured cells. Snijder er al. Nature 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19710653)


Drosophila reference genome Does anyone know the details about which line they are using to sequence as the Drosophila melanogaster reference genome?

That was surprisingly buried.

I found this in a paper describing genome build 3 - See "Materials and Methods".  I imagine that this is consistent through to the current build.  In any case it should get you started.

"Sequencing templates were made from P1, BAC and WGS DNA libraries using the D. melanogaster strain yellow (y1); cinnabar (cn1) brown (bw1) speck (sp1)."


Toll Like Receptors Vs Toll Receptors What are the major differences between them, apart from one being in humans and other in Drosophilla?

In Drosophila, Toll receptors are used during embryonic development as well as innate immunity. See The Drosophila Toll Signaling Pathway by Valance, et. al.

Toll-like Receptors are pattern recognition receptors found in organisms other than Drosophila that recognize common motifs found on pathogens.

Toll receptors were first discovered in Drosophila and orthologous receptors were then found in many other organisms, not only Human. Both will transduce signaling and will lead to transcription of genes.


Do women experience more bonding hormones than men after sex? Does Oxytocin (or any other bonding hormone) increase more so for women than for men after sex?

Someone told me that it increases 4-fold for men and 12-fold for women (unconfirmed).

Is there any observable or scientific relationship between sex, Oxytocin and the desire for a monogamous relationship with a sexual partner?

Does Oxytocin increase more so for women than for men after sex?

Answer: Yes, Oxytocin level shoot up for female after sexual. It is highest at orgasm, which is the main cause women could have multiple orgasm.

  Someone told me that it increases 4-fold for men and 12-fold for women
  (unconfirmed).

Answer: The level of oxytocin actually increase 5 times during sexual intercourse. Though some online article claim the male and female level as much you said, but it is not confirmed in humans.

  Is there any observable or scientific relationship between sex, Oxytocin and the desire for a monogomous relationship with a sexual partner?

Answer:

Take a look at this experiment done on people to test Bonding:

  Bonding is an important part of human romantic relationships, and
  research has suggested OT as a possible mediator of this effect. A
  2005 study by $Grewen\ et\ al^{4}$. found that couples who reported a greater
  amount of partner support showed higher baseline OT plasma levels.
  These couples also showed higher levels at 4, 7, and 10 min following
  warm partner contact. For women, OT levels increased sharply 7 min
  following warm partner contact, regardless of partner support, while
  male levels remained unchanged. This study demonstrates a
  relationship between supportive romantic bonding and OT, and shows
  that warm contact has a greater physiological effect on women than on
  men.[1]

A very famous study done on rats confirm that Vassopressin and Oxytocin is actually the reason behind monogamous relationship.

  Almost a decade ago, Thomas Insel, Director of the Center for
  Behavioral Neuroscience at Emory University, and colleagues at the
  National Institute of Mental Health and the University of Maryland
  implicated vasopressin and oxytocin in controlling the preference for
  particular partners in both male and female prairie voles. These
  investigators found that giving a male vasopressin causes it to stay
  with its mate, whereas blocking this hormone prevents a pair-bond from
  forming. The scientists saw similar effects in female prairie voles,
  with oxytocin determining the extent of pair-bonding. In contrast, the
  administration of these substances had no influence on social
  interactions in the promiscuous montane voles. Surprisingly,
  vasopressin and oxytocin are naturally found at similar levels in both
  prairie and montane voles.[5]

Source:

[1]. The role of oxytocin in mating and pregnancy

[2]. http://en.wikibooks.org/wiki/Relationships/Hormones#Oxytocin

[3]. The role of oxytocin in relation to female sexual arousal.

[4] Grewen, K.M., Girdler, S.S., Amico, J., Light, K.C., 2005. [Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact](Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact.). Psychosom. Med. 67, 531–538.

[5] http://www.smart-publications.com/articles/oxytocin-the-real-love-hormone


Change Genbank entry date with Biopython I can create a new Genbank record in Biopython with the following code:

from Bio import SeqIO, SeqFeature
from Bio.SeqRecord import SeqRecord
from Bio.Seq import Seq
from Bio.Alphabet import generic_dna
from Bio.Alphabet.IUPAC import IUPACAmbiguousDNA

my_sequence = "ATAGGGACUCATAGATA"
my_record = SeqRecord(Seq(my_sequence, IUPACAmbiguousDNA()))
my_feature_location = SeqFeature.FeatureLocation(2,5, strand=1)
my_feature = SeqFeature.SeqFeature(my_feature_location, type="CDS", id="Cre")
my_feature.qualifiers["foo"] = "bar"
my_record.features.append(my_feature)

print my_record.format("gb")

The corresponding genbank file then looks like:

LOCUS       .                         17 bp    DNA              UNK 01-JAN-1980
DEFINITION  .
ACCESSION   <unknown id>
VERSION     <unknown id>
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
FEATURES             Location/Qualifiers
     CDS             3..5
                     /foo="bar"
ORIGIN
        1 atagggacuc atagata
//

How can I change this bit UNK 01-JAN-1980?

So, the problem is that you are probably using wrong class for your record. Compare Bio.SeqRecord class with Bio.GenBank.Record class. Reason why in your GenBank format you have this reference date (01-JAN-1980) is because your record has intrinsically no date attribute, so SeqRecord.format set undefined fields to default (look through the source code to see where this happens).

What you want to do for creating GenBank record is following:

$ python
Python 2.7.10 |Anaconda 2.3.0 (x86_64)| (default, May 28 2015, 17:04:42)
[GCC 4.2.1 (Apple Inc. build 5577)] on darwin
Type "help", "copyright", "credits" or "license" for more information.
Anaconda is brought to you by Continuum Analytics.
>>> from Bio import GenBank
>>> from Bio.GenBank import Record
>>> my_rec = Record.Record()
>>> my_rec
<Bio.GenBank.Record.Record object at 0x1030b1890>
>>> my_rec.sequence = Seq(my_sequence)
>>> my_rec.sequence
Seq('ATAGGGACUCATAGATA', Alphabet())
>>> print(my_rec)
LOCUS                         bp
DEFINITION  .
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
ORIGIN
        1 atagggacuc atagata
//
>>> my_rec.date = '13-JUL-2015'
>>> my_rec.features.append(my_feature)
>>> my_rec.data_file_division = "ROD"
>>> print(my_rec)
LOCUS                         bp                    ROD       13-JUL-2015
DEFINITION  .
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
FEATURES             Location/Qualifiers
type: CDS
location: [2:5](+)
id: Cre
qualifiers:
    Key: foo, Value: bar
ORIGIN
        1 atagggacuc atagata
//

Notice, how print(my_seq) outputs data in GenBank format by default (since that is a GenBank record after all). I am sorry I cannot really talk on differences between GenBank.Record and Bio.SeqRecord and why/when use one object or another.

Anyways, looking up reference documentation is always a good habit: http://biopython.org/DIST/docs/api/Bio.GenBank.Record.Record-class.html


What is the evolutionary advantage of menstruation? I was wondering why woman have fertile periods. Based on some simple reasoning I would expect that if woman were always fertile this would increase the chance of reproduction(one of the important things in life). But having menstrual periods would decrease this chance because only the period close to ovulation would result in fertilization.

So why did evolution result in woman having menstrual cycles?

Human female ovaries only have a certain number of ova; none are manufactured in adulthood. Once they're gone (that's when menopause occurs), they're gone.

You can also ask, why did evolution result in a limited number of oocytes then? This kind of second guessing of physiology is endless.

In your scenario, an ovum would need to be released every few days in order to be fertile continuously. That alone would decrease the number of years that a woman could be fertile. Since a fetus needs about nine months to gestate, I think once a month fertility is more than adequate. The earth's population is already too large, which also translates as successful reproductively.

If a fetus could gestate in a month, I could see an advantage to constant fertility. But the disadvantages would also be great. How could a woman take care of so many babies? How could she possibly feed, say, six to nine babies a year with only two breasts? (Mammals that frequently have larger litters have more mammary glands.) How could her own body compensate nutritionally not only for the burden of feeding the fetuses but also of the babies?

Asking why didn't something evolve from a teleological standpoint rarely results in a satisfying answer. If constant fertility were advantageous, maybe it would be present.


Regulation of Glycolysis and other pathways at ‘irreversible’ reaction steps The hexokinase, phosphofructokinase and pyruvate kinase steps of glycolysis (1,3 and 10, below) are the only ones that are irreversible, and are also the steps where glycolysis is regulated.

Is it necessary for a regulatory step in glycolysis to be irreversible, and if so does this apply to metabolic pathways generally?

As far as glycolyis is concerned, the answer is straightforward. In certain cells and tissues there is a pathway working in the opposite direction — gluconeogenesis — in which the ‘irreversible’ steps of glycolysis are, in fact (and of necessity), reversed by a different enzymic reaction in which the position of the equilibrium is in the opposite direction.

Obviously if it is metabolically appropriate for glycolysis to occur it is inappropriate for gluconeogenesis to occur. The only way of turning e.g. glycolysis off while at the same time turning gluconeogenesis on is by regulating the activity of the different enzymes at these three steps.

Glycolysis is, therefore a special case in sharing many reactions with another pathway working in the reverse direction. What about pathways in which the interconversions only proceed in one direction. Classic examples are biosynthetic pathways that are regulated by what is known as ‘feedback’ or ‘end-product’ inhibition. An example (for which I happen to have my own diagram) is the synthesis of isoleucine from threonine in bacteria:

When the concentration of isoleucine increases to a certain amount (sufficient for the cell’s needs) this inhibits the enzyme threonine deaminase, preventing the wasteful conversion of threonine to isoleucine.

The main point is not the position of equilibrium of the threonine deaminase reaction (I haven’t checked it yet) but that it is the first unique step in the synthesis pathway. Hence regulating this step prevents the unnecessary removal of threonine in a way that does not allow the wasteful accumulation of intermediates.

Moral

There is an old party game in which you pass a pair of scissor to your neighbour saying “I pass you these scissors crossed” or “I pass you these scissors uncrossed”. The initiates then tell you whether you have performed the operation correctly. The uninitiated player assumes that what is important is whether the scissors are crossed. In fact, it is whether or not your legs are crossed. Beware of false associations.


Is collagen supplementation useless? When collagen is digested is it broken up into usable components that the body can use to produce its own collagen?

What evidence is there that supplementing with collagen type I & II etc.. can help connective tissue disorders?

What evidence is there that supplementing with collagen from animal products is not useful?

Regarding the use of collagen supplements to help prevent or treat a tendinopathy:
A rather inconclusive quote from a 2016  systematic review {1}:

glucosamine and chondroitin sulphate, vitamin C, hydrolazed type 1 collagen, arginine alpha-keto-glutarate, bromelain, curcumin, boswellic acid, and methil-sulfonil-methane were considered […]. preclinical results are very encouraging, however they are not fully confirmed by clinical studies. There are few clinical papers on the use of nutraceuticals in tendon disorders, and their methodological quality is poor. Furthermore, in most of the studies more than one supplement was administered at the same time. This may bias the results, and the effect of each single component cannot be determined. Furthermore, the interactions between nutraceuticals and drugs, or other dietary supplements (especially at high doses) has not been evaluated, neither their effects on chronic diseases. For these reasons, it is not possible to draw any definitive recommendations on the use of nutraceutical supplementation in tendinopathies.

References:

{1} Federico Fusini, Salvatore Bisicchia, Carlo Bottegoni, Antonio Gigante,3 Fabio Zanchini, and Alberto Busilacchi. Nutraceutical supplement in the management of tendinopathies: a systematic review. Muscles Ligaments Tendons J. 2016 Jan-Mar; 6(1): 48–57. Published online 2016 May 19. doi:  [10.11138/mltj/2016.6.1.048] PMCID: PMC4915461. PMID: 27331031. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4915461/


Has an artificial symbiotic relationship ever been created? Have 2 organisms ever been introduced to create a symbiotic relationship that doesn't occur in their natural environment?

Here are some examples:

symbiosis between genetic modified yeast cell populations (Shou W et al. 2007)
symbiosis between green algae and embryonic chick connective tissue (Buchsbaum R et al. 1934)
symbiosis between EcoBot II and microbial fuel cells (Ieropoulos, Ioannis, et al. 2005)


What is the relative power of GWAS studies in different species? I would like to know of any publication studying the relative power of GWAS studies in different species. For example, I've seen reports that say genotyping and GWAS in dog breeds is much more powerful than in humans due to the extent of linkage disequilibrium and other population genetics considerations. Some claims say that many GWAS studies in dogs are 10-20x more powerful than many GWAS studies in humans. I have also heard from pigeons (pigeon-omics) to be a similar case. I would like to know if there are other comparisons for other species and the relative power of discovery for GWAS studies compared to human. For example, are there any numbers for yeast, Drosophila sp., C.elegans, zebrafish and then also for plants like maize, rice, etc.?

Part of the increase in power to detect a genetic association via GWAS-genotyping comes from long haplotypes. Many dog breeds went through selective breeding bottlenecks 100-200 years ago. Many lab model organisms, such as flies, worms and plants, have recombinant inbred lines that aid in GWAS discovery as well. The price one pays for this increased power, say for canine GWAS, is not being able to pinpoint the casual variant. The association SNP(s) found may be far, far away from the gene responsible for the phenotype, because of that long LD.

Another aspect not to neglect is the phenotype. In humans, there may be a 3-fold range in phenotype p, while in dog that value is just 35% (1.35x). That may mean that the phenotype is difficult to measure (accurately) and to assign to a given allele with statistical certainty.

A third aspect to consider is the effect size of the association, say on a per (risk) allele basis.

Thus, while I am not aware of any papers specifically taking such elements as haplotype length, phenotype range and effect size into an analysis of GWAS power across species, I feel that one versed in genetics of the organism of choice can readily accomplish this for the specific trait(s) of interest.


Does severing the Corpus callosum, effect the brain's communicating ability? With serious epileptic seizures, a treatment is to sever the corpus callosum, which stops the seizures. However, does this affect the communicating ability between the two hemispheres? Or how does this affect the brain differently? What are the consequences in the brain?

Thank you in advance! (If I've got this all wrong, please let me know.)

Yes, it does; the corpus callosum is a major communication pathway between the hemispheres. Severing the corpus callosum is only done when seizures are severe enough to warrant it, and other options are ruled out for various reasons.

The condition of having a severed corpus callosum is often referred to as being a split-brain patient. There are some individual differences between patients, but hopefully searches using the keyword "split-brain" can help you find tons more information (summarizing it all here would give much too long of an answer).

One thing that is important to keep in mind is that although the corpus callosum is a very substantial connecting pathway between the hemispheres, it is not the only one, so the hemispheres are not completely severed. The cortex also communicates substantially with other brain structures that are not directly impacted by severing the corpus callosum.


Is there any evolutionary reason why male traits appear in the heterogametic sex and female traits in the homogametic sex? If you define male as the heterogametic sex, and female as the homogametic sex, then my question sounds like a tautology. But, what I'm trying to get at is why is it that the traits we associate with "males" (e.g. having an unlimited amount of possible offspring, greater average height, etc) appear in the heterogametic sex, and why traits that we associate with "females" (e.g. having a limited amount of possible offspring, shorter average height, etc) appear in the homogametic sex. Or, is it simply by chance that the homogametic sex became the female sex and the heterogametic sex the opposite?
As far as I understand it, heterogametic chromones allow for a greater chance of mutations being displayed, so I wonder whether there is something advantageous about this occurring in the male sex rather than the female sex. Perhaps it is because males are more "expendable" since they can have an unlimited number of offspring? Is this line of reasoning accurate, and are there any alternative explanations that go deeper than this?

The title question,

Is there any evolutionary reason why male traits appear in the heterogametic sex and female traits in the homogametic sex?,

suggests that male always is the heterogametic sex, but this is not true.  ("Male" is usually defined as the sex with the small, mobile gametes, i.e. sperm, as contrasted with the large, nutritive gametes, i.e. ova.) There are many species where females are the heterogametic sex, such as birds, most snakes, some fish, crustaceans, and insects.[a] These species use the "ZW" sex-determination system, which is essentially the inverse of the more familiar "XY" system.[a]  Other species don't have a heterogametic sex, but rather use lack of one chromosome as the determiner ("XO", "ZO"), and yet others use lack of one half of all chromosomes as the determiner ("haplodiploidy"). Others don't distinguish sexes by chromosomes, but use environmental stimuli.[b]
All this variety in forms of sex determination suggests that there are not substantial evolutionary advantages to having the heterogametic sex be the male.
[a] "ZW sex-determination system", Wikipedia.
[b] "Sex-determination system", Wikipedia.


Which is harder to contract - HIV or AIDS? I am working on mathematically modeling HIV and Tuberculosis Co-infection dynamics, and am working with 12 differential equations describing the behavior of all of the compartments and parameters.

Anyway, I just have one question:

Which is harder, in general: For a susceptible person to contract HIV, or a HIV+ person to contract AIDS?

Please pardon my ignorance.

Thanks.

Your question depends hugely on the factors at play.

The rate of transmission depends on the route of infection.  Wikipedia has a good breakdown showing the wide variability.  Are they getting a blood transfusion?  90%.  Mother-to-infant?  25%.  Male-to-female vaginal sex?  No higher than 0.3%.  Not to mention that the incidence varies massively between countries, as does the most common route of infection.
The rate of progression to AIDS also depends on a large number of factors including age, viral load, various genotypes, access to medical treatment, and, of course, long-term nonprogressor (LTNP) status.

The incidence of LTNPs is around 1 in 500, or 0.2%, which overlaps with but is at the low end of transmission rates for some routes of infection.


What are the differences between a benign tumor and swelling? What are the differences between a benign tumor and an injury related swelling?

And can swellings due to injury turn into a benign tumor?

The term tumor is used in the medical definition of inflammation. However it just denotes a temporary swelling that goes down once the inflammation subsides. This swelling is due to edema (accumulation of fluid). You have to understand that in practice no one uses the term tumor to denote an inflammatory swelling. So the term “tumor” denoting edematous swelling is of historical significance only.

In modern practice the term tumor is used only to indicate abnormal growth of any kind. Either benign or malignant.

In pathology an inflammation is classically described as having the following features:

Tumor : Swelling
Dolor : Pain
Calor : Warmth
Rubor : Redness


How did so many types of larvae become known as worms? How did it come to be that so many types of creatures typically known as worms are actually insect larvae? Silkworms are not actually worms at all, but larvae of a type of moth. Another example being the Maguey worm, which is supposedly the worm in some types of tequila and also not a worm, actually also a type of moth-larvae?
I find it curious that Wikipedia would have a creature with the word worm in its title, and then the first thing they tell you about it is that it is actually an insect. These are just the two examples I came across, there are probably more.

Excellent question. My zoology professor during biology undergrads explained this by clarifying that "worm" is a term that relates to one type of shape of animals. As such it does not carry any additional information on the relatedness of animals or their developmental stage.
This view also seems to align with wikipedia.


Efficacy of the 10-20 montage for EEG I am trying to better understand the relationship between the placement of EEG electrodes and the quality of the "brainwave" signals they produce.

There is the standard 10-20 system which has me wondering a few things:

Is the 10-20 system just a standard based on uniform distribution of the electrodes (so as to maximize brain signal collection)? Is it safe to assume one could increase the "density" of electrodes (again, in uniform distribution) and receive better quality signals? In other words, how does the placement & quantity of electrodes affect the quality of the information that can be obtain via EEG?
Is electrode gel strictly necessary? Is the gel used for adhesion, conductivity or both? I can't imagine it helps much with conductivity seeing the most of the scalp is (typically) covered with hair?

The placement in terms of location on the scalp determines what region of the brain is sampled. The electrode density determines how many locations are sampled. The spatial resolution of an EEG has been reported to be 7 mm (Im et al., 2006), meaning the variability in determined source and verified source (via fMRI in the study cited) is approximately 7 mm. Hence, increasing the density below 7 mm may not be too helpful. The 10-20 system utilizes an inter-electrode distance of 60 - 65 mm (American Clinical Neurophysiology, 2006), indicating it may make sense to use more electrodes when high resolution is needed. Note, however, that MRI and MEG have better spatial resolution than EEG and are methods of choice when you wish to do accurate source localization. EEG has excellent properties in the temporal domain, and a combination of MEG/EEG has great characteristics in both spatial and temporal domains.
Standardized EEG montages indeed promote uniformity so that different studies can be compared more efficiently.
Scrubbing with electrode paste primarily reduces impedance (increases conductivity). Hair and the skin don't conduct well and by applying a conductive paste impedances are substantially reduced. Mostly the technicians also scrape a little bit to ensure even better conductance by removing the fatty top layer of the skin. Also important is that differences in electrode impedances negatively impact recordings (American Clinical Neurophysiology, 2006). Impedance matching is hence necessary and using paste aids this purpose. So yes, conductive paste is essential.

Reference
- Im et al., J Neurosci Methods (2007); 161(1): 142–54


Is variation a result of Evolution? We know that the DNA copying mechanism that replicates DNA during cellular division is not 100% accurate and the resultant errors are the source of variation in the members of a population.

At the same time, we are also aware of the benefits of variation - how it is useful in ensuring the survival of a species over time and leading to evolution.

I would however like to know if 100% accurate DNA replication is possible (even if hypothetically) - because in my opinion, organisms can surely survive (atleast individually) without variation or evolution.

If it is so, is it possible that organisms with 100% accurate DNA replication did exist, but eventually their populations died out (due to natural selection) and we were left only with organisms that showed variation?

Putting in simpler terms, it is possible that evolution itself is the cause of variation that now causes further evolution?

There is previous research for that field of macroevolution.... Horse shoe crabs change slowly and tropical fish change fast.

You are right, it's not just random variation, it's fine tuned by DNA transcription processes which are too developed to be random, so the complexity of the processes leads scientists to think "WTF" regarding epigenetics, transgenerational phenotypic plasticity, paramutation, genetic drift, DNA mutation types, Specifically: "no systematic cross species studies of variation have been conducted (most focus on model organisms)", because the topic is so intense.

You don't have to change the DNA code of alleles to go from a chimpanzee to a human, most of the changes come from pre-existing genes that are varied to produce different results.

The texts for macroevolution fine-tuning of variability talk about: variability, gene flow, constriction, epigenetics, of traits of adaptive significance, of DNA mutations, their mathematical measurement... it can be summarized by this statement:

" variability has been a dilemma of evolutionary biology. Considering the pattern of increased genetic variation associated with environmental clines and heterogeneous environments, selection in heterogeneous environments has been proposed to facilitate the maintenance of genetic variation. No comprehensive models have been developed, likely due to the genetic and environmental complexity of this issue. " ref

Many books are devoted to the subject, so there is lots to read through, and there are mutation-control systems that fine tune variability, so it gets complex:

"... Epigenetic modifications, such as; DNA methylation, together with covalent modification of histones, are thought to alter chromatin density and accessibility of the DNA to cellular machinery, thereby modulating the transcriptional potential of the underlying DNA sequence" ref

There are genetic switches, which vary which DNA sequences are expressed by different species... Humans and chimps are 98% the same, and genetic switches can change the species selectively without having to change the DNA itself... "regulates when and where genes are turned on and off and how much protein they produce. The regulatory machinery works when proteins called transcription factors bind to specific short sequences of DNA that flank the gene, called transcription factor binding sites, and by doing so, switch genes on and off." ref

sharks ahve less less variability than humans and 1.5 times bigger genome...
"The researchers found that the white shark genome contained a lot of genes responsible for maintaining genetic stability — things like DNA-repair genes and tumor-suppressing genes. And when the researchers compared the white shark's stability genes with analogous genes in other vertebrates, they found small changes in the gene sequence that suggest a specific pattern of evolutionary adaptation for these genes in white sharks."

Only a few epigenetic processes for transgenerational epigenetic inheritance have been discovered, which vary species traits independently of the DNA sequence, so we don't even know how they compare between animal families.


What are the "minimum requirements" for a single cell? I saw a description of the "minimum requirements" for a cell at http://creation.com/origin-of-life in the section called "What are the minimum requirements for a cell to live?" and I'm wondering if this is scientifically accurate - and if not - what are the real requirements?

[note/warning - the link above is to a creationist site - I'm only quoting this source because I'm trying find the science involved and I didn't find other sources talking about all the necessary pieces. I'm not trying to promote creationism with this question so please don't attack the source or me for bringing it.  If you can find a non-creationist source which outlines these requirements, I'll be happy to update the question and remove this source.)

In summary it lists the requirements as follows:

cell membrane
way of storing information (DNA)
way of reading 2. to make components needed

RNA polymerase
gyrases to untwist DNA
ribosomes to make proteins
(a few others I omitted b/c I don't know if they're really important)

means of creating fuel (ATP synthase)
a means of copying the information for reproduction

The context of the question is similar to Can scientists create totally synthetic life? and a question I wrote What is the most complex biological organism (or precursors) that we have been able to synthesize from raw materials?.

I'm trying to understand what would be involved in making a cell from scratch. Somehow I found this source but I don't know if it's accurate.

So, to make cells from scratch you would need: amphiphilic molecules to form a membrane, a decent mix of simple molecules (sugars, nucleic acids, peptides) that serve as reactant and building blocks for more complex things, some simple catalyzer (metals, minerals, pepetides, aptamers, etc..) to run the reactions, enough energy to maintain lots of reactions running and keep them far from the equilibrium. Of course, lots of time...

An even more minimalistic approach would use a single molecule to do the enzymatic job while storing evolvable informations. In this case RNA alone has been proposed as substitute for proteins and DNA in a very minimal cell. In theory also DNA alone could do the same. However the minimal tasks needed to be done: maintain the self (to be compartimentalized), to grow (to have a flux of molecule not in equilibrium), to divide, to maintain the information stably enough to be useful for the next generation and at the same time prone too mutability to evolve.

One more point. Life itself doesn't strictly require to be compartmentalized.
You can think of a network of chemical reactions that have the ability to grow, to replicate its components etc but without a cell membrane. However I think that a cell-like form of life is somewhat more likely to happen.


Understanding conclusions that functional regions are under negative selection? I am reading in notes for a comparative annotation lecture that :

all DNA is subject to mutations
most functional regions are under negative selection (ie., mutations are often deleterious)

The conclusion was:

  that pieces of DNA with specific functions (especially genes) tend to be conserved against mutation more strongly than a DNA region with no specific function.

So if i understand it properly, since all DNA can accumulate mutations, the regions of genes that provide some fitness benefits avoid the negative selection of random mutations and are preserved (conserved?).

Also, the author placed in parentheses, (especially genes), therefore are there non coding regions that can provide benefits? Is he referring to "Selfish DNA" like Transposable elements that can have regulatory functions (or so i have heard).

Lets assume for simplicity that DNA is globally subjected to the same mutation rate (which is probably not a fully correct assumption).

Now let take a DNA region which is functional (what you meant by giving a fitness benefit), mutations in this region will occur as anywhere else in the genome. Some mutations will be deleterious and reduce the fitness of (or kill) the cell therefore, on the long run, cells that do not carry those deleterious mutations will propagate. This means that now if you look at the genome in the cell that propagated, certain genomic regions will contain less mutations than other because of the negative selection. They were "protected" against deleterious mutation.

Similarly, In multicellular organisms any mutations that reduces the fitness of the germline cells will be negatively selected (again functional regions will be more conserved).

The author was likely referring to regulatory regions. These are regions that do not encode proteins but are very important for gene regulations. Regulatory regions include enhancers, silencers, insulators and locus control regions (Maston GA, 2006). These regions will also be more conserved as deleterious mutations in regulatory elements could reduce the fitness of the cell/germline.


Identify this unusually-shaped, orange-colored fruit that grows in pairs? The photos below were taken on the island of Penghu in the Taiwan straight in October. This was in a public place and the small tree (about 3 meters tall, trunk perhaps 8 to 10 cm diameter) had probably been planted, so we can't presume it to be indigenous.

Each fruit was about 6 or 7 cm long, the skin was bright orange and seemed a bit waxy. The shape was a little bit like a banana-shaped American football in that it was divided into four quadrants. They attach to a stem in pairs and extend horizontally (sideways) rather than hang down.

Question: What could this gravity defying fruit-bearing tree be?

The first image is cropped, zoomed and sharpened in order to highlight textures.

The seed pods reminded me of the Apocynaceae, so I searched for "apocynaceae china" and found this University of Hawaii page where it is identified as Stemmadenia litoralis.  However, a little more looking it seems Tabernaemontana litoralis may be the preferred name.  There is some debate here.  This book may hold the final answer regarding the genus.

Your picture of the fruit is one of the best one I could find on the internet. There is another good one here with other pictures of the plant.

You were also correct that as a planted tree it might not be native.  This plant comes from Central America.


Why do two different E. coli reference genomes have different lengths? I've downloaded two different reference genome of E. coli (E. coli K-12 MG1655: U00096.1 and E. coli K-12 MG1655: U00096.2) and they have different lengths. I searched for the meaning of reference genome numbers in detail but I couldn't find anything that help me with my question: Why do two different E. coli reference genomes have different lengths?

U00096.2 is an updated version of U00096.1; you should preferably use the former for your analysis. In fact, even U00096.2 has been updated. The latest version is U00096.3. In general, the number after the dot (period) in NCBI accession numbers, denotes the version.

From NCBI:

  VERSION is made of the accession number of the database record
  followed by a dot and a version number (and is therefore sometimes
  referred to as the "accession.version")


What were the symptoms of Phineas Gage after suffering his brain injury? Phineas Gage was a construction worker who suffered a head injury due to an explosion at a construction site. A metal rod was pushed up his cheek and through his head.

I have heard he demonstrated six symptoms after the accident. What were they?

I have researched this for a while but all I can find is that he was very inappropriate in social situations.

Gage suffered a massive injury to the frontal cortex due to his accident in 1848 (Fig.1). Recent work using computer assisted tomography (CAT) has shown that contrary to popular belief, the injury was probably not bilateral, but confined to the left-lateral frontal lobe (Ratiu et al, 2004).

Fig.1. Original drawing of the wound sustained by Gage (left). Source: Harlow (1869) and the reconstructed injury using modern CAT scanning techniques on the original tamper and Gage's skull (right). Source: Ratiu et al., (2004).

The question of OP is not very particulate about the nature of symptoms (physical or psychological symptoms), or about the time window of interest after the accident (acute or chronic symptoms). I assume that OP is asking about the behavioral changes of the subject after he was physically fully recovered. The following is a formatted quote from the original publication written by his treating physician (Harlow, 1869) describing the subject's behavior approximately 6 months after the incident:

  His physical health is good [...], but says [he] has a queer feeling [in the head] which he is not able to describe. [...] His contractors, who regarded
  him as the most efficient and capable foreman in their employ previous
  to his injury, considered the change in his mind so marked that they
  could not give him his place again. The [...] balance [...] between his intellectual faculties and animal propensities, seems to have been destroyed. He is fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operation, which are no sooner arranged than they are abandoned in turn for others appearing more feasible. A child in his intellectual capacity and manifestations, he has the animal passions of a strong man. Previous to his injury, though untrained in the schools, he possessed a well-balanced mind, and was looked upon by those who knew him as a shrewd, smart business man, very energetic and persistent in executing all his plans of operation. In this regard his mind was radically changed, so decidedly that his friends and
  acquaintances said he was "no longer Gage."

The symptoms of Gage indeed match the current understanding of the functions of the frontal lobes. The frontal lobes are thought to be involved in a multitude of cognitive processes, such as executive function, attention, memory, and language, affect, mood, personality, self-awareness, as well as social and moral reasoning (Chayer & Freedman, 2001).

References
- Chayer & Freedman, Curr Neurol Neurosci Reports (2001); 1(6): 547-52
- Harlow, Bulletin of the Massachusetts Medical Society (1869) and see wiki page
- Ratiu et al., J Neurotrauma (2004); 21(5): 637-43


Do different emotions produce different tears? Do tears of joy, laugh, grieve, and others contain different things or are they all the same?

Basal tears

  are always in our eyes to serve the purpose of lubricating, nourishing, and protecting the eyes.

Reflex tears

  protect the eyes from irritants, including wind, smoke, or onions.

Tears produced by emotion

  Although these tears contain higher levels of stress, such as ACTH and enkephalin, and endorphin and natural pain killer, they can also work by directly calming the iris down while signaling the emotional state to others.

Secretion of tears

  The lacrimal gland, located in the outer part of the upper eye, is constantly secreting a protein-rich, antibacterial liquid. This fluid goes from the outer edge of the eyeball toward the cornea and lubricates the entire eye surface every time we blink.

Sources:

http://archopht.jamanetwork.com/article.aspx?articleid=625096
http://www.sciencedirect.com/science/article/pii/0002939481906516


Will you stop sweating if you exercise in a cold enough room? It's common knowledge that you will sweat from being in a very warm room. And you will also sweat from exercise, presumably because it raises your body temperature.

But if you exercise in a cold enough room, which magically adjusts its temperature to counteract your body temperature, will you then not sweat at all? And is it therefore possible to exercise without sweating... And not even have to take a shower afterwards?

Apparently you can sweat even in a cold enough room, without even doing exercise! The main causes of sweating include, among exercise and high body temperature, stress and anxiety. This condition is called cold sweating. See this article:

  The body normally produces sweat as a way to help keep cool. Sweating normally occurs with exertion such as when exercising or in high temperatures. However, there are other reasons for sweating. Sweating can be triggered by fear or anxiety, and this is often referred to as a cold sweat. It comes on suddenly and results in cool, damp skin. It is the body's reaction to stress as part of the "fight or flight" response that helps us to react in a dangerous situation.

So, even if you just think about doing heavy exercise, you might get sweat in hands or feet.

But cold sweating is not the only cause. It may also be caused by a more severe condition known as hyperhidrosis. See this article:

  Normally, your sweat glands produce perspiration that’s carried to the skin’s surface when the air temperature rises, you develop a fever, you’re exercising, or you’re feeling anxious, nervous, or under stress. When those factors are no longer an issue, the nerves that signal sweating are put on hold. For the 2% to 3% of the population who have hyperhidrosis, however, the sweat glands don't shut off. They sweat even when the circumstances don’t call for it: when they’re in air conditioning, or while they’re sitting and watching television. Some people even tell their doctors that they sweat in a swimming pool.

So, one might start sweating even in a cold enough room, if not because of body heat, then because of anxiety, hormones or medical conditions. Also, this condition does not work the way you are speculating. When the surrounding environment is very cold, the body prefers to shut off blood supply to skin than to cool it down through skin i.e. sensing cold environment, the body shuts off blood supply to skin and diverts it to core of the body. This is what causes more urination in cold environment and is called cold diuresis. Have a look at this answer for more information on this point.


Does the cellular response to every receptor work the same way? I heard somewhere that activating any receptor results in the same intracellular response (signaling) which involves NF-κB. If that is true, I hardly understand how the cells distinguish between different types of stimulis coming from different types of receptors. I guess I am missing the point... :S

Figure 1 - signal transduction - source

If you check this picture about signal transduction. What you can see that there are about 10 arrows pointing to the inside of the nucleus, and there are about 10 receptor categories involved. Afaik. there are much more genes in the nucleus, so how is it possible to regulate the expression of so many genes with only a few signaling pathways?

It's a complicated answer. More than 200 cell types, each type of cell inherits a unique expression of receptors, internal and external. Diffusion of signals through the plasma membrane and/or nuclear compartment may act directly as cofactors, activators, etc. The specific sequestration, and pattern of expression of external receptors also influence what signals become bound and relayed. The cell will also have a motif of internal/cytoplasmic/nuclear proteins expressed that complex or become directly activated by interaction with any of the above, etc. So the currently expressed set of internal, and external proteins determine not only how the cell interprets the signal, but also how they respond.

As for the actual genetic material, you'll find inherited motifs like DNA methylation, histone acetylation patterns etc. influence what parts of the DNA can actually be accessed. Per the above schema of signaling pathways, the signals received by each individual cell differ based on the actual cell type. In any case there are patterns of activators/repressors, enhancers/silencers that are switched on or off by these signals. Some journals are also introducing evidence insoluble receptors like EGFR+ligand can actually internalize and translocate to the nucleus and act as transcription regulators.

The final note, is that due to alternative splicing and transcription of proteins that promote or repress splicing sites, in a combination with the above concepts a cell can regulate for thousands of genes. This is a very general answer, however. The concept to take home, though, is that differentiated cells have their own specific motifs they express that make "reading" different signals possible, and also makes differing responses to what could be the same signal possible. These motifs also allow for the accurate expression of the relevant portions of the genome (not all genes are expressed at all times in all cells).


If DNA methylation inactivates genes, does DNA demethylation activate them? DNA demethylation can be passive or active. The passive process takes place in the absence of methylation of newly synthesized DNA strands by DNMT1 during several replication rounds – for example, upon 5-azacytidine treatment [23]. These pharmaceutical demethylating agents act via inhibition of DNMT1 and favoring its degradation by proteosomes [24]. This approach is currently used in cancer to demethylate tumor suppressor genes [25].

If we’re demethylating a tumour suppressor gene for cancer curing doesn’t this mean that we’re activating it (to stop the tumours)? I can’t seem to understand the function of DNA demethylation. I came across it when reading about genomic imprinting and haven’t been able to wrap my head around it. Please help.

Here is a series of articles explaining DNA Demethylation from Sience Direct.

In the most broadest of senses, DNA methylation adds methyl groups to DNA preventing the transcription complex from forming and transcribing the gene into mRNA. By demethylating the DNA, it allows the transcription complex to form and mRNA to be transcribed for translation.

When it comes to cancer, Most of the tumor suppressor genes are down regulated to allow for genes like stat3 to be upregulated. Ideally, by removing the suppression of these genes, they can reduce the levels of oncogenes and slow the growth of the cancer.

Think of it like this A -| B. Cancer decreases A so B can increase in expression A↓ -| B↑. By demethylating A, we  A↑ -| B↓.


Measuring depolarizations over the membrane Measuring the rest potential of a membrane is relatively easy and straight forward: put one electrode inside the neuron, the other one (the "counter electrode") outside the neuron.

Because everything is at equilibrium (steady state), it's not important where exactly inside the neuron you place the first electrode, and even less important where outside the neuron you place the counter electrode: in the extracellular fluid next to the neuron or inside a container filled with extracellular fluid placed anywhere. One may even connect the other electrode to the ground (a lightning rod), if one does it consistently (over all measurements).

But now consider you want to measure the spread of depolarization along the membrane by measuring the membrane potential at two different locations of the membrane: You place one electrode underneath the membrane at point $p_1$ (and its counter electrode to the ground). And you place another electrode underneath the membrane at point $p_2$ (and its counter electrode to the ground).

Now it seems possibly important where exactly inside the neuron you place the two electrodes: the distance from the membrane might make a significant difference. (But maybe not.)

What probably would make a significant difference: Since the ionic compositions of the extracellular fluid in the vicinity of $p_1$ and $p_2$ will differ, it might be important to connect the counter electrodes not to the ground (or to some volume of normal extracellular fluid) but to corresponding points $p_1'$, $p_2'$ directly opposite to $p_1$, $p_2$ on the other side of the membrane.

I emphasized might be important because in practice it may be not important. That's what my question is for:

  Is it OK, even for the measurement of the dynamics of depolarizations,
  to connect the counter electrodes to the ground (if only
  consistently). What would be the difference in the measured voltages,
  and can these be determinstically be cancelled out?

It is extremely important where you put your electrode when measuring such delicate structures as dendrites (which is when you want to compare voltage changes between two parts of a neuron). That is why you put your electrode inside the dendrite. Each recording electrode has its own ground that goes inside the bath, i.e. outside the neural tissue. Alternatively, you can observe fluorescence changes of a calcium or voltage dependent indicator that you have introduced inside them.

https://www.janelia.org/sites/default/files/Labs/Spruston%20Lab/Stuart_Spruston_2015.pdf


Does GC content determine codon bias or does codon bias determine GC content I was wondering if someone knows the answer to this quenstion, because I can't find a clear answer, maybe there isn't a clear answer :).

question
Which of these two is right? or maybe both influence each other

GC% determines codon bias
codon bias determines GC%

Thankyou,

Think about it this way, the G-C content is averaged over the entire genome, and varies between different species.  Whether you are dealing with prokaryotes, with relatively compact genomes, or with eukaryotes, with lots of non-coding regions, the open reading frames will, in general, be influenced by the average G-C content across the genome. Therefore we would predict that in species with lower G-C their open reading frames would be biased to using the codons in the genetic code that are higher in A-T. N.B. this also means that their tRNAs should also favour anticodons higher in A-T. In contrast, we would predict that in species with high G-C content, the open reading frames would be biased, in general, to using codons that are higher in G-C.
That is all G-C bias in codons is; for some amino acids like Met and Trp, there is only a single codon, but for other amino acids there can be up to six codons that can each encode the same amino acid side chain. It is in these ones with a higher number of degenerate codons that you are going to see the effect of codon bias.


Pedigree analysis : autosomal or mitochondrial I have tried a to decide if this is a autosomal dominant, recessive or a mitochondrial disorder.

Is it possible to know for sure, or do you have to use probability?

(English is not my native language)

No other pedigrees have had carriers marked so I did not expect this one had it either.

Auto dominant.

I:1 aa I:2 A-
II:1 aA II:2 aa II:3 aa II:4 aA
II:1 children could have got a from him and a from her the the disorder would be gone.
III:9 children got her dominant A

Recessive
I:1 A- I:2 aa
II:1 aa II:2 A- II:3 A- II:4 aa

Mitochondrial disorder
I read "transmission only accours through females"

Mitochondrial because all the offsprings have the same trait as that of the female parent. Lets go through the possibilities one at a time. Assuming you have no carriers (you do not have any carrier symbols) we can work out the following.

Autosomal Recessive?

This might be the case if we assume the male in the first generation is a carrier.

Autosomal Dominant?

This might be the case but it is unlikely. Looking at the first generation possibly yes, as 50% of offspring have the trait. Looking at the second generation however only 3 out of 9 offspring have the trait. Making autosomal dominant unlikely (but it is still a possibility.)

In the test, if you have to go with one option, mitochondrial inheritance is the best because there are no assumptions at all but if multiple options may be correct, you can have any of them.


How to find the age of a memory stored in the brain? Is there any way to find how old one's memory is?

One can find the age of stones, plants, animals, etc. So why not find the age of a memory stored inside one's brain?

We are only barely beginning to understand how the brain works, including memory. We do know that it is a very complex thing. There are many different kinds of memory; many different processes are involved in creating and recalling memories. One factor that plays into a naïve concept of "how old a memory is" is that "remembering" does not seem to be a passive activity; instead, every time we remember a memory we re-create it.

Having said that I don't see a theoretical reason why there wouldn't be a way to determine the age of a memory... but we currently don't know it.

Consider that we don't magically know the ages of stones, plants, or animals. We learned to figure it out from studying those things, seeing how they change over time, and deducing ways to use that knowledge to guess their age. For example, people discovered that in many climates trees alternate a growing season and a dormant season, and this results in the trunk having "tree rings" for each year they've lived. They've also seen that animals have specific life cycles and look different (if only in size) depending on their ages, and they can use that to roughly estimate an animal's age. Obviously this depends completely on the animal in question; different animals grow in different ways and we can tell their ages in correspondingly different ways, and not always to great precision.

For most of human history we were completely unable to tell the age of stones. Only the discovery of radioactivity, and that the atoms inside stones transmute into other elements over the millennia and that this allows us to tell how long it has been since the stone crystallized (i.e. the atoms got stuck where they are), enabled radiometric dating.

Similarly with memory, it is completely plausible that once we understand very well what a memory is, what its exact correlates in the brain are, and how those correlates change over time, it will be possible to tell how old a memory is. But we aren't there yet (see some articles at the end for where we are).

And while it's plausible that we'll be able to know the age of a memory once we understand it well enough, it is by no means inevitable. To give a counter-example, there is absolutely no way to tell the age of, say, a water molecule. We understand water molecules extremely well. They form and can be destroyed, so for every water molecule there is a certain amount of time since it formed, i.e. it has an age. But a water molecule is just an oxygen atom linked to two hydrogen atoms; its properties are dictated by chemistry and don't depend on how long it has existed. There is no way to tell the age of a given water molecule just from looking at it. Similarly, computers give a timestamp to a file when they create it, but if they didn't do that I don't think we could tell how long a file had been on the disk just from examining the disk itself. So it is certainly theoretically possible that once we understand how memory works, we'll find that we can't, in fact, know the age of a memory.

Here are some papers on memory to give an idea of what neurobiologists are looking at these days:

The Regulation of Transcription in Memory Consolidation
http://cshperspectives.cshlp.org/content/7/1/a021741.short
This paper looks at the role of DNA transcription in the consolidation of long-term memory (as such consolidation apparently requires new proteins being created)

Structural Components of Synaptic Plasticity and Memory Consolidation
http://cshperspectives.cshlp.org/content/7/7/a021758.short
This paper (more or less the same authors) looks at the structural factors involved in consolidating memories by strenghtening synapses and creating new ones.

The many faces of working memory and short-term storage
https://link.springer.com/article/10.3758/s13423-016-1191-6
This recent (2017) paper discusses "Working memory" and how the field doesn't have a single, coherent definition of that concept yet.

Functional neuroimaging studies of encoding, priming, and explicit memory retrieval
http://www.pnas.org/content/95/3/891.short
This 1998 imaging study looks at what regions of the brain light up in various memory-related tasks, and suggests such imaging studies can be useful to investigate brain function. They were right, but notice how general the areas they see are, and how they only can guess at what might be going on there.

The Molecular Biology of Memory Storage:
A Dialog Between Genes and Synapses
http://teachline.ls.huji.ac.il/72336/sphira/Kandelnobellecture.pdf
This is a very long lecture from 2000 from one of the authors of the above papers, summarizing their life's research on the molecular and synapse-level mechanisms of memory. These paragraphs give a historical overview of how scientists have thought memory works:

  In his Croonian Lecture to the Royal Society of 1894, Santiago Ramo´n y Cajal
  proposed a theory of memory storage: memory is stored in the growth of new connections[16]. This prescient idea was neglected in good part for half a century as students of learning fought over newer competing ideas. First, Karl Lashley, Ross Adey, Wolfgang Köhler, and a number of Gestalt psychologists proposed that learning leads to changes in electric fields or chemical gradients, which they postulated surround neuronal populations and are produced by the aggregate activity of cells recruited by the learning process. Second, Alexander Forbes and Lorente de No proposed that memory is stored dynamically by a self-reexciting chain of neurons. This idea was later championed by Donald Hebb as a mechanism for short-term memory. Finally, Holger Hyden proposed that learning led to changes in the base composition of DNA or RNA. Even though there was much discussion about the merits of each of these ideas, there was no direct evidence to support any of them [reviewed in 17].

  We were now in a position to address these alternative ideas by confronting
  directly the question of how learning can occur in a circuit with fixed neuronal
  elements. Kupfermann, Castellucci, Carew, Hawkins, and I examined the neural
  circuit of the gill-withdrawal reflex while the animal underwent sensitization or habituation, a form of learning in which the animal learns to ignore an innocuous stimulus to siphon when given with monotonous repetition. (We later also extended these studies to an examination of classical conditioning [20].) Our studies provided clear evidence for Cajal’s idea: learning results from changes in the strength of the synaptic connections between precisely interconnected cells [6, 7]. Thus, while the organism’s developmental program assures that the connections between cells are invariant, it does not specify their precise strength. Rather, experience alters the strength and effectiveness of these pre-existing chemical connections. Seen in the perspective of these three forms of learning, synaptic plasticity emerged as a fundamental mechanism for information storage by the nervous system, a mechanism that is built into the very molecular architecture of chemical synapses [95]

Notice how twenty years ago, this person was saying we can finally begin to answer century-old questions of what form memory storage takes in the brain to begin with.

A Putative Biochemical Engram of Long-Term Memory
https://www.sciencedirect.com/science/article/pii/S0960982216311393
Exciting 2016 article: they've maybe found one place where one memory might be stored! First line of the abstract:

  How a transient experience creates an enduring yet dynamic memory remains an unresolved issue in studies of memory.

Same idea in the first line of the abstract of this 2016 article on associative memory:

Neural ensemble dynamics underlying a long-term associative memory
https://www.nature.com/articles/nature21682

  The brain’s ability to associate different stimuli is vital for long-term memory, but how neural ensembles encode associative memories is unknown.


Help with identifying creature found in brazilian beach I don't know if this is the correct place, but I've been looking for someone
that could help me identify this creature I found while I was looking for shells. There are three mollusk-like "beings" stuck in some sort of big seed (it's definitely not a rock nor a part of their body). They
 can "spin" around with the arm that is stuck in the seed, and they continuously take some blood red hair-like tentacles in and out of a shell.
I shot a video of it,  the link is right below. Please ignore all background audio, I couldn't find somewhere without people.
This "being" was found today, at roughly 6pm, washed ashore in the beach I'm visiting - "Praia Grande" in Brazil.
Another peculiar thing is that tap water makes the "things" close for a while, and sea water doesn't do much. Also, as they dried, the single tentacle hair became multiple smaller ones. They keep coming in and out, without stop.

If anyone could give me a shine on what that animal is, it would be super helpful!

https://drive.google.com/file/d/1-rSk-WVb6pkS98Npp1VF3Aq8xxXPKiuc/view?usp=drivesdk

Those are gooseneck barnacles possibly pelagic gooseneck barnacles (Lepas_anatifera).

For comparison:

A beautiful picture and description can be seen here.


Which types of hydrogen bonds are known to exist in RNA secondary structures? I'm programming an implementation of an algorithm for pattern matching in RNA structures.
The algorithm assumes the following types of base pairs:

Plain: No base pairs (just the primary structure of the RNA)
Single: Each base can be connected to at most one other base
Multiple: Each base can be maximally connected to a number of other bases (where 'number' can be constant or infinite)

Although there is no problem with the implementation of the above types of base pairs (apart from the probable high computation complexity), I wonder if all of them were observed in real RNAs?

In particular, I'm interested in the following cases:

A base pair between two adjacent bases i,j.
One base (i) which connected to two different bases (j,k) (i is not adjacent to j or/and k).
One base (i) which connected to more than two different bases, all of them not adjacent to i.

Can these exist? Some of them?
If they can, how common is their existence?

By far the most common type of base pair is the Watson-Crick base pair in an RNA helix. Those are comparably easy to predict, e.g. Mfold and the Vienna RNA package can do this.

Base triples, three nucleobases that form hydrogen bonds to each other are not uncommon in RNAs with a complex tertiary structure. There is even a database of RNA triples, though this one also contains triples where not all three bases make contact with each other.

There are also quadruplexes, but there each base only makes contact with two other bases. I don't know if there are any structures where one base makes contact with more than two other ones.


Is it true that viruses cannot be seen with phase-contrast microscopy? There appears to be a lot of material on the internet claiming that viruses can be only seen with electron microscopes, and not with light microscopes. To the contrary, for example this old paper published in Nature states that viruses can be seen using phase-contrast (light) microscopy. Who's correct? What is the smallest thing I can see using a phase-contrast microscope?

It is true for most viruses. They have a size of roughly 1/100 of bacteria (or smaller), so they are too small to be seen in light microscopy. According to Wikipedia the maximum limit with light microscopy is around 1500x magnification (or making structures, which are at least around 200nm in size visible).

A lot of viruses are smaller, for example the influenza A virus is around 80-120nm, the HIV virus around 120nm and the rhinovirus which causes the common cold around 30nm. They would only be visible in electon microscopy. The measles virus on the other hand has between 350 and 400nm and should be visible in light microscopy. However, since you are very close to the region where you reach the diffraction limit for visible light, it is usually not used very much.


Parents that eat their own children I am told that there are some species, like fish or rabbits, that if let, will eat their own children. If this is true, how does a species like this exist? Shouldn't the fact that they kill their own lineage make them nonviable?

Yes, it is true.

Prairie dogs

Prairie dogs for example are known for frequent infanticides.

Many other species kill their babies too

But of course, such behaviour also exists in other lineages such as grey langurs, gerbilles, lions, giant water bugs and Bottlenose dolphins (just to cite a few examples).

How does that evolve

It will be impossible to provide a complete universal explanation to this behaviour because the evolutionary processes causing this behaviour varies from lineage to lineage. For examples, in lions, only males kill young of the females that are still nursing and they do so when taking over a new harem only. In prairie dogs, mothers cause infanticide preferentially on others' babies but also on their own babies.

Going into the details of how such behaviour evolves in every specific lineage would probably require writing an intro on kin selection and other fields of evolutionary biology which is way too much for a single post. You may want to have a look at the wikipedia article infanticide for a start.

  Shouldn't the fact that they kill their own lineage make them nonviable?

Of course, they don't kill all the babies. Only a fraction of them!


When is Pheophytin used in electron transfer to the q cycle in plants? If I understand it correctly:
(short version)
The Q cycle starts with PQH2 it removes the 2H(+) and gives one electron to Plastocyanin and the other to a stored Plastoquinone to charge it to Plastoquinone (-). This process is repeated and adds the electron to the stored Plastoquinone(-) to create a Plastoquinone (-2). This then gets 2H(+) to form PQH2. And the cycle begins anew.

But in a lot of pictures is shown that the excited P680 gives the electron to Pheophytin and that gives it to the Q cycle.

Please let me know when and where the Pheophytin interacts to give the electron.

Not sure if there is a definite answer. However, from structural studies, its proposed that essentially the Chlorophyll a and pheophytin(Pheo) are positioned ~10A away, and the transfer of a radical electron from the P680 center to Pheophytin does occur. The exact mechanism is possibly mediated by a tyrosine

Durant J.R et al (1995). Proceedings of the National Academy of Sciences of the United States of America, 92, 4798–4802
Oleg Victorovich (2006). Retrived:5/25/16. Site: http://samlib.ru/o/oleg_w_m/cdocumentsandsettingsolegmoidokumentythefunctionandthestructureofporphyrinmoleculesrtf.shtml

3.Zouni A et al (2001). Nature, 409, 739-743


Can a gene be inactivated using CRISPR if it is not in the interspace of short palindromic repeats? I have recently studied how CRISPR works but there is something that I do not understand at all. I have heard a lot of people claiming that with this method it is possible to modify any genome by inactivating, activating, removing or adding genes. However, as far as I have understood, DNA regions can only be modified if they are in the interspaces of short palindromic repeats. So, my question is whether a gene that is not in the interspace of short palindromic repeats can be modified or removed? And if it is possible to do so, how?

When people talk about genome editing with CRISPR, they are really talking about using CRISPR associated nucleases like Cas9 and Cpf1. These nucleases are useful since their sequence specificity is determined by a guide RNA and they can therefore be used to cut at specific sites in the genome. This actually has nothing to do with the repeats themselves.

See this answer for a brief overview of how genome editing with Cas9 works.


How can one relate in vitro studies of caffeine (dose expressed as concentration) to dietary intake of caffeine (dose in mass)? Having difficulty making the data in the below charts to apply to daily life. What is the right interpretation and implementation? How are the “in vitro” results of the below charts relevant to levels that cells would experience "in vivo" after the consumption of caffeinated beverages?

Link to the medical research article which the two above charts were taken from

In the mentioned study, they tried to support the evidence from earlier studies in which caffeine consumption was associated with skin aging and slow wound healing:

  Our research confirms our earlier observations that caffeine may have
  an adverse effect on the wound healing process, as well as on the
  aging process, of the human skin.

...and by "earlier observations" they mean another in vitro study.

In the study, they used 1, 2 and 5 mM caffeine solutions. 1 cup (~250 mL) of brewed tea can contain 95-165 mg caffeine (source), which makes it 2-3.4 mM, so much like the solutions used in the study. When you drink 1 cup of coffee (let's say, 2 mM caffeine solution), the caffeine, which is water- and lipid-soluble (StatPearls), will be dissolved in the body water and fat, which can together make ~50 kg in a 70 kg person. So, you would need to drink ~200 cups of coffee (~20 g caffeine) in ~2 hours (caffeine half-life is ~5 hours - source) to achieve 2 mM caffeine solution in the skin cells.

I haven't found any actual human clinical trial in which caffeine consumption would be associated with adverse effects on the skin. In a recent review: Coffee consumption and health: umbrella review of meta-analyses of multiple health outcomes (BMJ, 2017), they don't even mention skin or wound healing and regular drinking of 3-4 cups of coffee per day was not associated with an increased risk of various health conditions (except in pregnancy).


How many diseases can be linked to disruption in the microbiome of a human? I was listing to the radio and heard recent research found a link between children and higher cases of asthma when certain bacteria are missing from the microbiome. How many other diseases can be linked to a disrupted microbiome and are there ways in repopulating missing bacteria?

It is an open question and an active area of research. You will not be able to get a definitive answer to your question of number, as each new discovery will add to the total.

As for repopulating, we have not even determined all of the strains of microbes that populate us, many are very difficult to culture in vitro, and we do not know of all the functions for each species, so we do not have a clear picture of which need to be there, which don't, and whether or not some species work together to provide us with a benefit. For certain conditions such as Irritable Bowel Syndrome, one of the treatments that has been tried is fecal transplant.

Do a literature search for recent reviews. Nature Reviews tend to do detailed reviews, especially on topics as in the news as the Human Microbiome. That is probably the best first place to start. Then you can start to drill down into the reference papers that are cited in the review. That will generally give you a good state of play in the field.


Why are human bones usually curved? Is there any simple explanation as to why human bones are more curved than straight and are thicker at ends and thinner in the middle?

The slight curve allows bone to absorb shocks better.

This curve allows the bone to act like a spring and flex a little bit. One issue as bone get older is that they become harder and, therefore, more brittle which leads to the elderly breaking bones for a fall that younger individuals just get a bruise. Young children often get stick or "splitting" breaks where the bone does not break but separates as the bone is still soft.

The ends tend to be thicker as that is where the joints are and there are forces that need to be absorbed.

Of course, if the load applied to the bone is just too much or it is a sharp shock then bones will break, but really the skeleton is nature's design for a suspension system to allow us to do what we need to do walk, run, stand, etc

This set of slides makes good reading, with things like "less ductile", "elastic behaviour" and "strength in compression" worth looking for:

Mechanics of bones by Phillipe GILLET

A quick search gave many results but of these two shown the first seems very interesting from an engineer's perspective:

shock absorbing "goo"
shock absorbtion


How much is local blood non-Newtonian in Pathophysiology? I am studying the Barus effect / Merrington effect / die swell / extrudate swell, which is a characteristic of non-Newtonian viscoelastic liquids (Introduction to the phenomenon in this video) i.e. the medium responds to the stress $\sigma$ of irritator with a strain $\epsilon (= \Delta l/l)$ that increases until the medium ultimately fails in a local pathology

blood has both viscous and elastic components which it can apply in pathophysiological condition
\begin{equation}
\gamma = \gamma_{v} + \gamma_{e}.
\end{equation}

#1 Maxwell material model

total shear stress if blood behaves like Maxwell material in local pathophysiological regions
\begin{equation}
\sigma = \sigma_{v} = \sigma_{E} = \eta \frac{d \gamma_{v}}{d t} = G_{M} \gamma_{E},
\end{equation}
implying $\sigma = \eta \, d\gamma_{v}/dt$ and $\sigma = G_{M} \gamma_{E}$.

I am thinking when blood is not non-Newtonian etc in muscular pathologies and muscular infections. I want to evaluate how much blood is non-Newtonian in particular situations.
I am interested in muscles and their supply with necessities.

How much is local blood non-Newtonian pathophysiologically?

According to this conference proceeding blood is very nearly newtonian at normal shear rates. More accurately blood is very thick and a shear-thinning fluid, but the shear-thinning effects don't scale with a power law like other non-Newtonian fluids.

In terms of blood changing viscosities, I suspect that in living patients blood viscosity is quite constrained, not only by physiological feedback but by the fact that if the blood viscosity changed very much the patient would become nonliving. Blood circulates constantly, and when it stops circulating it coagulates(which complicates efforts to measure its viscosity, I imagine). Any local effects on blood viscosity would be 'washed away' by the fresh blood arriving every heartbeat. If there's no or very limited blood circulating to the muscular pathology you're interested in the blood viscosity is probably not as significant as the ischemic tissue death that's just about to happen.


Weird gelatinous substance in highland bog I recently went walking in the highlands in Snowdonia, Wales and we came across this:

Can anyone explain what it is? My guess was some kind of fungus but I'm not positive. The ground was very water logged and boggy.

It looked a lot like frog spawn, but it's autumn here and we wouldn't see frog spawn until Spring. There appeared to be no animals living inside or around it.

It's often called star jelly and there's a whole wikipedia article on Star Jelly talking about it:

  “Star jelly” (also called astromyxin, astral jelly, pwdr sêr, star
  rot, or star shot) is a gelatinous substance sometimes found on grass
  or even on branches of trees.1 According to folklore, it is
  deposited on the earth during meteor showers. Star jelly is described
  as a translucent or grayish-white gelatin that tends to evaporate
  shortly after having “fallen.” Explanations have ranged from the
  material's being the remains of frogs, toads, or worms, to the
  byproducts of cyanobacteria, to the paranormal.[2][3][4][5] Reports of
  the substance date back to the 14th century and have continued to the
  present day.

So the One show did a magazine piece on this the other day; a scientist did some DNA analysis of some of it.

The conclusion was that it's frog jelly (full of frog DNA). Apparently frogs have glands full of the components of the jelly in sacks in their bodies, when the sacks come into contact with moisture it expands massively (same process that allow them to produce frog spawn). When a frog is eaten (by a bird or fox) the jelly expands on contact with any moisture. The animal eating the frog either vomits it up or doesn't eat it in the first place and voila.


How much does the Hayflick limit/telomere length vary across taxa and within humans? Since they seem to be quite connected, I'm curious if anyone knows of research comparing the Hayflick limit (and presumably by extension telomere length) between different taxa. I've heard the Hayflick limit numbers 40-50 thrown out repeatedly for humans (probably relating to the WI-38 tissue line), but how universal is this really? I Know there are particularly long lived species, but has research been done to correlate this with telomeric length, or do they simply have slower cell division?
I suppose it is worth mentioning that a Hayflick limit of 40 rounds of division is massively different from 50, since each round of division conceivably could double the number of cells...

Many studies, including those of Hayflick himself, have found a strong correlation between a species' Hayflick limit and its maximum lifespan. For example, Galapagos tortoises, which can live over a century, have a Hayflick limit of 90-125, and mice, which live only a few years, have a Hayflick limit of 14-28.

However, the mechanism connecting the maximum number of cell divisions and maximum lifespan is not entirely clear. Cell division is associated much more with growth and development than with the maintenance of mature tissues. Cells that have stopped dividing can be perfectly functional for decades. Cells that don't stop dividing are called "cancer". So, while the correlation is strong, the reason for the correlation remains something of a mystery.

Rose, Michael R. 2005. The Long Tomorrow: How Advances in Evolutionary Biology Can Help us Postpone Aging. Oxford University Press, New York. pp 20-23


Is it possible for a substance to be absorbed by the hair or the scalp? I've heard that the aplication of Monovin A in the hair would allow it to grow faster. Monovin A seems to be only A vitamin, according to the first website.

Could the application of A vitamin in the hair make it grow?

I'm thinking it's not very probable that applying it to the hair and the scalp would affect the hair growth. References will also be useful.

As to the subject line, yes, lipid substances or any non-polar small molecule will enter the skin cells and the body below. The reason is because cell membranes simply consist of fatty substance that behaves like a solvent for other lipids.

As to the specific question about this product, Monovin A. This is a veterinary product and the producer, Laboratórios Bravet, intends it to be injected into animals in case of a vitamin A deficiency. The main ingredients is a retinol ester in the amount of 2,000,000 IU (which usually means retinol equivalents in this respect).[1]

Indeed, retinol is a lipid and long-chain esters like retinol esters are non-polar, too, and can readily be de-esterified by esterases, making vitamin A (=retinol, retinal, retinyl palmitate, retinoic acid) immediately available to the surrounding cells and, via transport in the blood stream, to the liver, which is the body's store for it. Daily doses of 25,000 IU are known to be toxic when administered over a long time. Doses of 50,000 IU can be dangerous over weeks. In general, it appears that single high doses are better tolerated than long over-exposure.[2][3] So, do the math and dilute the stuff such that you get at most one hundredth of an ampoule, else...

Now the effects. Indeed, hair loss is one of the symptoms of heavy vitamin A-deficiency, and logically, that symptom can be cured with vitamin A. That does not mean that more results in more. While retinoids are important therapeutic agents for the management of many skin diseases, notably acne vulgaris, psoriasis, ichthyosis, and palmoplantar keratoderma, there exists something like retinoid-induced effluvium which is a side effect of such medication with tretinoin (ATRA).

  Retinoid-induced hair loss (telogen effluvium) is among the most
  frequent and psychologically most distressing adverse effects of
  retinoid therapy, which results in premature termination of a
  clinically desired and often highly effective systemic therapy with
  retinoids.[4]

Since ATRA is readily produced from retinal, its concentration would be expected to be up, even if the original stuff was retinyl ester. In summary, I would expect no effect, or even hair loss, for you don't simply put such potent stuff on your head and elsewhere, and have no reaction from the body.

[1] http://www.bravet.com.br/pr-ceg-monovina.asp

[2] Vitamin A: Toxicity from Supplements In: Medical Sciences Bulletin 1995; Pharmaceutical Information Associates, Ltd.

[3] Hartmann S, Brørs O, Bock J, et al.: Exposure to retinyl esters, retinol, and retinoic acids in non-pregnant women following increasing single and repeated oral doses of vitamin A. In: Ann. Nutr. Metab.. 49, Nr. 3, 2005, p. 155–64. doi:10.1159/000086879. PMID 16006784

[4] K. Foitzik, T. Spexard u. a.: Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla. In: The Journal of investigative dermatology. Vol. 124, Nr 6, June 2005, p. 1119–1126. DOI:10.1111/j.0022-202X.2005.23686.x. PMID 15955085.


Advanced Higher Biology 2017 - EPT Index I was recently completing a biology past paper the Scottish SQA 2017 Advanced Higher Biology Qualifications. The question is as follows:

To solve this, I did:

EPT Index = 100*(striped stonefly + net spinning caddisfly + flathead mayfly)/(total number of taxa) = 100*(6+6+3)/(44)=34.09%

So, I answered C, however, the answer is B. What mistake have I made?

Well, you made a mistake: The numbers in the second table are irrelevant to the question as it is not about taxa but about individuals. And the ETP number is calculated from number of EPT taxa (and not individuals).

The correct answer was 3*100/7 = 42.9% ==> B good quality of water.


Sugar as a defence against bacteria? An answer on another SE site mentions that sugar "at a certain level acts as a preservative". I've always been taught that microorganisms eat sugar and expel acids, that is why sugary food are damaging to teeth. How is it that sugar acts as a preservative, then?

Googling the question I've found conflicting answers though I don't credit the sources as being especially reputable. What is the real reason that sugar can act as a preservative?

Sugar in high concentrations acts osmotic. This means that the water available in the cells is drawn towards the high concentration of a solutant (sugar), like in the image below (this is demonstrated with a plant cell, but the principle is the same for bacteria and other microorganisms):

Since microorganisms can not survive without water, they are not able to grow or reproduce. This effectively safes food. The same mechanism works when salt is used to conserve meat or fish.


What might this animal be? I have found two species of this strange looking animal on the Eastern shore of the Adriatic Sea and I was simply unable to recognise them.

This looks like an Aplysia, or "sea hare", a marine gastropod. Some of them sometimes get stranded and look like fat violet/green/brown blobs, around 10cm diameter. In the water, they swim slowly. I've seen some in Brittany (France) and in Algarve (Portugal).


What have the L-systems (Lindenmayer systems) been actually used for in biology? From Wikipedia:

An L-system or Lindenmayer system is a parallel rewriting system and a type of formal grammar.
L-systems were introduced and developed in 1968 by Aristid Lindenmayer, a Hungarian theoretical biologist and botanist at the University of Utrecht. Lindenmayer used L-systems to describe the behaviour of plant cells and to model the growth processes of plant development.

I tried to find biological research that has actually used this system but I could not find any. Perhaps this is because I do not know biology that well.
Are these models important? Still taught?
They do produce pretty pictures (again from Wikipedia)

Are these models important? Still taught?

Yes!! These models are extremely important, however, the application of L-systems most definitely isn't confined to just the scope of Biology. I myself first came across L-systems when taking Calculus in university, and then later in several Computer Science courses (I study Bioinformatics).

What's (probably) most significant to mention about L-systems is that they produce fractals, which is acheived by defining a substitution system and utilizing recursion.

Fractal mathematics can be used to describe extremely complex phenomena, starting with just a few simple rules and initial conditions (which is why it's so powerful/attractive to study). Also, fractals have the nickname of, "God's Thumbprint", or, "The Fingerprint of God", just from where they're found so prevalently in nature. To name a few, fractals can "easily" model:

Coastlines
Blood vessels
Brain structure (neuronal connectivity)
Plant foliage
Lightning bolts
Diamonds
Snowflakes

  I tried to find biological research that has actually used this system but I could not find any.

As you can see, some of these examples are biologically related, however, the use of L-Systems have been broadened to many other fields of science, such as mathematics (coding theory) and theoretical computer science.

Unfortunately, very rarely do biologists have the mathematical or algorithmic backgrounds to work with L-systems, since L-systems are more related to mathematics, algorithms and logic, than they are with (practiced) biology.


How does mutualism arise? How can a mutualism between two species arise? I have thinking about this for a while and I have come up with the following points
1.If mutualism gives one specie a competitive edge over its competitors then it could arise. Suppose you are being really pounded by your competitors and there is now way you can survive except if you give in to mutualism, even if it means "selling your soul".
2.The benefits received from the partner species outweighs the costs involved in helping it out.

I cannot think of any more examples. Please suggest a few; also point out if there are flaws in my reasoning.

I am afraid this question is too broad and I am voting to close. Evolution of inter-specific mutualism is a large subject. Here is not a complete answer but just a few comments on your two conditions

  1.If mutualism gives one specie a competitive edge over its competitors then it could arise.

This is mainly wrong. Mutualism is likely to increase if mutualistic behaviour offer increases the fitness of the individual performing it, you would expect mutualistic behaviour to increase. You would not really expect the same by comparing species ability to survive in relation to their level of mutualism.

  2.The benefits received from the partner species outweighs the costs involved in helping it out.

Again, you are talking about the benefit for a species. You should boil down your arguments to the individuals. It is true that mutualism can evolve only if the individual performing the mutualistic behaviour enjoy a higher fitness benefit than fitness cost (if any).