text:
Can someone identify this flowering bush from the US?
This bush is in Tennessee, USA.:

@DevashishDas , red horse chestnut is a tree...the Q. refers it as a bush...

Maybe the tree was young so looking like bush. young trees sometimes can flower.

Not sure about the ID, but those are definitely flowers, not fruits. You can see some of the fallen blossoms on the leaves in one of the photos.

Red flowering Japanese knotweed.

Polygonum cuspidatum, common name Japanese knotweed. A notorious invasive species.
It's actually a herbaceous perennial (those stems grew in just one season, and will die back to the ground at the first hard freeze), not a shrub. The red things are ripening seeds, not flowers.

Can you please add some reference to support your answer?

Polygonum cuspidatum? Google shows white flower for them.

It is quite showy as it booms in cascades of silver flowers in late August that turn an intense magenta and then to scarlet each year right at time of the solstice. --Bitter Orange and Japanese Knotweed


text:
Centriole genes Knock-out Experiment in Common experimental animals?
Anyone know of any experiments that have knocked out the genes for producing centrioles in a worm, mouse, fish, fly or whatever animal? Are the genes for centrioles even identified? It has been shown that centrosomes form with out centrioles so I'm curious how lack of centrioles would effect the system of an animal as a whole.

One of the chief components of centrosome is γ-Tubulin.
In this study the authors have reported the effect of γ-Tubulin knockout in mice.
Quoting the abstract:

Gamma-tubulin regulates the nucleation of microtubules, but knowledge
  of its functions in vivo is still fragmentary. Here, we report the
  identification of two closely related gamma-tubulin isoforms, TUBG1
  and TUBG2, in mice, and the generation of TUBG1- and TUBG2-deficient
  mice. TUBG1 was expressed ubiquitously, whereas TUBG2 was primarily
  detected in the brain. The development of TUBG1-deficient (Tubg1-/-)
  embryos stopped at the morula/blastocyst stages due to a
  characteristic mitotic arrest: the mitotic spindle was highly
  disorganized, and disorganized spindles showed one or two pole-like
  foci of bundled MTs that were surrounded by condensed chromosomes.
  TUBG2 was expressed in blastocysts, but could not rescue the TUBG1
  deficiency. By contrast, TUBG2-deficient (Tubg2-/-) mice were born,
  grew, and intercrossed normally. In the brain of wild-type mice, TUBG2
  was expressed in approximately the same amount as TUBG1, but no
  histological abnormalities were found in the Tubg2-/- brain. These
  findings indicated that TUBG1 and TUBG2 are not functionally
  equivalent in vivo, that TUBG1 corresponds to conventional
  gamma-tubulin, and that TUBG2 may have some unidentified function in
  the brain.

Another important gene is pericentrin. Fibroblasts from pericentrin knockout mice show abnormal spindles during mitosis have been studied.

In agreement with a model in which pericentrin is required for correct
  spindle orientation, fibroblasts isolated from PCNT knockout mice show
  a significant increase in cells with disrupted astral microtubules and
  misoriented spindles (Fig. 2; unpublished data; Zheng, G., personal
  communication). Spindle misorientation is shown by an increase in the
  angle formed by the pole-to-pole spindle vector and the cell–substrate
  adhesion plane in pericentrin knockout compared with wild-type
  fibroblasts.

Apparently both TUBG and PCNT deletions (individually) are not lethal.

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text:
How small does a nanobot have to be to "swim through the brain" and access any neuron it wants to?
I read on this question What is in the space between neurons in a brain? that there is actually not much empty space in a brain. But my question is slightly different. Is there a visual demonstration I can see of approximately how "packed full of cells" the brain actually is?
Obviously there wouldn't be a fixed answer as it is likely a continuum where the bigger you get the harder it is to swim through without being blocked by all the neurons/synapses. But what is a good ballpark size to be to swim through with relative ease?

Is there a visual demonstration I can see of approximately
how "packed full of cells" the brain actually is?
Yes. You can inject tracers in the CSF (Cerebrospinal fluid) or in the ventricles and monitor them. In this study, the authors have injected a fluorescent tracer in the CSF and used a direct imaging.

We used in vivo two-photon imaging to compare CSF influx into the
  cortex of awake, anesthetized, and sleeping mice. The fluorescent
  tracers were infused into the subarachnoid CSF via a cannula implanted
  in the cisterna magna for real-time assessment of CSF tracer movement.

You can also inject a radiolabeled tracer. The tracer should be a molecule that is not taken up by the cells. You can then visualize the space using Positron Emission Tomography (PET).
 But what is a good ballpark size to be to swim through with relative ease?
You may find this interesting: the abovementioned study shows that the "space" expands during sleep and CSF percolates deeper into the brain. This allows clearing of toxic metabolites. Having said that, some interior regions would be difficult to reach. Apart from neurons, there are several glia which occupy the space. I am not entirely sure about this but in interior regions there would be very less of extracellular space (I am just guessing it would be less than ~1µm. See the black regions in the figure below). Extracellular space is 20% of total brain tissue but it is not constant throughout. For more details refer to this book.

I wonder if you could repeat that experiment using labeled nanoparticles of known size, as they get larger they'd eventually stop moving throughout the whole space. But if that image is accurate, the space between the membranes doesn't look much thicker than the membranes themselves.

This is a SEM image from the book (that is linked). In the figure captions it is mentioned that "The scale bar is 1µm" but I am not able to find it. The ECS is as you can notice non-uniform (but certainly thicker than membrane in most places) :P
That injection experiment can certainly be repeated with nanoparticles (perhaps some kind of traceable ones like quantum dots).

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text:
Slicing cell cultures frozen in vitrified ice with a laser for CryoEM
Could a cell culture frozen in vitrified ice for CryoEM be effectively sliced into thin planes and resolved images produced? I was thinking if this could be done to get images from inside a cell.

Maybe I should take this over to physics. But this is something I'm interested in and not sure were to start.


text:
Recombination frequency as a function of genomic location in E coli?
Are there any databases or papers that give recombination frequency as a function of position in the E coli genome?

What kind of recombination do you mean?

Homologous recombination.

No, I mean: which process? There are several processes involving recombination in bacteria, which require enzymes and different substrates. For example, recombination-mediated DNA repair occurs at sites of DNA damage (which can happen at any location, albeit with unequal frequencies), while conjugational recombination is much more location-bound.

A recombination map of the E. coli genome was recently published (several years after question was asked).

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text:
Gene Sequencing and Plasmapper
Is there anything similar to this in Java (especially the circular map sequencing along with hover effect)?
For information I would like to convey that I am using Plasmapper and BioJava for achieving this, but, as the output is in image format, so I am not able to achieve the above said requirement.
Thanks...

Check these out. They provide the functionality that you want:

ApE
SnapGene viewer

Thanks, but I need a web version of this so that I could be able to implement it with in the code (Java Code).

@AbhijeetKumar. You can try using plasmapper then. It outputs svg. You can perhaps employ some libraries from d3.js for what you want.


text:
Is genetic drift necessarily deleterious?
I read that genetic drift is random variation in the relative allele frequencies of a population.

This question however seems to pin genetic drift down to increasing deleterious allele frequencies. Is the answer to this question correct? I don't think that increase of a deleterious allele necessarily indicates that genetic drift is operating; it suggests genetic drift, because one would think that such alleles should decrease in frequency rather than increase, but random chance in a large population can also increase the frequency of deleterious alleles.

Drift is a random element of evolution from one generation to the next, it is equally likely to spread a deleterious mutation as a beneficial one.
The reason the answer is D is because selection should remove a deleterious allele, while drift makes no distinction, and is therefore the only scenario where drift is expected to be a reasonable answer. However, it is possible for drift to contribute to all of those scenarios.

Personally I would prefer that the question you show there said probably rather than definitely - if a deleterious allele is linked to a beneficial one it can be spread by selection despite itself being deleterious


text:
Find protein homologs with BLASTp
I'm trying to find homologs of a set of proteins using BLASTp. I'm working with custom databases.
I'm using evalue of 0.00001 as threshold.
I would like to filter queries having hits with >90% identities. Because BLASTp output is based on HSPs, I cannot filter by %identities/query, only by HSP.
I would like to know how to do this and also if I'm following a reasonable strategy.
Here is an alignment example: qcovs=100 but qcovhsp lower.
qseqid           sseqid         pident length mismatch gapopen qstart   qend  sstart    send   evalue bitscore qcovs qcovhsp
HPNK_01698      HAPS_0519       81.88   596     75      5       630     1225    615     1177    0.0      889    100     49
HPNK_01698      HAPS_0519       49.17   301     115     8       84      366     201     481     2e-56    214    100     23
HPNK_01698      HAPS_0519       53.64   261     61      6       436     684     616     828     6e-49    191    100     20
HPNK_01698      HAPS_0519       46.61   251     62      3       332     510     584     834     6e-46    181    100     15
HPNK_01698      HAPS_0519       53.27   214     79      4       1       194     1       213     1e-45    180    100     16
HPNK_01698      HAPS_0519       55.96   218     60      8       550     764     643     827     1e-40    164    100     18
HPNK_01698      HAPS_0519       51.56   225     61      7       516     731     642     827     1e-38    157    100     18
HPNK_01698      HAPS_0519       49.57   230     77      6       484     713     643     833     1e-37    154    100     19
HPNK_01698      HAPS_0519       57.89   76      26      1       364     433     760     835     1e-13   76.3    100     6

Code used
Make database
makeblastdb -in $Hparasuisfastadatabase -out H_parasuis_strains_gb_ALL.fna_databaseBLAST -dbtype prot -parse_seqids

Run BLAST
blastp -db H_parasuis_strains_gb_ALL.fna_databaseBLAST -query 'out_2.fasta' -out HPNK_selected_vs_H_parasuis_strainss.tblastn -evalue 0.00001 -outfmt "6 qseqid sseqid pident length mismatch gapopen qstart qend sstart send evalue bitscore qcovs qcovhsp" -max_target_seqs 50

Thanks, Bernardo

If I'm not wrong, qcovhsp is a perc_identity for ONE HSP. I would have to calculate manually for each hit as an average for all HSPs perc_identity for one hit.

I even don't like hit_perc_identity because of its reductive information assumption. Average is normally influenced by extreme values.

What species are you comparing? How distant are they? If close enough, "real" homologs should be able to form a single HSP spanning most of the target sequences.

You can calculate the average HSP coverage for the entire sequence (from all alignments). You can also calculate average score per residue. The other option is to do an end-to-end alignment with tools such as stretcher.

Check out my new question related to BLAST: http://biology.stackexchange.com/questions/23958/tblastn-and-blastp-discordance-is-that-possible

First of all, if you want 90% identity, you can discard this hit. None of the HSPs pass that threshold. What's more, since you're working with proteins, there are no splicing issues involved and you should be able to get a single HSP spanning most of the query and subject sequences. Assuming, of course, you have a true homolog.
In your output, I see many small, overlapping HSPs, most of which have low identity. I can't be sure without seeing the sequence but it's a safe bet that what you have there are low complexity/repetitive regions and that's why you have so many separate HSPs. The only half way decent one starts at position 630 of the query sequence and is only 595 residues long, less than half your query protein. Either you have a very diverged N-terminal region or your HSP is just a conserved domain. Again, I would need to see the actual sequence alignment to be sure but that doesn't look like a true homolog (assuming your species are reasonably close which they must be if you're using a 90% identity threshold).
So, always assuming that your species are close enough to expect decent homologs, I would simply ignore the shorter HSPs and deal with those that represent more than, say, 80% of my query's length at >=90% identity. Shorter hits will most often be conserved domains or repetitive/low complexity regions. The thresholds you choose depend on the species you are studying.
If your species are not that close, don't use BLASTP at all. Instead, you can use something like hmmer. Collect a set of homologs from various species for each of your query proteins, build a matrix using these and use that matrix to search your database. You could also use Selenoprofiles which uses a similar approach.

They are strains of the same bacterial specie. I agree with the thresholds you suggest. Thanks


text:
B cell receptor editing
If a B cell contains two mu chains and two lambda chains and is self reactive can it go back and rearrange its kappa light chains? I'm not sure if it can only try to rearrange its lambda light chains or if it can go back and try to rearrange kappa chains as well.
Background info: the light chain is the smaller of the two types of polypeptide chain in an immunoglobulin molecule. There are two classes of light chain known as the kappa and lambda light chains. During B-cell development the light chain genes rearrange. First one kappa gene is rearranged; if this doesn't produce a functional protein then the kappa gene on the second chromosome is rearranged; if a functional protein is still not produced then the lambda gene is rearranged one chromosome at a time until a successful rearrangement is produced.

When I look at Wikipedia I can't find definitions of kappa versus lambda light chain. In the interest of making this question more broadly useful, would you mind adding some more definitions to your post? It might also help someone who is less of an expert do the requisite research to answer your question.

The short answer is no.
Here's a review article with some evidence:

B cell receptor editing in tolerance and autoimmunity
Section: Receptor Editing in Mice with Conventional Autoantibody Transgenes
If multiple κ rearrangements fail to yield a suitable L chain, the κ
locus undergoes rearrangement to a non-coding gene called RS in mice
(RS is referred to as the κ deleting element in humans). RS
rearrangement results in either deletion or inversion of Cκ,
consequently inactivating κ L chain expression on that allele. In cell
lines with λ rearrangements, one or usually both κ alleles are
deleted, whereas in κ-expressing B cells the fraction of RS
rearrangements is approximately 15%.

In summary: After a point with (probably multiple) κ rearrangement failures, both κ loci (usually) get deleted, leaving only λ. So if a B cell expressing a BCR with λ is self-reactive, it won't have the chance to rearrange its κ.
However, there's a lot more involved. For one, it's possible to get a functional and non-self-reactive λ chain BCR without repeated κ rearrangement failures.
Since the quoted passage might be confusing out of context, I'd like to mention briefly that your question's description of light chain recombination is very simplified. In reality, there are many additional mechanisms involved and many different paths to get a functional κ rearrangement, a functional λ rearrangement, neither, or even both. Moreover, there's a lot we don't know, since we learn one experiment at a time, and we can't always directly measure what we'd like to.
First, rearrangement has been observed to occur simultaneously in  κ and λ. This fact might explain why it's possible to get a functional λ chain BCR right away as mentioned above. Second, allelic exclusion (between both κs and both λs) doesn't always work as you and I might expect it to, and a developing B cell can express different BCRs simultaneously (even one with κ and the other with λ). Third, due to receptor editing, a B cell has multiple opportunities for a functional κ chain rearrangement on a single chromosome, meaning that neither λ nor the second κ is needed despite an initially nonfunctional κ rearrangement.
I highly recommend reading the review article!

authors: رنيم محمد صوافطة


text:
Pink E.coli cell pellet. Reasons?
I've harvested IPTG induced E.coli BL21DE3 cells' suspension culture by spinning at 5000 rpm/15 min/4 degrees C. The pellet after spin looked pale pink colored. What could be the reasons?

If you induced them with IPTG what additional genes had you added to induce?

That would be my question as well: What do you overexpress in the cells?

I've seen E. coli colonies with red fluorescent protein that were visibly red even without UV light. That assumes you have cells with RFP. I've heard of carotenoids making bacteria red too, but I don't know what would happen to make E. coli produce them.

There are a few possibilities why the cells can be pink, so it would be important to know which gene is overexpressed.


text:
Is "Cisternal Twins" an actual classification of twin types and if so, describe it
I always assumed my brother and I were identical twins. Now my mother, in her eighties, says we are cisternal twins, but I cannot find any references on the matter. Is there such a thing? If so, what traits make them so?
appended: also, we've been called mirror twins. In a study by a student, we learned that our fingerprints are nearly exact opposites.

Most likely she means fraternal, or dizygotic twins. http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Twins_identical_and_fraternal

that's not it; ty for the guess but I'd like something more definitive. I explicitly mean "Cisternal". I know what fraternal means.

Cisternal doesn't make sense in this context, so either your mother is using an obscure term (quite possible, these things change a lot) or just has the wrong word.
However, mirror twins are a known thing (and quite cool): http://www.twinsuk.co.uk/twinstips/4/140/twin-pregnancy--multiple-births/types-of-twins--identical-fraternal--unusual-twinning/.
She may have meant something like "chiral twins" or "cis-trans twins", which would be borrowing from a similar concept in chemistry to describe your mirror-image nature (but is, again, not a phrase I've heard in the twin literature.)


text:
What are the features on a microscope one needs in order to do lab work?
By lab work I mean urinalysis, blood work(live as well), fecals, cytologies, histologies and all other.
I have read(partly) a book(from 2002) on lab diagnostics and the author did not mention anything about diagnostics. I've spent a lot of time searching on google as well and I did not get anything.

It sounds like you need a microscope for standard microbiology lab tests. At a minimum, any standard wide-field/brightfield microscope would work. If most of your histology work involves colorimetric stains (e.g., H&E, gram staining), you don't need any fluorescence capability. If you are working with a lower budget, look at the new lines of LED-based miroscopes, which dramatically drop the cost (I think around $10,000).
If you plan on doing a high volume, in particular of fixed histology/cytology slides, then you may want to invest in some of the automated slide scanner microscopes. They have a small benchtop footprint and can be programmed to image large areas automatically, for later analysis.

Thank you for your answer. I'm not planing on doing high volume, I was thinking about an upright microscope in the price range 1000-2000 $.

Keep in mind that you will need it to have a camera to store the images, at least in a clinical or research setting. That will add quite a bit more expense. If you get creative, you can now use smartphone cameras for much less.

To more detail on the question I had in mind, I was thinking about which features such as phase contrast, darkfield, polarization, flurescence, DIC I would need.


text:
What is the most common way of administering loop diuretics and what is their time course of action?
I am reviewing some material on loop diuretics, and I am curious to know how these drugs are administered. Also, I am interested in knowing their time course of action once they are administered into the body.

I know that furosemide (there are more types of loop diuretics) can be given intravenously (but can be orally given as well (furosemide info sheet)). Effects of i.v. furosemide are pretty much immediate as it is carried quickly to the kidneys via the blood. After i.v. administration the effects wear off in about half an hour. t1/2 is about 2 hours, but likely depending on route of administration.


text:
Book Recommendations: GRE Subject Test In Biochemistry, Cell And Molecular Biology
There are probably a lot of really good answers that may vary significantly in terms of content.  I'm looking for a set of books that I can read in preparation for the GRE Subject Test In Biochemistry, Cell And Molecular Biology.  I have a Bachelors of Science degree, but never really studied any of the material on this exam (it's in a field which is not really related).  I'm interested in applying for a doctoral program in Biology, and would like to add something to my application so that it doesn't appear to come out of "left-field", as they say.  When I look at the questions from the sample exam in the link above, I can't tell whether they are introductory in scope or would require advanced study in particular areas.  Could somebody recommend a set of textbooks that would cover all of the ground for this test?  If one textbook exists which is sufficient, that would be wonderful, but I'm guessing that multiple texts will be required.  My goal is to learn the material necessary to do well on the exam as thoroughly as possible.
As an aside, I tried looking for study materials in online bookstores, but wasn't able to find anything that consistently got good reviews.  I don't think Princeton Review or Barron's have books on this subject, unless I overlooked something.  At any rate, I'm okay reading through a set of undergraduate university textbooks, but I really have no idea which ones would be good.

We're you able to find an appropriate book or selection of books? How did everything turn out? I am in the same situation and would like to know what books I should look for and the best way to study for the subject exam.

You can also try Lehninger Principles of Biochemistry. It covers all the topic except the part about cell motility and possibly, the 1-A-g ( I'm not too sure about it), but the book is for pretty advanced levels. I would not recommend it as a last minute reference book, but for thorough study it's great. Of course it's my personal opinion, so before you consider any book, I would rather advice you download a pdf copy of the same, to get a first hand experience.

Stryer's Biochemistry is a great book that pretty much covers all the requirements except those in A1 - Those are basic chemistry concepts which are not covered in Stryer. Any basic chemistry book will cover that. Make sure to verify, one-by-one, that all the test subjects are covered in Stryer. This answer is just a recommendation for a great Biochemistry book, not a guarantee for a one-shot success on the test.

For metabolism, I definitely recommend Biochemical Pathways: An Atlas of Biochemistry by Michal and Schomburg (eds). It is very extensive however, so memorizing its compounds and pathways takes much time and dedication. Generally, it works better as a reference book.

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text:
Clarification on BMI formula
In the BMI formula= (Weight)  X  703) / (Height^2) , what does 703 represent? What is a reliable source that I can cite for this answer?
weight= lbs    height= inches

I think it has to do with the conversion: normally the formula is used on a metric scale. the units are weight in kg and height in meters. 1 pound = 0.45 kg. 1 inch = 0.0245 meters. 0.45/(0.0245)^2 = 756. So I must say the 703 is kind of odd. But I think it's a conversion factor

It's a conversion factor.
$$ 1~lbs = 0.453592~kg \\
1~in = 0.0254000~m $$
$$ \frac{lbs}{in^2} = \frac{0.453592~kg}{(0.0254~m)^2} = \frac{703.069~kg}{m^2} $$


text:
Apoptosis vs necroptosis
I understand that apoptosis and necroptosis share the same upper part of the pathway, but I cannot seem to distinguish when is each one activated? From my readings, it seems that when procaspases 8 or 10 are unavailable, the cell will shift to necroptosis. What makes these procaspases unavailable and why does a cell second the necropotosis?

From my readings, it seems that when procaspases 8 or 10 are
  unavailable, the cell will shift to necroptosis. What makes these procaspases unavailable and why does a cell second the necropotosis?

This seems to be right.

Mice with a conditional deletion of caspase-8 in the intestinal
  epithelium (Casp8ΔIEC) spontaneously developed inflammatory lesions in
  the terminal ileum and were highly susceptible to colitis. Casp8ΔIEC
  mice lacked Paneth cells and showed reduced numbers of goblet cells,
  indicating dysregulated antimicrobial immune cell functions of the
  intestinal epithelium. Casp8ΔIEC mice showed increased cell death in
  the Paneth cell area of small intestinal crypts. Epithelial cell death
  was induced by tumour necrosis factor (TNF)-α, was associated with
  increased expression of receptor-interacting protein 3 (Rip3; also
  known as Ripk3) and could be inhibited on blockade of necroptosis.
Caspase-8 is a cysteine protease critically involved in regulating
  cellular apoptosis. On activation of death receptors, including
  TNF-receptor and Fas, caspase-8 is activated by limited
  autoproteolysis and the processed caspase-8 subsequently triggers the
  caspase cascade that finally leads to apoptotic cell death.
  Caspase-mediated apoptosis is important for the turnover of IECs and
  for shaping the morphology of the gastrointestinal tract 4.

2011 - Caspase-8 regulates TNF-α-induced epithelial necroptosis and terminal ileitis

Caspase-8 has both prodeath and prosurvival roles, mediating apoptosis
  and/or preventing RIPK1-mediated necroptosis depending on cell type
  and stimulus. We found that inflammatory stimuli (LPS, lipoteichoic
  acid, or TNF-α) caused an increase in caspase-8 IETDase activity in
  primary rat microglia without inducing apoptosis. Inhibition of
  caspase-8 with either Z-VAD-fmk or IETD-fmk resulted in necrosis of
  activated microglia. Inhibition of caspases with Z-VAD-fmk did not
  kill non-activated microglia, or astrocytes and neurons in any
  condition. Necrostatin-1, a specific inhibitor of RIPK1, prevented
  microglial caspase inhibition-induced death, indicating death was by
  necroptosis.

2013 - Caspase inhibitors protect neurons by enabling selective necroptosis of inflamed microglia.

Necrosis has long been described as a consequence of extreme
  physicochemical stress, such as heat, osmotic shock, mechanical
  stress, and freeze-thawing, which kill cells quickly and directly.
  Therefore, this cell death has been described as uncontrolled and
  accidental necrosis characterized by loss of plasmamembrane integrity
  and cellular collapse, though nuclei remain largely intact during this
  process (Krysko et al., 2008a,2008b; Vanden Berghe et al., 2010). Loss
  of membrane integrity and release of intracellular content grant
  necrotic cells the ability to induce an inflammatory response. These
  immunogenic endogenous molecules fall under the umbrella term
  ‘‘damage-associated molecular patterns’’ (DAMPs) (Garg et al., 2010;
  Kryskoet al., 2011). They include, in the case of accidental necrosis,
  HMGB1, IL-1a, uric acid, DNA fragments, mitochondrial content, and ATP
  (Tables 1and2)(Eigenbrod et al., 2008; Kono et al., 2010; Krysko et
  al., 2008a; Sauter et al., 2000). Because the nomenclature of DAMPs in
  the literature is confusing, here we define DAMPs as a family of
  molecules that are intracellular in physiological condition

2013 - Necroptosis: The Release of Damage-Associated Molecular Patterns and Its Physiological Relevance

Based on the articles above, I would say that capsase-8 is a signal that apoptosis works finely, and so the cell can kill itself whenever it wants. So if that signal is lost because of an infection, mutation or extensive cell damage, the cell has no choice, but to activate the necrotic pathway.

Figure 1 - cell survival and programmed cell death - source

During tumorigenesis, significant loss or inactivation of lead members
  in the caspase family leads to impairing apoptosis induction, causing
  a dramatic imbalance in the growth dynamics, ultimately resulting in
  aberrant growth of human cancers. Recent exploitation of apoptosis
  pathways towards re-instating apoptosis induction via caspase
  re-activation has provided new molecular platforms for the development
  of therapeutic strategies effective against advanced prostate cancer
  as well as other solid tumors.

2012 - CASPASE CONTROL: PROTAGONISTS OF CANCER CELL APOPTOSIS

These findings reveal that, although apoptotic/drug resistance is a
  formidable “stronghold” of cancer against chemotherapy, necroptotic
  susceptibility is an intrinsic “weak point” of cancer.

2007 - Targeting the Weak Point of Cancer by Induction of Necroptosis

Playing a central role in cell death, caspases are targeted by
  different viruses in the aim of prolonging cell survival. For
  instance, viral IAPs (inhibitors of apoptosis) interact with and
  inhibit the processed active caspases, either by blocking the
  catalytic part of the enzymes, or through E3 ubiquitin ligase activity
  from RING domains, targeting caspases for rapid degradation via
  proteasome. Baculoviruses, asfiviruses or irridescent viruses encode
  such IAPs. Another class of caspase inhibitors frequently found among
  poxviruses include the serine proteinase inhibitors serpins:
  CrmA/SPI-2. Crma targets cysteine proteases such as host Caspase 1 and
  Caspase 8.

viralzone - Inhibition of host caspases by virus

Pathogens specifically target both the caspase 8-dependent apoptotic
  cell death pathway and the necrotic cell death pathway that is
  dependent on receptor-interacting protein 1 (RIP1; also known as
  RIPK1) and RIP3 (also known as RIPK3). The fundamental co-regulation
  of these two cell death pathways emerged when the midgestational death
  of mice deficient in FAS-associated death domain protein (FADD) or
  caspase 8 was reversed by elimination of RIP1 or RIP3, indicating a
  far more entwined relationship than previously appreciated. Thus,
  mammals require caspase 8 activity during embryogenesis to suppress
  the kinases RIP1 and RIP3 as part of the dialogue between two distinct
  cell death processes that together fulfil reinforcing roles in the
  host defence against intracellular pathogens such as herpesviruses.
The MCMV protein vICA prevents caspase 8 activation, and this
  sensitizes cells to death receptor-induced necroptosis. In addition,
  the MCMV protein vIRA blocks necroptosis and MCMV-induced programmed
  necrosis by inhibiting RHIM (RIP homotypic interaction
  motif)-dependent interactions.

2012 - Viral infection and the evolution of caspase 8-regulated apoptotic and necrotic death pathways

One potential explanation for this is that this form of death evolved
  to provide a “backup” pathway. Indeed, cowpox virus produces the
  factor CrmA, a potent apical caspase inhibitor capable of blocking
  apoptosis (Ray et al., 1992; Gagliardini et al., 1994). Several viral
  encoded genes are similarly produced to prevent apoptosis, and thus it
  is clear that inhibition of apoptosis is an important means viruses
  have exploited to avoid immune clearance. Interestingly,
  cytomegalovirus induces RIP3-mediated necroptosis via the interferon
  regulatory factor DAI (Upton et al., 2012). This virus also produces a
  protein called viRA, a protein that disrupts assembly of RIP1/RIP3
  necrosomes and consequent necroptosis. Thus, while the physiological
  function(s) of necroptosis remains to be fully elaborated, it is clear
  that this cellular process has been around for a long time during
  evolution. It is likely that necroptosis may serve as an “Achille's
  heel” in tumor cells, and thus greater understanding of the process
  may reveal novel therapies for cancer therapeutics.

2014 - Grand challenges in cell death and survival: apoptosis vs. necroptosis

It seems like there is a 3rd pathway too, it is called ferroptosis.

TNF-induced necroptosis depends on receptor-interacting protein-1
  kinase, mitochondrial complex I and cytosolic phospholipase A2
  activities, whereas H2O2-induced necrosis requires iron-dependent
  Fenton reactions.

2009 - Necroptosis, necrosis and secondary necrosis converge on similar cellular disintegration features

The transition metal iron is essential for life, yet potentially toxic
  iron-catalyzed reactive oxygen species (ROS) are unavoidable in an
  oxygen-rich environment. Iron and ROS are increasingly recognized as
  important initiators and mediators of cell death in a variety of
  organisms and pathological situations. Here, we review recent
  discoveries regarding the mechanism by which iron and ROS participate
  in cell death. We describe the different roles of iron in triggering
  cell death, targets of iron-dependent ROS that mediate cell death and
  a new form of iron-dependent cell death termed ferroptosis. Recent
  advances in understanding the role of iron and ROS in cell death offer
  unexpected surprises and suggest new therapeutic avenues to treat
  cancer, organ dam
  - age and degenerative disease

2013 - The role of iron and reactive oxygen species in cell death
2012 - Heme induces programmed necrosis on macrophages through autocrine TNF and ROS production

Not just a 3rd, there are many more pathways (pyroptosis, MPT-RN, parthanatos, ferroptosis, NETosis).

Figure 2 - Signalling pathways of regulated cell death.
2014 - Regulated cell death and inflammation: an auto-amplification loop causes organ failure


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Why do we have five fingers?
Humans (and other humanoid mammals) have five fingers in each hand.
Curious to know, why five? Wouldn't more fingers be more useful?
Is there any evidence that it used to be different and natural selection caused those with five fingers to survive?

Related post

Thanks @WYSIWYG, missed it due to not knowing "digits" is used to describe fingers and toes.

Cost / Benefit. More fingers need more neurons devoted to controlling and coordinating them which means less neurons for other stuff. And I suspect the amount of coordination need probably increases exponentially which each additional finger. I'd also argue that the fact you can't move your pinky completely separately from your ring finger is a sign we're already on the limit of what we can support. The benefit of a sixth (or seventh, or eighth) finger on the other hand is probably pretty minimal (diminishing returns).

@Matt interesting, if you can elaborate with scientific quotes this might make a fair answer as well. :)

I found an interesting article in Scientific American (Coates, 2005), and I quote part of it:

The condition of having no more than five fingers or toes [...] probably evolved before the evolutionary divergence of amphibians (frogs, toads, salamanders and caecilians) and amniotes (birds, mammals, and reptiles in the loosest sense of the term). This event dates to approximately 340 million years ago in the Lower Carboniferous Period. Prior to this split, there is evidence of tetrapods from about 360 million years ago having limbs bearing arrays of six, seven and eight digits. Reduction from these polydactylous patterns to the more familiar arrangements of five or fewer digits accompanied the evolution of sophisticated wrist and ankle joints--both in terms of the number of bones present and the complex articulations among the constituent parts.

So Coates states that around 360 million years ago there were tetrapods with more digits (6, 7, 8), but that this was reduced to 5 about 340 million years ago. Losing things in evolution is generally relatively simple, yet re-gaining them is hard. So while there is still a tendency for evolution to create species with less digits, there are no examples of land dwelling species with more than 5 digits.
The author reasons that more digits do no good on land as more digits impair locomotion. Most polydactylous species were indeed found to be aquatic.

How do more digits impair locomotion?

@Nit: You need to coordinate all those digits as you walk making the process more complicated.

So, why we do not have three fingers?

Well, doesn't more digits create more traction? That's kind of the whole point of having fingers and toes, that an animal can create more surface are contact with any given object in a controllable manner. However, more digits are also more complex and would require more metabolism to keep alive as well.


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Why do chameleons move back and forth?
I was always curious, why do chameleons have this strange gait?

could you post a link to a video of the behaviour?

https://www.youtube.com/watch?v=KNsjrokwr-E - hmm they claim that it tries to imitate a leaf. but there is no wind :D

same with walking sticks I guess. They seem to try to blend in with the trees.

The movement you observed serves two functions:

Imitation of leaves to protect against predators
Improved stereoscopic vision while scanning for their own prey

Imitation of leaves (mimesis)
Chameleons in the wild live in trees and are surrounded by leaves. In order to protect themselves from predators they move forth and back to blend with leaves moving in the wind.
Also note that their torso shape resembles a leaf:

Why do they move like this even when there is no wind and they are not sitting on a tree? I suppose they just follow their instincts. Evolution "did not prepare" them for sitting in a cage. The lack of ability to know when to move and when not was not a evolutionary disadvantage so there was not pressure to get rid of it.
Improved stereoscopic vision
Chameleons are predators that use their tongue to catch prey e.g. grasshoppers. While they are looking for their next target, they scan their surroundings with both eyes independently, i.e. one scans the left hemisphere, the other eye scans the right hemisphere, thus during this time they have no stereoscopic vision.
Moving forth and back helps alleviating this. They can estimate the distance to their distance better through the use of motion parallax (closer objects seem to move more than object further away when we move sideways). Once they found a target they turn in its direction and then use both eyes to focus on it, preparing to shoot out their tongue.
(Disclaimer: I am not a biologist. This is from my own reasoning and the German Wikipedia article about Chameleons)

Predators are very good at spotting moving targets, as movements will easily stand out from inanimate objects and vegetation.
Most prey will prefer to hide or just run if they are spotted by predators.
But the chameleons prefer to blend in with the vegetation instead. This gives them the advantage that they may move in plain sight, and still not be recognized as prey.

I don't understand this explanation at all. Are you categorizing chameleons as prey or predators?

They go back and forth for the same reason that stick insects and caterpillars do. to imitate wind and foliage, leaf trembling, to ward of their predators. A possible additional reason is to gain added perspective of their environment.
Here is example of same principle in stick insects:
https://www.youtube.com/watch?v=EAIRjpaOXKs
https://youtu.be/gHoDKY8jL1g
https://www.youtube.com/watch?v=Rq7-BPuLXLo
They don't have the physiology or habitat where they can escape or hide from predators hence the open air hiding tactic.
They don't have running muscles and skeleton. They couldn't run if they wanted to (slower than a snake or bird) and they couldn't hide because trees also don't offer crevices like cliffs and walls do. Their behavior is good for catching more prey and for staying hidden.
They are related to Iguanadons, which are adapted to moving in the sea (cold). Chameleons often live in the shadows, 130 of 171 species are forest dwellers, and most of the others live in trees of savannas and steppes, only a few live on the floor.
They don't need to be warm to hunt, their tongue is still one of the fastest things in vertebrates, so they can hunt when they are cold.
Their prey is not very intelligent: birds, snakes and more rarely mammals. because they are too slow to run away, they don't have hiding places except for the branches, they have a very cautious walk which is disguised, with slow head movements, very active eyes, and ability to keep head still in between steps. hunters will tell you that animals are very oblivious when their head is moving, they generally need to stop to see you, and chameleons stop constantly. there was research to understand their slow muscles, the muscles have slow fibers, they have a heart which is not as capable as fast lizards. http://onlinelibrary.wiley.com/doi/10.1002/jez.1402630102/abstract

How does this answer the question?

Why do they use mimicry is tacitly the same question ... omitting stuff too simple to care to memtion .. as in what do the mimic... we know... why they do so is less trivial. The imitate leaves because of limited matbolism... the suck energetocally like a stock insect. To cut a lomg story short. They dont oscillate due to physiological processes do they... based on a broad look at species habits.


text:
Resource for finding what proteins bind?
I have two lists of proteins (including phosphorylated forms). I want to determine which members of each list act on which members of the other list. What online resources exist for finding out what a given protein binds or otherwise interacts with?
I am aware of Uniprot and Phosphosite which have proved useful but I am wondering if there are others that I am not aware of.
Again: the question I am trying to answer is "which proteins from list A interact with proteins from list B and vice-versa?"

"the question I am trying to answer is 'which proteins from list A interact with proteins from list B and vice-versa?'" You and every biophysicist on the planet.

Go to the NAR database site and look for protein domain databases. You have multiple options. Here is the link.

This is definitely a good resource. It looks like most of the tools are very specific. I am hoping to find something more general; like string-db.org

STRING is one available tool http://string-db.org/ and allowes you to do multiple sequences/names. I would also take an indepth look at what expasy has to offer http://www.expasy.org/proteomics. It is a large collection of bioinformatics tools (far too many for me to go through) and almost always has the tool you want.
(As a side note Expasy also has tools in genomics, structural bioinformatics, and many more, check the left hand tabs on the website for the full list!).


text:
Which agricultural crops attract rodents?
Are there any data on rodent populations per acre of different types of agricultural crops?

"Which agricultural crops attract rodents?" - I guess which they can eat :D corn, wheat, oat, etc... with high starch (and so energy) content. but almost everything I think.


text:
How to prepare sample for SDS PAGE?
I usually take my protein sample 0.8ml and sample buffer(2X) 0.2ml for my sample preparation in SDS PAGE. Am I using correct proportion? my protein sample concentration is 4.1mg/ml. What is the standard protocol?

Why do you dilute like this? If you do so, the final concentration of your sample buffer is 0.5x. For this dilution you need a 5x sample buffer.

@Chris. Yes, my final concentration become 0.5x. Is it effect on getting bands on SDS PAGE?

Surely it will affect the gel - the concentration of the ions is lower than it should be, so your gel can run funny.

@chris, Can you please give me protocol for preparing sample buffer? Because in different protocols showing different composition.

Sample preparation for protein gels is not a complex task. Simply mix the appropriate amount of sample buffer with your sample and load it. For a 2x sample buffer use equal amounts of sample and buffer, for 5x sample buffer use 4 parts of sample and 1 part of buffer (for examle 40µl + 10µl). Heat the mixed samples for 5 minutes at 95°C, cool them immediately on ice and load an appropriate amount of it on the gel. How much is possible really depends on the type of gel you use - 20-30µl should usually be possible.
Do not load too much protein, otherwise you will not be able to seperate them appropriately. I usually use between 20-30µg of total protein per well or as little as 50ng for purified proteins (this depends on the antibodies as well).
Have a look on this webpage for some further information.
For sample buffers I usually use the following recipes. I prefer the 5x, because I can load more protein, if the preparation is not very good. I also prefer the use of DTT to Mercaptoethanol, as it is much less smelly. If you have no DTT (or prefer mercaptoethanol) it can be replaced by an equal amount (200mM in the 2x, 500mM in the 5x buffer). If you use DTT, you need to make aliquots of the buffer and store it at -20°C, a working aliquot can be kept at 4°C for two weeks or so.
2x sample buffer:

4% SDS
20% glycerol
100 mM Tris-Cl, pH 6.8
2 mM EDTA (ethylene diamine tetraacetic acid)
200 mM DTT (dithiothreitol)
0.1 % (w/v) bromphenol blue dye

5x sample buffer

10% SDS
50% glycerol
250 mM Tris-Cl, pH 6.8
5 mM EDTA (ethylene diamine tetraacetic acid)
200 mM DTT (dithiothreitol)
0.25 % (w/v) bromphenol blue dye


text:
How hot can a beverage get without burning the tongue?
What is the maximum temperature that a beverage can be without burning the tongue?
I suspect there's a maximum temperature that the surface tissue of a tongue can withstand without being damaged (causing the burning feeling that lasts even after the heat goes away). So let's say I want to setup a device to keep my coffee to the right temperature to drink without damaging my mouth - I'm interested to know the highest possible temperature that will not damage the surface tissue of the tongue in a way that will result in lingering pain after the heat is gone.

I think its about 45-50°C, but why don't you try yourself? ;-) By fever/hyperthermia: "Almost certainly death will occur; however, patients have been known to survive up to 46.5 °C" so I think it is over 46°C, it's over nein-nein-nein.

Afaik the tongue is not more heat tolerant than other parts of the body, so the minimum temperature to cause burn is about drinking a beverage having 45°C temperature for a long time (more than 5 minutes). The pain threshold of tongue is around 47°C, so you will feel when it really burns.
According to studies the hedonic value of coffee has a maximum by 60°C, and it is significantly lower by safe levels (45°C). Frequent burns of mouth increases the risk of oral cancer. So I think this will be a hard choice... ;-)

A burn is an injury which is caused by application of heat or chemical
  substances to the external or internal surfaces of the body, which
  causes destruction of tissues. The minimum temperature for producing a
  burn is about 44°C for an exposure of about 5-6 hours or about 65°C
  for two seconds are sufficient to produce burns.

Thermal injuries

I. With the object of producing standard low-temperature burns in
  animals, and of studying the area of tissue only partly damaged in a
  burn, a burning iron has been made capable of applying temperatures
  from 45°-80°C. to the skin; with this the amount of heat and
  temperature causing skin damage has been studied, and the macroscopic
  and microscopic damage due to graded temperatures have been
  delineated.

Graded temperatures of 45°-80°C. have been applied to the skin of shaved, anæsthetised guinea-pigs, and in some cases rats, for times
  varying from 10 sec. to 6 and 10 min. Observations have been made of
  the development of erythema, flare, blanching, blueing, heat fixation,
  incipient blister formation, œdema, and edge wheal, as also upon the
  later scab formation and rate of epithelium regeneration.
Applications of 47°C. up to 6 minutes produce no visible change.
At 50°-55°C. applied for 1 minute and over, there is a critical temperature for the development of permanent and irreversible damage;
  in animals good scab formation occurs after burning at this
  temperature.
After temperatures of 60°-65°C. the epidermis can be peeled off from the exposed area, leaving a punched-out exposed surface area
  somewhat like the exposed human blister.

1943 - EXPERIMENTAL THERMAL BURNS, ESPECIALLY THE MODERATE TEMPERATURE BURN
According to Green the pain threshold of tongue is around 46-48°C.
1985 - Heat pain thresholds in the oral-facial region

In all experiments, the chosen mean preferred temperature for drinking
  was around 60 °C (140 °F). Black coffee drinkers chose a slightly
  higher mean temperature than drinkers with added creamer, and they
  also chose a slightly lower mean temperature when the flavor was
  stronger. In all cases, consumers tended to choose, on average,
  temperatures for drinking coffee that were above the oral pain
  threshold and the burn damage threshold.

2006 - At What Temperatures Do Consumers Like to Drink Coffee?: Mixing Methods

Overall, the available results strongly suggest that high-temperature
  beverage drinking increases the risk of EC. Future studies will
  require standardized strategies that allow for combining data, and
  results should be reported by histological subtypes of EC.

High-temperature beverages and Foods and Esophageal Cancer Risk -- A Systematic Review

AFAIK TRPV channels open at ~45-50⁰C. This is not really a heat that can cause burn. I have bathed many times in water @ ~>=60⁰ and it just felt relaxing (my epidermis was alright :P). It takes higher temperatures to actually cause a burn.

@WYSIWYG "I have bathed many times in water @ ~>=60⁰ and it just felt relaxing" - I seriously doubt that. Our boiler is set to 60°C and the maximum I am capable to tolerate is half cold + half warm, so about 40°C.

@WYSIWYG https://www.youtube.com/watch?v=0WniZ1ly5Ik watch this.

@WYSIWYG Just to mention, long exposure to more than 37°C can cause hyperthermia. Afaik. humans cannot bear more than 50°C air (non-scientific source), because they would sweat more than they can drink. So putting aside the burn injuries you would still die because of hyperthermia if you would bath in 60°C water (which has about 4000 folds greater volumetric heat capacity than air).

Bath is not such a long process. Face is of course more sensitive but legs and torso can tolerate ~60⁰C (Not too sure about the temp but its usually higher than what other people prefer. I don't use hot water often though. I'll check the temperature next time :P ).

@WYSIWYG Okay. :-)

Just saw this answer, +1 for good answer as well as appropriate username.

This depends on a lot of factors, including how you take your first sip. If you sip with air, you are altering the temperature of the liquid as you sip, as well as decreasing the volume of hot liquid in your mouth, so that the increased surface area of your exposed tongue can quickly alter the temperature of a borderline scalding liquid into a non-scalding one.
So, there is part of the answer: it depends on volume, and time in contact with the tongue.
Most coffee pots keep coffee at about 170°F (77°C) - hot enough to scald your mouth.
This article, while not scientific, does discuss why people like foods at temperatures that cause scalding, and what better temperatures are. But the public wants what it wants.
Safety experts recommend that water heaters be set at 120°F (49°C) because you will not sustain a first-degree burn on contact, which is important if one has mobility problems. At 120°F (49°C), it takes 8 minutes of contact to acquire a second degree burn. At 155°F (68°C), it takes one second.
So, to guarantee no scald on contact with a small volume of coffee, I would think 145°F (63°C) would be about right. (At 140°F (60°C), liquid will scald in 3 seconds. If you don't chug your coffee, this seems safe enough. If you chug, it will scald.)

I took the liberty of clarifying your temperature units, since I assume that you aren't talking about superheated coffee ;)


text:
Why does a pacemaker have a negative pulse?
Why is the first phase of the pulse from a pacemaker cathodic?

Welcome to Stack Exchange Biology!

Do you have a reference to back this up? In general neural implants are tested to see what the most effective pulse phase is. Often one polarity will stimulate the system, while the other inhibits it.Starting with the stimulating phase is deemed best. Then the opposite phase follows to clear the system from the detrimental effects of charge injection.

Hello Chris, thank you for your answer. but still I could not understand why negative peak is important for the stimulation rather than positive peak. As I can understand from electrochemical reactions, for cathodic stimulation, the energy level of free electrons in the metal are raised. It allows to transfer of electrons from metal to reactant species in solution.

Jan - I don't know which phase is most important either - it depends on the implant system and importantly, on the location of the implant. For example, in retinal implants the active phase depends on whether it is placed sub-retinally (anodic phase most effective) or epi-retinally (cathodic phase most effective). I did a quick search on pace makers and couldn't find anything on it - so please provide me with a citation that says that cathodic-first stimuli are most effective and I'll have a look. Interesting topic!

BTW: My answer on a related question may be of help to you: http://biology.stackexchange.com/questions/22020/mechanisms-of-extracellular-stimulation-of-neurons

Can you give some background to the question and your reason for asking?


text:
Is eating cooked food an evolved behavior or rather an intelligent one, passed down via culture?
I was just eating a rather rare steak when I started wondering whether eating foods cooked was something I would instinctively want to do if the practice hadn't been taught to me.
So, is cooking food an evolved behavior, inspired by nutritional value or health benefits, or is it a practice learned, and passed down through culture alone?

I think cultural. It is too a complex behavior to be simply evolved. In addition, many species will not even come close to fire. Plus, you have to learn cooking. lastly, the nutritional benefits are questionable although it is definitely beneficial for health as it kills germs. So in terms of evolution there could be a pressure on evolving this behavior, but again, I think it is too a complex thing to be hardwired into the brain.

@ChrisStronks I think there are nutritional benefits to cooking food, compare human teeth and digestive tracts to those in gorillas and chimps. We just aren't able to process raw food as well as they do, so cooking replaces part of the digestive process. This implies we've been cooking long enough to have an evolutionary effect, otherwise there wouldn't have been time to lose the large guts. It is speculated that spending less energy on digestive tracts allowed humans to develop larger brains. If true, it's an interesting interaction between a learned behavior (cooking) and evolution.

@user137: it is not the evolutionary consequence of cooking that is under question, it is the evolution of cooking itself that is questioned.

I think it is easy to decide this. Do we have an instinct to cook something after we killed it? I don't think so... At least I never felt it... There are stories about missing children have been living in the forest for many years, etc... If they cannot make fire (I think so), then there is no such an instinct, because without fire you won't cook... (Except if they have an instinct to build a microwave oven or use geothermal energy...)

@inf3rno having an instinct to do something is not the same thing as being able to do it, I am sure you would agree humans have an instinct to reproduce even if some fail. An instinct could be something as simple as preference, and on average humans prefer cooked foods, particularly meats and starches. Then you have things like language that is instinctual but still has to be learned.

@John Sure, but you have everything to reproduce when you are born, while you don't have the knowledge to make fire. Kids even try to touch fire, because they don't know that it burns. Even if preferences are instincts, it does not mean that they are not learned. For example I prefer blue over pink, because pink is a color for girls at least I learned that when I was a kid and now it is an instinct. My English is not good enough, but I guess reproduction is more than a simple instinct, it is a strong urge. So probably that is a better word for what I was talking about.

@inf3rno you prefer, not basically all great apes on the planet prefer, which is true of cooked food. language is a great example a human needs other humans to develop language, (if you don't learn at least language by puberty you will never have syntaxed language) but every human caries an instinct for language, and if two children with no language are put together for a while they will develop a complete language from nothing. Instinct is not just fixed action loops.

@inf3rno, touching fire may actually be evidence for it being instinctual most animals  instinctually avoid and fear fire. Not true for humans. Also learned and instinct are not mutually exclusive, plenty of instinctual behavior have learned components. not knowing how to do something does not mean you do not instinctually desire to do it.

@John "language is a great example a human needs other humans to develop language" - Sure and normally it is granted, because people live in families and groups. Afaik. the brain structure for languages are genetically coded just as the organs to make sounds.

@John Still it does not make sense to think that it is inherited to cook stuff. Without the capability to make fire all you can do is collect all your meat and pray for a wildfire. Maybe you get it maybe you starve to death. Not a solid strategy to survive. The first humans just ate what they found after a wildfire and learned that it is good. After a while they learned that they can make fire. And that's all. It is something easy to learn from others, no need to code it genetically. Maybe the digestive system changed because they started to eat cooked food instead of raw.

@inf3rno cooking predates Homo sapien by a wide margin, it may very well be the thing that allowed us to evolve, Again I don't think you understand what instinctual behavior is, just because something requires learning does not mean it is not instinctual, there are plenty of instinctual behaviors that have to be learned. There is no human society that does not cook their food. also yes the human digestive system is adapted to eating cooked food, as are our taste buds.

The headline of this question says "eating cooked food" but the text says "cooking food", which is a different question.  Human ancestors in an environment like the Okavango Delta would have encountered carcasses killed by seasonal wildfires.  I suspect intelligence would have permitted early humans to scavenge in fire-prone areas successfully where many other genera would suffer unacceptable risk.

Cooked food is a learnt trait rather than an evolutionary one. On a certain psychological level its a society norm so you would be hard pressed to find an individual who wouldn't mind eating completely raw meat/steak.
But, say if you chuck a few humans into the wilderness at an early age and not teach them how to cook meat they may not actually cook their food. As early prehistoric humans discovered fire they eventually noticed/learnt to cook food and passed on the knowledge . You would have to research the history of that since I don't actually know the details.
Cooking food makes more sense on a psychological level as we cook food based on our cultural upbringing, and our memories and knowledge. A human would prefer cooked meat based on his upbringing or understanding that eating processed meat is safer as it means food contains less pathogens. The way we cook food depends on where we are from (eg.An Indian would cook meat differently from, lets say an Italian because their environment provides them with different ingredients and/or devices, pans/pots)
I hope that wasn't too confusing.

If you just put people in the woods at an early age they'd die. Tool use and hunting are also learned behaviors that affected our evolutionary outcome, similar to cooking.

well yes you are right sorry, I meant it in a more elaborate format. As in raised with no social norms or inhibitions kind of way.

humans have been eating cooked food since before we were human, it is hard to argue something is cultural if we were doing it even before we were homo sapiens. especially considering there is no human culture that does not cook food. Use language as an example what language you learn may be cultural but language itself is an instinct.

Its almost certainly instinctual, humans along with other great apes (any many other animals) show a preference for cooked foods over raw in testing, the number that prefer it increases drastically if they are have sampled cooked foods before. So it is likely as built in as your desire for sweets and salt.
Just becasue something is instinctual does not mean you don't have to learn HOW to do it. Language is instinctual in humans, but what language you learn is up to your upbringing (the same is true in some birds), and denied another human to interact with until puberty you will not develop language. that does not make language itself cultural, just the particular language you learn.
No one would argue lions do not have an instinct to hunt, but they still have to learn how to be successful at it.
https://evolutionaryanthropology.duke.edu/sites/evolutionaryanthropology.duke.edu/files/site-images/Wobber%20et%20al_%202008_%20Great%20apes%20prefer%20cooked%20food%281%29.pdf

A study found that great apes prefer cooked food, which contradicts the notion that the preference results from human evolution.
Cooking food properly is generally beneficial for nutrient availability and taste, so the cooking itself is not what causes the animal preference: pulverising with a blender would have some similar effects on preference. Animal preference is based on sensation of sugar, fat, salt, aromatics, which generally are higher when the cells of the food matter have disamalgamated and volatilized.

As @John has pointed out above and in their other answer there exist solid biological evidence that humans (and other mammals) are better at digesting cooked food than uncooked one, and likely to prefer cooked food given a choice.
It is however harder to prove a causal relation that humans adapted to eating cooked food. Indeed, this would require that humans are exposed to cooked food during a reasonably long period of time (on an evolutionary time scale), and that those who are less adapted to digesting cooked food become less fit and gradually elimited from the population. It is more plausible to assume that cooking was discovered as a way of getting more benefits from food, and thus being more fit in respect to the human groups that were not cooking or were being uncapable of digesting cooked food. In other words, it is more likely learned than adapted behavior. But plausibility is not a hardcore scientific argument.
What further complciates this question is that our gut microbiota has certainly adapted to the cooked food. The gut microbiome is not encoded in human genome, but it is partially inherited during birth, and its further changes are mainly determined by the living conditions. So, it is safe to claim that this microbiome has adapted to humans eating cooked food, and it has certainly undergone genetic selection in this direction.


text:
Congenital blindness due to retinitis pigmentosa - does it exist?
Retinitis pigmentosa (RP) patients typically become blind after a period of years in which their eye sight slowly deteriorates due to photoreceptor degeneration. Generally RP patients develop night-blindness first, then tunnel vision, after which finally the central eye sight diminishes leaving them with basically no eye sight, barred some crude residual light perception. The wiki page on RP has more information when needed. Typically, the process from diagnosis of RP to (near) complete loss of eye sight takes years to decades.
However, Chebat et al. (2007) make mention that their study group, consisting of congenitally blind subjects, includes one person with RP (see table 1 in the linked article). Hence, this implicates that this particular subject was blind from birth due to effects of RP.
Is anyone familiar with newborns blinded by the effects of RP?

Reference
Chebat et al. Neuroreport 2007;18:1901-4

Just to be sure I understand the question, you're looking for case studies on a neonate that has already had a near total loss (or total loss) of vision from RP?  I'm not sure it would be diagnosed as RP at that point.

Can you link this article?

@AtlLED - correct, I am searching for evidence of congenitally blind folks due to RP.

@Chris - I linked the full-text article.

Thank you for linking the article.  I think I now understand where this question is coming from.  Was this prompted by Table 1?  Because even if RP is not showing symptoms at an early age, you are still "born with it."  As a genetic disorder, you are almost always going to see onset written as birth.

@AtlLED - yes - it was prompted by table 1! Interesting thought, but no - the authors are specifically including early / congenitally blind folks, i.e., visually deprived from birth

I have only ever heard of one case where RP caused blindness in a newborn. Unfortunately, I am unable to release the name or any details of the patient because of privacy issues and so forth.
Usually blindness from RP comes after a few years of life (as you said), making blindness from birth (or even early infancy) very rare.
I can tell you, however, that the formerly stated patient suffered from type I Usher Syndrome, if I remember correctly. I apologize for my inability to provide you with more specific details on this.
I don't know how much this will help in your search, but I sincerely hope that it does.
CDB

Perhaps I shouldn't ask new questions, but just to verify - is Usher's syndrome characterized by RP (i.e., is RP a symptom of Usher so to speak?) or is Usher's characterized as a syndrome with vision loss due to mechanisms related (but different) from RP? Thanks for your answer.

No problem, I'm happy to help. You are correct, RP is a "symptom" of Usher syndrome. Usher syndrome is a combination of hearing loss (usually due to a defective inner ear) and, of course, vision loss, which is due to RP.

Just to verify - this observation has never been published by any chance? Interesting observations ! :)

I don't believe this case specifically has ever been published. I have been searching for a similar article for a while because your question intrigued me so much (no doubt because of my past experiences with this patient), but so far I have found nothing. I am very sorry I cannot present you with even a name, as it is completely available to me, but, as I said earlier, certain privacy issues stand in my way. I will keep searching for an article that studies these observations.


text:
What is 'independent assortment'?
What is the definition of 'independent assortment'. I tried researching this term but came back with two results:

alleles assort themselves independently of different alleles
the alignment of homologous chromosomes is random along the metaphase plate; resulting in the daughter cell inheriting either maternal or paternal chromosome based on 50:50

Which is the correct term?

The term was pioneered by Mendel, who had no knowledge of chromosomes, so definition 1 would perhaps be the best answer. However, we now know that definition 1 arises from definition 2 (chromosomes are inherited independently of each other) and from the fact that chromosomes recombine (cross-over).
That said, independent assortment does not apply to linked genes, which tend to be inherited together. That is, they are not independently assorted.


text:
How to inactivate trypsin permanently by boiling?
I have to perform a hydrolysis of BSA with the enzyme trypsin. As a control I want to inactivate the trypsin enzyme. Can I inactivate it permanently by boiling (100oC) for 10 minutes, or does it it require 1 hour of boiling? After inactivation, I have to do a test (with an active enzyme) and a control with BSA at 37oC). At this point the inactivated trypsin (the control) should not be re-activated. So my questions are (1) whether I can irreversibly inactivate trypsin by boiling, (2) how long I have to boil it, and (3) if the boiling process will irreversibly inactivate the trypsin.

In my experience 10min at 100°C are sufficient, this is also supported by the paper linked below. Heat inactivation works by denaturing the protein and is therefore final.
Depending on what you want to do with you sample, it might be problematic, as this is probably also denaturated at least to some degree.
You can also chemically inactivate trypsin, either by adding fetal bovine serum (which is done in cell culture), which contains protease inhibitors as α1-antitrypsin and α2-macroglobulin or by using commercially available inhibitors. Trypsin is also inhibited by calcium and magnesium ions, so your reaction buffers shouldn't contain any of them.

A Simple Procedure for Effective Quenching of Trypsin Activity and
Prevention of 18O-Labeling Back-Exchange

The loading buffer for SDS-PAGE + heat(without dye) can also be used if little bit of SDS is okay. Or simply 2-mercaptoethanol + heat will also do [ref].

Since the purpose of this buffer is the denaturation of proteins, this will definitively work. The color helps during the loading and also forms the "running front" in the gel later.

You can consider these also:

Add 2-mercaptoethanol and heat at 95⁰ for 10 min [ref]
Add PMSF, incubate for some time and then heat for some time (lets say 70⁰ for 10min) to inactivate residual PMSF.


text:
When birds fly in V-formation, how is it decided which bird gets to be the 'lead bird'?
I've read on Wikipedia and in other sources that the lead position alternates due to flight fatigue, but does it alternate between a small cabal of of leadership birds, or does (almost) every bird get to sometimes go first?
Is the process different across different species?

Since this question is quite old (it jumped to the first page because someone just answered it) you probably won't read this comment, but it's worth mentioning this: the "lead" bird (at the front) is not the "leader" bird (who decides the direction). Normally, the "leader" bird is somewhere at the middle of the V.

There is an advantage for birds to fly in a V-Formation as stated by Portugal et al, 2013:

As a bird flaps, a rotating vortex of air rolls off each of its
  wingtips. These vortices mean that the air immediately behind the bird
  gets constantly pushed downwards (downwash), and the air behind it and
  off to the sides gets pushed upwards (upwash). If another bird flies
  in either of these upwash zones, it gets free lift. It can save energy
  by mooching off the air flow created by its flock-mate.

There is no advantage to the lead bird though, only the birds behind will get these free lifts by being in the upwash zones.
A study on Ibises determined that there was no clear lead bird and birds cycled between positions. Flying in a V-formation is a collective effort, there would be no benefit to always being in front, so the birds take turns. I would assume the same aerodynamics and the cycling of lead bird apply to all birds that generally fly in V-formations such as Geese. Otherwise the lead bird would just exhaust itself and not have enough energy to complete the migration, it would be the same situation as if the bird was flying alone.

By carefully observing the flock, the investigators learned that the
  amount of time a bird is leading a formation is strongly correlated
  with the time it can itself profit from flying behind another bird.
By working together, a flock of birds is greater than the sum of its
  parts. By not being selfish, individual birds can reap the collective
  advantage of aerodynamic wash-up, while also allowing for larger
  flocks, which result in yet more time for an individual to be in a
  backdraft situation.

Additional Reading:
http://phenomena.nationalgeographic.com/2014/01/15/birds-that-fly-in-a-v-formation-use-an-amazing-trick/
https://io9.gizmodo.com/why-birds-take-turns-at-the-front-when-flying-in-v-form-1683465294
References:
Portugal, Hubel, Fritz, Heese, Trobe, Voelk, Hailes, Wilson & Usherwood. 2013. Upwash exploitation and downwash avoidance by flap phasing in ibis formation flight. Nature http://dx.doi.org/10.1038/nature12939


text:
What is this bizarre in-growth in this red bell pepper?
I just chanced upon a rather strange red bell pepper (or capsicum?):

The green formation is bulbous to touch, just the like the outside of the bellpepper, and it has the same smell as one. I'm no biology expert, but I have a feeling that's a tiny ingrown bellpepper in there. My mom thinks it's a strange genetic experiment and wants me to throw it away!
What is that strange growth, and what might have caused it? Is this safe to consume?

These are "baby fruits" which are safe to eat. It's a quite common phenomenon.

This is very likely to be parthenocarpy, which is an “internal proliferation” and varies from an irregular fruit to an almost carbon copy of the larger pepper. What is known is that it shows up in seed lines through natural selection and is unaffected by weather, pests, or other external conditions. Please see page 27 of this document.


text:
Can we directly stimulate M cones in retina with current technology?
I wonder if we could try to see imaginary "supergreen" color by directly stimulating M cones. For this I suppose we'd need:

Non-destructively scan specific human's retina to locate exact positions of M cone cells.
Prepare a high-resolution image (on a retina-like display I guess), which would have light spots in some locations and dark in others, so that when the human we inspected looks at particular point of the image, these light spots were focused exactly on M cones.
Track the eye movements and adjust the image so that S and L cones avoided significant exposure to prevent misperception.

Is anything of this hard to implement with current technology, given typical human retina properties (M cones density, their apparent color etc.)?
If this is totally possible, has such an experiment already been performed?

You've probably seen the news reports by now, in which researchers targeted and stimulated individual cone cells in the eyes of volunteers: "The elementary representation of spatial and color vision in the human retina" Ramkumar Sabesan, et. al. (2016). This experiment is the first time that researchers have targeted and stimulated individual cone cells. The experiments mostly involved L- and M-Cones, though the published research noted the response obtained from S-Cones, too. The researchers used 543 nm laser light (25 nm bandwidth) and an optical tracking system similar to what astronomers use to correct atmospheric distortions. So, yes, the technology exists, but it looks like it is so new in this application that no one has performed other experiments with it, yet.

Technology is not advanced enough to achieve receptor-specific stimulation. Regarding your defined needs:
1) Identifying M cones: It is already challenging to distinguish cones from rods in the retina (Turpin et al, 2011), let alone identify the three classes of cones.
2) Your retinal-mosaic image would theoretically be possible, although very small pixels would be needed.
3) Eye tracking is doable, but not at this level of accuracy. Delays in the system will almost certainly result in transient activation of other receptors.

Regarding (1), there's a 2019 paper: Cone photoreceptor classification in the living human eye from photostimulation-induced phase dynamics


text:
Are fatty acids and glycerol lipids?
As far as I know, lipids are defined as biomolecules which are hydrophobic.
Triglycerides are composed of fatty acids and glycerol and are considered lipids but, are fatty acids alone or glycerol alone considered as lipids ?

From IUPAC Goldbook:

A loosely defined term for substances of biological origin that are
  soluble in nonpolar solvents. They consist of saponifiable lipids,
  such as glycerides (fats and oils) and phospholipids, as well as
  nonsaponifiable lipids, principally steroids.

That means that lipid does not mean any hydrophobic molecule.
Lipids can be amphipathic as you already know about fatty acids.
Glycerol is not a lipid; neither is it hydrophobic. Glycerol, if to be classified into one of biomolecular classes, it would be that of monosaccharides (in the form of sugar alcohol like sorbitol and xylitol).

I would rather classify glycerol as an alcohol, but this can be debated.

I dropped my answer and fully support this one. The wiki page on glycerol says it is a poly-alcohol and thus a sugar.

@Chris. Yes it is alcohol no doubt. I was talking about a biochemical class and it is one of the simplest sugar alcohol (like sorbitol, xylitol etc).

Instead of calling glycerol a monosachharide, shouldn't it be called derivative of a monosachharide as it doesn't have a ketone / aldehyde grp ?

@biogirl I didn't call it a monosaccharide. I said if at all it is to be grouped somewhere it would be in that of monosaccharides. And yes it is a reduced form of glyceraldehyde and dihydroxy acetone (which are the simplest aldose and ketose resp.). It would be called a sugar-alcohol (so yes it is a derivative).

Okay. Makes sense.

Glycerol is not lipid (short chain polyol, so it is polar and water soluble), but fatty acids (amphiphilic) and triglycerides (hydrophobic) are.

Lipids may be broadly defined as hydrophobic or amphiphilic small
  molecules; the amphiphilic nature of some lipids allows them to form
  structures such as vesicles, multilamellar/unilamellar liposomes, or
  membranes in an aqueous environment.

wikipedia - lipid


text:
How does the body really react to exposure to the vacuum of space?
I've seen sci-fi movies where the effects the body being unprotected in outer space are wildly different. In one movie, a guy radios for someone who's been ejected into space to breath all the air from his lungs immediately. In some movies, eyes are pulled from sockets. In others, ice crystals form, and the eyes begin to look a bit red... Sometimes the exposed person is a goner right away, sometimes they're shown to last for a minute or more. The Hollywood portrayals of space exposure just vary tremendously.
So I'm curious, what really happens to the human body in the vacuum of outer space?

With regard to the vacuum - Apparently nothing happens as long as you don't hold your breath, just like you shouldn't hold your breath when ascending after scuba diving and the pressure drops. See NASA's answer to the same question. Of course there's the radiation that does other funny things in space, see the NASA link.

And by "nothing happens" he means you pass out in 10-15 seconds from the lack of air and soon die. And btw there are many other reasons why you would die besides the lack of oxygen and radiation..

@zoran404 lol I guess he means "nothing spectacular happens" - no eyes bleeding or instant death.

If a person was in space without her spacesuit/helmet, she would feel a suffocation feeling, likely making breathing motions even though there is no air to breathe. She would also feel her sweat, saliva, tears, mucous, and any other water on her body boil off, though her body would maintain blood pressure, at least until her heart stopped. She would be unconscious within 15-20 seconds and dead within 90-120 seconds.
https://m.youtube.com/watch?v=ZrILTVRcW6A

Please add some reliable references to back up your statements here. And note that the person doesn't have to be teleported, their suit or airlock only needs to fail.


text:
How can eyeglasses improve vision beyond 100%?
The result of a vision test by my oculist yielded a result of more than 100% while wearing prescription glasses. I wonder, how can a person see better using eyeglasses?

What do you mean by 100%? Can you give us acuity measures? Like Snellen fractions (20/20 or 6/6 etc)? If you scored above the norm, say 6/20 that means you perform above the normative value. Those normative  values are simply averages and one can surpass that. Also with conventional corrections like glasses.

@ChrisStronks I wasn't told any measures or units. Just the result that was a percentage. Actualy I was too pleased at the moment to ask the doc this question.

maybe they meant you were shortsighted and your glasses made you longsighted (rather than "normal" sighted)?


text:
Why do plants fruit?
This is a two-part question:

What is the point of fruit if not to be eaten? It’s my understanding that organisms will adapt to survive and thrive. I understand that being eaten can spread seeds, but this just seems like too much of a risky tactic to rely on.
Following on from part one: If being eaten is the best way to spread seed, why do some plants avoid this (such as by being poisonous or thorny)?

I changed the name from "What's the point in bananas?" because, despite being an awesome title, the new one is a bit more biologically grounded.

A lot of times, the fruit flesh is good for more than just feeding people; it can provide a nutrient-rich environment for the seed itself to begin germinating in.  It's not too different from an egg, where the yolk is the part that turns into the chicken, in its entirety, and the egg white is purely food for the developing chick.

Fruit being eaten is a very useful attribute for a plant, just like pollenisation through provision of nectar is often better than wind dispersal. Seeds contain startch and sugar, so seeds are always attractive to animals, so plants with fruit actually dissuade animals from eating the seeds, and encourage the fruit to be eaten in such a way as to be dispersed by the right animal. Fruit are essentially designed like ideal dispersal devices for fruiting plant's and berries seeds, like wings are to designe to wind dispersed seeds. Fruit are the wings of the seed.

Seeds are spread by many mechanisms
Wind dispersal: When air currents used to spread seeds. Often these plants have evolved features to facilitate wind catching, for example dandelions. Aka, anemochory.
Propulsion & bursting: When seeds are propelled from the plant in an such as in these videos. This is called Ballochory.
Water: Similarly to wind dispersal plants can spread seeds by water movement/currents, aka Hydrochory. This is used by many algae and water living plants.
Sticky Seeds: There are many ways a seed can attach to the outside of an animal - by using hooks, barbs, sticky excretions, hairs. Seeds then get carried by an animal and fall off later. This is epizoochory.
Fruiting: Plants can use seed-bearing fruit to encourage animals to eat the seeds. They will then be spread when the waste is excreted after digestion. This is a process of endozoochory.
More than one way to spread a seed
From above you can see there are many ways to spread a seed. This means that many plants (those that do not use fruit) will want (from an evolutionary perspective) to avoid being eaten at all costs, and therefore evolve poison/taste cues that reduce the frequency of this. However, if investing in producing fruit bears a net benefit, ie many seeds are spread and successfully propagate, then the cost of fruit production is not a risk. A fruiting plant can minimize the risk by limiting reward (making fruit taste good and be nutritious) to only the right spatiotemporal moment when the seeds are primed for dispersal, if the fruit is eaten before the seeds are ready/present in the fruit then there will be no benefit of producing the fruit. (I expect this is why unripe fruit doesn't tend to taste so nice - it doesn't taste nice unless it's ripe because those where mutations made fruit taste good before the seeds were ready had no offspring, and those that time the ripening well were much more successful).
Producing an edible fruit is not necessarily the best way but is the way many plant species have evolved to spread their seeds. Evolution works by random mutation and selection, which can only work with the variation it has available - only if a mutation to produce fruit arises in a species and it improves fitness is it then likely to spread. It appears that endozoochory could be a very good methods of long distance dispersal.
Some interesting stuff
Interestingly, according to this blog post, unripe fruits taste bitter because they are full of tanins. Cranberries are an odd fruit because they taste bitter which means they are unattractive to animals, but they do float - which is a good dispersal method - because of an air-pocket inside the fruit that evolved. It could be the case then that once a mutation arrived for the air-pocket the fruit could just float away on water to a new location, and then using resources to make the fruit sweet and tasty became an unnecessary cost so was lost (to some degree).
This article contains this text:

Like many species of plants native to North America, the cranberry is specially adapted to wetlands -- water-soaked areas that create transition points between dry land and open water. But cranberries do not grow directly in the water. Instead, they typically lay their roots at its edge, taking advantage of the rich soils created by alternating layers of peat, sand, clay and rock.
  Other fruits are dependent on hungry creatures to spread their seed,
  so sweetness can help their chance of being eaten and transported
  elsewhere. Not cranberries. Because of their little air pockets, the
  fruit falls from the plant's long vines when ripe and lets the water
  transport it to distant beds.
This advantage dictated the fruit we eat today.
Blueberries and cranberries are close cousins and are in fact not
  berries at all; they belong instead to a class of fruits known as
  epigynous or false berries. Unlike a true berry, the fruit grows from
  beneath the rest of the flower parts and as the fruit ripens the
  flower stays attached and ripens as well.
Vorsa believes that at some point during the last ice age there were
  fewer animals to eat the fruits, and this might have driven the two
  species to diverge. The cranberries developed an acidity level five
  times higher than blueberries because it came to rely on water for
  seed dispersal. Cranberries did not need to produce large amounts of
  sugar that their blue-colored relatives required to entice consumption
  by animals in order to spread their seeds.

"the plant hasn't made it taste good because it doesn't want it to be eaten" be careful with this line of thinking. The reality of evolution is that the plants that made their fruit taste good, before or after their seeds were ready, died off. The ones that happened to have the right flavor at the right time managed to survive.

@zzzzbov that's what I'm getting at - I'm not suggesting plants "want" or choose. It's meant from an evolutionary perspective, ie as you say "The ones that happened to have the right flavor at the right time managed to survive"

@zzzzBov this is an important point that is typically assumed. This assumption should probably be adjusted based on target audience and the level of the question/answer. Physicists talk in the same way about what systems "want" to do. It's a fairly idiomatic way of describing a tendency or trend, but may be confusing to those with little scientific background.

@zzzzBov I will edit the answer next time I'm at the computer to clarify

I see no reason why a plant couldn't change the advantage gained from having animals eat the fruit and spread the seeds to restricting consumption by animals due to risk of seed destruction. Evolution is by nature dynamic! What worked a million years ago might not work today. If a fruit is appealing enough that most seeds get destroyed by being eaten but a variety evolves which is poisonous, bad tasting, has prickles or thorns or any other discouraging feature and that is enough to ensure survival then that variety will tend to become dominant.

It's also interesting to mention chili peppers, whose seeds can be digested by mammals, but not by birds. Birds lack the ability to sense capsaicin, the molecule that makes chili peppers hot.


text:
Evolutionary reasons why you cannot tickle yourself but you can masturbate
There are obviously good reasons that explain why you cannot tickle yourself (see e.g. here). This got me thinking why it is possible to masturbate...
Wouldn't it make more sense to not be able to do that so that you are more inclined to have real sex. Individuals who were not able to relieve themselves in this manner should have been more actively producing offspring. And the tickling example shows that self-produced sensations can be inhibited.
Does this make sense? I know that it is always hard to reconstruct evolutionary processes but are there reasons that explain this?

I am sure I saw a paper that suggested masturbation can enhance fitness via ejaculate quality

I guess tickling has an element of surprise.

When you watch porn you trick your brain to think you are actually having sex, so the brain doesn't think of it as self-produced stimuli. It's that simple... (If you don't have any porn you'll find it's much harder to trick the brain)

@Downvoter: Please give us a reason as is good practice here. How can I improve the question? Thank you.

I can tickle myself. (No pun intended.)

You don't need porn, though. People have been using their imagination for millenia.

Access to females is something regulated by an alpha male in chimps social groups. Most of males have to wait to be very old to have a chance to become alpha, and before that, mating will occure by chance on very rare occasions. Male chimps do masturbate. Regular ejaculation is said to avoid some cancers (prostate essentially) and masturbation is the most straitforward way to avoid those cancer in absence of mating oportunity.
This, of course, regards chimps but may tell us something about our ancestors and our evolution timeline.

As it is human males differ from animal by the fact that their organ is always outside the body. Could this be related to evolution from monkeys doing that since hundred thousands years ago ?

Is there any evidence that masturbating discourages (young) men from having sex? If not then there is no evolutionary reason to stop it.

I think there is a bit of a logical leap here (or at least in the title).
The simple answer is that there are many biological phenomena for which there is no logically satisfactory explanation. For instance: why do people have wisdom teeth? We come up with some hand-wavy explanations about ancestral diets, but at the end of the day we just have wisdom teeth (or at least most of us do) and there isn't a great immediate causal pathway that tells us why this rather inconvenient thing exists in modern humans and hasn't been lost.
Getting back to the question at hand, there are a number of assumptions that seem to come along with this question:

Most importantly, why is it assumed that there must be an evolutionary "reason" for a biological phenomenon? In many/most cases there is no such reason. Most (molecular) evolution is neutral and random.
Why is it assumed that there is an equivalence between tickling and sexual stimulation? (then again, a cursory google search suggests there is a relationship...)

Both tickling and masturbation are phenomena that seem to occur in primates. However, this does not require that there be a link between them even if they appear to be similar superficially. Furthermore, it is not logically required that either of them satisfy any particular purpose, even if we can imagine a possible purpose (as some of the commenters have).
Of course, there are lots of reasons why these things exist if you're willing to drop the evolutionary mumbo-jumbo. For instance: both of these things can be fun and God loves us and wants us to be happy. This is the same as the platitude from Ben Franklin on why booze exists. Substitute your favorite demiurge.
These arguments are not much different from arguing that constant ejaculation leads to better sperm on evolutionary time scales. There is equally good (better?) evidence that having to produce more sperm leads to a higher prevalence of birth defects and other disorders. So maybe masturbation is bad from one reasonable point of view, and is in fact a deleterious vestigium like wisdom teeth. The "scientific" answer depends a bit on which literature you pay attention to.
Evolutionary answers of this type tend to be this kind of just-so stories. They give an air of precision and authority with uncertain logical backing, and they don't even have the folksy philosophy as a consolation.
This may not be an answer in the fashion the OP intended, but hopefully it does at least give a perspective on thinking about these kinds of questions.