Origin of human intelligence and thought I've been debating this topic with a friend of mine and we can't get to a common answer. She argues that we don't descend from any Chimpanzee or Orangutan because, if we did, they would also have the cognitive thinking ability that we have. I am arguing that a high protein diet allowed the first humans to have the possibility to develop a higher memory, intelligence and other mental procedures.

But after all, what would be the real origin of the intelligence? And if animals do have intelligence too, why isn't theirs as advanced as us.

How is

"we don't descend from any Chimpanzee or Orangutan because, if we did, they would also have the cognitive thinking ability that we have"

not equivalent to

"We are not related to the chimpanzee or orangutan because, if we did, they would also have [the same amount of body hair]/[the same sized mouths]/[the same muscular strength] that we have"

?

Any related species are going to differ in some respects (otherwise they would not be different species, after all), and it is plain to see that intelligence is one of the ways in which species can differ.

Regardless of that (if your friend thinks intelligence is special in a way that hairiness is not), you can make your argument even while sticking to talking about intelligence, and there is no need to go into the reasons for changes (increases) in intelligence to see that.

To make the point with your friend, it might be best to point to two different animals that

she recognizes as related, and that
she also recognizes as having different levels of "cognitive thinking ability".

In light of such an example, her argument falls flat (unless she further considers only human thinking ability special, in which case you will have a harder time!)


potency in preformed germ-line In organism that have a preformed germ-line like Drosophila where germ cells are pre-allocated in the oocyte, are there technically no adult pluripotent stem cells since germ line cells can't be developed from somatic stem cells?

In almost all metazoa, the pro-germline cells get segregated from other stem cells at an early stage of development and they thrive and differentiate in their neighborhood. This is important in order to preserve the germline. This post provides some basic explanation.

However, even drosophila have adult multipotent stem cells and help in the formation of midgut as reported by this study.


What kind of worm is this in my food? (Tuna sandwich from canned tuna) Can I have some assistance identifying this worm which was in a tuna salad sandwich I purchased from a local co-op in Minneapolis MN?

Looks like a maggot (fly larvae) of some sort — see for example the following image:

That particular image is of a common green bottle fly maggot, which has a distribution consistent with your posted location.


How to write 100% phenotype ratio? I am not quite sure how to write 100% out come for the phenotype ratio after using "Punnett Square". The result from the each alleles, the dominant allele completely(100%) took over the recessive allele.
How can I express my phenotype ratio?

(Let's say....Purple flower→dominant White flower→recessive)

Phenotype/ Purple flower 1: White flower 0
Phenotype/ Purple flower 4 :white flower 0
Phenotype/ Purple flower 4

The phenotype ratio would be 4:0.

You did not include the complete example including the genotypes, but an example that might produce this result is:

P is a dominant allele that produces purple flowers, and pp homozygotes are white.

    P    p
  -----------
P | PP | Pp |
  -----------
P | PP | Pp |
  -----------

The genotype ratio is 2:2:0 (2 PP : 2 Pp : 0 pp) meaning there are 50% PP and 50% Pp.

The phenotype ratio is 4:0 (4 purple : 0 white) meaning there are 100% purple and 0% white flowers.

To keep things simple, you do not need to reduce the ratio to the lowest terms (in other words, the sum of the numbers in the ratio should equal the number of boxes in the Punnett Square). It would not, however, be incorrect to reduce the genotype ratio to 1:1:0 and the phenotype ratio to 1:0.


Which is the correct term haploid daughter cells or haploid parent cells? Meiosis 2 begins with 2 haploid parent cells and ends with 4 haploid daughter cells (gametes). Gametes from the opposite sex can now merge together and fertilize.

If I were to refer to a specific haploid daughter cell merging with another to produce a zygote; are these daughter cells from Meiosis 2 still called 'daughter' cells or are they now called parent cells?

"Parent" and "daughter" terminology is indeed relative. Any parent cell has been a daughter at some point. However, in the case of the zygote there is no "parent" strictly speaking since it is the result of a fusion between two cells, that you may call "daughter cells" only if you are referring to the previous meiosis event.

In this particular case, there is no cell division, so no "daughter" is formed, so no point in calling the haploid cells from M2 "parents" either.


How to typeset gene regulatory networks I have a relatively simply gene regulatory network I would like to visualize, complete with the common arrow and bar symbols used to show, respectively, which genes enhance or repress with other genes. Is there a way to typeset a gene regulatory network using something like LaTeX or Graphviz?

For very simple networks, I guess something like Photoshop or Illustrator would probably be the quickest solution, but these programs become very tedious as the size of the network grows even a little bit. What do people typically use for this type of task?

If you have simple 1:1 connections or can list your data in that manner, you can try Cytoscape (freely available). There are numerous plug-ins to customize what you have in mind in terms of visualization.


How was the Huntington's disease gene's location found? I read in the book "Why we get sick." by Nesse and Williams that:

  Steady detective work and fabulous luck have enabled geneticists to
  pinpoint the Huntington's gene on the short arm of chromosome 4.

I want to know what was the "detective" work and the fabulous luck - the whole story of the discovery of the location of the gene.

A Google search for "Huntingtons disease gene discovery" yielded this page at the Nature Education Scitable website. The following citations are provided regarding the molecular basis of HD:

  Huntingtin (HTT) was the first disease-associated gene to be
  molecularly mapped to a human chromosome (Gusella et al., 1983)2. Ten
  years later, scientists identified the DNA sequence and determined the
  precise nature of the HD-associated mutation in HTT (MacDonald et al.,
  1993).

Gusella et al. used restriction fragment length polymorphism (RFLP) analysis to locate a RFLP marker linked to Huntington's disease on chromosome 4. From the introduction of their paper:

  We have now identified an anonymous DNA fragment from human chromosome
  4 that detects two different RFLPs in a HindIII digest of human
  genomic DNA. This polymorphic DNA marker shows close genetic linkage
  to the Huntington's disease gene in two separate families, although a
  different haplotype of the marker segregates with the Huntington's
  disease gene in each family. We infer that the Huntington's disease
  locus resides on human chromosome 4.

Further details given in the paper might justify the description given in the question. "Fabolous luck" could refer to the discovery or availability of suitable families and pedigrees for the genetic studies. The "steady detective work" would be the genetic mapping and fieldwork required to establish the link. The following quotes describe some of the efforts spent on the project:

  The success of any genetic linkage project depends in large part on
  the quality of family material available for study. We initially
  invested considerable effort in identifying a useful family from the
  National Research Roster for Huntington's Disease Patients and
  Families at Indiana University. An American family of reasonable size
  was selected and blood samples were obtained (...). Subsequently, a
  substantially larger Huntington's disease family was located. This
  pedigree stem from a unique community of interrelated Huntington's
  disease gene carriers living along the shores of Lake Maracaibo,
  Venezuela. (...)For the past three years an expedition has spent one
  month annually in Venezuela collecting pedigree information, tissue
  samples, and clinical data. (...) In Venezuela, many family members
  were examined for three consectuvie years. Permanent lymphoblastoid cell lines were
  again established for each individual to act as a permanent source of
  genomic DNA. In both families each individual was examined by at least
  one neurologist experienced and knowledgable about Huntington's
  disease.

The Scitable page also summarizes the approach and results described in the paper. For the RFLP analysis, several DNA probes were tried, of which one, "G8", resulted in a HD-linked pattern:

  James F. Gusella and colleagues carried out a study to determine
  whether they could identify a DNA probe that would show an
  HD-associated restriction fragment length polymorphism (RFLP) when
  used in Southern blot analyses of chromosomal DNA digested with the
  restriction enzyme HindIII (palindromic recognition sequence
  5'-AAGCTT-3'). The team identified one probe out of 12 tested, called
  G8, that showed a specific RFLP pattern associated with HD in two
  large families with a history of the disease (Gusella et al., 1983).
  Using the G8 probe, they next identified two HindIII sites (called H1
  and H2) that were palindromic within this chromosomal region. DNA
  fragments at these sites vary in length among different HD lineages.
  Because researchers used two large pedigrees in these experiments,
  they were able to obtain statistical support for their discovery
  (Figure 3).

However, at the time the origin of the G8 probe DNA in the human genome was not known, so human-mouse somatic cell hybrids were made to identify where the G8 probe DNA belonged. This showed that the G8 probe corresponded to chromosome 4, and indicated that the HD gene would be found there:

  Researchers found that the G8 DNA probe hybridized only to Southern
  blots using chromosomal DNA from human-mouse somatic cell hybrid lines
  that contained human chromosome 4. Therefore, researchers determined
  that the G8 DNA probe is located on human chromosome 4, and they
  concluded that the HD gene is located on chromosome 4 near the region
  corresponding to the G8 DNA probe (Figure 5; Gusella et al., 1983).


To understand synthesis of e-NOS and n-NOS with respect to Ca and calmodulin I found this sentence in my notes interesting

  E-NOS and n-NOS are Ca-calmodulin dependent ferments.
  They are synthesized in small concentration as a response to physiological signals which increases the level of Ca2+ in cell.

Does it mean that e-NOS and n-NOS are synthesized by mediation of Ca and calmodulin?

I remember how RNS can be derived from nitric oxide and superoxide.
Are e-NOS and n-NOS expressed on macrophages after induction by cytokines and microbial products, notably interferon-gamma and lipopolysaccharide?

Does it mean that e-NOS and n-NOS are synthesized by mediation of Ca
  and calmodulin?

Calmodulin is activated by binding to calcium and NOS is activated by binding to Ca2+-calmodulin. The binding changes the structural conformation which renders the enzyme active. See this.

  Are e-NOS and n-NOS expressed on macrophages after induction [...]

Macrophages generally express iNOS upon induction by cytokines. The activity of iNOS is shown to be different in humans compared to mice; humans have low activity [ref]. However mouse macrophages have been shown to express eNOS constitutively and eNOS-knockout mice show reduced NFkB production and iNOS induction.


How much mechanical stress can a skeletal muscle bear? In the movie- Saw, for the last trap Bobby was told to insert metallic hooks into his pectoralis major muscle. In his fake story Bobby has raised himself successfully, but when he was "really" trapped, his muscles were broken under his own weight.

Is it true, that muscles can be broken so easy? When human is pulling up on the bar, aren't these muscles undergo much more tension, because of lever effect made by his arms?

Also, what if Bobby insert hooks under his ribs, would he die immediately due to pneumothorax?

The question is biological, no interest of how it was possible to overcome trap with mechanical means.

The skeletal muscle is not isotropic and therefore the effect of stress would be different from different axes. The strength also depends on the density of fibers and the composition of tendons (aponeurosis) that connect the muscle tissues; these can change (positively) with long term exercise [ref].

In this article the authors show the effect of different mechanical stresses on the skeletal muscle tissue — digitorum longus, from rabbit hindlimbs.

  Tests were performed on extensor digitorum longus (EDL) muscles,
  chosen for its regular cross-section and low pennation angle (Lieber
  and Blevins, 1989). To ensure that only muscle tissue was tested,
  aponeuroses were carefully dissected away

Figure from the same article by Morrow et al. (2010)

You can notice that the yielding point to longitudinal extension is somewhere near 180kPa. It can be assumed that a hook into the tissue on pulling would generate longitudinal extension stress (unless the hook pierces through the muscle tissue or has sharp edges that can rip the muscle transversely). The stress in the Bobby situation would be: $$\frac{\text{weight (mass)}\times \text{gravitational acceleration}\ (9.8\ ms^{-2})}{\text{area of the muscle covered by the hook} \times \text{number of hooks}}$$

This is the best I can answer your question based on data; this cannot be directly extrapolated to the Bobby situation because:

The muscle tissue is different
The strength of the tissue depends on how much has Bobby exercised his muscles.
There would be additional mechanical stresses in other directions because of his movement while being suspended from the hook.

Ribs are not very strong bones and attempt to hook something on it may cause punctured lungs, not pneumothorax. Death will depend on the severity of the wound.


How do the three mechanisms of the 1000X improved "new" vancomycin work together? The BBC News article Ultra-tough antibiotic to fight superbugs says (in part):

One hard-to-treat infection that has been worrying doctors is vancomycin-resistant enterococci or VRE.
It has been found in hospitals, can cause dangerous wound and bloodstream infections and is considered by the WHO to be one of the drug-resistant bacteria that pose the greatest threat to human health.
Some antibiotics still work against VRE, but the 60-year-old drug vancomycin is now powerless.
The Scripps team set out to see if they could revamp vancomycin to restore its killing ability.
They made some strategic modifications to the molecular structure of the old drug to make it better at attacking bacteria where it hurts - destroying cell walls.
Three changes in particular seem to be important, increasing the strength and durability of the drug.
Lead researcher Dr Dale Boger explained: "We made one change to the molecule vancomycin that overcomes what is the present resistance to vancomycin. And then we added to the molecule, two small changes that built into the molecule, two additional ways in which it can kill bacteria. So the antibiotic has three different, we call them 'mechanisms', by which it kills bacteria. And resistance to such an antibiotic would be very difficult to emerge. So it's a molecule designed specifically to address the emergence of resistance." (emphasis added)

Unfortunately I haven't been able to see the PNAS paper. The link in the BBC article just gives me this:

However the title in PNAS seems to be stated in the Genetic Engineering & Biotechnology News article Vancomycin Modified to Combat Growing Antibiotic Resistance Threat as "Peripheral Modifications of [Ψ[CH2NH]Tpg4]Vancomycin with Added Synergistic Mechanisms of Action Provide Durable and Potent Antibiotics"
It sounds to me that the first change was to keep the original vancomycin's original mode of action but to make it more robust against adaptations in the vancomycin-resistant strain, but I'm not sure if that's correct.
The other two differences sound to me like two new mechanisms that were not there before - it almost sounds like they could just as well be on different molecules administered simultaneously, and that their presence on the vancomycin molecule is primarily for issues of delivery.
Are these two new changes essentially independent modes of actions that could be on separate molecules, or do they need to reside on the same molecule as the primary mechanism?
The article puts the word "mechanism" in quotes. I'm trying to understand if these are independent or work together at the molecular level - in other words do they operate together in such a way that they need to be on the same molecule?

This is typically for a paper under embargo - it can be accessed by registered journalists so they can cover the original article when it is published. The paper is now published, so I changed the first answer.

Before I go into the details, it is necessary to have a short look at the working mechanism of Vancomycin and the way bacteria got around it (which took exceptionally long given that the drug is used since 1959 in the clinic):

Vancomycin works by inhibiting the proper crosslinking of the bacterial peptidoglycan in the cell wall. This is achieved by binding to the substrate for the peptido glycane synthesis, a D-alanyl-D-alanine end of a peptide. Cells then burst due to osmotic pressure.

Resistant cells have a D-alanyl-D-lactate ending of this peptide (all details can be found here or in the introduction of the paper) which lowers the effictivity of the drug by a factor of 1000. Interestingly, this resistance mechanism seems not to have evolved in pathogen bacteria itself, but has been "borrowed" from bacteria which produce Vancomycin and need this as a self-defense (for more, see reference 2).

Vancomycin forms a pocket around the d-Ala-d-Ala substrate, which is impaired in the resistant form. Overcoming the resistance means finding a variation of Vancomycin which effectively binds both of the variants and thus inhibits proper cell wall crosslinking.

To achieve this, Okano and his colleagues chemically modified the structure of Vancomycin with several different functional groups at different sites of the molecule, see this figure from the paper (figure 4 from reference 1):

Changing these residues changes the sensitivity against these modified Vancomycine quite a lot, as can be seen in the sensitivity table in the figure.

When they changed the molecule, they did not only change the binding pocket to allow binding to the different peptide substrates, they also introduced two other independent mechanisms against the bacteria. The most active compound (named 18 in the paper, seen above from figure 11) shows:

  Compound 18, which incorporates the redesigned pocket modification for
  dual d-Ala-d-Ala/d-Ala-d-Lac binding (blocks cell wall synthesis by
  ligand binding, including inhibition of transpeptidase-catalyzed
  cross-linking), the CBP disaccharide modification (blocks cell wall
  synthesis by direct transglycosylase inhibition without
  d-Ala-d-Ala/d-Ala-d-Lac binding), and the C1 quaternary ammonium salt
  C-terminal modification (induces membrane permeability), exhibited the
  most potent inhibition of cell wall synthesis in the assay of all
  compounds assessed.

Okano and colleagues also tested the different modifications one by one to see, which one has which effect and also tested the effectivity on resistant bacteria. The resulting table shows that the strongest effect is only achieved when all three modifications are present in the molecule.

Since these are independent mechanisms, it will also prolong the time until resistance against the new version of Vancomycin (given that is has a tolerable toxicity in humans and can be introduced into the clinic) will take a while to develop. Despite the optimism in parts of the paper this resistance will eventually develop, although it is quite complicated to overcome three different mechanisms.

References:

Peripheral modifications of [Ψ[CH2NH]Tpg4]vancomycin with added
synergistic mechanisms of action provide durable and potent
antibiotics
Glycopeptide antibiotic resistance genes in glycopeptide-producing
organisms.


Identification of a Kakadu bird This species of bird was spotted in Kakadu National Park, NT, Australia. It looks a bit like a lemon-bellied fly catcher, but I think my bird here is a tad bigger than the fly catcher, but I am unsure.

I was hoping one of the more ecologically proficient people here could help me out.

Note: This is the 3rd related question on this topic, so feel free to close-vote-for-whatever-reason, but I am generating a photo album with all the birds I have spotted there (heaps!), and a few of them I can't identify with the limited resources I have.

It is great bowerbird (Chlamydera nuchalis). It is much bigger than the mentioned flycatcher. I have seen both species and there is no room for confusion. Most of the pictures online are birds perched on the ground next to their "buildings", but I found a picture that should convince you.

Notice:

-Stout bill

-Patterned wing coverts

-Marks on the undertail coverts


Are there any examples where 'magic bullet' drugs have worked in cancer treatment? Magic bullets are drugs that can be administered on a micro local scale. In this context administration/binding would occur in or near the tumour by exploiting the different surface antigens that cancers expose. Basic lectures teach that a "magic bullt" drug could attach via an mAb (attached to the pro-drug) and then a conjugated enzyme cleaves or converts the pro drug to a drug. This would eliminate a lot of side effects from chemotherapy.

Use in clinical trials. Some mAbs have started to be used in clinical trials, almost 40 years after they were first proposed. My question is simply; have there been any cases of mAbs being used as a successful treatment for any disease? If not, what makes the R&D of this drug type so difficult?

There are, indeed, several such mAb based treatments. From the Mayo Clinic:

  The monoclonal antibody drug rituximab (Rituxan) attaches to a specific protein (CD20) found only on B cells, one type of white blood cell. Certain types of lymphomas arise from these same B cells. When rituximab attaches to this protein on the B cells, it makes the cells more visible to the immune system, which can then attack.

(...)

  Cetuximab (Erbitux), a monoclonal antibody approved to treat colon cancer and head and neck cancers, attaches to receptors on cancer cells that accept a certain growth signal (epidermal growth factor). Blocking this signal from reaching its target on the cancer cells may slow or stop the cancer from growing.

(...)

  The monoclonal antibody bevacizumab (Avastin) targets a growth signal called vascular endothelial growth factor (VEGF) that cancer cells send out to attract new blood vessels. Bevacizumab intercepts a tumor's VEGF signals and stops them from connecting with their targets.

(...)

  Ibritumomab (Zevalin), approved for non-Hodgkin's lymphoma, combines a monoclonal antibody with radioactive particles. The ibritumomab monoclonal antibody attaches to receptors on cancerous blood cells and delivers the radiation.

(...)

  Ado-trastuzumab emtansine (Kadcyla) is one such drug approved to treat HER2-positive breast cancer. Ado-trastuzumab emtansine contains an antibody that attaches to the HER2 receptors on the breast cancer cells. The cancer cells then ingest the antibody, which releases a few molecules of chemotherapy.

It does eliminate side effects, although the treatment is not side effect-free.

Personally, my suspicion with this approach is this: At its heart, cancer is a problem of uncontrolled cell division. Most cells in the body do not divide rapidly, and this slowing down of proliferation is integrated into differentiation into whatever tissue the cells are in. The most obvious cells that divide rapidly are stem cells (themselves carcinogenic!). Furthermore, it seems to be a common theme in cancer that the less differentiated (or more de-differentiated) you are, the more easily you divide, and hence the nastier the cancer you generate.

As such, the worst cancers out there are going to be very undifferentiated, and express few eligible surface markers. What's more, tumors evolve. If you start selecting against cells which express your marker, you will encourage the tumor to simply evolve and stop expressing that marker. Back to the benchside to look for a new marker - meanwhile your patient gets worse and worse.

This is why generalized chemotherapies (or radiotherapy) are so attractive. They attack the rapid division of cancer cells, and the cancer cells cannot evolve to lose this property, because if they did, they would not be cancer cells.


Which two organelles absorb acid? I stain an unknown acid with purple dye. Later, you find the cell in two organelles. What are they?

I am guessing that one of them is lysosomes, because they break down unwanted elements. What would the second one be? Mitochondria?

The principle of staining works in such a way that acidic dyes stain the complementary basic components of the cell hence acidic dye rather than staining lysosome which is acidic will stain the relatively basic components of the cell.


What is the relationship between protein-protein interaction networks and metabolic networks? I am trying to find out how these networks can be linked together. I know that Protein-protein interaction networks and metabolic networks both fall under the Intra-cellular type of biological networks that describe the cellular functioning. But what is the relationship between them?

Thank you very much.

In short, proteins in Protein-protein interaction networks perform a function by directly interacting with one another.  They may for instance bind to one another forming permanent or momentary complexes (e.g. insulin binding to insulin receptor or the pieces of F0-F1 ATPase combining), or they may chemically modify one another (e.g. protein kinases adding a phosphate to the residue of another protein).

Proteins in a Metabolic network might never be in physical contact one another. They effect one another by producing chemical compounds which are utilized by other enzymes, forming a network of chemical transformations.

Of course an enzyme in a metabolic network might also have its activity modulated through interacting with other proteins in a protein-protein network.  The two terms are of course not mutually exclusive, but describe different sorts of relationships between proteins.


Any idea what this fish is? Bought this Fish at the pet shop today. Forgot it's name.
That pink fish

Your fish in question is a zebra danio GloFish; they're genetically engineered to have flourescent coloration. The giveaways for me were the shape of the body (minnow shaped, with zebrafish belonging to the minnow family), its size (small), and the striped pattern running along the body, parallel to the lateral line. Since the fish in your picture is in motion, it's a bit difficult to see, but it's definitely there (can be seen closer to the head).

And here's another image, where the coloration is closer to what you have. (IMO, the previous image has a strong contrast, especially with the black background)

This zebrafish is suffering from a bent spine, which accounts for the misshapen body. (source)

Also, it seems that the fish in the background is a black-skirt tetra.


Can anyone identify this microorganism? I was examining some rainwater from my backyard in Richmond, VA, and found this microorganism. I took some pictures of it at 400x and 1000x (see below). The microorganism is attached to some moss and appears to be using it as an anchor while hunting/feeding. While feeding, it stretches out and searches for food, and once it catches something, it snaps back into itself. I also got some pictures of the microorganism while resting.

I'm not sure what this is and would appreciate any input. Thanks!

They seem to be rotifers, the fuzzy (supposedly rotating) mouthparts are part of what convinces me. The behavior you mentioned of latching on the moss with their 'tails' is also a characteristic behavior of rotifers. They are also able to retract their bodies just as you mentioned.
Here are some images of rotifers that might support the argument.

I am least certain about the last image but I am making the assumption for now that it is either some variety of circular/retracted rotifer or a completely different kind of microorganism.
Stay curios!


What is the name of this red and blue striped spider (?) - Brazil, Rio de Janeiro Anyone knows the name of this thing? I found it in our bathroom. It is maybe 10-15 mm.

It looks like a spider but the colors left me puzzled

This appears to be some species of jumping spider (family Salticidae) in the genus Psecas.

For example, some red/blue striped species of Psecas:

]

 Sources: Top: Alchetron.com (image: Edwards, 2001)  |   Bottom: Tree of Life (image: Maddison 1994)

Wikipedia lists the following species from Brazil:

Psecas chapoda (Peckham & Peckham, 1894) – Brazil
Psecas chrysogrammus (Simon, 1901) – Peru, Brazil
Psecas viridipurpureus (Simon, 1901) – Brazil
Psecas zonatus (Galiano, 1963) – Brazil

Psecas chrysogrammus is my best guess given my limited knowledge of the specimen, this family, and arachnid literature.

We likely can rule out P. viridipurpureus (see here) and P. chapoda (see here) because of the longitudinal striping pattern of the dorsal abdomen of these two species.

I couldn't find any definitive or reputable sources regarding P. zonatus.

The sketch of P. chrysogrammus here seems to indicate that this specific species has the horizontal striping seen in the OP's specimen.

Salticidae.org provides these sources for P. chrysogrammus ID info:

M. E. Galiano 1963b. Las especies americanas de aranas de la familia Salticidae, descriptas por Eugene Simon. Redescripciones basadas en los ejemplares tipicos. Physis, Buenos Aires, 23 (66): 424, t. 32, f 14-18.
Simon E. 1901a. Histoire Naturelle des Araignees. 2(3-4) Paris: 460, f 528, 533(=H).


In what range do humans generally interpret sound best? I am currently working on a speech recognition frameworks. A generally used feature used in speech recognition are MFCC features, which uses the mel scale to extract features with.

The mel scale visualises how humans interpret different frequencies of sound compared to each. The graph shows that by linearly increasing the frequency from 0 -1000 will the sound/pitch be interpreted as linearly increasing. When the frequency is linearly increased beyond 1000 hz, is the sound not interpreted as linearly increasing but logarithmic increasing.

How MFCC make use of this:
When training the system, are audio files processed using band pass filters with center frequencies that are mel distant, meaning that they will be (somewhat) linearly increasing at the beginning and end up being logarithmic increasing.

How do I interpret this:
It seems to me that the human auditory system is very susceptible to sounds the range 0-1000 and not much above, but 1000 hz isn't much and I guess conversation must in somewhat higher range. So why are humans more susceptible to sounds in these ranges?

I work on voice recognition too. Yes, very brilliant query about sound perception that I can clarify and not answer completely. Most of the text belongs to DSP SE forum, i.e. Voice rec, MFCC, filter, BP, audio processing. You may have confused the readers except for the image and the final paragraph.

I had to rephrase it to clarify it to myself:

Why are humans unable to hear pitches on a straight maths scale, they hear logarithmically? We hear according to a mystery ratio called MEL distribution, a well studied summary of many subjects perception of pitch, averaged to:

0.01% Humans have Perfect pitch, 95% are relative pitch, and 5% are tone deaf. MEL varies by the type of listener. Tone deafness is hereditary, ( info about biology and brain structurehere) and the rest of humans probably follow a gradual distribution of poor to good pitch differentiation, and they also hear amplitudes differently.

As you can see from the wiki page, there is no explanation for MEL theory, it's either neurological, a soundwave energy balance, or because of the ear anatomy.

To answer the title question, your graph shows humans have a continuous response to frequency spacings through all their perceived sound. However volume tests show amplitude sensitivity peaks at about 3kHz, which you can see on inaccurate amplitude perception and equal loudness contour graph.

MEL studies of Steinberg are stagnant since Volksmann, same as Donald D Greenwood suggested in 2009, they overgeneralize and the field needs to be developed a lot further under a different study name than MEL scale, which isn't english.

Why can they hear voice well under 1000Hz?

At least 1/2 of the sound energy of voice occurs below 1000Hz, same reason bass requires a lot of energy.

So humans can hear sub 1000Hz sounds from further away, but the more sound data you have the clearer the voice is, and computer should use nearly all of possible human voice frequencies to measure formants and N/M consonants to best accuracy. Sub 1000Hz may contain enough vowel subharmonic frequency bands at different spacings to represnt the vowels of sound basically, but it is less clear and realistic if the voice is filtered at 1000Hz, the subharmonics of AEIOU go multiple octaves above middle C male/female voicebox peak, near 440Hz.

The sub 1000Hz components are generated by the voice box, which changes tone at a slow rate, whereas the 2000-3000Hz sounds, i.e. Frictives, S,F, and N aspirated P, k, don't require very as complex sound processing to interpret (for digital sound filter processing)

The 625-1000Hz pivot component of the equation doesnt appear less straight under 1000Hz if the graph is from a parametric frequency view.

To resolve your query, Biologists would want to know:

1/Structure of the ear as a reason for sound perception imbalance
2/Child learning and adult learning of complex pitch tasks
3/Brain structures used in pitch recognition
4/Evolution of ears and psychoacoustics, reason for a hearing peak at 3k which is the same as rustling leaves
5/Physics energy and mathematical reason for MEL distribution (ask on DSP SE)

As a Voice rec researcher, you should think outside of the box. Computers don't hear like humans. Frictives like F and S have peaks around 3000-4000HZ, they are the highest and easiest to recognize and similar in all accents. Formants from vowels can peak from 400 to 500HZ roughly in men and women, at 700hz for children.

Vowels are vague and vary by accent are are the least precise element in voice-rec. That's why voice recognition hinges a lot on formants and accents which have energy peaks below 1000HZ, and timbral graphs which change wildly wether it's AEIOU sounds.

As a side not for voice-rec,
English is tougher to recognize than French because of the stress time, swingy nature and the 2-3-4 vowels per syllable, and perhaps that's why French have lost the wild traditional accents faster (I know I speak both since I was 0). Voice rec of French and other syllable time languages is easier.

I don't know why MEL is used at all in voice-rec filters. Perhaps because people use the same intonations as they hear from MEL, so the PC must know too, else because the programmers don't know enough about real sound physics, and have implemented it as a rough power-balancing graph for filter results? else some other physics reason. Other power-related filter shapes should work fine, as DSP SE if this has a known physical basis of if it uses human psychoacoustics for digital audio inaccurately:
mel-frequency cepstrum (MFC) is a representation of the short-term power spectrum of a sound, based on a linear cosine transform of a log power spectrum on a nonlinear mel.

Humans don't need perfect pitch for anything except music. Relative pitch, we nearly all have ok, and it makes sense because biologically relevant sounds, animal calls, physical signals of water, trees, voices, add together to make a continuous freqency spectrum that we have to measure all the frequencies by a similar rating of importance to interpret best. Voice contains lots of micro-expression subtones that represent clear psychological states that humans benefit to hear, and rustling leaves and other sounds all should biologically benefit from a high relative pitch clarity.


Quantity of toxin release by pathogen in host I came across these lines from this paper:

  Pathogenic microbes exert a broader sphere of influence by releasing a bolus of toxin that can act upon many cells within a given tissue and/or diffuse away to modulate one or more types of cells at multiple locations within the host.

What does this line mean? Does it mean that the pathogen releases multiple types of toxins or does it mean that the pathogen releases just one type of toxin in a large quantity?

As I commented, a bolus is a single (often large) dose of a drug or compound given (released) all at once. Please read the very next sentence after the one you quoted:

  For example, the lethal and edema toxins of Bacillus anthracis disseminate within the host bloodstream and act upon both immune and nonimmune cells.

This gives an example of a pathogen releasing multiple toxins, although there are other pathogens such as Clostridium tetani which release a bolus that consists of only one toxin. So, it can be one or the other.


Is there any reason to use an upright microscope over an inverted microscope? I've never actually owned an inverted microscope, but it seems it has only advantages compared to an upright microscope: taller, heavier samples; no crashing the objective into the glass slide; easier to operate, etc.
Why then do people still use regular, upright microscopes? Is there a disadvantage I'm missing?

As already mentioned in the comments, cost is one of the primary reasons when you're looking at simple light microscopes. Inverted scopes have more complex optics, along with the convenience factor of being able to examine larger samples, generally having a more stable frame, etc. All this leads to higher cost.
An advantage I can think of for smaller upright scopes is the ability to use them as a dissecting scope, where the sample is opaque and you need to see it from above. Another advantage is this:

Many fluorescence microscopes are upright, as there is a significant amount of extra equipment that needs to be mounted in addition to the eyepiece, including lasers, stage motors, and cameras and other detectors. This can take up a lot of room, and for convenience's sake it's often easiest to mount it up top where it is accessible.


Help identifying an insect by its remains Yesterday i hiked in Bolsena lake, Italy. I felt this insect moving into my ear. So i smashed my ear and this is the result. Please tell me that there are no risks related to Lyme desease or similar.
Sorry for the bad quality of the photo.

It is probably a beetle.
The shape of legs and the two big eyes are an insect thing.
Lyme desease is transmitted by ticks, so i would not worry.


Classification and differences between homologous, homoplastic, analogous, derived and ancestral traits? My question is contextualised for basic phylogeny knowledge. Here is my understanding: similar or identical traits between any two species, at the basic level, can be either homologous, meaning the trait is developed from a common ancestor, or homoplastic, meaning that the trait was independently developed.

Homologous traits can be either ancestral or derived, and derived traits are a subset of ancestral traits as derived traits need to be from the most recent common ancestor.

Homoplastic traits can be analogous, meaning they developed independently without any common ancestor or commmon initial trait, or can be traits that arose due to convergence, where species with the same (distance/close) ancestor independently developed the traits.

Please evaluate whether my understanding is correct.

This vocabulary is common in textbook but not in the peer-reviewed literature

First please note that while those terms are often used in intro class to evolutionary biology, they are actually rarely used in the peer-reviewed literature.

No trait value is fundamentally derived / ancestral

Note also that any given set of shared trait could be called ancestral or derived depending on the size of the tree that you consider. A trait is therefore not fundamentally ancestral / derived, it depends upon what other trait value you compare it to. Per consequence, it would easier to have a tree under our eyes to discuss these terms.

Note that there is one exception to that. Traits that are shared with LUCA are fundamentally ancestral!

Two states in different lineages can be fundamentally homologous / homoplastic

In general, when we are interest in a given trait, we display a tree so that all homologous trait states appear ancestral. While it is true that homoplastic trait state are necessarily derived when shown, homologous trait state can be shown as derived from a yet more ancestral trait state.

Analogy vs homoplasy

Many think of an analogy as a synonym of homoplasy. However, have a look at @GerardoFurtado's answer for the subtle difference between the two.


Does exhalation help us speak, and if so, how? Everyone knows that we breathe in oxygen and breathe out carbon dioxide. That's how the respiratory system works. But we also use the respiratory system to produce sound and language. When we speak or emit sound, our glottis opens up, and depending on whether the sound is vocalized, our vocal chords vibrate. We then use articulators (tongue, lips, teeth) to shape the sound we produce.

But what kind of air is emitted in the first place? When our glottis opens up, what kind of air is passing through, and why does it pass through? The most obvious answer, which is my first guess, is that carbon dioxide is passing through our glottis and our trachea, and that we use this to create sound. In this way we would be using the product of respiration for a separate purpose: to create sound and communicate.

This is only a guess. But a logical one. The question, to put it most simply, would be, do we utilize our natural cycle of exhalation to produce sound and speak? Or is something else going on?

Not including water vapor, argon and trace elements, inhaled air at sea level: ~79% nitrogen, ~21% O2, ~0.04% CO2. Exhaled air: ~79% nitrogen (the body doesn't "use" inhaled nitrogen), ~16% O2, ~4% CO2

It is this exhaled air we use to speak. However, there is a very minimal increase (and I do mean minimal) in the CO2 concentration and decrease in the O2 depending on how fast we speak, how often we stop to take breaths, etc. compared to plain, expired breath. This is because the inhaled air is being held back in the lungs and released more slowly as we speak, giving more time for O2/CO2 exchange to occur. However, it will mostly occur in what's called "dead space" and the %CO2 will be changed for a few breaths thereafter as well.

To demonstrate this, speaking until we're "out of air" should make us slightly dizzy because maximal exchange will have taken place at a certain point, after which our blood CO2% will rise, and our blood O2% will fall.

After that, the higher serum CO2 will cause us to take a deeper breath, a 'cleansing breath' if you will, to jump start the return to normalcy in blood gasses. It is very, very hard to resist this deep breath (which is why breathing has a voluntary and an involuntary component, i.e. you can't hold your breath until you die.)

Breathing


What is phenotyping of blood during transfusion process? Thallaesemic patients are advised to have only "phenotypically matched blood".I mean the transfusion problems arise mainly due to "grouping problems" like mismatch b/w ABO & Rh+/- so what do this phenotyping mean? Isn't "grouping" of blood enough?

Statutory declaration- the link provided in the q is only to clarify in which context the q is asked & nothing more, like promoting Egyptian Gov. Health Service...(or any other CRAZY INTERPRETATIONS like that)**

In response to the above q. many have commented that the process is only limited to Middle Eastern countries....I think the term 'only' will be better substituted by 'mainly', the reason to which , is explained later ....

Now, the main clarification lies in the fact that,

  ....there are more than 600 known antigens besides A and B that
  characterize the proteins found on a person's red cells. A combination
  of some of these less familiar but commonly occurring antigens are
  absent from the blood of an extremely small percentage of the
  population. There are also a few antigens that almost all people have
  on their red cells but that some lack. - One In A Million
  American Rare Donor Program

Now patients receiving a 1st time transfusion normally do not show any reactions or cross-matching problems with these blood subgroups but during repeated transfusion process like in case of thallaesemia , the receiver's blood gets sensitized against the donor's blood & the problems ensues...

  Dr Therese Callaghan said, “All other antibodies are unexpected and
  are of two distinct types, alloantibodies (which target an antigen
  that is not present on your own red blood cells) and autoantibodies
  (which target an antigen that is present on your own cells).

  “Patients receiving a transfusion for the first time do not normally
  have problems with matching blood types and antigens. However it is
  during subsequent transfusions when more care needs to be taken. If,
  during a later transfusion, the blood contains the same antigens as an
  earlier one, the patient’s immune system recognises the transfused
  blood cells as ‘foreign’ and the antibodies (formed after the first
  transfusion) will destroy the blood cells the patient has been given.
  This is called a transfusion reaction and can cause serious illness or
  even death if not treated quickly. That is why matching the blood
  phenotype is so important.”

Now coming to "Why mainly in Middle-East ??"

These rare blood groups are distributed into major 30 discrete system, which mainly  are present in different ethnic groups & communities...mainly living in Middle-Eastern states & Asia...& also in African countries...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3353626/table/T3/

Intersted people may also check the following articles (or simply search Google)

To Provide Phenotype-Matched Red Blood Cells or Not – That is the Question!

13.3: Pre-transfusion testing- Joint United Kingdom (UK) Blood Transfusion and Tissue Transplantation Services Professional Advisory Committee

& for a complete picture plz browse through- Immunohaematology


harvesting fertilized eggs from Tetraodontidae species? I would like to know how easy/difficult it is to harvest fertilized eggs from Tetraodontidae species such as Tetraodon nigroviridis or Takifugu rubripes compared to zebrafish? Ultimately, I would like to know how much material would be obtainable from Tetraodontidae eggs to extract DNA from the nuclei.

I know zebrafish lay lots of eggs, and other model fish species like medaka lay much fewer of them, but I couldn't find any information about Tetraodon nigroviridis or Takifugu rubripes after some googling.

For DNA extraction, you would need only a few eggs. PCR would then give you all the copies of your target gene(s). A quick Google Scholar search on Takifugu fecundity revealed a paper by Yang and Chen (2008). They found that T. obscurus produced an average of 320.8 oocytes mg$^{-1}$ ovary wet weight. In comparison, T. ocellatus produced 125.2 oocytes mg$^{-1}$ ovary wet weight. Takifugu rupripes and other species are likely in a similar range, which is plenty of tissue for DNA. Kusakabe (1962) published on the fecundity of T. rubripes but the paper is in Japanese and is not readily available to me.

Beware: T. rubripes ovaries are highly toxic. Why not use other tissue instead?


Neuroscience of confusion How does (neuro)science characterize "confusion" that occur to "healthy" persons when engaged on a particular mentally-intensive task?

I would exclude the case where we are rationally and with clear arguments deciding one out of many choices (but remain undecided due to lack of sufficient resource/information). My thinking is more towards the case where, for example, we are trying to understand a mathematical problem and its solution, or an abstract reasoning, but in the process get lost: even have no clear idea of what part is 'not understood', or where to start learning (the parts involved) so that we can understand the original problem.

I am aware that I am unable to make my question very clear, I am actually confused how to formulate my thoughts.

Here's an article I found that seems to attempt to address this question, using a kind of machine-learning approach involving "Long Short-Term Memory" (LSTM)-Recurrent Neural Networks (RNN), to classify EEG from participants who were watching either "easy" or "difficult" online lectures - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5620019/ .

It's not a complete account of their process, but the manuscript suggests that gamma-1 frequency bands in the frontal lobe (using a single EEG electrode) were the most valuable feature for distinguishing between trials in which participants were thrown into the middle of a challenging lecture, vs. trials in which participants were viewing the introductory background material at the beginning of the lecture. I'm interested in the same question as the one you proposed, so I hope to see more responses to your post!


What is 'refractile' cell morphology? I can't find a definition for 'refractile' (not 'refractory', and not explicitly in an optical context).

As in:

  A tumour cell phenotype features increased proliferation, anchorage- and growth factor-independenth growth and ‘refractile’ cell morphology

It's not in any of the dictionaries I can access online, nor in the Oxford Dictionary of Biochemistry and Molecular Biology. Any help would be appreciated, thanks.

From the Biology Online Dictionary, refractile refers to:

  ... the ability of cellular granules to refract or scatter light.

Tumor cells can be more "dense", as they are usually rapidly dividing, and so need extra ribosomes to maintain protein production, may have a higher DNA/RNA content reflecting increased transcription and duplication, more mitochondria to power the cells, etc. This can alter the refractive index of a suspension of tumor cells as compared to organ-matched normal cells, for example.


Why do we get 'bags under our eyes'? Why do these circles form around the eyes if somebody is tired? And why does fatigue express itself around the eyes this way? Can I get eye bags very quickly in another way?

http://www.todayifoundout.com/index.php/2014/06/causes-dark-circles-eyes-sleeping-people-really-tired/

http://www.top10homeremedies.com/how-to/how-to-get-rid-of-dark-circles-fast.html

According to the Mayo Clinic website:

As you age, the tissue structures and muscles supporting your eyelids weaken. The skin may start to sag, and fat that is normally confined to the area around the eye (orbit) can move into the area below your eyes. Also, the space below your eyes can accumulate fluid, making the under-eye area appear puffy or swollen. Several factors can lead to this, including:

Fluid retention due to changes in weather (for example, hot, humid days)
hormone levels or eating salty foods
Not getting enough sleep
Allergies or dermatitis, especially if puffiness is accompanied by redness and itching
Heredity — under-eye bags can run in families

Of the list above, the most common reason is likely heredity.
Sources:

Mayo Clinic, as linked above
http://www.allaboutvision.com/cosmetic/puffy-eyes.htm


In theory, would it be possible to create an injection of Vitamins, Minerals, sugars etc so that eating was no longer necessary? I am wondering, out of pure curiosity, whether with current medical & biological science, (or indeed with accepted probable future developments in those areas), in theory, would it be possible to create an injection of vitamins, minerals, sugars etc so that eating was no longer necessary, and in fact, an average life with average energy usage could be continued?

I am not a biological professional nor academic, so apologies if this is on the wrong Stack Exchange site, however I thought this was closest to the mark. If there is somewhere more appropriate please direct me, and I shall delete the question and post it there.

Also, if no, would there be certain parts that you couldn't replicate in an injection or something of the like?

NB: This doesn't have to be an injection, any simple method of ingesting or attaining everything the body needs. This could be a pill, or anything. I simply used an injection as an example.

Thank-you very much.

Edit:
Having found this question,
Has there ever been an attempt to create nutritionally tailored food for adult human consumption?
I would like clarify. This has given me a lot of information, however, I am looking for any method APART from food. Thanks.

The quantity of nutrients the body requires takes much more physical space than can be included in a simple pill or injection (used only a few times a day).  But nutrition can be provided by IV (intravenous administration), and it is used today for some medical conditions.  When the IV completely substitutes for normal digestion, it is called total parenteral nutrition (or TPN).  The procedure is simple and reliable enough that it can sometimes be used outside of a hospital setting and be self-administered by users at home.


Does "RT-PCR" denote "real-time PCR" or "reverse transcription PCR"? I often find the term "RT-PCR" used in articles without any further qualification. Searching for the meaning of the acronym sometimes leads to "real-time polymerase chain reaction" and sometimes "reverse transcription polymerase chain reaction." I understand that reverse transcription PCR uses a reverse transcriptase to convert RNA to DNA, which is then amplified by the usual PCR method. I'm not sure I understand what real-time PCR is, but it sounds to be distinct from reverse transcription PCR. Are these distinct methods that happen to have the same abbreviation? Or do they somehow mean the same thing? What is usually meant by the acronym "RT-PCR"? Is there some context I can use to distinguish them?

Real-time PCR is used to quantify a PCR target by measuring some indicator of target amplification in real time after each amplification cycle, thus it is sometimes(often) called quantitative PCR (qPCR). The key to distinguishing between reverse transcription PCR and real-time PCR in the context of a paper or protocol is to look at the starting material being used and the data output.
If the source material is RNA, it needs to be reverse-transcribed into cDNA before PCR amplification. And if they're showing quantification of a specific target, it's likely a real-time PCR of some sort. Quantification of a gene target from normal DNA is likely a standard real-time PCR (aka qPCR). Quantification of an RNA target (like gene expression from mRNA), is likely quantitative reverse transcription PCR (RT-qPCR). The same goes for if the starting material is cDNA (end product of an RNA reverse transcription reaction). Lastly, any mention of Ct or Cq values (or delta-Ct, or delta-delta-Ct) generally indicates a real-time quantitative methodology.
If they are citing the use of RT-PCR to simply confirm the presence or absence of a target (sometimes called endpoint PCR) or to amplify it for downstream applications like sequencing, with no mention of specific target quantification, it's likely a standard reverse-transcription PCR.
There are exceptions to some of these rules, but it should help get you through most literature with some idea of what methods are being used.
Edit: In the past few days, I've seen multiple papers using "RT-PCR" as shorthand (I guess) when they were talking about RT-qPCR or rRT-PCR. Like I said, always exceptions to the rule. But as long as you read the methods it should be simple enough to figure out.


Is the amount of dNTPs rate limiting for very long PCR products? I'm using the Q5 system and I'm PCRing a product that will have a final length of around 9500 bases. I have noticed that the product is there but very faint. The primer seems to be used up.

So my question is, can the dNTPs be rate limiting in a long reaction? That is, can all the dNTPs be used up in the first PCR cycles and maybe not be available for the later exponential rounds?

It seems you have about 1000 times the amount of dNTPs to the amount of primer (200 µM compared to 0.2 µM). So maybe...or is my basic chemistry off. Any precedence?

200uM dNTPs in 50ul reaction mix could produce more than 10ug DNA if all dNTPs were consumed whatever the length of PCR products is. You could detect as low as 5ng DNA fragments by conventional electrophoresis using EtBr. You probably could see a clear band when you load more than 100ng of a DNA fragment. Therefore I am not worried much about the dNTP concentration.

The longer PCR products you amplify, the more difficult it is to amplify. Then you may not get enough efficiency to detect your PCR products. You might want to try lower annealing temp if you do not get any none-specific bands with/without some additives such as DMSO, betain, etc., or use more stronger enzymes. Also touch down PCR may be useful to get specific bands efficiently.

When you increase dNTP concentration, Mg++ effects may be muted because dNTP could chelate Mg++ as Chris mentioned in the comment column.


How do scientists create specific mutations? Suppose I want to create a mutant like Antennapaedia how will I go about accomplishing it ?

I know that radiation and certain chemicals are mutagenic. So do scientists subject animals to such mutagenic chemicals and then wait for their progeny to see what mutation it has got ? Are there any specific protocols to create a specific type(for eg.homeotic) of mutant or is it pure luck ?

Sorry if I am being too naive!

Thats basically the oldest method to induce such mutations. For this purpose either radiation (x-rays) or mutagenic chemicals (like Ethylnitrosourea) have been used for this purpose. This method is undirected, so you never know what the outcome will be untill you see the off-springs. Using this method to get specific mutations is relative difficult. Its used for the detection of genes which deliver visible phenotypes (for example it has widely been used for the analysis of pigmentation in mice, since you can easily spot mutations).

Newer methods can target genes directly and either introduce or remove sequence areas. These techniques make use of homologous recombinases. In short you bring in you gene of interest in the modified version on a plasmid into the cell which you want to change. The plasmid also expresses the recombinase (this can be under a cell specific promoter to target specific cells) which then recombines the DNA between the plasmid and the genomic DNA.

An example for that is the FLP-recombinase system (image from the Wikipedia article on it):

Other examples for site specific altertions are the Cre-LoxP-System or the Crispr/CAS-System.


What is the simplest autotrophic cell? Very simple cells, such as Nanoarchaeum equitans, require a host to provide certain essential ingredients for life. Complex life-forms (like humans) require a whole ecosystem of other life-forms to survive (either externally, to provide food, or internally, in a symbiotic relationship).

What is the simplest cell that has been discovered so far that can live in an environment where there are no other life-forms, not even in a decomposed state? Does such an organism exist, or is all life inextricably dependent on other life?

If by "simplest" you mean smallest genome, then according to Brock's Biology of Microrganisms (13th ed, p 319) the smallest autotroph is Aquifex aeolicus, a chemolithotroph bacterium. It's genome is 1.5M bases, about 1/3 of that of E.Coli, and was sequenced in 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9537320).

The genome is densely packed though and still carries some 1,500 open reading frames. The authors of the genome sequencing paper states that "metabolic flexibility seems to be reduced as a result of the limited genome size", which I guess is some evidence of "simplicity".


Are 2 eyes necessary for 3D vision? To start off: I'm not a biology student, but a computer science major

It has always been my understanding that humans have 2 eyes so that we can have 3D vision: the left eye see more of the left side of an object than the right eye and vice versa, this helps us to estimate depth among other things.

Now when I close one eye, I still am able to perceive depth: I assume this is because my brain fills in the blanks? For how long does this work? Do people eventually lose the depth perception (or at least is diminishes significantly) when they lose a single eye?

If so, how low does it take? If not, clearly we are capable of perceiving everything with one eye: why do we then have two (besides redundancy and a larger field of view? What is considering the evolution of man better in having 2 eyes as opposed to 1 or 3,4,..?

It seems like you suffer from a misconception. "The left eye sees more of the left side of an object..." is not how distance perception works. Otherwise we wouldn't be able to estimate the distance from flat objects, such as traffic signs and shooting targets.
The actual mechanism is parallax estimation, or Binocular disparity. In a nutshell, the closer an object is to your eyes, the bigger the difference of its position on the left and right eye's retina will be.
You may perform a simple experiment: find a place where several parallel wires hang in the air: a train line or aerial phone/power line. Look at the wires normally, and they will appear just as black lines in the sky, with no distance perception. Now tilt your head to the side, and you will instantly gain a feeling which one is closer, and which one is further away. Why the difference? Because any shift of a horizontal wire gives the same picture, meanwhile for vertical wires the difference is obvious.
When you close one eye, your brain loses the ability to estimate parallax. However, it is left with several options:

Visual cues. If one object overlaps another, it's obviously closer. If two objects look the same but one is smaller, it's probably further away (or a child). If you know the expected size of an object (a mountain/a horse/a fly), you may get the feeling of distance as well.
Focusing distance. When you focus your eye on a near and far object, the feelings are different.
Memories. You remember what you've seen with two eyes.

Of these, only (3) depends on previous binocular vision. (1) and (2) are available even to those who were born with one eye. However, parallax estimation is much faster and more precise. With a single eye you will be able to hit a fly on the wall, but catching it in the air will be extremely difficult.


Evolutionary Midways Given that the mechanism of natural selection is sensitive, how do species survive in an evolutionary midway? The ability to breath in air requires complex protein systems. An animal that is developing these organs would not be able to utilize its function until it fully evolves. While it doesn't, wouldn't the wasted resources used in growing half-developed lungs be.. wasted? Or is all evolution continuous?

It is a common question

Statements of the kind "Evolution is impossible because of intermediate state" are common from religious extremists literature. There is therefore a lot of resource online that already debunk this type of statement but I guess, I'll just quickly write one more! Of course, I am not suggesting that you are taking an opinion-based position, you might well be genuily seeking for an understanding of the world.

Quickly speaking there are a series of concepts that are necessary to understand in order to answer this question.

Fitness landscape and fitness valley

The term "evolutionary midways" is not used in biology but one can rephrase it with the concept of fitness landscape and fitness valley.

Fitness landscape

The fitness landscape is the function that maps fitness (generally represented in y-axis) to phenotypic trait value (typically multi-dimensional but often represented on a single axis for simplicity). Fitness landscape may also refer to the mapping from genotype to fitness but we will not be concerned with that for this answer.

Fitness valley

A fitness valley refers to a region of low fitness on the fitness landscape. The movement from one locally high fitness state to another locally high fitness peak might well get through a region of low fitness. This is what you call fitness valley and on the fitness landscape and this is what you are interested in.

Is there always a fitness valley?

Let's first consider reasons for which a population might not experience such fitness valley

Logical Fallacy: Argument to ignorance

It is common for a layman to assume that intermediate states ought to be associated with low fitness. In reality the intermediate states might well be neutral or only slightly deleterious (and therefore be mainly affect by genetic drift) or might even be directly beneficial. It appears to be a mistake to assume such fitness valley are more common than they are in reality just because you fail to imagine how a trait may have evolved. In philosophy of logic, this is called an argument to ignorance. Of course, fitness valleys do exist. So, when they exist, do populations ever manage to get over them?

Assuming there is a fitness valley (for a given trait), can populations just "jump over it"?

Do populations need to get through an intermediate state?

Darwin framed his theory into the idea that evolution is a very gradual process. As we know today, this is far from being true. Evolution can actually occur through a big steps. There are single mutations that double the amount of genetic material, there are single mutations that completely affect the physiology or anatomy of an individual. There are cases of horizontal gene transfer (transfer of genetic material between species) as well that can cause sudden important change without having to get through intermediate stages. It is sometimes wrong to assume that there must be intermediate steps.

If there is a fitness valley and the population will not "jump over it"...

Let's assume a fitness valley (for a given trait, for a given population) and let's assume that the population will not "jump over it" thanks to a mutation of big effect.

Shifting Balance Theory

There are a number of different forces that affect evolutionary processes. Layman often think of natural selection as being the only force causing evolution but this is wrong. Genetic drift is another very important process that affect evolutionary process. Genetic drift refers to the random sampling of individual at one generation to build up the successive generation. The relative importance of drift to natural selection in driving evolution of a population depends on the effective population size. Have a look at Why is the strength of genetic drift inversely proportional to the population size?. Genetic drift can typically randomly yield a population toward a fitness valley, from which natural selection will yield the population to either come back or start climbing the opposite fitness peak. This concept is called shifting balance theory. There has been a lot of work on shifting balance theory suggesting that it well be much more common than previously thought.

Phenotypic flexibility

One may wrongly assumed that if a mutation occurs to make, say, a bone a big longer, then one organism would simultaneously need mutations that would make muscles, nerves and other tissues longer accordingly. In reality our developmental process is very flexible to an environmental change or to a mutational change. This flexibility is very much used in medicine and agriculture. If a bone gets a bit longer, muscle might just stretch a little more and end up developing in accordance to the new mutation. It would therefore be wrong to assume that because we are made of a complex interaction of traits, that a mutation cannot bring anything that would not be beneficial. If you are interested in the evolution of complex system you might want to have a look at the post How did the cardiovascular system evolve? for example.

Source of information

I would recommend that you have a look at a very short and introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example and you will be able to understand much more about what evolution is and how it occurs.


Combining gene expression data from two species I currently have two sets of gene expression data. The first is a dataframe of genes identified by Annotation id CG numbers (for example "CG10005") in one column and a numerical variable of interest associated with each of those genes in the other (the important part is that the genes are identified by the CG number). The second dataset is this study from multiple species where genes are identified by "GLEANR" ID's like this one: "dsim_GLEANR_10060".

I would like to extract all of the values from this study for the D.melanogaster and D.simulans data, then link that to the Annotation ID's in the first dataset (to connect my variable of interest to the sex bias in expression for each species). The trouble I am having is connecting the orthologous genes within the second study to each other, and then connecting them to the CG identifiers in the first study.

Does anyone have any suggestions on resources which can be used to get this all to link up?

This is the FlyBase page for the example gene: Dsim\GD10095. There, you have a section "orthologs", linking to OrthoDB. So my suggestion is: Find the list of synonyms for D. simulans on FlyBase (perhaps here?), download the Drosophila section of OrthoDB, and finally find the 1:1 orthologs.


In flowering plants food is transported in which form? In flowering plants food is transported in which form? I searched on google and found that it is sucrose. Why not glucose/fructose/starch?

This is a homework question but I will answer it (forgive me moderators ;).

You will get your answer from this answer:

  Sucrose and starch are more efficient in energy storage when compared to glucose and fructose, but starch is insoluble in water. So it can't be transported via phloem and the next choice is sucrose, being water soluble and energy efficient sucrose is chosen to be the carrier of energy from leaves to different part of the tree. Another problem exists, glucose is highly reactive and this may result in some intermediate reactions while transporting glucose. Being a complex structure, sucrose is not as much reactive as glucose. So plants uses the sucrose as a medium to transfer energy. Inside the cells, sucrose is converted back to glucose and fructose.

Once again:

Glucose- too reactive: CANCEL
Fructose- too reactive, again: CANCEL
Starch- insoluble in water: CANCEL
Sucrose- no problem: ACCEPT


What kind of spider is this? First time I have ever seen one This was taken 07/06/19 in Cape Breton, NS, Canada.

I would say that it is about an inch (2.5 cm) in length and seemed to be pretty uniformly grey. The belly was the same colour as the legs, it had a few small brown spots but I couldn't tell if that was an actual marking or maybe just environmental.

It was just hanging out right beside the handle of the door exactly where you don't want a spider to be.

In usual spider fashion it has dipped and is now...somewhere :(

It appears that you have a leafcurling sac spider:

They are observed all over east and west north america:

Here is the eye arrangement from bugguide:

I labeled with arrows the two thin dots at the top, which are eyes that point upward, which are easily visible in your picture. Would need a front-facing photo to see the rest of the eyes.
The spinneretes out the back of the abdomen are also diagnostic of clubionids.
The colours can span dark yellow to light brown, and the jaws are dark and sometimes the entire front face is dark as well.
A gallery of clubionids filtered on only Canadian observations is here:
https://inaturalist.ca/taxa/121774-Clubiona/browse_photos?quality_grade=any&place_id=6712


Why the major gene model can be supported by finding de novo mutations in affected cases? I found a sentence which I can't fully understand in a publication on the genetics of autism.

  The unified major gene model is supported by the significant increase
  in damaging de novo mutations found in subjects with ASD as compared
  to their unaffected siblings.

Is it saying under the major gene model, the de novo mutations comprise the majority of genetic risk?

It helps to give context and a source citation in questions like this. With some research I identified the source of the quote as Torre-Ubieta, "Advancing the understanding of autism disease mechanisms through genetics".

The quote comes from a section of the paper discussing the main two different genetic models of ASD: (1) the polygenic (many genes contributing small influences) model, and (2) the major gene model, where a variation of a single gene is responsible. The first two sentences of the paragraph having the quote are:

  The unified major gene model62,63 is supported by the significant increase in damaging de novo mutations found in subjects with ASD as compared to their unaffected siblings44,49. Further support for this model is seen in the phenomenon that there are more inherited SNVs that disrupt protein function in conserved genes transmitted from the mother to individuals with ASD than in unaffected siblings73.

The sentence in question (the first) is simply citing evidence supporting the second kind of model; it is not claiming that the majority of risk is due to de novo mutations.  As to how de novo mutations support the major gene model, it helps to consult the papers cited in the sentence.  Review of citations 44 and 49 show that those with ASD often have rare de novo mutations that look to be gene-disabling, whereas their unaffected siblings do not.  This suggests that disabling of a single gene can bring on ASD, and thus fits with the major gene model, but does nothing for the polygenic model since it supposes one gene difference has only small effect.

Let me add that the two models are not mutually exclusive: a polygenic model might explain the observed familial occurrence of ASD, while a de novo major gene model might explain why only a few in a family are affected.


What is the point of DNA sequencing? This is a very very basic question. I've looked at methods such as chromosome sequencing and shotgun sequencing. Wikipedia says that:

DNA sequencing is the process of determining the precise order of nucleotides within a DNA molecule

For instance, with methods such as shotgun, we already have the original DNA. If we have access to the original DNA itself, don't we ALREADY know the sequence of nucleotides?

Why exactly do we need to 're-build' the DNA with methods such as shotgun and chromosome walking, when we already have the original DNA available? If we have the original DNA, don't we already have the original sequence of nucleotides?

It makes me think that these techniques for 'DNA sequencing' is sort-of pointless. But, obviously I am misunderstanding something.

Thanks in advance, any simple pointers would be great.

No, you don't. Having the DNA in your hand means that you have access to a macromolecule, not more.

Think of the DNA as a book (or a library). From holding the book in your hands, you don't know what the content is. You have to actively read the book to get this information.

Sequencing a piece of DNA is basically the same. Your readout is the sequence of the bases which is essential to understand (or do research on it) a certain piece of DNA. With this knowledge you can see where genes start and end, define introns and exons (for eukaroytes) and so on.


Are mutations accumulating far faster than selected out? I just want to see the mutation accumulation rate in human populations. Versus the rate at which mutations are selected out. Just wanted to check if the genome is deteriorating

Welcome to Biology.SE

Is the rate at which new mutations occurring higher than the rate at which alleles fix today in humans?

Human populations are exploding! Genetic diversity within a population is a function of the effective size of its population. As the population expansion in human is extremely recent, we ought to expect that our genetic diversity is much lower than what would be expected from our population size and structure. Therefore, yes, genetic diversity is currently increasing, or in other words, more mutations appear than there are alleles that fixed.

Is the genome deteriorating?

I am not sure what you mean by "the genome is deteriorating" but the answer to "Is the genome deteriorating?" is likely no!

Actually, larger populations tend to suffer from less drift load and as such our mean fitness would rather be increasing. However, given the population size, I doubt that would make such an important difference.

On the other hand, medicine is greatly affecting our environment and is reducing the strength of purifying selection. As a consequence, modern populations would eventually be less fit than our ancestors if placed in the environment experienced by our ancestor (that is an environment with little to no medicine). But this will not be true in our current environment.

Prerequisite to understand the answer

This answer felt quite introductory but it actually contains all the following concepts:

Allele
Allele fixation
Genetic drift
Effective population size
Population structure
Drift load
Purifying selection
Genetic diversity (typically defined as the expected heterozygosity)
Effective population size
Environment (and even niche construction)

If any of the above concept is unclear to you (and I very much suspect that at least the term "drift load" will be new to you), then you might want to start with an intro course to evolutionary biology and population genetics.


How well does it actually work to surgically reroute the optical nerve? Two publications, Roe et al, 1992[1] and Metin & Frost, 1989[2], describe results pertaining to the ability of a region of cortex to process information from a different sensory mode than the one that it normally does.

Specifically, they describe studies in which:

input from the retinas of newborn rodents was rerouted, by
surgical methods, to parts of the cortex other than the visual;
the rodents were allowed to mature;
the responses of cortical cells in the new target region to visual stimuli were assess.

Now it's 20 years later, so I'm sure there have been many others.

Something of which these publications seem to make no mention is the behavior that developed in the test subjects. For example, did they appear to be completely blind from a behavioral standpoint?

Is anyone aware of any publication, relating to these studies or other, similar experiments, which addresses this question?

Roe AW, Pallas SL, Kwon YH, Sur M. 1992. Visual projections routed to the auditory pathway in ferrets: receptive fields of visual neurons in primary auditory cortex. Journal of Neuroscience, 12(9): 3651-64.
Métin C, Frost DO. 1989. Visual responses of neurons in somatosensory cortex of hamsters with experimentally induced retinal projections to somatosensory thalamus. Proceedings of the National Academy of Sciences USA, 86(1): 357-361.

At least two follow-up studies have investigated the behavioral consequences of the re-routing of the optic nerve to the auditory cortex. In these animals the visual cortices were ablated, and the optic nerve re-routed by combined lesions of the superior colliculus and ascending auditory pathways to the thalamus. These lesions induce retinal axons to form permanent ectopic (i.e., re-routed) projections to the auditory thalamus and cortex. These ectopic visual projections result in the formation of retinotopic maps in the auditory cortex and in visually responsive neurons with receptive field properties reminiscent of cells in the visual cortex.

These re-wired ferrets and hamsters were shown to have functional vision, as shown by their ability to tell light from dark and to recognize simple visual patterns. Visual pattern recognition was absent in control animals that were blinded, but not re-wired. Visual function, as measured by grating visual acuity in re-wired hamsters and rats, was however not as good as in control animals with normal vision (Frost et al., 2000; Melchner et al., 2000).

References
- Frost et al., PNAS (2000); 97(20): 11068–73
- Melchner et al., Nature (2000); 404: 971-6


Mechanism for earthworms to get into a roof gutter While cleaning accumulated muck from a roof gutter on my house, I found a few earthworms living in the muck. I am intrigued about what mechanism may have allowed the earthworms to reach that location. Some hypotheses:

Live worm crawls up a downpipe
Live worm dropped by an overflying bird
Cocoon is stuck to the outside of a bird (feet), falls off while the bird is overflying the roof
Cocoon passing through bird digestive system and deposited on the roof

What is the likely mechanism for earthworms to reach that location?

I would say that the reason why a given organism reaches a given space relies on four main factors:

Morphology and physiology: can that organism reach that place physically?
Food distribution: is there enough food to reproduce and spread in that specific spot?
Habitat: does that habitat fulfill its environmental/physiological needs? Is it environmentally safe for that species?
Abiotic factors: wind, water, etc...

I know it's a very general answer, but consider that the main goal of every organism seems to be to survive, spread and reproduce as much as we possibly can.

For example, if the gutter accumulates moss, earthworms will most likely crawl up the wall and into the gutter to feed on the precious organic matter. Also, gutters, due to its function, tend to be wet at times, and earthworms need a moist environment, so it seems like an ideal spot for them (earthworm climbing up).

  Live worm dropped by an overflying bird

Seems likely too: the term ornithochory defines seed dispersal by birds. I guess it could also be applied to dispersal of other animals (at least anthropochory can be applied to both seeds and reproductively capable animals dispersal by humans, in this case, earthworms being transported by the bird's beak). I think the most likely scenario in this case is food availability and a good environment to proliferate and make more earthworms (mostly because it would take a couple of clumsy birds to drop their prey on top of your gutter to establish an earthworm colony up there although it depends on the specific earthworm species and whether it is parthenogenetic or not, of course, but still within the realms of possibility).

When it comes to species distribution, it normally tends to be a mixing of different mechanisms rather than one single specific mechanism.


How well do Eppendorf cups seal? I am considering to send some samples overseas in Eppendorf cups. They are the standard plastic cups of 1 to 2 mL capacity. Of course they may tip over during their journey and I'd like to know how well they seal or if there is any danger that anything leaks from inside the cup. The samples are fixed in alcohol if that is relevant.

I have never had  problem with tubes leaking. However, if you are worried about them getting somehow popped open in transit, you might consider wrapping the lid in parafilm. Alternately, there are lid locks that you could use like these.

@Chris has a good point about screw-cap tubes, they could also work, and are probably a lot sturdier, in case of actual damage.


Why does throat 'burn' when you've got a common cold? Apart from pain when swallowing, there's also a persistent feeling of throat 'burning' in the same area.

What causes it and why does it feel that way?

If you've been sneezing or coughing a lot it is probably micro abrasions in the throat. I don't recognize any other burning sensation.


Which biological process causes the feeling of having "Butterflies in the body"? If someone is under stress, he or she may feel a strange feeling in the belly; it can be said that he or she feels that butterflies spread through the belly.

For other emotional reactions like being in love, similar, but different feelings can be caused.

What causes this symptoms? Is it because of the muscle tension varies, is it an electric current through the nerves?

These sorts of behaviors are mediated through activation of the sympathetic pathway of the autonomic nervous system.


What the name of this fish? Well saw this on a fish group on facebook. Noone can give a decent answer so I came to you guys hoping you can help us? The one who posted lives in the Philippines and he said he caught it in the river that is somewhat connected to sea.

This fish called neon velvet damsel fish (Neoglyphidodon oxyodon)

Check wikipedia


Can viruses survive Super saturated salt solution? As we know there is less evidence of biological activity in Dead Sea ( Lake full of salt water).

Also, our blood cells do not survive in too much salt water as they shrink and die.

So I was thinking that about if viruses survive a super saturated salt water.

And if they survive then which thing is making them survive and giving them the tolerance capacity?

And if they get killed then how they get killed?

This issue was studied in Virus inactivation by salt (NaCl) and phosphate supplemented salt in a 3D collagen matrix model for natural sausage casings International Journal of Food Microbiology Volume 148, Pages 128–134.

Saturated NaCl was tested on 4 types of virus, foot-and-mouth-disease virus (FMDV), classical swine fever virus (CSFV), swine vesicular disease virus (SVDV) and African swine fever virus (ASFV) at four different temperatures:4, 12, 20 and 25 °C for a period of 30 days.

For ASFV, but not the other 3 viruses, saturated NaCl had a significant effect of inactivating the virus, on a days timescale.


Function of the Auricle in heart What is the function of the auricles (conical appendages through the atria) present in the heart?

Do they have any other function than increasing the volume of blood the heart can hold?

The left auricle is a decompression chamber when atrial blood pressure is high (in systole or in some pathological conditions) [1, 2]. Some research claims it also plays a role in cardiac regeneration because it contains cardiac progenitor cells [3].

Probably the right auricle has less important function; also there are fewer studies about it.

References:

Al-Saady NM, Obel OA, Camm AJ. Left atrial appendage: structure, function, and role in thromboembolism. Heart. 1999 Nov;82(5):547-54. PubMed PMID: 10525506.
Bansal M, Kasliwal RR. Echocardiography for left atrial appendage structure and function. Indian Heart J. 2012 Jul 27;64(5):469-75. doi: 10.1016/j.ihj.2012.07.020. PubMed PMID: 23102384.
Leinonen JV, Emanuelov AK, Platt Y, Helman Y, Feinberg Y, Lotan C, Beeri R. Left atrial appendages from adult hearts contain a reservoir of diverse cardiac progenitor cells. PLoS ONE. 2013 Mar 12;8(3):e59228. doi: 10.1371/journal.pone.0059228. PubMed PMID: 23555001.


Is the SRY gene the sole responsible of biological male sex? It's very well known that the Y chromosome is what determines maleness, but more specifically this seems to happen thanks to the SRY gene located on it. Some individuals have an XX karyotype, but because of unequal crossing-over between X and Y chromosomes during meiosis in the father, one of the X chromosomes ends up containing the SRY gene, and the individual develops into a male (De La Chapelle Syndrome).
So I was wondering, is the SRY gene all that's really needed for an individual to be, unquestionably, a male? It's kinda odd how XX males have male genitalia but are classified as intersex solely because their karyotype is a typical feminine one (which should be irrelevant given how they also possess the SRY gene).

To my knowledge, the SRY gene is the only gene that cause variance in sex determination in humans. Of course, many genes are then involved in sex determination cascade but none these genes have variance in humans. Because environmental variance has no impact on gene determination in humans (to my knowledge and despite a few highly criticized articles) and therefore, nothing else than the SRY gene explains the sex determination.

The genes that are involved in the cascade of sex determination are not necessarily on the sexual chromosomes. On the Y chromosome, there are some genes that are male beneficial (beneficial for the male function) but these genes are not involved in the sex determining system.

In all species, the sex is determined by the environment and/or the genes. The best way to look at it is by reaction norms. On the below picture, think of the x-axis as being the temperature. Then, if you ask the question "Does the temperature influence the probability to develop into one sex or another?" One should answer. "It depends on the range of temperature you're looking at!" If you look at only very high temperature (far right) or very low temperature (far left), only the genotype explains the sex determination. If you look at mid-range of temperature, then both the genotype and the environment determines the sex.

N. Perrin and L. Beukeboom are writing what is probably going to be a very good book that will obviously interest you. I think the book is going to be publish in 2014 only. Here is the amazon link to pre-command it.


Two-fold cost of sex and r/K selection theory This article cites a bunch of articles (I haven't been through them) that the effect of the two-fold cost of sex is "reduced" in stable environment or in K-selected environment. It says:

  [..] the infamous ‘two-fold’ cost may be reduced or, perhaps more accurately, more easily balanced in K-selected species. The ‘cost of males’ is with respect to reproduction. Abugov (1985) argued from life history theory principles that the two-fold cost of sex might be easier to pay with K-selection. The two-fold fecundity advantage of asexual reproduction is always a two-fold fitness advantage, regardless of whether it is in a K- or r-selected environment. However, a survival advantage is worth more under K-selection than under r-selection. Consequently, it is easier to balance the two-fold cost under K-selection if sexually derived genotypes have a survival advantage.

I think that k-selection, k-selected environment and stable environment describe (more or less) the same kind of environment. Let me know if this sounds wrong to you. Here is wiki for r/K selection theory

From the same article K-selection is defined as:

  K-selection might favour slower development, greater competitive ability, delayed reproduction, higher survival rates, lower resource thresholds, leading to ‘efficiency’ (rather than productivity) and constant population sizes at or near carrying capacity of the environment.

It sounds really strange to me. Can you please help me to understand why the two-fold cost of sex is lower in stable environment than in unstable environment?.

r/K selection has become more of an heuristic for characterizing a species' strategy of reproduction and less a matter of predicting what sort of species will emerge from a given environment as it had originally been proposed by MacArthur and Wilson in 1967. The paper you cite tries to determine whether rotifers become more r or more K selective in different environments.

The thought here on k-selection is not almost from the definitions of the term, which is why it isn't explained in the paper.

In R-selected strategies, many more offspring are produced, but less investment is made in each one.  Think about a cockaroach laying thousands of tiny eggs.  The hatchlings might be eaten by their own mother; they are so 'cheap' the insect who layed the eggs doesn't have any anxiety about their survival.  In extreme cases, most of these hatchlings will not reproduce, they may even be a bit of food for the ones which do reach maturity.

In k-selected strategies, very few offspring are produced.  In addition to the 'cost of sex' limitation, they are invested in so heavily that the female may stop being fertile for a while.  An example would be how female mammals which are lactating are not fertile or seasonal mating like many birds do; the females turn off reproduction so that they can focus on the success of one or two produced offspring.

k-selection is advantageous over R-selection when more of their investment pays off.  If one out of ten R-offspring survive and one out of four k-selected offspring survive, then for these competing rotifers, the k-selected strategy is advantageous.

The cost of sex is that its half as efficient as asexual reproduction because males don't really reproduce - they only provide genetic material for females.  You can argue r/K selection independently of this factor, but the article is suggesting that k-selection can be so advantageous as to also give sexual selection an advantage over asexual selection.  I think asexual reproduction could be k-selected as well, but that seems to be the point being made here.

The reason that k/R has toned down in importance in the past couple of decades is that it has been found that individual species can adapt to shift their k/R strategems.


Does a large effective population size result in faster decay of linkage disequilibrium (LD)? I am thinking about an invasive species that was introduced into North America just a few (<20) generations ago. Using microsatellite genotypes (105 loci), I have identified almost no significant linkage across the genome. I'm tempted to speculate that this has something to do with rapid population expansion that has caused LD to decay that quickly, but I'm not sure whether this is a reasonable train of thought. Can anybody think of why this might or might not be the case?

It is certainly possible as yes, rapid population growth will reduce LD.  From Slatkin, 1994:

  In a rapidly growing population, however, there will be little chance of finding significant nonrandom associations even between completely linked loci if the growth has been sufficiently rapid.

Or Nature Reviews, 2002

  Przeworski... showed that population growth tends to decrease the extent of LD, especially for longer periods of growth. By contrast, population subdivision tends to increase the extent of LD, especially when a sample contains individuals from several strongly differentiated subpopulations.

See also box 1:

  Rapid population growth decreases LD by reducing genetic drift.


Is Hypericum Perforatum (St. John's wort) a C3 or C4 plant? I've been curious as to which photosynthetic cycle St. John's wort uses to synthesise glucose and more complex carbohydrates. I know it probably won't be the crassulacean acid metabolism (CAM) cycle seeing how that applies mostly to plants that require a limited amount of water as opposed to St. John's wort which tends to prefer moisture. I suspect the answer to my question will be C3 seeing how they dominate in the plant kingdom and I know that St. John's wort requires relatively cool climates to grow successfully -- a trait characteristic of C3 plants seeing how high temperatures tend to cause excessive and wasteful photorespiration.

It's C3, according to the Illinois plant information network.  (See CO₂ fixation on this page.) This is the best I could find.


Can TGF beta family induce all somatic stem cells? I think this is not possible.
Conclusion about this preview article TGF-$\beta$ family signaling in stem cells:

  While TGF-$\beta$ family signaling regulates stemness of normal and cancer stem cells, its effects are diverse and depend on the cell types and physiological state of the cells.

Can TGF-$\beta$  induce all somatic stem cells?

Signalling in the TGFβ pathway normally puts a brake on the progress of cells through the cell cycle - it counteracts the action of myc for example, partly by regulating the expression of myc. In Burkitt's lymphoma myc escapes this regulation because of a chromosomal translocation, tipping the regulatory balance over to uncontrolled cell growth.

This anti-proliferative action of TGFβ signalling is so critical that you might expect it to be ubiquitous in cells, and the expression atlas entry for the TGFβ receptor is consistent with this.


Are platyhellmintes and annelids segmented? Are the organisms of platyhelminthes unsegmented worms or segment? And what about those belonging to annelida?

I guess Platyhelminthes are unsegmented and annelida are segmented but i am not sure about it?

Here are the first sentences from the wikipedia articles for platyheminthes and annelids:

  The flatworms, or Platyhelminthes, Plathelminthes, or platyhelminths (from the Greek πλατύ, platy, meaning "flat" and ἕλμινς (root: ἑλμινθ-), helminth-, meaning "worm")2 are a phylum of relatively simple bilaterian, unsegmented, soft-bodied invertebrates.

  The annelids (Annelida, from Latin anellus, "little ring"),2[n 1] also known as the ringed worms or segmented worms, are a large phylum, with over 17,000 extant species including ragworms, earthworms, and leeches.


Size of deoxyribonucleotide What is the diameter of each type of deoxyribonucleotide (if the types are significantly different in diameter, if they are fairly similar one value would suffice)? I.e., if a hole was to be created through which only a single deoxyribonucleotide could pass at a time, how small would it have to be?

DNA is about 20 angstroms wide, so each of the two strand is about 10 angstroms wide. That width is the average between a larger purine unit and smaller pyrimidine unit, so let's round up to 12 or 13 angstroms for the larger unit.