In the transition to multicellularity what function becomes specialized first?

Lyons & Kolter (2015) On the evolution of bacterial multicellularity. Curr Opin Microbiol 24: 21-28; emphasis mine:

  Multicellularity is one of the most prevalent evolutionary innovations
  and nowhere is this more apparent than in the bacterial world, which
  contains many examples of multicellular organisms in a surprising
  array of forms.

  cell-cell adhesion to form a new evolutionary unit, and intercellular
  communication leading to coordinated activity (...) are the minimal
  requirements to redefine a group of cells rather than any single cell
  as an "individual."

  [M]ulticellular magnetotactic prokaryotes (MMPs) [are the only known bacteria] without a unicellular phase in their lifecycle.

  [The key features of multicellularity are: cell differentiation,
  intercellular signaling, extracellular matrix, tight cell-cell
  junctions, coordinated movement, division of entire structure (Table
  1).]


Are there any mutagens that can undo the mutations they cause?

It is possible but extremely unlikely.

When a base undergoes tautomeric shift the DNA does not contain a mutation yet, just an unmatched pair. The mutation will only becomes inscribed into the DNA permanently after the DNA is replicated or wrongly repaired.

In order to reverse the mutation you would need to provoke a chemical change to that specific base using the same or another mutagen and as most of them are unspecific the likelihood of obtaining both the correct mutation to reverse the effect AND at that specific location is extremely low. Just for the location itself (i.e. that base pair), in human you have ~0.000000033%  chances (1/3 billions) to mutate that base. This is assuming equal probabilities across the genome and a single modification event which is of course not true but shouldn't modify much the conclusion. I am not even speaking about provoking the chemical modification that will reverse it which will even further reduce that probability.

Such induced or natural mutations will actually only rarely appear in the genome permanently as the cell has multiple DNA repair mechanisms (see this wiki). So in this case the modified base does not need to be reverse as the cell will make sure to repair it directly but using mechanisms not based on mutagenesis.


How does salinity affect the bonds of an enzyme?

Sodium Chloride is not "polar". It is an ionic compound and dissociates into the respective ions in water (because of the latter's high dielectric constant).

Hydrogen bonds are similar to of dipole-dipole interactions (van der Waals) but much stronger and are therefore classified as a separate type of bond. However excess salt can lead to ion-dipole interactions (which are stronger than H-bond) that may prevent the formation of the hydrogen bond.

Ions such as Cl - can act as chaotropes (cause disorder)[ref]. K+ is also chaotropic while Na+ is kosmotropic (reduces disorder). However both Na+ and Cl - affect the entropy of water very slightly. So the effect of NaCl should be mostly due to ion-dipole interactions.


That looks like what I would call a "daddy long legs", also known as harvestmen. These are arachnids of the order Opilones. There are some 30 species of harvestmen found in the UK. The webpage https://harvestmen.fscbiodiversity.uk/ has a very useful identification tool and based on it, I believe your photograph shows a Leiobunum sp. A:

Please visit the site itself for more details as it doesn't allow copying.


What is the life-span of the various organs in the human body?

Perhaps you can infer relative lifespan from the age at which organs start declining in someone of average health.

Skin, muscles, bones, eyes, and ears start to visibly decline around age 40.

Kidneys become smaller and their ability to filter blood starts to decline around age 30.

Brain function begins to decline around 70, even in the absence of neurodegenerative diseases such as Alzheimers.

I don't think any organs can be passed through people for centuries, since decline of virtually every organ is observed even in individuals in perfect health. There may be two exceptions: The digestive tract and liver seem to be the most long-lived and are very little affected in healthy elders, probably because they regenerate their cells.

Reference


Relation between carbon dioxide assimilation and the ambient and intercellular partial pressures of carbon dioxide

After more research, I've found this to be true and the reason why. Discrimination against ¹³CO₂ isotope comes from two reasons; kinetic effects (diffusion and enzyme fractionation), and thermodynamic effects (1). ¹²CO₂ and ¹³CO₂'s diffusion rates are different, carboxylation reaction's discrimination value is 30 per million, and the diffusivity of ¹³CO₂ is 4.4 per million less than that of ¹²CO₂ (2).

When stomata are fully open

  they place no place no limitation on diffusion of CO₂, C3 leaves should discriminate against ¹³CO₂ by 30 per million, with respect to the atmosphere. When stomata are sufficiently closed that they become the sole source of limitation, the discrimination should be 4 per million. Intermediate cases give intermediate discriminations. (2)

It's known that when CO₂ is abundant in the atmosphere, stomata start to close because their job is to balance the CO₂ uptake and water loss by transpiration. This, combined with the previously mentioned information, to my understanding, means that, when they are more closed, CO₂ in the intercellular space gets consumed more. This lessens the carboxylation reaction's effect on the ¹³CO₂ discrimination because the CO₂ in intercellular space becomes more limited compared to the free diffusion of fully open stomata. In other words, carboxylation reaction has less CO₂ molecules to choose from intercellular space because free diffusion doesn't supply a constant flow of CO₂ molecules, making it use more ¹³CO₂.

(1) Farquhar et al., 1989, Annual Rev. Plant Physiol, Carbon Isotope Discrimination and Photosynthesis

(2) Farquhar et al., 1982, Aust. J. Plant Physiol, On the Relationship between Carbon Isotope Discrimination and the Intercellular Carbon Dioxide Concentration in Leaves


Common ancestry of our cells to the first unicellular cell

What it seems you're struggling with here is a lack of clear definitions.
Yes, the unity of core cellular mechanisms implies an unbroken line of descent back to the origins of life. But that does not in any way mean the cells are actually the same. I think that you would find it instructive to learn about the puzzle of the Ship of Theseus, which is the essence of the issue you are dealing with. In short, once changes can happen (e.g., mutation, as you note), it's possible to have both continuity and a fundamentally different item.
Beyond this, it's also worth noting that at every step we are dealing not with individuals but populations, even likely back into the murk of abiogenesis (when the populations would be various chemicals and protocells of some sort), and that genomes are also modified in a much wilder variety of ways, e.g., all the various forms of horizontal gene transfer.


Identifying type of inhibitor from $K_m$ and $V_{max}$

Competitive inhibitor competes for the active site. Therefore it will interfere with the binding of the substrate thereby increasing the apparent KM.

A strictly non-competitive inhibitor does not compete for the active site. It however inhibits the catalysis by reducing the available molecules of active enzyme, E0 (if it is a perfect inhibitor), thereby lowering the Vmax.

There can be mixed inhibitors too and there can be different kinds of mixed inhibition. For example an inhibitor that interferes with catalysis and can also compete for the active site.

Depending on how you define KM, a non-competitive inhibitor may or may not change it. If such inhibitor can bind to the enzyme at non-active site and reduce its kcat, it changes the KM as well as Vmax in case of Briggs-Haldane kinetics.


Which predators only eat some parts of their prey? (Warning — graphic content)

In the pictures shown above only the soft part of the animals have been eaten. This is common for most predators as these are the easiest parts to eat.

Correct me if I am wrong but the animals seem to not have severe bite marks around the neck. This means the predator was not big. You can pretty much rule out anything around the same size or bigger than the sheep.

To exactly identify what killed them just from a carcass is hard, and even harder over the internet. However, it looks like you are dealing with feral dogs, coyotes or wolves, although with wolves and dogs there would generally be more scarring around the neck of the sheep.

Dogs: I have seen this behavior in dogs. These are normal tame dogs that have discovered the kick of hunting. Where I come form in South Africa the farmers tend to shoot dog packs if they see them on their land. This is because it is a common problem for the packs to attack chickens, sheep or even calves.  They get an immense kick from hunting the sheep but in most cases don't eat it, not like the photos shown at least.

Foxes: Although it may be hard to believe foxes have also been known to kill sheep. However, in your case it is not likely to be foxes. Foxes hunt alone and tend to kill lambs.

Coyotes: Coyote packs have almost identical behavior to dog packs. The difference being that they pick one sheep and kill it quickly. They do not do it 'for the kick' like dogs and rather for the food. Judging from the photos I would say it is possible that this was done by wild Coyotes, if they are found in your area. Coyotes are also not very shy, and will often hunt close to where people live.

Wolves: While possible, I would rule out wolves because of your geographical location. Wolves also tend to be more shy and will stay away from places with lots of people, like a city.

Source:
http://www.omafra.gov.on.ca/english/livestock/sheep/facts/02-029.htm


Aerobic vs anaerobic respiration comparison

I think the reason as to why glucose concentration is faster in the aerobic case than the anaerobic one, is perfectly explained by Chris. To summarize:-

  The energy requirement of the organism in both the condition remains more or less
  constant. Since aerobic respiration generates more energy per glucose,(38ATP)
  it takes more time for the same concentration of the glucose to be
  depleted, than it takes in the case of anaerobic respiration where
  less energy is released.(2ATP)

The non-linearity in case of anaerobic respiration can probably be explained thus:-
In the aerobic case, glucose is oxidised to water and carbon dioxide, both of which do not influence the respiratory process. The first step of glycolysis, the phosphorylation of glucose has a very negative free energy change, i.e. is practically irreversible. Therefore a dip in glucose concentration will not affect the rate of energy release and therefore the rate of energy released will stay constant resulting in a linear graph. But in the anaerobic case, the final product is un-metabolised ethyl alcohol. The conversion of pyruvic acid formed as a result of glycolysis to ethyl alcohol is not so strongly irreversible(smaller free energy change), and at high product concentrations, becomes considerably reversible. This means that the ethyl alcohol produced will affect the rate of glucose metabolism, and will retard it by negative feedback (Le chatelier's principle). This will lower the speed of glucose utilisation at low concentrations of glucose, i.e. high concentrations of ethyl alcohol. This reduce the value of slope at lower concentrations of glucose in the graph, and hence produces the non-linearity.


How to set threshold in ImageJ for quantifying relative fluorescence?

You need to normalize both images to the background. This can be done in many softwares including photoshop.

When I was learning this starting to do it with something more simple like SDS page protein bands helped me a lot. The principles are the same you are still subtracting background. Look at this tutorial:

http://m.youtube.com/watch?v=JlR5v-DsTds

However, when analyzing intensity values in fluorescent microscopy the most important parameter is area of your analysis. This needs to be an objectively applied as much as possible, and that can be by increasing the number of replicates whose area you analyze. Your going to look at pixel intensities for many many cells and average those intensities. Using the imagej cell counter plug-in is helpful to see how to determine cell area.


Converting Ensembl Compara gene tree DNA alignment to corresponding amino acid alignment

As a general rule, both within and without the world of bioinformatics, public FTP sites contain README files tat explain what each file offered by the FTP server contains. The file README.protein_trees states:

Compara.gene_trees.{release}.emf.gz
                        contains the peptide alignment for every genetree in emf alignment format
Compara.gene_trees.{release}.fasta.gz
                      contains the peptide alignment for every genetree in fasta format

This means that both Compara.gene_trees.57.emf.gz and Compara.gene_trees.57.fasta.gz contain the protein alignments. I had a quick look at the files and it looks like Compara.gene_trees.57.fasta.gz actually contains nucleototide sequences but Compara.gene_trees.57.emf.gz does indeed contain a protein alignment:
$ zgrep -m 1 AAAAASAAAT Compara.gene_trees.57.emf.gz.crdownload
SAAA-AHS-AGTAAAAA--AA--AAAAASAAAT-ASAATAI-SASSA-ASAAT-V----AAASVAA-HAFAS---ASAAASAAAAA-TIVAAAAX-SAASIYSAAAA-YAA--AASAS-ASAASAS-ASAASSSSSARS-AAS

So, to answer your question, the file you want is the .emf.gz one.


Is cancer a defect of the immune system?

Cancer is uncontrolled division of abnormal cells. This is caused by mutations in a cell which causes a cell to divide more frequently and the lack of control by intracellular AND extracellular mechanisms. The extracellular mechanisms include growth inhibition by hormones, local factors, contact and also the immune system.

These cancerous cells could be immune system cells and then, in that respect, the cancer could be considered an immune system disorder. Or the cells could be of different origin, but due to the lack of a functioning immune system (particularly NK cells), the cells may divide uncontrollably whereas otherwise they would've been tagged for immune or self destruction. Or a cancer may be caused by a virus; in this situation an immunocompromised patient is more susceptible to a cancer caused by this oncogenic virus. In these cases the risk of cancer is increased due to a compromised immune system. So cancer risk may be increased in these circumstances but cancer still is not an immune disorder.


Why our body does not produce polyunsaturated fatty acids?

Simply, it’s because our bodies add double bonds in MUFAs by delta 9 desaturase which adds double bonds between delta 9 and delta 10 carbons, hence additional double bonds can be formed between existing double bond and the carboxilc group but cannot be formed between the existing double bond and the omega carbon. As a result, our body cannon synthesize parent omega 3 alpha linolenic acid and parent omega 6 linoleic acid, but can form timnadoneic acid which is an omega 3 PUFA


How do neurons send electric pulses even though they are surrounded by liquid which is mostly water?

Neurons have sodium, potassium, as well as some calcium channels all over the surface of the cell (I'm giving a very generalized explanation here). The "electric pulses" that you are mentioning is more of electrostatic potentials generated from the interactions of cations and anions flowing in and out of the channels. Water at the specific pH surrounding the cations is a good conductor of these electrostatic interactions.

You have to remember that there are large negatively charged anion proteins inside the neurons which attract the cations (sodium ions for example) to rush into the cell. Once threshold is reached all gates open and an action potential is produced.


Whether de novo mutation can be inherited or not?

De novo mutations can be inherited if they occur in the germline cells, those responsible for making the sperm or the egg. If you have a de novo mutation in a blood cell or a skin cell, this doesn't pass on to the next generation. But when you test the blood for mutations, it can also mean that the same mutation is present in the germline! However, if the parents are not sufferers of the dominant disease, it means this mutation is not present in their somatic (non-germline) cells. It's likely that the mutation occurred de novo in either the parent's germline during their lifetime (during the production of their sex cells in adulthood).

If your parent has a mutation in their germline, and it is passed on to you, the zygote is formed from both your parents (half of your alleles are from the mutated parent) and this zygote creates ALL of you, including your blood cells and your skin cells. This is why we can test your blood to guess what must have been the case in your germline. Of course, you may have accumulated mutations independently in the germline in the meantime, or accumulated mutations independently in the blood cells! So it's not completely the case that testing blood will tell you about the state of the germline. But you must understand that ALL of you is created from a single cell, the zygote, so at this point there is a 'bottleneck' that forces all somatic and germline cells to share the same genetic makeup.

Also, please consider that humans are diploid, i.e. have one copy from the mother and one copy from the father. And that these recombine and only one copy goes into the sex cell. This may help you think about your problem.

I trust this will help you better understand your questions.


Can we detect the origin of a 1000 year old dead body after grave excavation?

Adding to comprehensible's answer, 99.9% similar DNA still leaves 0.1% of different DNA. Within this 0.1% would be enough differences to be able to find the differences that comprehensible mentioned. This is also how the ancestry tests that are so popular these days work.

Additionally, for that type of place-of-origin analysis, my impression is they commonly look at isotopes of chemicals found in the bones, and matching it to profiles found in other regions.

For example, let's say that an area we're interested in has high levels of isotope X but low levels of isotope Y in the water and food, which we discovered from examining the archeological record. If we find someone in that area whose bones have low levels of isotope X and high levels of isotope Y, we can conclude that this person traveled here later.


The reason chlorination still works is that it is aspecific, just as @AliceD mentioned.

The way chlorination works is mainly by oxidizing biological molecules. Chlorine, along with other halogens, is a strong oxidizing agent. It breaks down the phospholipid bilayer membrane, proteins and enzymes. There is no way organisms can overcome this, unless it uses none of the chemical molecules that react with chlorine, which is virtually none.

On the other hand, antibiotics inhibit particular enzymes and proteins in a particular way and by making one or two amino acids different in the protein, the microorganisms can easily overcome this.

Reference - http://www.sswm.info/sites/default/files/reference_attachments/TUE%202011%20The%20Chlorine%20Dilemma.pdf


How are the correct tRNAs transported to the ribosome?

The only way I can imagine this happening is that all types of tRNA+amino acid reach the ribosome, bombarding the ribosome, and the ribosome will 'accept' only the one that matches what it is waiting for.

Yup, basically.  This is an extremely cool figure showing the process. There are various elongation factors that aid the process, such as EF-Tu, which essentially waits until there is a good codon-anticodon match before hydrolyzing GTP and allowing the tRNA/amino acid to enter the ribosome.

This process can be particularly salient when you look at a concept such as codon-usage bias.  Certain tRNAs are more common in the cell, so if a given mRNA uses codons to match those tRNA instead of matching other degenerate but less common anti-codons, translation will occur faster.  This is more obvious in organisms such as E. coli where growth is paramount.


Why must the alcohol decolorizer be used for 30 seconds or less for Gram staining?

The crystal violet stain will be removed if the decolorizer is left on too long.  I'm assuming that the crystal violet complexes that are retained in the gram positive bacteria's peptidoglycan layers end up being washed away (perhaps from overdehydrtation).


Are there fungi that are directly beneficial for humans?

Saccharomyces boulardii.

https://en.wikipedia.org/wiki/Saccharomyces_boulardii

S. boulardii is a yeast, closely related to S.cerevesiae (if not the same organism).  There is a lot of solid data showing use of this fungus as a probiotic can help treat or prevent intestinal infections.

Systematic review with meta-analysis: Saccharomyces boulardii in the prevention of antibiotic-associated diarrhoea.

  RESULTS:  Twenty-one randomised controlled trials (4780 participants),
  among which 16 were new trials, met the inclusion criteria for this
  updated systematic review. Administration of S. boulardii compared
  with placebo or no treatment reduced the risk of antibiotic-associated
  diarrhoea (as defined by the study investigators) in patients treated
  with antibiotics from 18.7% to 8.5% (risk ratio, RR: 0.47; 95% CI:
  0.38-0.57, number needed to treat, NNT: 10; 95% CI: 9-13). In children, S. boulardii reduced the risk from 20.9% to 8.8% (6
  randomised controlled trials, n=1653, RR: 0.43, 95% CI: 0.3-0.6); in
  adults, from 17.4% to 8.2% (15 randomised controlled trials, n=3114,
  RR: 0.49, 95% CI: 0.38-0.63). Moreover, S. boulardii reduced the risk
  of Clostridium difficile-associated diarrhoea


Why does Taq polymerase add 3' adenine overhangs?

Non-templated terminal addition by certain DNA polymerases is apparently dependent on the base stacking between the incoming base and the existing duplex (Fiala et al., 2007*). This was verified by using a non-base-pairing (but better stacking) nucleotide analogue called deoxyribo pyrene nucleoside triphosphate (dPTP). Adenine seems to have a higher efficiency of base stacking compared to other three bases:  A (1.0), G (0.7), T (0.6), and C (0.5)

It was also verified that the preference for dATP did not depend much on the terminal base-pair of the duplex with the incorporation probabilities being:

79% dATP 16% dTTP, 3% dCTP, and 2% dGTP when the last base pair is A-T (A is 3'), and
81% dATP, 8% dTTP, 8% dCTP, and 2% dGTP when the last base pair is G-C

Fiala, Kevin A., et al. "Mechanism of template-independent nucleotide incorporation catalyzed by a template-dependent DNA polymerase." Journal of Molecular Biology 365.3 (2007): 590-602.

*They had used the Dpo4 polymerase from Sulfolobus solfataricus as a model because it is a known lesion bypass polymerase and its kinetics and structure are well studied.


How do I reverse my insert within a plasmid?

Design your 5' primer upstream of ProDpro. with a Spe1 cut site added to the end (plus a few extra random bases to allow for better cutting). Add an Xba1 cut site to the end of the 3' primer, again with a few extra random bases on the end to allow for better cutting.

Amplify the insert, PCR cleanup, digest, cleanup again, and you should be able to easily clone into the Xba1/Spe1 digested vector that has been gel purified.


Some more hours of literature research finally produced a result:

As published by Khan et al. 2006 6x-His-tag has two distinct dissociation constants of koff1 = 6.3 10-3 and koff2 = 1.8 10-3.


There are definitely examples! For one, you might consider sickle-cell anemia to fall into this category.

The mutation that causes this disease leads to abnormal strands of hemoglobin that distort the shape of red blood cells, to the point that those cells can directly disrupt blood flow.

Interestingly, carriers of the sickle-cell trait actually have some protection against malaria, which explains the high incidence of the allele despite the dangerous consequences of the disease.

You can find many other examples in the category of autosomal dominant disorders (though note that sickle-cell is considered recessive, though carriers can still have some negative effects). Because these disorders only require one copy of a gene to cause illness, there is often some toxicity of the mutated protein, whereas in what you refer to as "passively" harmful mutations, one healthy copy can often compensate, fully or partially. Of course these are general statements and there will always be exceptions, but I hope thinking about it this way can guide your curiousity!


Does the 'President' have 2 Billion Leaves?

One way* to come up with an estimate of how many leaves - or needles, in the case of Sequoiadendron giganteum - is simply to count the number of leaves on a twig (or a number, to get a good average), then the number of twigs on a branch, and then count the branches on the tree, after which it's just multiplication.

Now one reason that the number seems so high is the way the needles grow.  Unlike for instance pines, which have long needles arranged in sparse clusters of 2, 3, or 5, or spruce & fir, which have medium needles arranged along the branches, the sequoia has lots of tiny needles arranged on twiglets.

Link with picture of sequoia needles: https://www.monumentaltrees.com/en/trees/giantsequoia/giantsequoia/
Picture of pine vs spruce & fir: https://www.finegardening.com/article/fir-vs-spruce-vs-pine-how-to-tell-them-apart

*But I don't know whether it's the way used to get the number in the link.


Why do we have two kidneys but one liver?

Your organs can be grouped into two categories.
The digestive tract organs, which are singular.
These form from the endoderm.
The liver and pancreases are all direct outgrowths from the digestive tract which is again singular.
Everything else which comes in pairs.
These form from the mesoderm or ectoderm.
Even the brain and heart are paired organs, the heart starts as two organs and fused during embryonic development. The whole circulatory system starts perfectly paired, (embryonically and evolutionarily) but then specific parts close off to create the complex circulatory system of "higher" animals so we can have a high pressure section and low pressure section.
The spine is also sort of singular but is basically the the line splitting the left from right half of the body. Everything that branches off the spine does so in pairs.
The real questions is why you have two lungs and one spleen. They are the only organs that breaks the rules. The lungs are an outgrowth of the digestive tract and the endoderm, but is paired. The spleen is part of the circulatory system, but singular. Now the most primitive lungs are singular, it split later likely as animals got larger and needed more lung capacity and also needed a tight connection with circulatory system (paired). The spleen is the weird one, and likely harkens all the way back to before vertebrates existed, it predates the closed circulatory system, and develops on the midline of the body just like the spine and digestive organs. Just like how the spine is the midline dividing the nervous system into pairs the spleen divides the circulatory system into pairs.
https://www.researchgate.net/figure/Embryology-of-the-gallbladder-A-In-the-early-embryo-liver-specification-occurs-in-the_fig1_303959093
https://embryology.med.unsw.edu.au/embryology/index.php?title=Cardiovascular_System_-_Spleen_Development
https://embryology.med.unsw.edu.au/embryology/index.php/Gastrointestinal_Tract_Development#Germ_Layer_Contributions


Mechanism by which water flows through xylem

-
NO,for capillary action 2 things are of importance 1) the radius of capillary tube[R] ,2)the tension force between molecules at surface of liquid [T] (for water=72.8 dynes/cm= 728 X 10^-6 N)

-
height to which the fluid will rise due to cap.effect, H=(2T cosα)÷(ρgR)

-
[ρ=density of liq,here water =1000kg/m³]

-
numer.=constant(for given liq) denomin.=variable R

-
so if capillary was in effect for trees 100s of meters tall the deno. wud have to be small while the ρg is a fixed value here for water = 10000 units the R wud have to be impossibly small

WHAT HAPPENS IS the transpiration of water droplets from the stomata causes a suction as no air can enter to fill in for the water lost the water as to rise up taking more of it from the soil


Did the Great Oxygenation Event also cause a mass extinction?

The proposed mass extinction due to Great Oxidation Event is actually an elucidation by scientists.

After reading many articles online, although there are evidences of GOE, every article states the extinction of most anaerobes as something that should have happened as a fact (Because $O_2$ is considered poisonous for obligate anaerobes). To better understand this, imagine if there was a spike in Carbon Monoxide in the atmosphere, for Oxygen dependent organisms like us, inhaling $CO$ is harmful and therefore a spike in $CO$ would be toxic and lead to death.

Here are some excerpts, which state the extinction of anaerobes being factual more than anything else:

From Arizona State University, Origins Project >>

  In a relatively short amount of time, Earth went from having very
  little oxygen to what may be the highest levels of atmospheric oxygen
  it has ever had. This event had wiped out most of life on the planet
  to which the oxygen was poisonous. Some of these anaerobic organisms
  were though to have survived by burrowing into the earth where oxygen
  levels were survivable.

From Slate.com - Bad Astronomy Blog >>

  At some point, though, as cyanobacteria flourished, the minerals and
  other sinks became saturated. They could no longer absorb the oxygen
  being produced. It built up in the water, in the air. To the other
  bacteria living in the ocean—anaerobic bacteria, remember—oxygen was
  toxic. The cyanobacteria were literally respiring poison.

  A die-off began, a mass extinction killing countless species of
  bacteria. It was the Great Oxygenation Event.

From Imperial College London >>

  The permanent introduction of oxygen into the atmosphere fundamentally
  changed the ecology of the planet. The first impact was on anaerobic
  organisms, which didn’t need oxygen to survive. The rise in oxygen
  levels was poisonous to them and led to most them becoming extinct.
  Some managed to survive, but they retreated deep into the subsurface
  where there is no oxygen.  This was one of the first mass extinctions
  in the history of our planet, and it was also the catalyst for the
  evolution of oxygen-based life – us!

As a result, based on what I have read so far, we really dont have any stone cold proof that rise in oxygen lead to mass extinction of anaerobes. The mass extinction is what scientists consider should have happened as we know $O_2$ is poisonous for strict anaerobes.


These are lacewing eggs. Lacewings lay their eggs on stalks.

From wikipedia  :


Using proportion or a diversity index when dealing with just two strains

Extended upon the suggested statistic

The proportion $p$ is definitely not a good measure of diversity. A proportion of 0 or 1 both indicates no species diversity as only one species exist. If one species, never reach a frequency of 0.5 in your data it might be reasonable though. Otherwise, something like $p(1-p)$ could be a statistic of interest.

If you're willing to use $2p(1-p)$ (instead of the above $p(1-p)$) as index of diversity, then you could make the point that it can be easily extended to $S$ species with $1-\sum_{s=1}^S p_s^2$, where $p_s$ is the frequency of the species $s$ by analogy to the genetic diversity within populations (see Nei 1973).

Note that these statistic will be sensitive to the sample size. For example, if you sampled only one individual, then this individual can only belong to one species and your measure of diversity can only be zero. You might want to compute an unbiased estimator for this statistic.

Your goal is to reduce the reader's cognitive load

Your goal is to use a statistic that will communicate easily. If your readers are going to be very much used to Simpson's or Shannon's indices, then even a mathematically simpler index might end up leading to an extra cognitive load onto the reader.

IMO, it will be hard to give a more definite answer without knowing 1) who are going to be your readers (which journal are you aiming to publish in) and 2) what are the exact data manipulation and interpretation you are aiming to do based on your results. For example, if it makes the comparisons among graphs easier by using a simpler statistic over a more complicated once, then choosing the simpler statistic is a good idea.

Good statistical analysis

In any case, it is essential that you to try out (and you did) different measures of species diversity and make sure that your conclusion is robust to these different measures and explain in your methods that the chosen statistic won't matter. That will make your point and your choice of statistic much stronger.


Definition of species - location of gene

The position of a gene is not always fixed neither within nor between species. There are Copy Number Variation for example. A great part of the variation within humans is due to CNV. I agree that it is important to consider other genetic variations than only the alleles though. CNV, position of genes, regulatory sequences and other stuff are important too in the description and the functionality of a lineage.

The concept of species is a poor concept which is old as Aristotle and important in the christian culture but we have to accept that this concept is not a natural category. For french speaker people this podcast(Follow: Biodiversité: Plus qu'une simple histoire de conservation/Pierre-Henry Gouyon) is of interest. You won't find the perfect objective definition of what is a species. Here and here are posts that discuss the definition of species.


It is hard to say for certain, but the insect hanging from the spider looks like it may be a member of the family Elateridae, commonly known as a "click beetle". As far as I know, they're harmless and no threat to a spider.

The close binding of the legs with silk suggest that the click beetle(if that is indeed what the insect is) may have been a meal prior to the spider's death, or packaged for later consumption.

Given the amount of debris in the webbing surrounding the spider's corpse, including some pieces of some sort of grass leaves, it seems likely that the webbing become tangled during or after the spider's death.  The placement of the click beetle is likely coincidental, although I suppose it is possible, given the positioning, the size of the click beetle, and what we can conjecture would be the size of the wound if that black material is seepage from a wound on the spider's abdomen, that some force actually punctured the spider's abdomen with the body of the click beetle.


Which is the proportion of metagenomics reads that cannot be mapped in any genome?

I think this will vary greatly depending on the source environment. Your example (marine viruses) is probably due to the large diversity of ocean viruses of which most have no reference genome.

Referencing the Human Microbiome Project:

A total of 57.6% of the high-quality microbial reads could be associated with a
known genome (ranging from 33–77% for anterior nares and posterior fornix, respectively).

Other papers describing more recent k-mer based approaches for classification report between 40-90% classified to a known reference. See:

http://www.nature.com/articles/srep19233

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4401624/


What is the best alignment definition for the Multiple Sequence Alignment (MSA) problem?

In your case both answers are equally valid.

The scoring matrix, for example DNAFULL (http://rosalind.info/glossary/dnafull/) usually contains various penalties for wrong alignments.

Also the introduce gap score should NEVER be set at 0 as it will cause the aligned sequences to be filled with artificial gaps!

The only thing the algoritms try to optimise towards is the score, therefore you need sane values for calculating the score and those you propose does not result in usefull alignments.


Can someone tell me what these cocoons are?

I think you are actually looking at dried bottle gourds, a squash relative.  These are probably in the genus Lageneria.  These come in an extreme variety of shapes, and have been put to many ornamental uses. They were important as containers for early cultures.  Good background here and here.  Search for "dried bottle gourd" images and you'll see plenty.


Is there a free software for manual sequence annotation?

You might find some success with using WebApollo or JBrowse

WebApollo allows you to perform many manual annotation functions for your genes, such as editing exon boundaries, fixing coding sequences, and merging or splitting gene predictions, which looks like what might have been done in the UCA-At2g42245. It can also be used for adding various attributes, GO terms, pubmed info, or generic attributes. WebApollo actually uses JBrowse, but JBrowse itself has very flexible options for displaying annotations. The part about highlighting the alpha helix/beta sheets is not built in, but JBrowse can be configured to do lots of different renderings, and I could provide more details if you are interested. Disclaimer: I'm a WebApollo developer/JBrowse contributor.


Does a cell suspend or exit cell cycle at G0?

It is actually suspend and yes the words do differ. This is because the cells that enter the G0 stage is not actually exiting the cell cycle because when situation demands it will divide. It is metabolically active and therefore the word suspend suits better


How heavy are all foreign microorganisms in and on the human body?

Edit: Matters Arising

In this Nature News article, Scientists bust myth that our bodies have more bacteria than human cells, and in the bioRxiv pre-print article, Revised estimates for the number of human and bacteria cells in the body, a new estimate of the ratio of microbial cells on the human body to human cells that make up the body has been revised down to close to 1-to-1, with there being slightly more microbial cells to human cells.

It should be noted that near 90% of the human cells taken into account were red blood cells and platelets.

- Revised estimates for the number of human and bacteria cells in the body, Sender et.al. bioRxiv preprint.  doi: http://dx.doi.org/10.1101/036103

Note: Preprint articles have not been refereed. The information in them is subject to change, may not pass review, and in the end my not be accepted for publication.

  Readers should therefore be aware that articles on bioRxiv have not been finalized by authors, might contain errors, and report information that has not yet been accepted or endorsed in any way by the scientific or medical community.
  - bioRxiv.org: What is an unrefereed preprint?

Original Post

  The human body contains trillions of microorganisms — outnumbering human cells by 10 to 1. Because of their small size, however, microorganisms make up only about 1 to 3 percent of the body's mass (in a 200-pound adult, that’s 2 to 6 pounds of bacteria), but play a vital role in human health.

From: NIH Human Microbiome Project defines normal bacterial makeup of the body

Additional Information on Microbiome and Obesity

From Cell

Altering the Intestinal Microbiota during a Critical Developmental Window Has Lasting Metabolic Consequences

From The American Journal of Gastroenterology Supplements (a Nature Press Journal)

Disclaimer

  This article was published as part of a supplement sponsored by the Gi Health Foundation, a nonprofit 501(c)(3) educational organization dedicated to increasing awareness of the effect of gastrointestinal disorders in the United States. The foundation's goal is to provide health professionals with the most current education and information on gastrointestinal health.

Impact of the Gut Microbiota on the Development of Obesity: Current Concepts


In protein-protein interactions what is the difference between a binding site and an interface?

A protein-protein interaction (PPI) binding site is a type of interface. If it has been established that the interface is a PPI binding site, then the terms can from that point forward be used interchangeably. But the word "interface" is very generic and does not have any specific scientific meaning so the nature of the interface must be defined or else the term is fairly meaningless.


Can Naegleria fowleri enter through wounds into the bloodstream?

No, Naegleria fowleri is a free-living excavate form of protist that lives in warm fresh water. Fowleri finds its way into the brain by eating through the olfactory neurons in the nose where it multiplies itself greatly by feeding on nerve tissue.

Once it penetrates the nervous tissue, fowleri's feeding  results in significant necrosis of and hemorrhaging in the olfactory bulbs. The protist then climbs along nerve fibers through the floor of the cranium via the cribriform plate and into the brain.

Since the protist travels by feeding on nervous tissue, fowleri could not enter the brain via bloodstream.

Just some more facts about Naegleria:

Death usually occurs within 14 days of exposure due to destruction the autonomic nerve cells of the medulla oblongata.
Luckily for everyone this disease is rare. There were only 300 cases as of 2008


Is this mammalian embryo blastocyst, gastrula or only phase between them?

Again, the thing (2) is idealized and probably does exists at all. It is an idealized picture. It is really a mistake to call such a thing blastocyst like Wikipedia does. The thing should be fixed not to confuse other people.

There should be real pictures instead of such idealized ones.


Effect of Ethanol on Brain Volume Measurements

I just spoke with my histological colleague about your question. He said that you should be fine for gross examination but not for microscopy. Why? He says, "When working with specimens, the higher resolution microscopy you try to achieve, the more 'potent' the fixative needs to be. A preservative will preserve what tissues are there. However, fixatives (like paraformaldehyde or glutaraldehyde) bind proteins together and, thus, are used to try to 'fix' a tissue posthumous in the manner that it was structured in life. For gross examination, a preserved specimen (without prior fixation) can act as a decent voucher for macroscopic evaluation of its internal organs; however, it will not suffice for any type of detailed histology at the light microscopy or electron microscopy level."

So, the short answer is that it depends on the type of work you need to accomplish.


Why didn't a concept like "pointers" in Computer Science evolve in the genome?

Short answer: Pointers already exist within the genome, in terms of transcription elements (such as repressor/activator systems). These systems can remotely activate a specific gene for transcription based on concentrations of specific chemicals within the cell.

The problem with LINEs are that they are thought to be ancient retroviruses which lost their capacity to infect other cells, instead jumping around within the genome. They are therefore parasitic in nature, and they reproduce by inserting multiple copies of themselves into the genome. It makes more sense to think of LINEs as nearly inactivated retroviruses instead.


What are good data on the Human Metabolic Model and where can I get them?

As far as I know, there is no one model officially known as "the Human Metabolic Model", but the Recon 2 model, described as a "consensus" model and the most comprehensive to date in Thiele et al. 2013, A community-driven global reconstruction of human metabolism (http://www.nature.com/nbt/journal/v31/n5/full/nbt.2488.html) is available at http://humanmetabolism.org/?page_id=75

Tissue-specific models are also available. See for example  Wang et al.:  Reconstruction of genome-scale metabolic models for 126 human tissues using mCADRE. BMC Systems Biology 2012, 6:153:


Dominance by silencing the other allele

The mechanisms by which dominance work are still very much unknown. One type of mechanism that will be of particular interest to this question is the modifier of dominance where the protein product of an allele silence the expression of the other allele in order to cause dominance relationship.

Is the pattern you describe possible?

In such system, I can imagine a case where allele A1 would silence A2 which would silence A3 which would silence A1. I can't think of any reason such a pattern should not exist. However, I am not aware of evidence of such pattern.

The interesting case of SI in Arabidopsis thaliana

This type of dominance (dominance through silencing the other allele) has been reported in the self-incomtability locus of Arabidospsis theliana (Durand et al. 2014). At this specific locus there are 6 alleles but they have a very hierchical relationship where A1 silences all other alleles, A2 silences all alleles but A1, A3 silences all other alleles but A1 and A2 etc..

Related posts

Evolution of dominance of alleles
What determines if a gene is dominant or recessive?


Mud tube, metallic green, bee-like - sounds like a mason bee to me.

There are several metallic green mason bees (Osmia spp.). As Wikipedia explains:

  Mason bees are named for their habit of using mud or other “masonry”
  products in constructing their nests, which are made in naturally
  occurring gaps such as between cracks in stones or other small dark
  cavities; when available some species preferentially use hollow stems
  or holes in wood made by wood-boring insects.

One example here:

Photos at http://www.laspilitas.com/insects/megachilidae/osmia-mason-bee.html


What animal / bird can be heard in this evening sound recording from Western Washington, USA?

I asked the same question on another forum here: http://www.birdforum.net/showthread.php?p=3454684.

It looks like another possibility is a barred owl. It also sounds somewhat similar.


The cell line is most likely genetically male. On the English (US) site, the Description box has several sections, of which one is DNA Profile. In there, it lists amelogenin as X, Y. This gene is located on both the X and Y chromosomes (AMELX and AMELY, respectively), which have distinct PCR-detectable sequence differences. It is often used in helping to determine the gender of unknown samples in the realm of forensics - it is not 100% accurate, so other genetic tests (such as for SRY) are also performed.


Woodpecker pecking, an effective evolution?

My question is quite simple, were woodpeckers gifted with a positive form of evolution?

Though this has been addressed in comments, it's an opportunity to address a popular mind frame about evolution, that is anthropormorphizing it.

Evolution does not think or bestow in the sense that a philanthropist might. Evolution does not doom or treat unfairly as a dictator might. Evolution is merely the process of predominantly random changes in genetic material that result in a change in the expression of that genetic material. If it is a change that radically affects expression of a critical gene (say, that encodes the structure of hemoglobin), the organism experiences a lethal point mutation and ceases to exist. Evolution for that organism stops there; if death occurs before reproduction, the mutation is lost.

Evolution seems beneficial because the environment exerts selective pressures on life: if two animals (say, birds) in the same habitat (say, woodlands) eat the same food (say, larval insects), competition for resources exists, decreasing the numbers of both animals. However, if a mutation (say, a marginally different beak shape) allows even a slight chance that the animal will have a competitive advantage, it is kept in the population. A staggering number of mutations similarly either harmless or advantageous may eventually allow two animals to inhabit the same habitat without competition - a net gain for both animals.

But there's no gift involved. Just a mind-numbing number of non-lethal mutations over a mind-numbing number of years, under the influence of the selective pressures of the environment. You don't see all the mutations that were deleterious, resulting in countless deaths and dead ends because you are standing in one point in time, seeing what exists around you now. The woodpecker seems almost fantastical.

  Were [woodpeckers] given an improper and doomed form of evolution?

Evolution follows the same principles for all species: predominantly random mutations without rhyme or reason or form. If you want to speak of doomed animals, look to mankind's effects on the environment in the last 2000 years, or the last 20. When ecological niches are wiped out, that, not evolution, dooms an animal. The Monarch Butterfly is a poignant example of dooming a species by destroying it's habitat.

A great way the understand selective pressures of habitat is to read about marsupial evolution in Australia. The effect of ecological niches on evolution is very clear.


If I've understood the graphs correctly, then I think you are right on both questions. The difference between 1 and 7 is just that the alleles are in LD in 1 but not in 7


To build on busukxuan's answer, there are a lot of single-celled organism responses that kind of resemble memory:

Slime mold uses an externalized spatial 'memory' to navigate in complex environments - essentially, a slime mold leaves behind a trail, which it then avoids, allowing it to avoid where it has traveled in the past.

If you apply a periodic stimulus to Physarum, it will anticipate the next stimulus: Popular, openly accessible summary Paywalled journal article.

If the amoeba Dictyostelium sees an increasing cAMP gradient, it will follow that gradient - and then be less sensitive to a reversal in the gradient: Cellular memory in eukaryotic chemotaxis

In fact, even bacteria have some memory - they can figure out whether or not they are going up a chemoattractant gradient by making a comparison with the signal they observed a few seconds ago: Temporal comparisons in bacterial chemotaxis


Which direction are wild beehives combs oriented?

I've usually observed wild Indian Bees (Apis cerana) orient their hives in an East-West direction. The entrances are usually oriented towards the Sun.

This is purely from my own observation (in South India) and not from any research.


It means that the direction in which the normal double-strand is wound up (which is also helical) and the direction on which the double helix itself is twited to reach the supercoils are opposite to each other. Have a look at this image from the Wikipedia, I think it makes this clearer:

The first show a DNA ring with the normal helix-coiling. The second show the supercoiling of the coiled ring molecule. Imagine a rubber band. This you can twist around its band axis to get the coiling and around its vertical axis to get the supercoiling.

For linear DNA molecules, this looks like this (taken from here):


Why must a planet be in a star's "habitable zone" to have life?

Your question is not complete. I would suggest to slightly change the title to something like:

"Why must a planet be in a star's “habitable zone” to have life as we know it from our experience?"

You are right, when you are assuming that there could be another than carbon based life as we know it from our planet Earth.

There are many hypotheses that life could be based on Si or other elements.

But carbon is still the easiest element to create bounds with other
elements and carbon too. Why? Here is the answer from wikipedia Carbon-based life:

  There are not many
  other elements which even appear to be promising candidates for
  supporting life - for example, processes such as metabolism - but the
  most frequently suggested alternative is silicon.3 This is in the
  same group in the Periodic Table of elements and therefore also has
  four valence bonds. It also bonds to itself, but generally in the form
  of crystal lattices rather than long chains. Silicon compounds are
  generally stable but do not support the ability readily to re-combine
  in different permutations in a manner that would plausibly support
  lifelike processes.

There is a great documentary from a physicist Brian Cox published by BBC this year called Wonders Of Life which deals with the basic questions how carbon based creatures were "born" on this planet ;) + other interesting things about life.

Brian talks there why the first organisms were created probably in water and how it could be.

Why water?
http://www.pbs.org/wgbh/nova/evolution/liquid-of-life.html

  And why is water the best liquid to do the job? For one thing, it
  dissolves just about anything. "Water is probably the best solvent in
  the universe," says Jeffrey Bada, a planetary scientist at the Scripps
  Institution of Oceanography in La Jolla, Calif. "Everything is soluble
  in water to some degree." Even gold is somewhat soluble in seawater.
  (Before you get any ideas about extracting gold from the oceans, I
  should add that, according to Bada, the value of dissolved gold in a
  metric ton of seawater comes to about $0.0000004).

If you take a route that there could be a different form of life outside of habitable zone, then many things are possible. E.g. life on asteroids, ouside of solar systems, life in other dimensions, life based on silicon or some other elements, energy based life? Or even dark matter and dark energy based life or gods/God-like creatures and all kinds of sci-fi ideas ;).


Can dolphins actually communicate linguistically?

Dolphins and orcas do have dialects. Of course there are species specific dialects and it has been shown that orcas reared with bottlenose dolphins tend to learn the latter's dialect. Dolphins of the same species also seem to have regional dialects, as mentioned in this BBC post (I personally do not trust in non-research articles much, but nonetheless in this case the article indicates a certain possibility of a phenomenon). However, this page also reports the same finding and this source seems to be much more reliable. There are citations too that are at present inaccessible to me. Both the sources say that bottlenose dolphins from Shannon estuary in Ireland, "speak" different dialect compared to those from Cardigan Bay in Wales.

The actual research work is this:

  Hickey, R. (2005) Comparison of whistle repertoire and characteristics between Cardigan Bay and the Shannon estuary
  populations of Bottlenose dolphins (Tursiops truncatus) with
  implications for passive and active survey techniques. School of
  Biological Sciences, University of Wales, Bangor

Apart from having regional dialects, the cetacean communication also seems to have other features of a "language". I am pasting excerpts from this article which basically reports a study on the acoustic communication or codas in sperm whales. This may apply to dolphins as well.

  Individuals within social units have preferred associates among
  members (Gero et al. 2008), indicating differences in the way an
  individual interacts with other members of its unit. These preferred
  associations among unit members suggest the possibility of an
  individual discrimination system.

  .... most adult animals within a social unit shared the most common coda
  types, with the exception of the mother-calf pair whose repertoires
  were different from those of other unit members and each other. Apart
  from the mother-calf differences, the repertoire similarities of other
  members did not support the hypothesis of individually distinctive
  coda type repertoires. This sharing of coda repertoires suggests that
  they allow group membership recognition, at either the unit or clan
  levels. This hypothesis is further supported by the fact that social
  units seem to form groups preferentially with other units of their own
  clan (Rendell & Whitehead 2003b).


Does body absorb nutrients less efficiently if we ingest the same amount at the same time, opposed to spreading over a larger period?

LARGE MEALS AND ABSORPTION

When consumed in usual amounts, the percent of absorbed macronutrients (carbohydrates, proteins, fats, alcohol) should not differ significantly when coming from one large or several small meals.

As an example of the composition of a single large meal, let's imagine something that fits into Acceptable Macronutrient Distribution Ranges (AMDR) in a 2,000 calorie diet: 250 g of carbohydrates, 70 g of proteins and 80 g of fats.

Most carbohydrates are digested into glucose and fructose. Glucose, when absorbed as the only carbohydrate (ingested as glucose or starch), can be absorbed at the rate 60 g/min, but the addition of fructose can increase the absorption of both together to as high as 126 g/min. When fructose is absorbed as the only carbohydrate or in the excess of glucose, it's absorption limit from one meal can be as low as 5 g or as high as 50+ grams. Certain sugar alcohols (see Table 4) (sorbitol, isomalt..) can trigger diarrhea when consumed in amounts greater than ~20 g/meal.

Virtually all ingested protein is absorbed by healthy humans (Surgery Journal). The rate of absorption depends on a type of protein: about 10 g of whey protein and 3 g of egg protein can be absorbed in one hour (JISSN).

At least 60 grams of fat consumed at once can be normally absorbed, concluding from a study in which they investigated the relationship between the amount of fat consumed and atherosclerosis.

In conclusion, the amount of macronutrients (except fructose and sugar alcohols) consumed with a single meal does not seem to significantly affect the percent of macronutrients absorbed, but it prolongs the time in which they are absorbed.

LARGE MEALS AND DIET INDUCED THERMOGENESIS

After eating one large meal, more of the consumed calories will be lost as heat than after eating several small meals:

  Consuming the same meal as a single bolus eating event compared to
  multiple small meals or snacks was associated with a significantly
  higher DIT [diet induced thermogenesis]. (Nutrients, 2016)

  TEF [thermic effect of food] was measured by indirect calorimetry
  for three hours following each meal and was found to increase
  systematically, in a nonlinear fashion, as meal size was increased.
  (Metabolism, 1984)


What is the diet preference of American cockroaches?

American cockroaches (Periplaneta americana) are omnivorous and opportunistic feeders, and as a result, they eat a large variety of foods. They will eat almost anything.

Favorite foods: They are particularly fond of fermenting foods$^{4,6}$ and also prefer sweets$^2$.

Common foods they eat: plant materials, dead animals, sugar, oil, cheese, beer, tea, soap, leather, bakery products, paper, starch in book bindings, manuscripts, glue, hair, flakes of dried skin, soiled clothing, glossy paper with starch sizing and generally most human or pet moist food or other organic matter $^{1,3,5}$. They have also been observed feeding on dead or wounded cockroaches of their own or other species as well as their own cast-off skins and egg-capsules$^6$.

 According to EOL:

 Some of [their food] items, such as cellulose, can not be digested by normal means. However, like cows and other grazing animals, cockroaches have a symbiotic relationship with a bacteria that allows them to digest such substances.

As a result, they could almost certainly survive on just wood and water.

Citations:

 {1}  Bell, William J. and K.G. Adiyodi. (1981). American Cockroach. Springer. pp. 1, 4. ISBN 978-0-412-16140-7.

 {2} Barbara, K. A. 2014. American cockroach. University of Florida Institute of Food and Agricultural Sciences. Retrieved 11 February 2017. http://entnemdept.ufl.edu/creatures/urban/roaches/American_cockroach.htm .

 {3} Jacobs, Steve. "American Cockroaches". The Pennsylvania State University. Retrieved 11 February 2017. http://ento.psu.edu/extension/factsheets/american-cockroaches .

 {4} Jones, Susan C. 2008. Agricultural and Natural Resources Fact Sheet: American Cockroach (HYG-2096-08). Ohio State University. http://ohioline.osu.edu/hyg-fact/2000/pdf/2096.pdf.

 {5} Milne, L. & M. Milne. 1980. National Audubon Society Field Guide to Insects and Spiders. Knopf, New York, NY. p 393. ISBN: 0-394-50763-0.

{6} Periplaneta americana: Palmetto bug. Encylopedia of Life. Retrieved 11 February 2017. http://eol.org/pages/1076920/hierarchy_entries/51102706/details .


The situation you described is entirely normal. $V_{max}$ is the same, so when described with a graph of initial reaction rate vs. substrate concentration, both curves will asymptotically approach the same maximum level. $K_M$ is higher in one than the other, so the exact shape of the curve as it goes from 0 to $V_{max}$ is different. As you may know, you can interpret $K_M$ as the substrate concentration that causes the initial reaction rate to be half of $V_{max}$. This means the substrate with the higher $K_M$ will have a shallower first half of the curve.

You can read more about these parameters and initial enzyme kinetics in Berg biochemistry or at khanacademy.


What is the difference between cytosol and cytoplasm?

IMO, the definitive answer to this question is given in a paper by J. S Clegg.  He traced the origin of the term cytosol to a book chapter by H. A. Lardy, and confirmed by email that Lardy had indeed coined the term. Their definition of cytosol is as follows:

  ... that portion of the cell which is found in the supernatant fraction after centrifuging the homogenate at 105 000 x g for 1 hour.

Thus cytosol is a centrifugation term, (ie a fraction obtained by centrifugation)  and  ' should not be applied, in any context, to the intact cell' (Clegg, 1983).

The cytosol  may roughly be though of as the 'soluble' portion of the cellular extract obtained after everything else, including the microsomes, have been sedimented. (For those not familiar with subcellular frationation, centrifugation at 100 000 g for 1 hr is the 'standard' method of sedimenting microsomes. If your enzyme is found in the 100 000 g supernatant fraction, you can be  pretty sure it is soluble).

When we are referring to the cellular aqueous fluid  that 'holds'   the organelles and other  components we should use the term cytoplasm.

At the bottom of Clegg's article, the editors of TIBS have supplied the following quote, attributed to F.H.C Crick & A. F. W Hughes (1950):

  If we were compelled to suggest a model for the structure of cytoplasm we would propose Mother's Work Basket -a jumble of threads, beads and buttons of all shapes and sizes, with pins and threads for good measure, all jostling about and held together by "colloidal forces".'

In being a  centrifugation fraction,  the term  'cytosol' is very like  microsome: the intact cell contains neither cytosol or microsome.

Ref

Clegg, J. S. (1983) What is the cytosol? Trends in Biochemical Sciences 8, (Dec, issue 12), pp 436-437


Human Demography - Where can I find this statistic?

The CDC has some good stuff. http://www.cdc.gov/nchs/data/nhsr/nhsr051.pdf

But keep in mind that number from your book is likely based on yearly findings in which more than half the women would not be able to have children due to age, voluntary contraception, or other conditions. So it is not reflecting how many children they have over their lifetime. Even in the CDC study more than half the women had no children but few had no plans to have children, couples are moving their first pregnancy to later and later in life, which is going to make it look like few are having children at all on first glance.
 And it's probably not accounting for death rates, the poorest people tend to have the most children but they also have the fewest number live to maturity, which is why they tend to have more (not necessarily consciously mind you) .


How to assess if biological measurements follow a normal or a log-normal distribution

From personal experience, nearly all count data whether from microarray or reads from RNAseq of some kind, requires a log transformation of the counts. Usually a small fraction is added to all values before doing so to zero protect. Log2(counts + 0.5) or some such.   This is independent of the treatments. If you log transform one sample, you will do the same for all samples. To examine for normality, a simple way is to look at the histogram of counts (by all samples or by each sample) before and after transformation. Roughly bell shaped -> proceed.

Pictures below from my data. Although the data are from RNAseq, microarray data should be similar.

R code here:

hist(t$counts,breaks=100,main="Histogram of Raw Counts from RNAseq")
hist(log(t$counts + 0.5,2),breaks=100,main="Histogram of Log2
transformed Counts from RNAseq")


where can I find estimated costs of laboratory equipment?

The best way (if you're buying new) is to contact the manufacturer/distributor. Sales people get inquiries like this all the time, and are generally more than happy to accommodate you (because they get commission on any sales they make). Most items have customized pricing depending on the customer, their order history, the number of items being ordered, add-ons like maintenance contracts, reagents, etc. Many complex instruments like flow cytometers have many customization options, including the number and type of lasers, different types of filter sets, tube vs. plate-based acquisition, type of computer, licenses for software, etc. Sales people know their company's product lines the best, and are willing to talk to you to figure out your needs and then recommend the product that works best for you, which may not necessarily be the one you were originally thinking of.

You can always ask to not be added to any email lists, and if you are added, commercial emails (in the United States, at least) are required to have an unsubscribe link in every email. Check out the CAN-SPAM Act of 2003 for details.


Why do Phobia exist if they aren't advantageous?

I think the fault in your reasoning is the assumption that phobias are not advantageous to us. As an example of a potentially useful phobia, consider the fear of heights. Now consider two different ancestors: one who was afraid of heights and one who was not. Generally speaking, the ancestor who was afraid of heights would likely avoid such environments and thereby reduce the likelihood of, say, falling off a cliff or high precipice. In evolutionary terms, we would say that natural selection confers an advantage to the phobia-possessing individual(s). This website in particular has some interesting reading:

  Others believe that phobias exist because of evolutionary development to avoid danger in order to improve survival. There are several stimuli that are shared by the most phobic people (heights, insects, crowds, etc.) These phobias, with a couple of exceptions, relate more closely to pre-technological societies. Thus, some scientists, such as Martin Seligman, believe that people are inherently "prepared" to fear certain objects. ((5))) In other words, our phobias relate closely to the perils of our ancestors, as through natural selection, those who feared the dangerous stimulus survived while those who didn't, died off. Prepared fears appear to be very easily conditioned. Some scientists, such as LeDoux, believe that preparedness and the ease of conditioning are the result of certain preexisting neurological connections that exist evolutionarily. These connections are turned on with relative ease.


Is there already discovered non-carbon form of life?

In a word, no.  There are some good chemical reasons to expect all life to be carbon-based.
Of course, it is no longer a silly fantasy to imagine an artificial intelligence that might qualify as life.  (Still FAAAARRRR in the future, though, if ever.)


This papers tables shows that cell penetrating peptides are placed before their cargo peptide and do not need to be on a side chain.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1576229/table/tbl1/


Does the fact cordyceps mostly affect insects have something to do with chitin being polysaccharide?

My initial guess was no but there might actually be some evidence for this. For example, host-switching between fungus and insects apparently happens within relatively small taxa of cordyceps, suggesting that host specialization is not too dramatic.
Moreover, there does seem to be some evidence that chitin is a relatively important metabolic input for at least one cordyceps species.
I don't know that we could say that chitin is the thing that allows the host switching or that it is the most important nutrient for cordyceps or anything like that, but it looks like it at least helps.
It's worth noting that ecological characteristics may play at least as large of a role. The phylogenetic study noted that host switching likely occurred from cicada nymphs (which hibernate underground) to truffles (which have their main mass underground), so it's possibly just an opportunistic jump in the soil environment.
It would be interesting to see if there is a "chitin sensor" mechanism in cordyceps that yields a signal to cordyceps that there is a host to invade. But I don't think that I saw anything that suggests that (though it's far from unprecedented in biology).


In an RNA microarray, a hybridization event between a probe and target sequence would indicate a presence of the transcript within the sample. The probes are oligonucleotide sequences found on the microarray chip. The target sequences are representative of the entire transcriptome. The targets are found within your biological sample and have gone through many rounds of amplification in addition to labeling with fluorescent dyes. The fluorescently labeled target when bound to the probe can then be detected using a scanning laser.


What is the highest competency possible for E coli?

This is a great question as I just made my own "homebrew" chemically competent cells.

There are a vast variety of E. coli strains that are commonly used for cloning. They may be transformed chemically by heat shock method, or electrically by electroporation (a brief summary may be found here). These can be made in the lab manually, or purchased commercially from reputable vendors (I recommend Invitrogen/Life Tech, NEB, Promega).

Chemically competency is achieved using Hanahan's method or some a variation thereof. The method involves washing the bacteria in a series of buffers containing various di-valent cation chloride salts (CaCl2, RbCl2, etc). Commercially available E. coli are sold as "regular" and "ultra" competent, ranging from 106 to 106 for regular, and the highest I've seen is 1010 cfu/µg DNA. For maximum efficiency, especially since a small plasmid such as yours will be easy to transform, electroporation is a more efficient technique, but requires specialized equpment. Electroporation can yield >1010 cfu/µg. For standard cloning practices, regular or high efficiency chemically competent E. coli are perfectly adequate. Since you mentioned you are creating a library, you certainly want to go with ultra high efficiency chemical transformation or, if you have the necessary equipment, electroporation. I have not seen electroporation efficiencies reported > 5x1010.

Transformation efficiencies are standardized by reporting a rate as the number of colony forming units (cfu) per µg of some control plasmid, typically pUC19. Transformation efficiency is very sensitive to many factors, including heat shock time, cooling times, thawing time, amount and size of plasmid DNA. All things being equal, the size and quantity of DNA are important for your purposes. Transformation efficiency generally increases with quantity of DNA, but there is a saturation point, and evenetually having too much DNA decreases the yield. Also, efficiency decreases linearly with plasmid size. For example, pUC19, the control vector, is ~2.7 kbp, and your library plasmid is ~6.6 kbp, so you should expect for the same mass of DNA you will have lost 60% transformation due to plasmid size. This loss is due to the physically larger size of DNA being more difficult to move into the bacteria.


Why can you graft two unrelated cacti successfully, but you cannot do this on garden trees?

Firstly, different genera of trees can occasionally be successfully grafted. For example, quince, genus Cydonia, may be used as a dwarfing rootstock for pear, genus Pyrus.

However, it is true to say that this is the exception rather than the rule.

In the case of plants in the family Cactaceae, I would suggest that grafting is usually successful for two main reasons:

Genetic similarity. Plants in the family Cactaceae while known to be morphologically often very different, have relatively little genetic diversity. This will increase the likelyhood of a successful graft.
Ease of aligning vascular cambium. This is required for a successful graft, and in Cacti this is quite easy to achieve since the cambium is clearly visible when you prepare the scion and stock.

It is also possible that Cacti readily form callus tissue, which would also aid in the grafting process.

Nyffeler, R., 2002, doi: 10.3732/ajb.89.2.312 Am. J. Bot. 1 February 2002 vol. 89 no. 2 312-326


The biology behind tree pruning and hedge trimming

The difference has to do with the concept of "thinning and heading" and how plants respond to abiotic damage. Thinning refers to the removal of a branch or shoot all the way back to the node which it originated from. This is the primary type of pruning used on trees - either to limit growth or to increase the amount of light permeating to lower branches. Late winter is generally the best time to do this, just before the tree breaks dormancy, since plant pathogens are generally less abundant. By pruning in late winter, this also reduces the amount of time that the wound is exposed before the tree begins active growth.

In contrast, "heading" refers to the partial removal of a branch, usually 1/2 to 1/3 back to the node.  The purpose of heading is to stimulate shoot growth on the remaining branch - hedges being a primary example. Because new shoots and leaves are desired, heading is usually performed at the height of stem growth (in most climates late spring to early summer).

The biologic processes behind this are complex (botanists are just beginning to understand how plant behavior adapts to predation) but in very general terms, plants respond to damage in two ways: by compartmentalizing the wound; and by stimulating growth on the remaining tissue. Many types of woody plants produce latent (or adventitious) buds, which lie dormant within the cambium tissue. Normally these buds are suppressed by auxin hormones produced in the meristem by active shoots. When the meristem is removed (such as through heading the branch), these buds rapidly develop to produce new shoots and leaves. Most species used for hedges are selected because of this ability.

So long story short: thinning is best performed in late winter, when the plant will quickly be able to seal off the damage while limiting the production of unwanted water sprouts and suckers. In contrast, heading is usually done in early summer, when the hedge can vigorously produce new growth and fill out any gaps.

Some resources:

http://extension.wsu.edu/maritimefruit/Pages/PruningBasics.aspx

http://puyallup.wsu.edu/~linda%20chalker-scott/horticultural%20myths_files/Myths/Wound%20sealer.pdf


Can different bacteria strains of same species have different genomic sizes?

Yes, and one could argue that the differences between two strains of the same species are entirely due to their collections of genes (and therefore different genome sizes).

Take the plant pathogen Pseudomonas syringae, for example. There are many different strains, categorized by the plant hosts they cause disease on. This host range is determined by different collections of virulence genes in their genomes. So although they are the same species, they can be remarkably different in their genomes. See this (open access) paper by Baltrus, et al for more information.

A point to remember... "species" is a manmade concept, and there can be different definitions. Some species can have less than 90% similarity at the genome level!


How does water buffer a sudden drop in temperature?

From pure biophysical viewpoint the question

"Why does water buffer sudden temperature changes?" can be answered in the following way:

Water has relatively high specific heat capacity. This is the measure of the energy required to raise the temperature of one kilogram of a substance by one kelvin without a change of state occurring. "Relatively high" means that water can absorb more energy without noticeable (for the cell) increase in temperature.

Here are some heat capacity values from the above-linked Wikipedia article:

  Animal (incl. human) tissue   3500 Jkg-1
  Water at 25 °C    liquid  4181.3 Jkg-1
  Methanol  liquid  2597 Jkg-1
  Ethanol       liquid  2440 Jkg-1
  Paraffin  wax solid   2500 Jkg-1
  Graphite  solid   710 Jkg-1

Water has relatively high thermal conductivity. This means that the absorbed heat is quickly distributed over the complete cell volume, leveling down the focal temperature increases in cell. Here are again some values for comparison:

  Water 0.6 Wm-1K-1
  Wood 0.2  Wm-1K-1
  Paper 0.05  Wm-1K-1
  Glycerol 0.3 Wm-1K-1

The follow-up questions:

"Why does water have relatively high heat capacity?" and "Why does water have relatively high thermal conductances?" are not within the scope of this site. However, here exactly comes your explanation with hydrogen bonds in play (from Wikipedia):

  Hydrogen-containing polar molecules like ethanol, ammonia, and water
  have powerful, intermolecular hydrogen bonds when in their liquid
  phase. These bonds provide another place where heat may be stored as
  potential energy of vibration, even at comparatively low temperatures.
  Hydrogen bonds account for the fact that liquid water stores nearly
  the theoretical limit of 3 R per mole of atoms, even at relatively low
  temperatures (i.e. near the freezing point of water).


It obviously can do that, causing a rubella encephalitis. A specialized form seems to be the "Progressive rubella panencephalitis", which is very rare with only 20 cases described since its first description in 1974.

About rubella encephalitis more papers are available, see these for a start:

Neurological aspects of rubella virus infection.
Mumps encephalitis: return with a vengeance.
Neurological Aspects of Rubella Virus Infection


why dead mouse doesn't bleed when we cut their skin?

From personal experience, extracting organs/tissues of over 1000 mice I can give some hints:
Mice blood coagulates quite fast after death. If you need to extract blood, you are under time-pressure and many scientists extract the blood directly after death from the heart using a syringe. If you are not fast, you miss the chance of drawing blood as this can't be done after coagulation. Others cut up the thorax (post mortem) and then directly draw blood with a syringe. I personally never tried this technique but I spectated that mice bleed a bit, directly after death, when opening the thorax, however it's not much.
After drawing all blood from the heart, mice don't bleed, no matter where you cut, potentially because of low blood content remaining. (Un-?) Fortunately, I never had to cut mice that were alive.. so I cannot tell you what would happen if they were alive.
Edit: Also, in theory, the smaller an animal is, the higher becomes the diffusion/volume ratio and surface-tension/volume ratio. This means smaller animals need less active blood circulation and and their blood vessels might have a small diameter, so that most blood would be kept inside by surface tension if these vessels were cut.
Edit due to comment:
The extractable blood from mice is around 1.5 ml, and I have seen opening of the thorax within seconds post mortem with minor bleeding. Afterwards, the majority of blood (1.5 ml) was extracted directly from heart with a syringe. As this was post motrem, I cannot exclude the possibility that coagulation of blood in small peripheral vesicles already affected the observation or how heart beating would affect it. I cannot say what would happen in live mice and I am happy that I don't have this knowledge.


Can you use a microscope without an eyepiece?

Yes, you can. I have a microscope where the data can be transferred to a screen on a computer instead of going to the eyepiece. This microscope has both an eyepiece and the option to redirect the image to a screen. However, I also have a microscope with a screen only. So, I suppose you can have a microscope without an eyepiece.

I have never come across a microscope that has neither an eyepiece nor a camera but I don't know whether it's possible or not.


Most viruses of human concern are "enveloped", that is, they are surrounded by a lipid membrane. This membrane is usually what determines the shape of the outer layer, and is intrinsically flexible, so most human viruses would be able to deform a bit to fit through a hole. Additionally, the size of individual enveloped virus particles tends to vary quite a bit as seen in this image from a previous answer:
You can also see that biologically active proteins stick out of the membrane. These are likely to break off if the virion experiences any significant forces. My experience with coronaviruses has been that even relatively mild purification procedures remove the spikes from most particles, let alone forcing them to deform through a hole. So, while they might pass through a small hole without rupturing, it's likely their ability to infect cells would be greatly reduced.
In the case of non-enveloped viruses such as adenoviruses or picornaviruses, their outer layer is composed of many copies of a "capsid protein", linked together according to quasi-equivalence. The capsid proteins need to join together over a range of angles, so they should be able to tolerate some flexing. Again, though, any extra proteins that stick out for biological functions (such as the adenovirus' fibers) will likely be damaged or detached, which would remove the virus' ability to infect cells.


A reservoir host most obviously is a long-term carrier organism of a given pathogen that doesn't exhibit the disease caused by the pathogen.

A vector is literally any agent that transfers the pathogen to another organism. If you think about it, a reservoir doesn't have to be a vector i.e. there's no route of transmission they participate in, but a vector can certainly be a reservoir, such as bats, who often act as a vector for the pathogens they house (think Rabies). On the flip side, ticks are common vectors for Lyme disease, but small rodents actually act as the reservoir for B. burgdorferi (1).


My first thought was this:

According to Wikipedia (citation provided)

  Between 50 and 70 billion cells die each day due to apoptosis in the average human adult. For an average child between the ages of 8 and 14, approximately 20 billion to 30 billion cells die a day.

For every cell that dies a new one must be born, so there must be at least between 50 and 70 billion cell divisions to replenish these cells in an adult human (no net growth).

But then I remembered erythrocytes. Wikipedia again:

  Adult humans have roughly 2–3 × 1013 (20–30 trillion) red blood cells at any given time, comprising approximately one quarter of the total human body cell number

and...

  these cells live in blood circulation for about 100 to 120 days

So approximately 1% of erythrocytes are destroyed every day and must be replaced. That's 2-3 x 1011 cells formed every day, which dwarfs the cells replenished due to apoptosis (5 - 7 x 109).

  Through this process [erythropoiesis] erythrocytes are continuously produced in the red bone marrow of large bones, at a rate of about 2 million per second in a healthy adult.


Do cats ingest everything that they lick off themselves during grooming?

Cat licking is partially to clean themselves (including of odors that might attract predators) but is also used as a cooling mechanism (they sweat little and so use evaporation of saliva as a cooling mechanism), socialization, and to help spread oils. Most hair in short haired cats passes through the digestive tract with no issue. Source The hair that is unable to pass through the cat will accumulate in the stomach and be coughed up as a hairball (generally every 1-2 weeks) source.
For more on a cat's digestive tract see here. Note also that the human digestive tract can manage all manner of weird things to and just allow it to 'pass through' and this is the 'default' behavior for many digestive tracts.


One possible answer for your question could have to do with the level of exercise the subject is doing.

While the nasal passage is the main route for breathing, it provides cleaner air and allows for more even and slow respiration rates, a greater volume of air can pass through the mouth LaComb.

There is no discomfort in mouth breathing during exercise because mouth breathing can deliver greater amounts of oxygen and release greater amounts of CO2; it is the preferred method of breathing for increased activity.

Secondly, discomfort in oral breathing stems from a perception of breathlessness due to stimulation of receptors in the oral mucosa. When patients were required to breath orally with humidified air, no instances of breathlessness were reported (Source).

Based on these two studies, when exercising oral-breathing is required to deliver adequate amounts of O2. Therefore, nasal-breathing is not required and an obstruction of the nasal passage is not percieved. When exercising in a pool, discomfort of oral-breathing is diminished due to the humidity of the surrounding air. When not exercising, and breathing orally in low humidity air, discomfort is felt due to the stimulation of receptors in the oral mucosa.


What makes a strong polyadenylation signal a strong signal?

Just expanding on aandreev's comment.

Polyadenylation is initiated by binding of CPSF (Cleavage and Polyadenylation specificity factor) after its binding to the AAUAAA motif.
From the introduction of this article:

  CPSF (cleavage and polyadenylation specificityfactor) binds to the
  AAUAAA hexamer via its 160-kDa subunit and possibly its 30-kDa subunit
  (Keller et al., 1991; Murthy & Manley,1992; Jenny et al.,1994;
  Barabino et al.,1997). CstF (cleavage  stimulation  factor) binds to
  the U- or G/U-rich element downstream of the cleavage site, and
  stabilizes the binding of CPSF to the AAUAAA sequence of the pre-mRNA
  (reviewed in Colgan & Manley,1997; Wahle & Kuhn,1997).

Any alteration in the CPSF binding site will lead to reduced polyadenylation efficiency. Polyadenylation efficiency also depends on other factors such as secondary structure and presence of proximal CstF sites.


Is there a comprehensive list of human circadian-like processes, hormones or gene expressions?

There isn't a central/master website that I'm aware of, as it's still an area of active research.  I did a bit of work in the field about 10 years ago, and at that point we were still working out the circadian rhythms in the yeast mating cycle.

Since then, the field been enumerating more and more involved processes: mRNA expression, mRNA degradation, micro RNA, mRNA transport and translational regulation, then protein translation and protein regulation... Given that any single gene can be regulated at one or more of these points, and that there are at least a few different circadian cycles and they can even conflict... well, it's a bit of a mess.  Oh, and don't forget that different organs and cell types have different responses, so then you have to cross check 50 cell types.

I'd start with this review paper, which can give you an idea of what kinds of papers to search for.  If you decide you want to know about individual genes, a lot of scientists in the field have made their datasets available online in various gene expression databases.  There are several databases running currently, and maybe one of them will be specialized in circadian expression.

Circadian topology of metabolism
Joseph Bass
Nature 491, 348–356 (15 November 2012) doi:10.1038/nature11704
Published online 14 November 2012
http://www.nature.com/nature/journal/v491/n7424/full/nature11704.html


Do plants have distinctive DNA genomes from each other like humans do?

Short answer: Yes!

Now for the longer answer. Yes, they do have distinct genes in general, but what you may see as different plants can also sometimes be clones. For example Quaking Aspen Trees which commonly grow in clonal colonies.

If you had a massive database of genetic material from plants you would be able to trace it. You may be able to, by doing sampling, work out where a sample was located geographically.


Worm type bug inside of stick? What is it?

It looks to me like the larva of a case-bearing moth. Despite the common name, the case is made by the larva, as seen here. What you are watching is the larva creeping out, then moving forward, bringing its case with it. Larvae of other moths make cases out of various kinds of hard materials, such as pieces of stick or grains of sand. Have a look at the possible duplicate noted above, which has helpful info.


phylogenetic analysis of gene enrichment?

Phylogenetically analyzing genes that are not present in every species may present you with some problems, but it is completely feasible to simultaneously analyze the relatedness of the species (based on your enrichment score), and the relatedness of the scores themselves.

Forgive me if this is too 'simple' an analysis, but you have not said what you have tried.

My choice of approach would be to use R (open source stats package) to generate a heatmap of your matrix of data. There are plenty of options for the method of clustering, but the defaults tend to produce quite a nice heatplot, with hierarchical cluster analysis performed on both dimensions of the data (you can specify only 1, or even none, if you prefer). I have used the following code to simulate some data to generate the below heatmap;

# generate 10x10 matrix using random data
x <- as.matrix(data.frame(rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10)))
# use heatmap function on the data. "labRow" and "labCol" simply remove the labels.
heatmap(x, xlab="Genes", ylab="Species", labRow="", labCol="")

Because it is randomly generated data there are no patterns really, but if you were to stick you real data in there it would look better no doubt. (In an actual analysis you will want to leave the labels on, I was just simplifying the plot). The function can handle missing values, so you could put all the genes you want to analyze in there, even if not all species have them.

Using this method you could see the most closely related species by gene enrichment, and also which are the most closely related genes (in terms of enrichment for your TF).


Where can I find clinical trial data published in JAMA?

Online repository

Today, most journals (although t may depend on the field) require author to upload their data. The paper you are interested in was published in 1967 (internet was invented in 1969). It is very likely that the data have not been uploaded. It is also possible that the data have never been compiled numerically but is only on paper.

Ask the authors

Your best chance is to contact the authors directly and politely ask if they can give you their data. The author might be hard to contact as well as they may have changed university, be retired or even dead.

Possible loss of data

If you can contact the authors, then it is not unlikely that the data have just been lost. The loss might be due to a flood, to a technical issue or just because they don't know where it was placed.


I understand that Robin Holliday was the first to discuss the possible role of DNA methylation
in the control of Gene expression. In his paper "The inheritance of epigenetic defects"
he presents what is one of the first modern formulations of what we now regard as epigenetics. The term "epigenetics" itself was coined by Conrad Waddington although this predated our modern understanding of heredity.

Holliday, R., The inheritance of epigenetic defects, 1987, Science, 238, 4824


Good question! As you write Vitamin A is quite important vision as it is an integral part of the light sensitive rhodopsin protein. Rhodopsin is necessary for a type of photoreceptor, the rod. It is located in outer segment of the photoreceptor. Vitamin A is also required to other opsins that are needed for the cones to function.

When someone has Vitamin A deficiency it does not mean that they have no Vitamin A. For example instead of having i.e. 100 Vitamin A you only have 30 (arbitrary numbers!).

In the retina, you have the very light sensitive rods and the less light sensitive cones. Rods need a lot of rhodopsin (and hence Vitamin A) as they have to detect small levels of lights (it is thought that a rod can detect a single photon!).

Cones, on the other hand are not so sensitive to light. During the day there are tons of photons*. Since you need less Vitamin A for cones to function, you will see the symptoms of Vitamin A deficiency later compared to rods.

Hence, when you still have a bit of Vitamin A but not enough (e.g. 30 instead of 100) you will first notice it in systems that need Vitamin A the most. It turns out that this are the rods. And yes, if you had 0 Vitamin A you would be blind. But since Vitamin A is needed for many other processes, you will probably be dead at that point.

*Personally, I find it hard to grasp just how large the difference in Illuminance (and hence photon numbers) is for example between day and night. See here for a comparison. As you can see, our visual system has to deal with an enormous dynamical range of illuminance. The fact that we usually don't even think about these differences in light intensities in everday live is testament to how fantastic our visual system is in dynamically adapting to the huge differences in input.


What is this beetle? Found in heather in snowdonia

I believe it's the Violet Ground Beetle -
Carabus violaceus. This is a close relative to the Carabus coriaceus posted by Jon.

The purple colour is a give away, but as in many insect groups there are often very similar species. As pointed out in the comments to this anwer, this is the case for C. violaceus and C. problematicus (differences)

There are websites  like observado.org where sightings can be added as a species or for instance "unknown beetle", where they are reviewed (depending on the availability of the volunteering experts) or identified.


Why is western blotting used to confirm positive ELISA HIV tests?

One reason a Western blot is more specific than an ELISA - even one using the same set of antibodies - is background.

Antibody-linked colorimetric reactions aren't completely on/off. There's always some background reaction. The antibodies are a little bit cross reactive, or non-specifically sticky, or the colorimetric coupling enzymes aren't completely washed away, etc. There's a number of reasons you'll get a small amount of signal even in the abscence of the desired reagent.

So imagine how this non-specificity looks in an ELISA assay. You're only getting a single readout. Any non-specificity/background in the assay adds noise to your output level. Hopefully for any decent assay the noise is normally well below the threshold for crossing over into a "positive" readout, but if the noise is Normally distributed, there's always a small chance that the noise will exceed that threshold. (There's also those non-normal failure modes, where you mess up a wash step, or you get a bad tube of antibody, etc. Negative controls help, but only so much.)

In contrast, think about how non-specificity/background looks in a Western blot. If you get non-protein linked background, the presence of this background will be across the entirety of the blot. It's very obvious that something went wrong with the assay in those cases. Even if you get random spots and not overall background, the chance you'll get a random spot at just the correct molecular weight is very, very unlikely.

An additional benefit is that Western blots first separate the proteins prior to doing antibody-linked detection. This means if there's some protein in the sample which cross-reacts with the antibody, it's very likely it will migrate at a different molecular weight and not be counted as a false positive. (As opposed to ELISAs, where every signal counts toward the total.)

These effects mean that if you're looking for low false positives (as you would with an HIV test) a well-done Western blot is likely to give a more confident signal than a well-done ELISA would. (At the cost of time and effort.)

A final issue is that combining the two will give you more confidence in a positive result than either one alone, especially if you use different antibodies for each. The final confidence in a positive result is not just the confidence from the Western blot, but the confidence that both the Western and the ELISA report positive results, so there's a benefit of doing both, even if they were equally specific.