What is the mechanism behind cats' geolocating homing behavior?

It is explained with path integration in behavioral neuroscience. Not only cats, but other mammals, birds and even insects use path integration to return to a starting point.

Here is a relevant excerpt from the book Beyond the Cognitive Map: From Place Cells to Episodic Memory (by A. David Redish):

  Path integration is the ability to return directly to a starting
  point (sometimes called a home base or reference point) from
  any location in an environment, even in the dark or after a
  long circuitous route (Barlow, 1964; Gallistel, 1990; Maurer and
  Seguinot, 1995). Sometimes called dead reckoning, this ability
  has been shown in gerbils (Mittelstaedt and Mittelstaedt, 1980;
  Mittelstaedt and Glasauer, 1991), hamsters (Etienne, 1987, 1992;
  Chapuis and Scardigli, 1993), house mice (Alyan and Jander,
  1994), rats (Tolman, 1948; Alyan et al., 1997; Whishaw and
  Maaswinkel, 1997), birds (Mittelstaedt and Mittelstaedt, 1982;
  von Saint Paul, 1982), and even insects (Wehner and Srinivasan,
  1981) and arthropods (Mittelstaedt, 1983), as well as dogs, cats,
  and humans (Beritashvili, 1965).

  Path integration in animals has been the subject of argument
  for more than a century, including a notable debate in 1873 between
  Alfred Wallace and Charles Darwin in which Wallace suggested
  that animals find their way back via sequences of smells
  and Darwin argued that animals must be using dead reckoning
  (see Wallace, 1873a, 1873b; Darwin, 1873a, 1873b; Nature, 1873;
  Forde, 1873; Murphy, 1873). The carefully controlled experiments
  of Mittelstaedt and Mittelstaedt (1980) and Etienne (1987) have
  demonstrated conclusively that this ability is a consequence of integrating
  internal cues from vestibular signals and motor efferent
  copy.

emphasis mine

Cats, dogs and rodents can use taxon navigation as well along with path integration. Here is a relevant excerpt from Neural compass or epiphenomenon?
Experimental and theoretical investigations into the
rodent head direction system (by Matthijs van der Meer):

  “Internal allocentric” navigation. This type of navigation relies on a mapping of praxic commands to an allocentric spatial representation, allowing the animal to make a direct return to a home base after a complex outward path in the absence of cues, an ability referred to as path integration, discussed in detail in the next section. Returning by following an odour trail back, or navigating to a cue indicating the home base would be taxon navigation, but behavioural experiments have provided convincing evidence that rodents are able
  to do this without using external cues. As mentioned above, this ability requires some mechanism of continuously updating at least one’s directional heading (a “homing vector”) relative to the home base. This is an allocentric representation which does not need to be related to any external cues, unlike the next class of strategies; the reference point or direction can in principle be set to any location the animal desires.

emphasis mine

Further reading:

A connectionist model of path integration with and without a representation
of distance to the starting point (ROLAND MAURER, University of Geneva, Geneva, Switzerland) - Copyright 1998 Psychonomic Society, Inc.


How do molecules signal pre synaptic neurons to activate?

Activating a neuron generally means depolarizing the neuron, sometimes depolarizing enough to trigger an action potential. In general, molecules activate neurons by binding to their cognate receptors in the neuron cell membrane. Sometimes the receptor is, itself, an ion channel. Other times the receptor initiates a cascade of events in the neuron's cytosol that end up modifying the cytoplasmic portion of an ion channel and thus opening the channel. In both cases, the channel is usually specific for positively charged ions (cations) (e.g. Na+ or Ca2+) whose concentration is greater outside the neuron than in the neuron's cytosol. Activation results when these cation channels open and allow positively charged ions to flow into the neuron. This entry of positive charge reduces the neuron's cell membrane potential, making the potential less negative. If enough positive charge enters, the neuron may be depolarized enough to trigger an action potential on the neuron's axon. This is what is usually meant by activating a neuron. It depends on the three-dimensional structure of the molecule (often a neurotransmitter) and the structure of the receptor. The binding of a signaling molecule to its receptor is usually non-covalent, often mediated by hydrogen bonds.


The maximum temperature for E. coli to survive is dependent on the strain. E. coli from warm areas can easily survive 45 °C and more. The minimum number of E. coli to ingest in order to become ill is also dependent on the strain. Whether you become ill at all is also dependent on the strain. You harbor many billions of E. coli in your digestive tract without becoming ill, so without further information on the released strain, it's really hard to tell.

One of the suggestions from the WHO Guidelines for drinking water quality is to boil the water in order to desinfect it.


Where does extra blood come from to fill your muscles during exercise?

The blood comes from the body's reservoirs:

spleen (mostly erythrocytes) [1]
liver [2]
veins (probably the most important blood resevoir as they contain 50-60 % of the volume) [3]

In pathological situations, if hypovolemia occurs, blood can also come from:

splachnic vascular bed [5]

But what attracts the blood into the muscle? The phenomenon is called active hyperemia:

  Active hyperemia is the increase in organ blood flow (hyperemia) that is associated with increased metabolic activity of an organ or tissue. An example of active hyperemia is the increase in blood flow that accompanies muscle contraction, which is also called exercise or functional hyperemia in skeletal muscle. Blood flow increases because the increased oxygen consumption of during muscle contraction stimulates the production of vasoactive substances that dilate the resistance vessels in the skeletal muscle [4].

References:

The human spleen as an erythrocyte reservoir in diving-related interventions. Kurt Espersen, Hans Frandsen, Torben Lorentzen, Inge-Lis Kanstrup, Niels J. Christensen. Journal of Applied PhysiologyMay 2002,92(5)2071-2079;DOI: 10.1152/japplphysiol.00055.2001
Lautt WW, Greenway CV. Hepatic venous compliance and role of liver as a blood reservoir. Am. J. Physiol. 1976 Aug;231(2):292-5. PubMed PMID: 961879.
Michael J. Gregory, Ph.D. The Circulatory System. Licensed under CC-BY-NC-SA-3.0
Richard E. Klabunde, PhD. Cardiovascular Physiology Concepts. Active Hyperemia. Available from http://www.cvphysiology.com/Blood%20Flow/BF005.htm (accessed 03.08.2014)
Blaber AP, Hinghofer-Szalkay H, Goswami N. Blood volume redistribution during hypovolemia. Aviat Space Environ Med. 2013 Jan;84(1):59-64. PubMed PMID: 23305001.


The Sydney Funnel Web Spider's venom is called δ-atracotoxin and it is especially toxic to primates. It is a peptide toxin, which means that it has the potential to be digested in the stomach before having any physiological affect. However, many peptide toxins are not inactivated by swallowing--you don't want to be eating any Botulinum toxin.
Characterization of insecticidal peptides from venom Australian funnel-Web spiders (Vonorax et al. 2006) harvested venom from Hadronyche infensa, the Darling Downs funnel-web spider. This spider is closely related to the Sydney Funnel Web spider and also produces δ-atracotoxin.

An oral ingestion activity test was undertaken using crude H. infensa venom.

The ingestion test was performed with insect larvae, which are susceptible to the venom when injected. (Aside: there's a lot of interesting research on the toxin's effect in insects). They didn't find much:

Oral ingestion activity test of crude H. infensa venom
No effect was observed in this test, even though approximately 4 times the dose required for lethality by injection was orally consumed by the larvae.

I don't think anyone has performed a study of toxin ingestion in primates (if they have, I couldn't find it). The researchers don't speculate as to why the toxin has no effect when ingested. As expected, the toxin had no effect on (non-primate) mice:

Effect of atracotoxin-Hv1 on newborn mice
All mice in both test and control groups survived without apparent toxic effect beyond 24h post injection.

Whether this is applicable to other spider venom depends on the nature of the venom. A non-peptide, low molecular weight venom able to be absorbed by the lining of the esophagus could be very toxic by ingestion.

Further reading:
Scanning Mutagenesis of ω-Atracotoxin-Hv1a Reveals a Spatially Restricted Epitope That Confers Selective Activity against Insect Calcium Channels (Tedford et al. 2004)
Isolation and pharmacological characterisation of δ-atracotoxin-Hv1b, a vertebrate-selective sodium channel toxin (Szeto et al. 2000)
(for more info on peptide toxins): Cyanobacterial Peptide Toxins


Copper for cell incubator to prevent contamination

First thing I'd do is replace the HEPA filter. A copper plate/foil may help, and it certainly won't disrupt the flow of heat, as copper is incredibly conductive (that's why they make electrical wires out of it), and poking holes would help with the airflow, but a new filter will probably make the most difference. I've never used a full-copper incubator, and the few serious contaminations I've had to deal with were related to the HEPA filter and poor TC practices.

If you haven't already, I'd institute a good routine cleaning program as well. Change the water bath each week (make sure you're adding fungicide to the water), and wipe down the whole incubator with bleach followed by an alcohol rinse each month. Make sure you clean all the bleach off, as it corrodes metal if left on very long. At the same time, clean and autoclave all of the removable components like shelves, rails, and water pans.

Good luck!


Has any flying creature evolved into a sea creature?

Clarification of the question
The following feedbacks from the OP are his comments below

By creature of course I denote animals
I meant animals that can fly (not glide) and control their flight
By sea creature I mean those animals that either breathe in water with gills (e.g. fish) or the ones that have to surface to breathe (e.g. whales).

Answer
Water beetles are the perfect example.

They live underwater, some of them very rarely (if ever) surface as they capture air under their abdomen and can breathe it for a long time while underwater. Just like dragonflies, butterflies, flies, bees, ants, bugs and many others, beetles are Pterygota and therefore have flying ancestors.

Answer before clarification
It all depends what you mean by "sea creature" and "flying" as well as by you mean by "semi-aquatic" and "semi-terrestrial" and also what you mean by "creature".
Here are examples of eventual interest to you.

Birds that are good swimmers, including those that can't fly anymore such as many penguins. No birds can breathe the air dissolved in the water though.

Insects that evolved a larval stage in the water while the ancestors are fully terrestrial. I don't think any insect can breathe under water however several species can carry quite a lot of air with them underwater (such as water beetles) or many just stick their butt out of the water to breathe (like culex mosquito larvae).

It is unclear whether by the use of the term "creature", but if you accept examples from non-animal forms of life, you'll find examples of seed dispersal through water while ancestors used air, you'll find plenty of examples of parasites too.

If by "creature", you meant "animal" and by "flying", you meant high level of control flight and by "sea creature", you meant animal able to breath air dissolved in the water, then I personally can't think of an example of a flying animal evolving into a sea animal.
None of these examples are as pleasant for you as an example of a big flying bird evolving gills that now live in deep sea though but unfortunately, I can't think of such case.
For fun, you might want to have a look at the post How many times did terrestrial life emerge from the ocean?

Your usage of the term "creatures" as well as the phrase "according to evolution theory" and also the phrase "many sea creatures of the deep past" make it feel like you don't have much knowledge in biodiversity, evolution and evolutionary time scale. You might want to get some intro knowledge on the subject. Understanding Evolution by UC Berkeley is a very introductory and pretty short free online course on evolutionary biology if you are interested in.


Does a man contain all the genes needed to make a woman?

This answer also involves some speculations as the question is about a good theoretical framework for a science fiction.

You can find in this post about how sperm can be used to produce embryonic stem cells. It would still require an oocyte for doing that.

The question now is- Can you produce oocytes from a male?

You may fuse two X bearing haploid spermatids to form a diploid cell with XX. This cell will also have mitochondria and ribosomes — seems like a decent candidate. Gametogenesis has not been shown to happen in-vitro. Moreover a zygote will need a lot more cytoplasmic resources that you can get from a fused spermatid.

Plus there are imprinting issues as already pointed out by Chris.

Conclusion: Next to impossible

For your question "Does a man contain all the genes needed to make a women": yes he has but does not have the biological machinery to do that (exclusive of the womb).

However if you choose to send a female astronaut for this mission then there may be some hope. As Chris said, there are problems with homotypic fusions because of imprinting issues. But with a supply of ova there can be other ways:

Make clones using SCNT: limitation is that there would be very little variability.
Erase imprinting marks and fuse two oocytes: This has not been done yet but this is possible. At this moment we have technology (still incipient for therapy grade), for targeted genome editing. The basic principle involves fusing a DNA-endonuclease with a sequence specific DNA Binding Domain (DBD). Examples include Zinc Finger Nuclease, TALENs and Crispr-Cas. This study demonstrates an engineered system that can deaminate RNA in a sequence specific manner. Based on a similar principle it should be possible to link DNA-(cytosine/adenine)- methyltransferase or DNA-(cytosine/adenine)-demethylase to a sequence specific DBD 1. This system can be used for targeted epigenetic modification. This would have a little more variation than cloning because of meiotic recombination. Limitation is that there won't be any males, this would perhaps become an Amazonian Planet.

Make sure that your space-shuttle has a good biolab facility :P

1 Imprinting is generally implemented by DNA methylation which happens mostly on cytosines.


No single factor is considered to be the reason for the aerial spinning behavior (Hester et al., 1963; Norris and Dohl, 1980; Norris et al., 1994). The various factors include leadership or dominance, alertness, acoustic communication, courtship display, defining positions of members in the school, and dislodging ectoparasites. The most notable ectoparasites are remoras and whalesuckers (order Perciformes, family Echeneidae). ... Hester et al. (1963) suggested that the aerial maneuvers executed by spinner dolphins are involved in the removal of remoras. ... While aerial spinning maneuvers may not have developed specifically to remove ectoparasites like remoras, dynamically it is plausible that this proves to be an added benefit.

--Dynamics of the aerial maneuvers of spinner dolphins


Does anybody know what this shark is eating?

The fish in this image is Helicolenus dactylopterus. Shown below;

This fish, is more formally known as a Blackbelly Rose-Fish. This fish, is one of the Goblin Sharks' many prey in the deep sea.

In the photo you posted it looks as if the Goblin shark effortlessly and oddly so caught the fish - it did. This is due to how it consumes most of its prey:

  When they approach it their jaw goes out similar to how a human can stick out its tongue. Then with a sucking motion they draw they prey into their mouth where very powerful teeth are waiting to consume it.

Goblin sharks are quite terrifying...


I'm a bit confused because your title and your question description don't seem to align perfectly (-omics data versus host-pathogen interactions). If you are interested in host-pathogen dynamics, in my opinion, the best general introductory text in this area is Keeling and Rohani Modeling infectious diseases and humans and animals.


How does a new species survive without suffering inbreeding?

Well, speciation is a process, not a single event thing.

Usually what happens initially is geographic isolation of some members of a species, so in that sense the inbreeding is something that is influencing and you can also think of it as causing the speciation process. The presence of special harmless or semi-harmless disadvantagious mutations - which increases in frequency from this isolation - influences how the species is going to evolve, but eventually shapes this species to better cope adapt to some environment, or evolves the new species out of existence.


Does DNA Ligase look for complementarity in sticky ends?

If I understand correctly you are preparing your cloning vector by digesting it with two enzymes that are 31 bp apart. If you have a high background of recircularized vector see if there is a unique restriction enzyme site within that 31 bp.  If there is, and if the fragment you are trying to insert also lacks that site, then a simple approach would be to inactivate the ligase, and digest the reaction with the third enzyme.  That should drastically reduce the background of recircularized vector.
If after gel purifying the vector backbone after the double-digestion, you get a  significant background of recircularization, then you can easily test your hypothesis about ligase ligating mismatched sticky ends: both of the starting sites should be gone and any sites in-between them should be gone.  Have you tested this?


Are males taller than females in humans?

Are males taller than females?

Best data I could find come from the Statistical Abstract of the United States (1999) > Section 3. Here is a table reporting the percentage of the male and female population which height is lower than a given threshold

Note that this data collection was done among students in US universities and is therefore not representative of the whole world or even the whole country.

Does height follow a bimodal distribution?

A difference in height between males and females is often used as a classical example in introductory statistic class to exemplify a bimodal distribution as seen in this picture

and on these (a priori fake) data

However, Schilling et al. 2002 argued that while the difference in mean height between the sexes is real, this difference is too small relative to the variance in height within each sex to be clearly depicted on a graph.

Note that I found this non-peer-reviewed paper which shows real data that display a truly bimodal distribution of height.

Genetics of height

The question why are they taller? is very broad. I will just focus to give you some hints about the genetics of height in humans. First, you want to make sure you understand the concept of heritability.

Evoy and Vissher 2009 report a heritability coefficient of 0.8. This estimate is impressively high - only a few phenotypic traits have such high heritability. They also review articles discussing that 50 loci are correlated with variation in height (actually, today, more than 500 loci are known to contribute to height, see the link in AlexDeLarge's comment to this answer). However, these loci are not sufficient to explain the whole heritability observed (common missing heritability issue). Yang et al. 2010 provide evidence that the remaining heritability is due to incomplete linkage
disequilibrium between causal variants and loci of weak effects. In short, height is a highly polygenic trait.

Related post

You should have a look at Is there a genetic reason explaining the difference of the height of male and female? for more information.


Are there any animals that maintain white fur year round?

Polar bears (Ursus maritimus) have white fur all year long.

There are probably several other examples. @L.Diago gave sheep as example. There are also all white troglodyte species.


Do insects respond to the detection of dead insects?

Yes, it is a common behaviour and is called necromone signaling (Yao et al 2009, see references in paper for many examples), and is probably used to avoid predators, parasites and disease. The chemicals used are often similar (unsaturated fatty acids), and seem to have an old evolutionary history (~400 million years). Many groups of species can also detect infected, not yet dead, conspecifics. Removal of dead individual is also common in e.g. ants (necrophoric behavior).

The paper referred to earlier (beside reviewing earlier evidence) also provides experiments of detection/avoidence in isopods and Tent
caterpillars (Malacosoma americanum), where they show avoidance based on crushed conspecifics, unsaturated fatty acids and (for isopods) intact corpses.

Naturally, the same type of compounds are used by e.g. species of carrion beetles (Silphidae) to find their animal hosts, but then for the purpose of reproduction.


Your teacher is indeed correct.

In the first round you would get two identical molecules of the dsDNA.

In the second round you would get 3 identical molecules and one molecular with an A substituted for a G in one of the strands.  ie.

No error (3 of the 4 molecules):

------G-------
------C-------

One mismatch (1 of the 4 molecules):

------A-------
------C-------

So there are a total of 8 strands of DNA after the second round and one of those strands has the mismatch.  1 / 8 = 0.125 = 12.5%

In round 3 you would have 8 dsDNA molecules and only one of those 8 dsDNA molecules would have the mismatch.


How can neuronal signals faithfully be reproduced by scalp electrodes?

EEG has been recorded beginning in the late 20s, by people who were fairly clueless about electricity. While the strength of the EEG is indeed weak, it is readily observable with even such comparatively primitive technology.

The first thing you should take note of is that EEG measures the aggregate field. It does not see single neurons. It sees the synchronized activity of large neural populations of neurons - tens, hundreds of thousands of neurons at the very least, and probably more on the order of tens and hundreds of millions of neurons. This aggregate activity creates activity on the order of microvolts. This activity is then relayed (via the differential amplifier technique) to a powerful amplifiers. Modern EEG amplifiers have very large input impedances, and are thus able to amplify these weak signals. However, it still only observes mass action of large groups of neurons, not e.g. single action potentials by single cells.

Next, direct EEG analysis is comparatively uninformative for many reasons, including those you mention: that the scalp, the skull, and the other intervening tissue attenuate the signal. Thus, very often, extensive preprocessing is applied, such as averaging over many recordings. However, at least two features are already visible in the waking EEG. The first is the power-law structure of the frequency spectrum (although this is reinforced by the filtering characteristics of the tissue; the tissue filters higher frequencies more than lower ones). The second is the alpha wave, which is a large activity pattern coming mostly from visual areas. However, this is a very coarse feature; it tells us little beyond if the subject has their eyes open and is attentive, or has them closed/is inattentive.

Lastly, it is indeed generally assumed that deep sources (such as subcortical areas) are not picked up by the EEG (but only by e.g. MEG).

A good introduction to the topic is the book Electroencephalography by Niedermeyer and Lopes da Silva.


Sneezing itself is a part of long story of human evolution.

Sneezing for early humans was as common as eating is for us. Early humans lived in caves which were full of dust and insects so whenever they wake up from sleep they sneezed intentionally to remove the dust and small insects from their nose, slowly this behaviour of early humans was proved to be beneficial and muscle memories remembered the Activity as a daily routine work and performed it to remove dust and any irritant in their nose or nasal cavity.
As they evolved they passed on their daily routine works to their descendants and this was also passed on , this way sneezing was slowly incorporated into the muscle memories and it exists till now as a way to relax is from external allergens.

There are several other theories too about evolution of sneezing and it itself demands great research .
 There is also a video on Veritasium on YouTube regarding the Sneezing whenever one sees light , this video too discusses this theory.
You should check that out too.


Calculating the frequency of a recessive allele in case of three segregating alleles

Welcome to Biology.SE

A few issues about your post

You should always limit your post to a single question.

Make sure to define what the function f() and p() mean.

Use points (.) instead of comas (,) for the numbers.

You should show how you made your calculations otherwise we can't tell what is right and wrong.

Your question

  is $p = f(AA) + \frac1{1}{2} f(Aa)=\sqrt{f(AA)}$ correct?

$$f(AA) = p^2$$
$$f(Aa) = 2pq = 2p(1-p)$$
$$f(Aa)/2 = pq = p(1-p) = p - p^2$$
, therefore

$$f(AA) + f(Aa)/2 = p^2 + (p - p^2) = p = \sqrt{p^2} = \sqrt{f(AA)}$$

So, yes you are correct


Finding Regulatory Elements: How Have People Been Doing This?

As it can be seen from (more or less recent) discovery, most of the regulators were discovered through specifically designed experiment to exhibit one particular factor. Several examples include:

The discovery of Sp1, the first eukaryote transcription factor to be discovered (as described in the video linked in the comments)
The discovery of the Lac operon in E. coli.

None of these were intended to be screens for regulatory sequences in general. If you are looking for regulatory sequences of a specific gene, the technique of reporter gene, combined for instance with a random mutagenesis screening can provide you with a mapping of regulatory elements.

The following article might be of interest to perform a screen based on UV-mutagenesis: UV mutagenesis in Escherichia coli K-12: Cell survival and mutation frequency of the chromosomal genes lacZ, rpoB, ompF, and ampA.

If your question is more general: "all the regulatory sequences associated with one gene", then this question is generally unanswered, and can probably be better tackled first using bioinformatics analysis (such as promoter prediction, etc).


Is consuming sugar with food as beneficial as consuming glucose (~half of the amount of sugar)?

You have it backwards. One sugar molecule is equivalent to two glucose molecules, though the actual structure of sugar (Sucrose) is a Glucose + Fructose combination.

While Glucose is metabolized via Glycolysis into two molecules of Pyruvate (which are then used in the Citric Acid Cycle), Fructose enters the Glycolysis metabolism at a later stage as shown here:

The GA-3-P is then turned into 2-Phosphoglycerate and then into 2x Pyruvate.

The end result is that a single Sucrose molecule (Glucose + Fructose) [aka - Sugar] is equivalent to 4x Pyruvate, whereas Glucose alone is equivalent to 2x Pyruvate. Or, if you prefer, a single Glucose molecule results in about 32-36 ATP produced, whereas Sucrose will result in 64-72 ATP produced - with ATP being the primary energy carrier of the cell.


What confuses me about "homologous gene"

Can you please directly cite your textbook. Either your textbook is wrong or you massively misinterpret it.

The concept of homology refers to the concept of shared ancestry. From wikipedia

  In biology, homology is the existence of shared ancestry between a pair of structures, or genes, in different taxa. A common example of homologous structures is the forelimbs of vertebrates, where the wings of bats, the arms of primates, the front flippers of whales and the forelegs of dogs and horses are all derived from the same ancestral tetrapod structure.

I would add that a common counter example are bats wings and bird wings (which is an analogy).

Two genes are homologous if they both derive from the same ancestral gene. Of course, as ultimately, all genes are related, the concept only make sense by comparison to other structures that are more distantly related or relative to a time point in time.

For more information, just have a look at any good introductory course or textbook to evolutionary biology (for example evo101 > homology)


This is an immature "True Bug", order Hemiptera. You can tell this from the general shape of the wings, and from the big "beak", a feature of the Hemiptera.

Within Hemiptera, it's possible that with those enlarged front legs, it could be an Assassin Bug, family Reduviidae.


Plant identification - variegated ivy-like

Found an answer myself, so here it is.

This is Ceropegia linearis ssp. woodii, also known as hearts on a string or hearts entangled.

More information about the plant can be found at https://www.rhs.org.uk/plants/details?plantid=5862


Need help distinguishing between a primary and secondary source

Too long for a comment: Although this is a review article which summarizes the findings of other researchers, considers this as a primary article. The author gives you all the resources he used in the reference section of this article and summarises their finding. Additionally, review articles in renowned journals (and Genome Research is definitely such a journal) are peer-reviewed. Primary vs. secondary sources would be more the comparision of research articles and news articles. In my observation, news articles hardly ever name the sources or the original articles about which they report. Plus they sometimes have problems of getting the message wrong.


Aspirine irreversibly inhibits the enzyme cyclooxygenase. This enzyme facilitates the reaction from arachidonic acid to prostaglandin G2/H2. The further reaction leads to the generation of Thromboxane A2 which is important for the activation and aggregation of platelets. See the figure (from here) for an overview:

Thromboxane A2 usually stimulates the activation of new platelets and increases their aggregation, with a shortage of this compound these activations are not possible and the coagulation of blood is reduced.


Why is a magnesium ion essential for ATP activity in enzymic reactions?

As far as I know there are two main reasons for this:

promoting a nucleophilic attack

  In general, Mg2+ interacts with substrates through inner sphere
  coordination, stabilising anions or reactive intermediates, also
  including binding to ATP and activating the molecule to nucleophilic
  attack (wiki)

 - assists in the leaving a pyrophosphate group and may also facilitate the cleavage of the bond between the α- and β-phosphates by its electron-withdrawing effect. (source)

  wouldn't the presence of mg hinder release of phosphate?

As with all reactions this is dependent of the concentration of the molecules
involved as stated here:

  The Gibbs free energy change (ΔG) due to ATP hydrolysis depends upon
  the concentrations of the various participants in the reaction. When
  the concentrations are farther from their equilibrium values, the
  absolute value of ΔG is greater. Under “standard” conditions (i.e.
  concentrations of 1M for all reactants except water which is taken at
  its characteristic concentration of 55M) the Gibbs free energy of ATP
  hydrolysis varies from -28 to -34 kJ/mol (i.e. ≈12 kBT, BNID 101989)
  depending on the concentration of the cation Mg2+. The dependence on
  Mg ions occurs because the positively-charged magnesium ions help to
  stabilize the ATP molecule. However, in the cell the conditions are
  never even close to the standard state values. (source)


Where can I find a compendium of microorganisms?

I do not know how complex of a key you want, but this one is a good identification guide for beginners. It contains a lot of common freshwater pond algae, what they look like, and some basic characteristics. From here, you can identify your specimen and then be able to look them up further. Hope this helps!


What would cause E. coli to change from filamentous growth to normal growth?

Expression of sfiA (sulA) causes filamentation during the SOS response, so presumably sfiA is induced, as part of SOS, in response to some sort of DNA damage. Once the DNA damage is repaired the SOS genes, including sfiA, will be repressed again and normal growth will resume.


STRING ID - allelic differences and splice variants

STRING does not distinguish between different products of the same gene. E.g. for human, the protein identifier you see (ENSP...) corresponds to the longest splice form for each gene (ENSG...). Therefore, STRING won't help you if you need to distinguish between splice forms.

Splice forms are merged because for most sources of evidence, there is little data for the interactions of individual splice forms.


Do different microscopes and attached cameras differ in crop factor between each other?

Thus the conversion will make the results just more difficult to interpret.

I'm not personally familiar with this specific measurement, but in general, unless there is a specific convention in how to report a measurement, an absolute measurement should make the results easier to interpret, not more difficult (vs. % of image area). From a quick search, it seems like absolute measures of area, volume, and density are typically used when reporting chorionic villi measurements, so there isn't a convention to do it another way.


Why our bees might have suddenly disappeared

We call it Colony Collapse Disorder (CCD).

Consequences

The phenomenon is observed worldwide and is pretty serious. Northern Ireland lost 50% of its beehives for example. Between 1997 and 2003, 10 millions beehives were lost. Many cultivated crops are pollinated by bees and we don't quite have an alternative today. In 2005 a study showed that the worth of crops that are pollinated by bees is around 200 billions dollars.

Causes

Why? The short answer is "we don't know". There are a number of possible factors and the general consensus is to think that there is not a single factor that is causing the decline but it is a combination of different factors. Possible factors include:

Pesticides
Pathogens
Fungicides
Antibiotics
Miticides
Climate Change
migratory beekeeping
loss of genetic diversity through too intense selective breeeding
malnutrition
parasitic phlorid fly

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The wikipedia article for CCD is very complete. You should have a look at it!


What are the differences between mammal and insect digestion of cellulose?

Update 2 (interpreting "faster" in terms of efficiency because it seems easier to measure)

The question has been updated but I still don't see a reference for insects being more efficient than mammals. Therefore I investigated this and did not find convincing evidence that it is the case.

Granted, the means of measuring efficiency are not necessarily comparable, but nonetheless it appears that ruminant cellulose digestion efficiency is comparable to overall distribution of cellulose-digesting bacteria.

(Overall, in both clades, the vast majority of species do not appreciably digest cellulose, so I focus on those that do.)

This paper suggests that while termites have remarkable ("nearly 99%") efficiencies they are a dramatic outlier among insects. In different groupings efficiencies range from 12-68%, 40-90%, and 11-50%.

This paper suggests that the "digestibility" of cellulose by cattle is in the range 0.7-0.8 (that is, 70%-80%). It is observed that the rate is higher in sheep (and goats?), though comparable figures are not provided. Other figures in the paper are in terms of animal body weight gain, which is unfortunately a poor measure due to the high energy cost of just living for warm-blooded animals.

If I interpret these numbers correctly, this means that ruminants in fact compare favorably to most celullolytic insects in their cellulose digestion efficiency. The very high efficiency of termites specifically is likely a facet of their being little microbial factories with legs; they are definitely an outlier among insects.

In conclusion, I don't think that there is any particular intrinsic advantage for insects in cellulose digestion.

Update

I went back and read the linked post and realized that much of my answer was covered there and thus somewhat duplicative.

What is not covered is the insect/animal comparison. I do not see the source material for the assertion that insects are more efficient at cellulose digestion, it might be true or be somewhat trivially true but I would need to see where you got this information to assess it.

I would suggest doing a little initial research to maybe get closer to an answer. For example, here is a review on cellulose digestion in insects, and here is a resource for mammals, here is a comparison between the two.

Original

Neither insects nor mammals (as far as I know) have the appropriate digestive enzymes to digest cellulose efficiently on their own. However, some special animals like termites and ruminants have assemblages of microbes in their gut that can break down cellulose. These enzymes are called cellulases.

However using these assemblages efficiently requires an extremely specialized gut system such as the rumen.

So you might get humans to digest cellulose by making transgenic humans with cellulases in their digestive system or completely redesigning the human digestive system. Possibly there would be a way to supplement with cellulase the way some people do with lactase.

A different concern might be that human physiology isn't set up to support that style of nutrition. For example I imagine that diabetes incidence would increase. But it's hard to predict.

If the idea is to feed a growing population of earth in a less carbon-intensive way, there are likely less complicated ways to do that by altering diet to e.g. less meat, popularization of sea vegetables, etc. But that's just my opinion, maybe you had something else in mind.

Hope that helps.


The two structures are tautomers of one another:

Tautomers are often considered the same compound even though they are really constitutional isomers. Technically they are called 7H-xanthine and 9H-xanthine, respectively (thanks to gilleain for the links).


How does coconut water solidify into hardened coconut meat?

There are three types of endosperms encountered in botany - nuclear, heliobial and cellular. The endosperm of Cocos nucifera is both special and interesting.

Initially, the cocunut is a nuclear liquid endosperm. Meaning, it is a coenocytic liquid tissue with lots of rapidly dividing nuclei. The reference I cite here (although pretty old), states that it is safe to assume the fluid to be the 'sol' phase of cytoplasm. At some point, gelification of the sol surrounding the nuclei occurs and cellular boundaries start to appear.

These cells and nuclei start to settle down on the endothelium (inner lining of the integuments) and the cells divide to produce a columnar sort of a covering over the it. This is what forms the characteristic coconut meat. Development of the cellular endosperm is by coalescence of these deposited cells and nuclei at the antipodal end (bottom end of the fruit) and continues towards the top end. You might have noticed that the meat is thicker at the bottom but thins out towards the top.

The cells right above the endothelium stay meristematic for a long time while the columnar cells on top of this meristematic layer grow radially inward.

If the terminology seems confusing, the bottom end is the antipodal end. End. in the diagram stands for endosperm - the coconut meat. The Sh. is for the shell, which is the thickened inner integument. The inner lining of this shell has been referred to in this answer as the endothelium. Mic. stands for micropyle where the stalk (pedicle)  of the fruit is. It is at the micropylar end that the embryo is placed. Remember! The coconut meat is not the growing embryo.

How does the meat harden?

As said, initially the deposited mass of cells and nuclei is jelly like and slowly hardens after proper cell wall synthesis etc. The hard white coconut meat that can be grated, is end stage of maturation and is formed when the above said tissue architecture has been established.

What happens to the coconut water?

After the cellular endosperm has reached its final state a little water is still left in the coconut. This water is opalescent compared to the clear water found in younger fruits. Interestingly this water is now totally devoid of nuclei.

  Whether the decrease in liquid is the result of its incorporation into the endosperm cells or due to evaporation due to drying and cracking of the pericarp remains uncertain.

Sorry for the anticlimax. But this has been quoted from a 1955 paper. I was unable to find newer papers. Little work has been done in morphological botany in the recent past, but I'm pretty optimistic the answer would lie somewhere in literature.

References:

V.M. Cutter, Jr., K.S. Wilson and B Freeman. Nuclear Behavior and Cell Formation in the Developing Endosperm of Cocos nucifera. American Journal of Botany (1955), 42 (2), 109-15.
A. Abraham, P.M. Mathew. Cytology of Coconut Endosperm. Annals of Botany (1963), 27 (3): 505-512.
The Hindu (2002) : Mystery behind coconut water, R. Subramaniam.


Just flying from the waist: filter approach:
If there is a data source that has the expression data for cells in multiple tissues for any organism i would use that to find the housekeeping genes by sorting which genes are expressed in the greatest number of cells (think excel or XML). Next, I would check which of those genes are also found in/similar to the respective gene (homolog I thin its called) in the plants (using genome browser, e.g., ensembl and blast or just look it and click on the button to bring you to the plant genome). If your model organism does not have sequenced genome... get primers and see if you can sequence it for yourself to see if its there. Then check to see if its a single copy. Hardest part is finding an expressome database spanning multiple tissues in an organism to find housekeeping genes - then hoping they are conserved to the plant. Alternatively, you can consult literature to find housekeeping genes.

You probly just wanted a listing of the genes... sorry.


How different can the Tm be between 2 primers?

The default parameter provided by "primer-blast" is 3 degree (max difference between the melting temperatures of the pairs) .
that said I think it really depends on the application. in case of cloning (in my experience) you can allow wider ranges of delta Tm between primers (in this case I used to use the average Tm of the two primers as annealing temperature). you accept to have a bad efficiency but eventually you can pull out your insert from the gel and clone it in a vector for a prep.


This animal is a sea cucumber. It is probably a "sweet potato" sea cucumber (Molpadia arenicola). Here is a useful link describing this animal with pictures quite similar to yours:
https://mexican-fish.com/sweet-potato-sea-cucumber/


Are any organisms known to use meiosis I to create non-identical offspring asexually?

In automixy the meiotic cells give rise to diploid offsprings. This can happen by diploidization of the haploid cell (1n->2n), which will produce homozygotes or endomitosis prior to meiosis (4n->2n) which produces heterozygotes. Examples:

Cnemidophorus uniparens : 4n->2n
Sphyrna tiburo: 1n->2n

I don't know of any case where there is fusion of similar gametes to form a diploid cell. It is difficult for two ova to fuse in natural conditions because the vitelline membrane has to be dissolved.
Experimentally a haploid ES-cell can be fused to ovum to form a progeny. Haploid ES cells undergo diploidization and when injected in blastocyst, can develop properly (Ref). In fact haploid androgenic-ES cell line had been made in this study by injecting sperm into an enucleated oocyte. These androgenic-haploid cell lines can be fused to ovum to give rise to viable offsprings.

Also see this question. Similar topic


Can a Translocation of chromosomal parts occur between an autosome and an allosome?

In short, yes. A quick scan of a few abstracts gives both clinical and model organism examples.

  [I]f it occurs in between allosomes,what could be the effect of Robertsonian Translocation between an X and a Y...

It seems Robertsonian translocations are not ubiquitous amongst the chromosomes and only involve 13, 14, 15, 21 and 22.

HTH.


Good question, but I'm not sure if anyone really knows the answers. The governments of Japan and the U.S. have both been very secretive at best, while an army of propagandists have made it very difficult to distinguish between truth and fiction.

Any health effects are likely to be too small and gradual to make headlines. For example, suppose there was a 1% increase in thyroid cancer in California due to Fukushima radiation. How could investigators prove there's a link with Fukushima radiation?

Adding to the confusion is the fact that the Pacific Ocean and neighboring land masses are being battered by more than nuclear radiation. Ongoing reports of mass dieoffs of various creatures are variously linked to radiation, global warming, pollution or unknown causes. One famous example is the "melting starfish" disease.

A lot has been written about increases in radiation in tuna. For example, see Is Tuna Safe to Eat Post Fukushima?. Some sources say we shouldn't eat any seafood from the Pacific Ocean, period. Others say "Don't worry." The propagandists particularly like to focus attention on radiation that originated from atomic bomb tests.

When investigating the amount of radiation in North America, keep in mind that the levels are presumably increasing, as contaminated water is still being dumped into the sea (hundreds of tons a day, according to some sources).

You can glean more specific information from the Internet, but it's just very hard to know how truthful or accurate it is. I wanted to write an article about this very topic but gave up in frustration. I decided it might be better to wait until there was more irrefutable evidence - like several new extinct species. ;)

You might get a better feel for the potential damage by doing some research on a similar event that has received even less publicity - the dumping of nuclear wastes off the coast of East Africa. For example, read the article You are being lied to about pirates.

Regarding the effects of cesium on human health, you can start with Public Health Statement for Cesium. But you should solicit similar information from several other sources before reaching any tentative conclusions.


Frequent urination caused by sound of running water

Very simply put, its the power of suggestion. You urinate, flush, wash your hands umpteen times together each day. So when you hear the sound of running water, you naturally feel the need to urinate.

Apparently, the sound of running water also help patients with lower urinary tract symptoms urinate (reference)


Is there a PSI-BLAST for nucleotide sequences?

If you have a non-coding gene sequence (e.g. regulatory sequence) this answer should hold your solution:

Background theory

Firstly you must realize that PSI-BLAST is built for detecting "romote homologues",  (i.e. those that have a very "distant evolutionary relationship" to your query) - from a database of sequences. It is therefore known to be a "sensitive" analysis which can recruit distantly related matches but has a small chance of recruiting some false matches - "rogue homologues".
Secondly PSI-BLAST is known as a "profile method" that is it uses multiple sequences that are cumulatively recruited with each "psi-blast iteration", to build an empirical profile of amino acid residues along the positions of your query. This is in the same family of analyses as "Hidden markov models" (HMMs) in that HMMs use multiple sequences to build an empirical profile that is able to recruit distant homologous, except the "profile" includes probabilistic pathways to all the recruited sequences.

My Answer

I suggest you use a software package called HMMER. Indeed this method shares critical theoretical similarity to PSI-BLAST as well as functionality in your case (searching for remote nucleotide sequence matches in a database vs. a nucleotide query), it also does not assume your sequence is protein-coding - here is the wiki description:

  HMMER is a free and commonly used software package for sequence
  analysis written by Sean Eddy.1 Its general usage is to identify
  homologous protein or nucleotide sequences. It does this by comparing
  a profile-HMM to either a single sequence or a database of sequences.

Other possible answers

If you are afraid of using HMMER, then here is a list of all alignment software tools represented in a table that allows you to focus on only those that use nucleotide sequence as input:

http://en.wikipedia.org/wiki/List_of_sequence_alignment_software


Most likely to assist in maintaining neutral buoyancy. Many fish have reduced weight of heavy structures (evolutionary wise)like bone to assist in maintaining nuetral buoyancy. The swimbladder struggles to maintain  buoyancy near the surface for some herring

https://www.researchgate.net/publication/231918276_The_herring_swimbladder_Loss_and_gain_of_gas/amp


I don't have access to Provine's book, and I can't describe the details of the hooded rat experiments, but here is an attempt to explain the importance of the work.

Darwin published “Origin of Species” in 1859. He proposed that modern species were all descended from ancestral species, and that evolution proceeded by natural selection. He believed that evolution proceeded gradually by an accretion of small changes (gradualism). The origins of hereditary change were, of course, unknown to Darwin.

Mendel’s work (published in 1865) was rediscovered in 1900, and gave rise to a school of thought referred to as mutationism.  Mutationist theories emphasised the importance of single factor changes with large effects, and placed these “leaps forward” at the centre of the mechanism for the generation of new species. This was in contrast to the biometricians who argued, in the Darwinian tradition, that natural selection acted on populations in which there was continuous variation. Extreme mutationists believed that continuous variation within a species had no relevance to the evolution of new species. Their view was that within a species most genes were fixed (100% wild-type allele), and that only mutations could create new species (‘hopeful monsters’). T.H. Morgan, for example, was a strong proponent of the mutationist theory, so this wasn't some minor controversy.

Sewall Wright joined the laboratory of W.E.Castle as an assistant in 1912, when he was 23. Starting with black and white hooded rats (white rats with black ‘hoods’) they instigated breeding programmes and showed that they could progress gradually, through a number of generations, towards all white or all black rats. The importance of this work was that it demonstrated that there was underlying genetic variation within this strain of rats that could be acted upon by selection (selective breeding) resulting in  gradual changes in coat colour. This provided strong evidence for the gradualist school.

By the 1930s the modern synthesis began to emerge, which combined mutationist and gradualist ideas: natural selection acts upon populations (gene frequencies etc.) but mutation provides the raw material that creates new variations in the population. Key to the acceptance of the modern synthesis was the development of a mathematical treatment of population genetics. This led to the current view of phenotypic  traits influenced by multiple loci, with natural populations harbouring genetic variability which can be acted upon by selective forces. We have all accepted this and so of course it is difficult to think ourselves into the controversies that existed in genetics at the beginning of the twentieth century.

Here is an article in which Sewall Wright refers briefly to his work with Castle, placing it in historical context. It also describes subsequent work with guinea pigs. This is a quotation from the article which underscores what I have written:

  From assisting Prof. Castle, I learned at firsthand the efficacy of mass selection in changing permanently a character subject merely to quantitative variability. Because of this and a distaste for miracles in science, I started with full acceptance of Darwin's contention that evolution depends mainly on quantitative variability rather than on favorable major mutations. Thus, I have assumed that species are typically heteroallelic in tens of thousands of loci in which the leading alleles differ only slightly in effect, a situation that is maintained in a continually shifting state of near-equilibrium by the opposing pressures of recurrent mutation, diffusion and weak selection. Only a few loci at any time can show fairly rapid changes in allelic frequencies from strong selection.


Why is the consumer/producer biomass ratio higher in the oceans?

The paper you cited suggests an explanation:

Such inverted biomass distributions can occur when primary producers have a rapid turnover of biomass [on the order of days (34)], while consumer biomass turns over much more slowly [a few years in the case of mesopelagic fish (35)]. Thus, the standing stock of consumers is larger, even though the productivity of producers is necessarily higher. Previous reports have observed inverted biomass pyramids in local marine environments (36, 37). An additional study noted an inverted consumer/producer ratio for the global plankton biomass (16).

To explain/clarify this a bit further: there are two main processes that affect the consumer/producer ratio. One, which you have identified, is efficiency (how much of the biomass is transferred from one trophic level to the next). The other is turnover rate (rate at which biomass leaves a trophic level), which is the reciprocal of the residence time (the average length of time that a unit of biomass spends in a trophic level before transitioning to another trophic level/compartment).
At equilibrium, the biomass in a trophic level is equal to (inflow/turnover rate) or (inflow $\times$ residence time). If consumers at a particular level consume one tonne of biomass per month (assume 100% efficiency for now) and the residence time is 6 months, the standing stock or quantity of biomass at that level will be 6 tonnes. Taking some of the numbers from the paragraph above: suppose the residence time for phytoplankton is 4 days while of consumers is 400 days. If the consumers have a 10% efficiency for taking up phytoplankton biomass, then the consumer biomass will be $(400~\textrm{days}/4~\textrm{days}) \times 10\% = 10$ times higher than the phytoplankton biomass.


How can haired mammals synthesize vitamin D?

According to "Melanocyte biology and skin pigmentation" (Yin and Fisher, 2007), the exposed parts of mammal bodies, such as their noses have melanocytes that can be locations of vitamin D production.

According to this Wikipedia article, the secretions in woolly animals also produce vitamin D.

This is further explored in "Vitamin D(3) synthesis in the entire skin surface of dairy cows despite hair coverage." (Hymoller and Jensen, 2010), where they found that cows synthesise vitamin D all over their body, where they dispute an idea that vitamin D is manufactured in the fur secretions, and ingested via grooming.


Why do mutations not take place in mRNA of higher eukaryotes?

The premise of the questions suggests that mutations cannot take place in the mRNAs of higher eukaryotes.
To answer your question I think it is important to consider two viewpoints:

First, from a theoretical point of view, since DNA and RNA are as you pointed out composed of nucleic acids, they both can be mutated if enough energy is provided (UV light, chemicals, etc) which invalidates the premise of the questions.

Now, from a practical point of view, as you mentioned most mRNAs molecules have a short half life typically in the minute to day range whereas DNA molecules exist during the whole existence of the organism.

While it can occurs that mRNAs are mutated people are not interested to study this aspect for the following reasons:

You pointed out in the comment section, a mutation in a mRNA molecule might lead to translated malformed protein which can easily be degraded. It will be only one mRNA transcript from thousands transcripts. With a short half life, the mRNA an proteins will be degraded which will not have a long standing impact of the cell/organism. As such it will be very difficult to observe a phenotype which will affect the whole host.

Thus RNAs mutations have only transient effects which will not affect the host in the long term. RNAs molecules are not more protected than DNA molecules just that they are short lived so the host is protected from the effects of RNA mutations.

Hope this helps!


How do ribosomes contribute to their own synthesis?

The most important parts of the ribosome are not made by other ribosomes - 5 rRNA (ribosomal RNA) of the ribosome actually do most of the direct work of creating the protein and are made by RNA polymerase ( a protein, but not the ribosome).

Then there are 92 ribosomal proteins, which as a rule bind to ribosomal RNA to support their structure and keep everything going.  These are all made by ribosomes.  They are thought to have appeared later in the evolution of the ribosome though I imagine that it would not be possible to constitute a working ribosome without each one of them.

these numbers are for the eukaryotic ribosome, the prokaryotic ribosome has 3 rRNA and 52 ribosomal protein components.

http://en.wikipedia.org/wiki/Ribosome


Design arbitrary degenerate primers (with non-binding criteria)

If you already know the basic sequence i.e. the fixed regions in the primer; for e.g. the known nucleotides in the sequence -  NGATWGCTSATNGC, then you can implement your algorithm like this:

Fix the max length of the primers. Lets say 20nt.
Generate all combinations of primers (20nt): that is pretty straightforward. You will have  4N × 2(R+Y+S+W+K+M) × 3(B+D+V+H) number of combinations, where each alphabet denotes number of such instances. Chek this site for the nucleotide codes.
Calculate the Tm of the primer-template pairs. UNAfold has a nucleotide hybridization Tm calculator. You can specify parameters like salt concentration etc. There are other such tools too. These can be run on the commandline.
Discard all primers have Tm below the acceptable limit.
For those that exceed the acceptable Tm, keep dropping a base from the 3' until the Tm reaches within the range.
If primer length goes below 14nt then discard the primer.
Now with all these selected primers check for parameters like self hybridization, GC clamp etc (OPTIONAL). You can use primer3 for these purposes by running it on the primer_check mode.
Download the nr/nt BLAST database.
Adjust BLAST parameters for short nucleotide search: Decrease the word length, increase e-value cutoff etc (See this biostar post and BLAST help).
BLAST your primers against the database in plus-minus mode.
Worry only about cases where there is significant alignment at the 3' of the primer as only these can cause extension.

These instructions can be automated using any language or shell script.

Questions on script writing would be off-topic in this site. You can ask specific doubts about coding in stackoverflow.


tools to reconstruct the transcriptional regulatory circuits?

Inferring transcriptional / regulatory networks from empirical data is an active area of research, and to my knowledge there aren't many mature tools for this type of analysis. I see mostly mathematicians, statisticians, and engineers working on this problem, probably because of the intense quantitative theory involved. Even if mature tools do exist, I doubt they're tailored for the typical biologist--more likely, they are geared toward scientists with a more quantitative background.

That being said, I am aware of 2 or 3 pieces of software that may provide a starting point for the curious or the adventurous: AIRnet (described here), iBioSim (described by Barker's PhD thesis, currently the second hit on this Google search), and maybe Ingenuity Pathways Analysis (which requires a paid license). The only one of these tools I've even tried to use is iBioSim, and at the time (2 or so years ago) it was a very kludgy process.


How does MSMA kill crabgrass with only minimal damage to lawn grasses?

Please consider this a sort of comment — I tried looking up for articles related to MSMA mode of action but almost all the articles are about its toxicity in mammals.

By what I understand, trivalent arsenates act as phosphate analogs and therefore interfere in phosphorylation reactions including DNA synthesis [Ref].

The weed is affected perhaps because of its relatively higher growth rate. Also the already established lawn grasses would have good population size to regrow out of the damage.


The key to understanding this is to digest the fact that there are two gates blocking a normal sodium channel. These gates are called the activation gate (on the extracellular side) and the inactivation gate on the intracellular side. Both of these together, or any one of these alone, if closed, can block the sodium current from entering the cell.

In the resting state, the activation gate is closed and the inactivation gate is open. There is no influx of sodium. Owing to a neurotransmitter release, there is depolarization of the plasma membrane around the channel. As soon as the potential reaches a fixed threshold value, there is a change in the conformation of the sodium channel. The voltage is sensed by a biophysical voltage sensor, a part of the channel.
At the threshold potential, both the gates respond by reversing their state. But owing to the biophysical structure, the response of the activation gate is faster than the response of the inactivation gate. What happens is that the activation gate quickly opens allowing the influx of sodium ions, generating the action potential. The inactivation gate is closing but before it closes, the activation gate has been open for some time and the action potential is already fired due to considerable depolarization.
After some time, the inactivation gate also closes completely, blocking the sodium influx. By this time, the potential is at the peak of the action potential, the potassium channels have opened, and the re-polarisation phase begins. Here the inactivation gate is closed, thouh the activation gate is still open above the threshold potential. As the potential dips below the threshold, again the gates reverse their states but they respond with different speeds. First, the activation gate closes while the inactivation gate is still closed, and then the inactivation gate opens. In this way, during repolarisation, no sodium influx occurs since atleast one of the two gates is always closed.

I hope I answered your questions. Here are further links to understand this in greater detail.

Wikipedia
Mechanism of sodium channel inactivation
Basics of Voltage-Gated ion channels in Neuroscience
Mechanism of Voltage gated Channels in general(Detailed)

A more technical and biophysically accurate version of the diagram.


What are limiting factors for intron length?

I think the above values (500-750 kb) are wrong.  http://www.bioinfo.de/isb/2004040032/ shows that most introns are less than about 10 kb (and personal experience in Drosophila confirms that - I've rarely seen an intron bigger than about 5 kb).  There are some very large ones, but since it's nearly impossible to detect the splicing reaction, particularly if they're very large, it's not clear whether they are spliced as one BIG intron or are instead recursively spliced (in little steps, as in http://www.genetics.org/content/170/2/661.full.pdf+html).  I think its safe to say that we don't know how long the biggest introns can be.


Our muscles give us the ability to move our arms but....?

I am a bit confused as to what you are asking. You don't move your arm, like your suggesting, ever. No one does, and no one can. You contract your muscles which happen to move your arm. The movement of the arm is the result of your muscles contracting, not the cause.

How it happens is that your brain sends a signal to your muscles (which you cant feel). The muscles get excited and they contract. The instant your muscle contracts your hand begins to move. In the end your bones are like sticks, and your muscles are the ones that pull the stick in different directions, in order to achieve flexion and extension.

Might i suggest you read up on the musculoskeletal system (http://kidshealth.org/teen/your_body/body_basics/bones_muscles_joints.html) ?


When writing about past research should I use the species name they employed or the modern version?

3. is right thing to do. You can mention in the introduction that "Campylobacter fetus, which was previously known as Vibrio fetus [Ref] ........."

You should not use the old name anywhere again (also for the sake of consistency), once you have made it clear that the species was renamed, in the Introduction.

I don't think there is any written convention like that (As such usage of any obsoleted terms is to be avoided and the standard nomenclature as described by ICZN/ICBN etc should be used).


Calcium ions and bacterial transformation

DNA has an overall negative charge. The phosphate heads of the lipid molecules that make up the cell membrane, along with the LPS molecules on the outer membrane, are also negatively charged. This means the plasmid is normally repelled by the cell membrane.
What Ca2+ ions do is shield the negative charges on each side, making the overall situation electrostatically neutral.
This site has a nice animatic for this process: http://www.dnai.org/b/index.html


Exactly what kind of spider is this in Louisville, KY?

It is an Orb Weaver (Neoscona crucifera). It is found from Maine to Florida in the east, to Minnesota in the Midwest, to Arizona in the southwest, and in Mexico.

Females are about 9.5–19 millimeters (0.37–0.75 in) long, while males are somewhat smaller. The upper surface of the abdomen is brown and hairy. The legs display alternating light and dark brown bands. The undersurface of the abdomen is black, with two white spots.
This species is relatively variable in color and sometimes pattern, but is most commonly seen sporting a rusty-red or golden orange color. The orb-shaped web is very large and is often constructed on buildings and other man-made structures, especially near outdoor lights. This species is most conspicuous in late summer and early fall.

For many years, this kind of orb spider would build a very large web every night just outside the back door (near a light.) While fascinating to watch, if was a lot less fascinating to forget it was there in the morning and walk face first into it. But I prefer to live and let live, so... :)


Is Zeiss Primo Start microscope worth the price for student use?

I'm defenitly no fan of the Primostar. It's made to order for Zeiss, probably by Meji.

It's a fine microscope allright, but compared to the gray and beige Standards, it's a toy.

And those gray and beige Standards were already kind of toys, compared to the former black GF stands...

Being a "home user" there are far better and at the same time much cheaper  alternatives availlable on the second-hand market.

In Europe, a Standard 14, basicaly equipped (4,10,40,100 achromats, 0.9 condenser, build in 6V/10W HAL illuminator, binocular) can be bought for anything between 100 and 200 Euro.

This is a universal platform, designed with flexibility regarding applications such as DF, FC, DIC, fluorescense... in mind. The same can't be said to that extend regarding the Primostar.


Is there a maximum amount of antibodies your body can keep?

Antibodies are simply proteins and like any other protein have a relatively short "life", so after clearing out an infection, they are not retained for long (most of them anyway). What the body keeps is memory cells which can produce a much more rapid response if they come in contact with the same pathogen again.

You could see it as a selective process: the body produces immune cells, one or more specific cells for nearly every potential antigen that might exist in the world (there are more steps involved of course but they are of little relevance here). Only those which are used at some point mature into memory cells.

Unfortunately, I just realised that I can't explain why the immune system goes through this selective process; producing cells equivalent to memory cells in the first place would make the immune response much stronger. One explanation I can think of for why the body produces naive cells first is that either a) their production or b) their maintenance is less costly.

The other explanation I could think of is that even immune cells in the periphery which have undergone the proofing mechanisms of immune cell development already, may not be perfect and target body cells every now and then - in that case it would be devastating if they would go all-out like a memory cell.

From my three explanations, only alternative b) would mean there could be a limitation to how many vaccinations our immune system can bear (if memory cells take more effort to maintain than naive cells, having too many of them may overstrain whatever systems maintain them). Otherwise I don't see any limiting factor for how many memory cells you can retain; except if their numbers become so large that your lymph nodes swell and that causes problems.

Edit note: I'm not aware of any research about that question and couldn't find anything either.


How is a very small quantity of poison able to kill a large organism?

"Cyanide" doesn't refer to just one compound, but given the lethal dose you mention of "half a gram" you are probably referring to potassium cyanide, with a molecular weight of about 65g/mol, so 0.5 gram is about $10^{22}$ molecules. Potassium cyanide becomes hydrogen cyanide in the stomach, and hydrogen cyanide is the gas (at body temperature) that causes toxic effects.

The toxicity of cyanide containing compounds is because they bind with high affinity to cytochrome c oxidase, an enzyme that is part of the mitochondrial electron transport chain. The result is that electrons cannot be efficiently transferred to oxygen molecules. The effect is roughly the same as if oxygen was not present in the inspired air.

$10^{22}$ is a huge number. That's about 250 million molecules per human cell in an adult (taking # of human cells from Bianconi et al). Even so, it isn't likely that cyanide molecules be perfectly bound at every molecule of cytochrome c oxidase, just that there is enough to cause massive brain damage or stop the heart.

By comparison, cyanide is not even close to the most toxic substance. Toxins that target neurotransmission can be much more potent. For example, the IV LD50 for botulinum toxin is about 2 ng/kg, so something like 125 ng for an average adult, equaling only $5\times10^{11}$ molecules.


How do I calculate the change in allele frequency in a haploid population under selection?

Here is my full derivation to the book example you gave, hopefully it'll help you clear up what went wrong:

You need to remember that after there is selection acting on the population, you no longer have a total of 1 after selection. Think of selection as "killing" individuals, which means the total is now 1 minus what has been "selected out". sy is what is selected out, therefore the new total is 1-sy. Which means you now divide each of your frequencies by 1-s*y (see picture).

Please comment if you need more explaining.


Polar amino acids in this case stabilize the helical structure within the apolar milieu of the membrane by making intra- and inter-helical connections. Thus the side chains of polar amino acids turn to one another while apolars face the apolar membrane. This would be definitely supported if you could find alternating apolar - polar segments in the sequence of helices.


Is gene only the portion of a single strand which codes for a particular protein?

None of the highlighted regions in your figure, is a gene. A gene is a section of DNA which gives rise to a product. Basically, a gene has an orientation (5'→ 3') i.e. it is essentially a single stranded region. However, the strand that mechanistically contributes to RNA synthesis (template) has the reverse-complementary sequence of the gene (in other words, anti-sense). Therefore, a gene, as it is annotated is not a functional entity but a genomic representation of a product. Some viruses (such as M13 phage) have a single stranded genome; for them the transcript is always antisense to the genomic DNA region.

Same section of dsDNA can harbour multiple genes in both orientations and this is clearly seen in viruses which have an highly compact genomes. Other prokaryotic and eukaryotic genomes also have overlapping genes.

Some related posts:

On which DNA strand is TATA box present?
Do transcription factors bind to both strands of DNA?
Which DNA elements belong to the definition of a gene?

  Does that mean only the indicated region of molecule A is a gene? Or,
  does the Indicated portion of molecule A + Complementary portion
  present in molecule B comprise a single gene, such that A is sense and
  B is non-sense strand of the same gene?

If the molecules A and B are expressed from opposite strands, then they are considered products of different genes, even if the gene region overlaps.

The situation is more unclear if both the molecules are expressed from the same strand and the transcribed region overlaps. Sometimes they are classified under the same gene (splice variants) and sometimes they are not.

These are some lines from the human genome annotation file which tells the location of genes in the genome (+ and - denote opposite strands):

chr1    HAVANA  gene    1567474 1570639 .   +   .   gene_id "ENSG00000189409.8"; transcript_id "ENSG00000189409.8"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "MMP23B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "MMP23B"; level 2; havana_gene "OTTHUMG00000074713.4";
chr1    HAVANA  gene    1590786 1594063 .   +   .   gene_id "ENSG00000272004.1"; transcript_id "ENSG00000272004.1"; gene_type "antisense"; gene_status "NOVEL"; gene_name "RP11-345P4.10"; transcript_type "antisense"; transcript_status "NOVEL"; transcript_name "RP11-345P4.10"; level 2; havana_gene "OTTHUMG00000185638.1";
chr1    HAVANA  gene    1603429 1604850 .   +   .   gene_id "ENSG00000269737.1"; transcript_id "ENSG00000269737.1"; gene_type "antisense"; gene_status "NOVEL"; gene_name "RP11-345P4.7"; transcript_type "antisense"; transcript_status "NOVEL"; transcript_name "RP11-345P4.7"; level 2; havana_gene "OTTHUMG00000182604.1";
chr1    HAVANA  gene    1604714 1605836 .   +   .   gene_id "ENSG00000269227.1"; transcript_id "ENSG00000269227.1"; gene_type "pseudogene"; gene_status "KNOWN"; gene_name "RP11-345P4.6"; transcript_type "pseudogene"; transcript_status "KNOWN"; transcript_name "RP11-345P4.6"; level 1; tag "pseudo_consens"; havana_gene "OTTHUMG00000182605.1";
chr1    HAVANA  gene    1570603 1590473 .   -   .   gene_id "ENSG00000248333.3"; transcript_id "ENSG00000248333.3"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "CDK11B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "CDK11B"; level 2; havana_gene "OTTHUMG00000078638.4";
chr1    HAVANA  gene    1592939 1624167 .   -   .   gene_id "ENSG00000189339.7"; transcript_id "ENSG00000189339.7"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "SLC35E2B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "SLC35E2B"; level 2; havana_gene "OTTHUMG00000078639.1";
chr1    HAVANA  gene    1634169 1655766 .   -   .   gene_id "ENSG00000008128.18"; transcript_id "ENSG00000008128.18"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "CDK11A"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "CDK11A"; level 2; havana_gene "OTTHUMG00000000703.14";
chr1    HAVANA  gene    1634175 1669127 .   -   .   gene_id "ENSG00000268575.1"; transcript_id "ENSG00000268575.1"; gene_type "processed_transcript"; gene_status "NOVEL"; gene_name "RP1-283E3.8"; transcript_type "processed_transcript"; transcript_status "NOVEL"; transcript_name "RP1-283E3.8"; level 2; havana_gene "OTTHUMG00000183552.1";

Not evident in these examples but there are many overlapping genes in opposite strands. Anti-sense lncRNAs would be an example to have a quick look at.

Bottomline: A single gene is on one of the DNA strands, not both.


Can anyone ID this flower plant by the photo?

It seems like it's either a Paeonia brownii or Paeonia californicus.  According to Wikipedia, these are the only peony trees native to North America, but there aren't any that are native to Canada specifically.  I guess these are the closest you can get.  I added some images to hopefully help you out a bit.

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

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


What would happen if one eats silica gel?

Usually, nothing happens if you eat silica gel. In fact, you eat it all the time. Silica is added to improve flow in powdered foods. It occurs naturally in water, where it may help confer resistance against developing senility. Silica is just another name for silicon dioxide, the main component of sand.
Mayby you think if silica is harmless to eat, why do the packets carry the warning? The answer is that some silica contains toxic additives. For example, silica gel beads may contain toxic and potentially carcinogenic cobalt(II) chloride, which is added as a moisture indicator. You can recognize silica containing cobalt chloride because it will be colored blue (dry) or pink (hydrated). Another common moisture indicator is methyl violet, which is orange (dry) or green (hydrated). Methyl violet is a mutagen and mitotic poison. While you can expect most silica you encounter will be non-toxic, ingestion of a colored product warrants a call to Poison Control.


How can we decide at which level does natural selection apply?

Natural selection favors genotypes that produce phenotypes that survive to reproduce.  To the extent that natural selection drives the instincts that drive predation, the (essentially tautological) answer is that, "It has proven selectively beneficial for that particular genotype to eat whatever it's eating."

Indeed, nature has shown us a variety of solutions to these selective pressures.  Cannibalism is not hard to find.  In the extreme case, mothers from diverse species are known to kill and eat their own offspring, which at first glance may seem like the height of failure when it comes to propagating one's genes.  And yet we can hypothesize a number of selective advantages of that behavior.  (E.g., the mother can produce large litters when food is plentiful, and then adjust for shortages to shore up a smaller litter when food is scarce.)

We also know that there are selective pressures against eating similar animals.  For example, pathogens that kill an animal are likely to afflict its genetic relatives, and so that could drive the aversion of some carnivores (including humans) to eating close relatives.

There are plenty of examples of evolved symbiotic organisms.  Alligators don't eat plovers, and sharks don't eat remoras.

But it is hard to imagine selective pressure for altruistic behaviors that don't benefit a particular genotype.  E.g., if there are mammals to be eaten, the lions that eat them will survive and the ones that don't will die.  If the entire class Mammalia is under pressure, population dynamics trump evolved behavior: If prey become scarce, predators will become scarce.  But if any predators survive, it will be the greedy ones.


Why does BLAST reduce word size for short proteins?

No, the search won't be less reliable. It will only be more sensitive, more capable of finding matches. To understand this, you need to understand how the BLAST algorithm works, what the word size means.

When you use a word size of $N$, BLAST starts by looking for a match of length $N$ between your query and target sequences. If such a match is found, BLAST then attempts to extend the match as far as possible. So, for example, consider these two sequences:

> query
CRKKL
> target
CRAKL

As you can see, they are quite similar:

query           CRKKL
target          CRAKL
                ** **

Now, what happens if you try to find the target sequence with BLAST using the query sequence and a word size of 2 ($N=2$)? BLAST will take the first
$N$ characters of the query and try to match them against the target:

CR
CR
**

It will then try to extend:

CRK
CRA
**

It will find a gap and apply the gap penalty, but continue matching since the next characters match1, thereby increasing the overall score of the alignment:

CRKK
CRAK
** *

And so on and so forth. BLAST starts by matching the first $N$-sized word and then attempts to extend the alignment.

Now, what if we were using $N=3$?

CRK
CRA
**

Because the word size is now 3, we need at least three matching residues to match in order to attempt to extend the alignment. Since there is no 3-letter match, the target is missed.

So, decreasing the word size is better for finding small protein matches because it can use shorter matching sequences as an alignment seed.
As a general rule, playing with the word size is a question of finding the right balance between specificity and sensitivity. Decreasing the word size helps you find more matches (increases sensitivity) but it will also find more divergent sequences (decrease specificity). Increasing the word size will reduce the number of matches (decrease sensitivity) because you need a longer perfect match to start extending the alignment, but will increase specificity for the same reason.

If you raise the word size to something close to the size of the query, you will only find almost exact matches. That might be what you want to do and it is what algorithms like BLAT which are designed to find near exact matches (for example, mapping a sequence to the genome it came from) do. Usually, however, we want less than perfect matches since we are looking for homologous sequences and not the exact same query. In such cases, we will decrease the word size for smaller proteins to increase our chances of finding homologs.

1 This is a bit of a simplification. The rules for extending alignments are a more complex but it serves to illustrate the point.


Do "virgin" ant queens ever shed their wings?

Good question. I tried to find a few articles to validate my answer, but it would appear that very few professional studies have been done on the matter. One of my hobbies a few years back was ant keeping and I have had several colonies started from queens over the years, so I can share some of my personal experiences.

Anyway, back to your question. For the most part, no. An infertile queen will keep her wings and either find a safe place to lay eggs like a fertile queen or just walk aimlessly until she dies/is eaten. However, there are some rare instances where an infertile queen will shed her wings after the nuptial flight and find a safe place to nest and even in some occasions will lay eggs that are, of course, unfertilized and will therefore die or become male drones.

On the subject, the same is true vice versa. In rare instances, a fertile queen will NOT shed her wings, find a nesting place and even raise a colony all with wings on. Most of the time, however, her first workers to emerge promptly remove them.

I hope this answers your question.

CDB


How much does the distance between a transcription factor binding site and a promoter influence transcription?

That really depends on your system. At least for yeast the difference influences the strength of the activation ("Analysis of Transcriptional Activation at a Distance in Saccharomyces cerevisiae").

For bacteria such long distance regulations have recently been identified. Before that it was thought that this does happen only in eukaryotes. See the paper: "Long distance relationships: enhancer-promoter communication and dynamic gene transcription."

I eukariotic cells the regulatory sequences (transcription factor binding sites and enhancers as well as silencers) can be really far away. An example for this would be the rs12913832 in intron 86 of HERC2, which influences the expression of the OCA2 gene, which is about 21 kB away. Both genes are not related in their functions. Normally three transcription factors interact here in the regulation of OCA2, HLTF, LEF1 and MITF, which leads to the formation of a DNA loop between the enhancer in HERC2 and the promoter in OCA2. The polymorphism reduces the binding of HLTF to the enhancer and hinders the formation of the loop which results in reduced expression of OCA2 (the whole story can be found here: "HERC2 rs12913832 modulates human pigmentation by attenuating chromatin-loop formation between a long-range enhancer and the OCA2 promoter.")

This paper ("Essential role of microphthalmia transcription factor for DNA replication, mitosis and genomic stability in melanoma.")analyzed (among other things) the binding sites for the microphthalmia-associated transcription factor (MITF) and their distance from the transcription start site. Figure 1 a/b of the paper is shown below. Interestingly a lot of the binding sites where pretty distant.

To go deeper into the topic, the following reviews are interesting to read:

Long distance relationships: enhancer-promoter communication and
dynamic gene transcription.
Enhancer and promoter interactions-long distance calls.


How can electric fields inhibit tumor growth?

In a PNAS paper by Palti's group (2007) they explain the hypothesis behind the technique:

They reason alternating currents of 100 kHz to 1 MHz specifically affects dividing cells and thereby targets cancer cells. Note that this is the same basic idea as chemotherapy and radiotherapy, which also target dividing cells mostly. The mechanism of action of alternating electric fields on dividing cells is though to be the result of a specific effect on the  bridge separating the daughter (cancer) cells during cell division (Fig. 1). They think it interferes with spindle tubulin orientation and induces electrophoretic effects (Kirson et al., 2007), resulting in a pile-up of cytoplasmatic organelles at the cleavage furrow. This is thought to interfere with cytokinesis, and to lead to cell destruction** (Kirson et al., 2004).

Note it is the frequency that differentiates between the various effects of current stimuli. At very low frequencies (1 KHz) electric fields stimulate excitable tissues through membrane depolarization. At higher frequencies this excitatory effect is lost. At very high frequencies (>1 MHz) tissue heating results (e.g., microwave ovens).  Hence, alternating electric fields of intermediate frequencies (10 kHz to 1 MHz) were considered not to have any meaningful thermal effects (Kirson et al., 2004).

Fig. 1. Palti's electric field hypothesis. Source: Kirson et al. (2007)

References
- Kirson et al., Cancer Res (2004); 64: 3288-95
- Kirson et al., PNAS (2007); 104(24): 10152–57


Techniques to find out which species are endangered

Based on the IUCN Criteria for endangered status there are two broad categories of models to help in determining endangered status. Note that no one methodology is used to determine the status of any species. Rather, a panel of experts consider all available evidence (including numerous modelling studies) and essentially make a determination based on their own judgement.

Range Estimates
Estimating the range of a species uses two primary techniques. The first is an expert range maps drawn by people very familiar with the species distribution, which involves essentially no modelling. The 2nd is ecological niche modelling, aka. species distribution modelling. See 1 and 2 for introductions on the latter. Note that the IUCN guidelines have criteria based on total range size, and well as the amount of fragmentation and patchiness of the range.

Population Size Estimates
Since it is usually impossible to count all individuals of a species, models are used to estimate total populations. These usually fall in the realm of mark-recapture models. There are numerous variations on the basic model form which account for things like an open population, varying birth and death rates, and varying capture probabilities.

1: Elith, Jane, and John R. Leathwick. "Species distribution models: ecological explanation and prediction across space and time." Annual review of ecology, evolution, and systematics 40 (2009): 677-697. https://doi.org/10.1146/annurev.ecolsys.110308.120159
2: Araújo, Miguel B., et al. "Standards for distribution models in biodiversity assessments." Science Advances 5.1 (2019): https://doi.org/10.1126/sciadv.aat4858.


How does HIV know to attack specific immune system cells?

The CD4 receptor is a protein complex that harbors very specific chemistry. A virus is able to bind with the receptor if it harbors a particular protein/set of proteins that are able to interact with the receptor. The virus is basically disguised as something the CD4 receptor recognizes, and from there it is internalized within the cell via a process called endocytosis. You can google viral endocytosis to learn more.


Are "constraint trees" in phylogenetic analysis cheating? How can I correctly use them?

I understand where you are coming from when you say that it feels like cheating. However, there are a coupled of things to keep in mind. First let's consider why your tree topology might not reflect concordance with intuition/species trees:

1) Presence of artefacts such as long-branch attraction

2) Lack of sufficient phylogenetic signal/presence of non-phylogenetic signal (due to, for example, convergent evolution in the sequences)

3)Horizontal gene transfer (unlikely in animals).

4) Incomplete lineage sorting/deep coalescence (hemiplasy).

Only in the case of 3 and 4 does your tree reflect true relationships among taxa that genuinely differ from the species tree. Cases 1 and 2 are artefactual. In cases 3 and 4, it would not be appropriate to use a constraint tree to get a species-tree concordant topology because the resultant topology would not reflect the 'true' relationships among taxa (i.e. would be 'cheating'). In cases 1 and 2, I would argue that it is appropriate to use a constraint tree to get the species-tree concordant topology (depending of course on what you want to use the tree for) because you know that the your current topology is species-tree discordant because of artefacts and is therefore not reflective of the 'true' relationships among taxa. Of course, you are unlikely to know a priori what factors (1-4) are causing your bad topology (though you can do some tests for long-branch attraction for example -- see Cladistics 21 (2005) 163–193).

What you can do is test whether the log-likelihood of your non-constrained tree and your constrained tree differ significantly. You can use tree topology tests such as the  Kishino and Hasegawa (KH) test. I don't know about RaxML, but IQ-TREE has excellent topology testing: http://www.iqtree.org/doc/Advanced-Tutorial. If your constrained topology is significantly different (statistically) from the ML topology, then you probably should not use the constrained tree. I am by no means proficient in phylogenetics concepts so I would take my advice with a grain of salt, hopefully some of the other members can illuminate the issue a bit further.


Where in the digestive tract are melatonin pills dissolved? Same question for gelatin capsules

Unless specially coated or formulated, most pills break apart in the stomach. Note: "break apart", not necessarily absorbed.

Take a gelatin capsule with rice or melatonin and immerse it in warm water. Massage gently with your fingers. Watch the clock.

When the rice is fully exposed, or the melatonin starts to break apart and dissolve, add that amount of time to the instructions. Be sure to take it with at least 4 ounces of water.


Why do sperm have centrioles and do female eggs cells even have centrioles?

Oocytes do not have centrioles. During fertilization, the centrioles of the sperm become the centrioles of the zygote. Only one pair is needed, as there is only one cell (i.e. zygote) right after fertilization.


Does the growth in size of hippocampus of London taxi drivers affect their net number of brain cells?

The study you linked was very interesting, and there is a reason that the authors of this paper and many others like it refer to grey matter density or grey matter volume.

From another study on grey matter (density), Neurolinguistics: structural plasticity in the bilingual brain,

  Whether grey-matter reorganization in this region is related to changes in neuropil, neuronal size, dendritic or axonal arborization will be revealed by methods other than whole-brain magnetic resonance imaging.

Meaning, there's really no way to know without autopsy and histological studies whether this means more neurons, increase in neuron size, more dendrites, more connections between neurons, etc. So, the answer to your question is, no one knows exactly.

Histopathological studies are usually done on diseased patients (e.g. Alzheimer's), not healthy taxi drivers.

However, one mouse study of loss of hippocampal grey matter did correllate MRI studies and histopathological studies, with the result that

  no changes in the number or volumes of the somas of neurons, astrocytes or oligodendrocytes were detected. A loss of synaptic spine density of up to 60 % occurred on different-order dendrites in the ACC and hippocampus...

Loss is not the same as gain, however, so the definitive cause cannot be ascertained yet.

Stress-Induced Grey Matter Loss Determined by MRI Is Primarily Due to Loss of Dendrites and Their Synapses


What did Francis Crick and James Watson discover that Rosalind Franklin didn't?

There were staff migrations and personality issues, information leaks between researchers and other factors. Her boss annoyed her. Watson and Crick used her geometry of a helix with previously known DNA nucleotides and phosphate from other researchers. She actually had discovered and photographed the helices.

Franklin had obtained the basic structure, shape and measurements of DNA.

Franklin:

She used careful hydration from 75-90% in order to obtain her best pictures. Hydration makes the DNA expand into a visible helical configuration. She used cylindrical Patterson map calculations to determing DNA's density, unit cell size and water content. From this she deduced the basic dimensions of DNA strands, and that the phosphates were on the outside of what was probably a helical structure. Her research was briefed/presented in an internal meeting/seminar at the college and was published officially in 1953 in support of Watson and Crick's presentation.

Watson and Crick:

Watson and Crick suggested a basic framework of a helical molecule for DNA,  Without elaborating precisely. Watson and Crick combine all the findings of other scientists, for the bases and acids of DNA, with Franklin's helix into a synopsis into a correct helical molecular structure. The phosphate and CAGT were already known, and they arranged it into a helix.
Judge for yourself if their research was brilliant research, if it is a discovery, or if it is laying the last pieces of a puzzle assembled by other researchers.

Watson and Crick stayed friends with Franklin after 1954 and shared friendly correspondence and some road trips, and helped with her health issue.

full pdf at .edu source here

If you check that publication, what may seem dishonest is that they iamge a photo by Franklin in support of their work, but only as a blurred photo, when they actually had access to all of her best photos. I haven't been able to find if Franklin published her photos independently in Nature or another magazine.

It was obviously not her best work.

Franklin obtained undenatured DNA gel from a Swiss researcher at Berne university, Rudolf Signer.

She used careful hydration from 75-90% in order to obtain her best pictures. Hydration makes the DNA expand into a visible helical configuration. She used cylindrical Patterson map calculations to determing DNA's density, unit cell size and water content. From this she deduced the basic dimensions of DNA strands, and that the phosphates were on the outside of what was probably a helical structure.
Her research was briefed/presented in an internal meeting/seminar at the college and was published officially in 1953 in support of Watson and Crick's presentation.

The Nobel Prize in Physiology or Medicine was awarded to Watson, Crick and Wilkins in 1962. The prize was not awarded to Franklin; she had died in 1958, and although there was not yet a rule against posthumous awards, the Nobel Committee generally does not make posthumous nominations. Watson suggested that she should have won the nobel prize for chemistry in his book, and Franklin is known through his distorting lenses. Ideally it would be interesting to know what Franklins personal letters and documents told of her research. Perhaps there is an autobiography of franklin? if not there should be one! She had differences with the lab director, professional or personal, we don't know, so she changed labs after only 2 years, leaving Watson and Creek and the research at King's. In july 25,2020 it will be the centenarian of her birth... She is older than Watson and Crick and would be 99 today. Perhaps she was not fond of helices?