Which Geologic time scale is the most accurate? I kindly ask to show me some pictures that is a generally accurate geologic time scale.

In google, a lot of geo time scales are different.

On what i have searched there are 2 major eons which are

I.Precambrian eon
 1. Archean eon
 2. Hadean eon
 3. Proterozoic eon

II.Phanerozoic eon

Palezoic
Mesozoic

3.Cenozoic

But along with it Precrambiann is further divided to proterozoic eon, archaaen eon and hadeon eon are ERAS of but it clearly says its an EON.

And how about in Phanerozoic eon?

Kindly please clarify the following. Thank you!!

According to these Wikipedia pages - https://en.wikipedia.org/wiki/Geologic_time_scale#Table_of_geologic_time, https://en.wikipedia.org/wiki/Precambrian - the Precambrian is a "supereon" not an "eon".

The ICS International Chronostratigraphic Chart, ambiguously, puts "Eonothem/Eon" over both the "Precambrian" column and the "Hadean - Archean - Proterozoic" column, with the next column over being "Erathem/Era", which corresponds to what's in the other periods.

It seems clear that 1) the Hadean, Archean and Proterozoic are considered "Eons" like the Phanerozoic is (with their sub-divisions all being called "Eras"), 2) the Precambrian is a larger period of time that encompasses the Hadea, Archean and Proterozoic, and 3) there might be some disagreement as to how to name the period of time the Precambrian is; Wikipedia says "Supereon", which makes sense, but the ICS chart doesn't include that word and seems happy to have it share the name "Eon" with its immediate subdivisions. But the name is just a name, the more important things are how the different periods relate to each other, which is covered by 1) and 2).


Can I use TBE to elute a plasmid shipped on filter paper? I'm receiving a plasmid shipped to me dried on sterile filter paper, as described in this question. This protocol and many others like it call for eluting the DNA from the paper using TE buffer.
My question is can I also use TBE to elute, as I already have a bunch on-hand? And in general, what concentration should the buffer be as I never see that mentioned in any of the protocols (including the AddGene version).

In my experience it does not matter if you use water, TBE or TE buffer. Even with a little EDTA in it, it will not mess up enzymatic reactions as the concentration is way too low. TBE/TE buffer usually contains 1mM of EDTA which can chelate 1mM of bivalent cations.
Since you not use the DNA undiluted (which also binds a lot of magnesium needed for most enzymes btw.) this really doesn't affect you in reality (been there, done that multiple times).
Additionally, I would recommend not using this DNA directly but transform it into bacteria first and then do a proper miniprep so you have enough material to work with (maybe even do a few restriction cuts and run it on a gel, to ensure the right identity) and a stock you can go back to if something goes wrong.


Why would evolution favor blue as a color in bugs? This question arose when I saw a metallic blue - black bug some while ago. I can't remember the species name now, but a quick google search will show that such bugs do exist. I'm down with green and black - camouflage, right? But what is the case for blue color? What kind of an advantage does it provide so that they have survived to this date?

Similarly, you could ask

Why are bees yellow?
Why are some frogs so colourful?
Why widowbirds have such long tails?
Why do peacocks have such a tail?

There are a number of reasons why such traits could evolve. The main reasons are:

Sexual selection (esp. intra-sexual selection when it comes to colors)
Mimicry (esp. batesian mimicry)
Aposematism

I let you investigate further by yourself through reading the linked wikipedia articles.

For the specific beetle, you have seen, it will be impossible to address the question unless we know the species.


snail motion and snail tracks I took a picture of a snail whose tracks are not continuous. What is the reason? Does the snail lift itself from the ground during its motion?

During particularly dry weather some snails will only touch the ground with part of their "foot" at once. In effect moving more like a desert snake in the image below. They do this to reduce moisture loss. Even though it is still a continuous motion it leaves a discontinuous trail. the same number of these points of contact are present the entire time at no point does it leave contact, think of it more like high stepping. This behavior is sometimes called "jumping" even though it has nothing to do with actual jumping.

http://www.molluscs.at/gastropoda/index.html?/gastropoda/morphology/locomotion.html


Protein PTM site prediction Is there any in silico analysis method to predict post-translational modification sites on a given protein?

There are actually a lot of these sites available, I have used some of the one listed below. Additionally there are some huge list of other services available in this field from ExPASy, you can find it here and the Center for Biological Sequence Analysis, which can be found here.

ExPASy - FindMod
The Eukaryote Linear Motif resource for Functional Sites in Proteins
Phosida


Autoclaving media Question 1.When I autoclave media should I close the cap tightly or slightly?

I put all tools in plastic bag when I autoclave, should I close slightly the plastic and when it finish I close tightly the plastic? The air steam need to go inside the bag?
I read some document told me autoclave 21 minute, but in my lab everyone operate 35 to 40 minute, What you think?
Thank for your help.

For the media bottle, it is better to keep the cap a bit loose to avoid to pressure inside the bottle. A good way is to had autoclaving tape on the side so that it is clear that the bottle has been autoclaved. As Chris mentionned below once autoclaved, use gloves, and close the bottle firm after you open the autoclave and do not wait until it has cooled down completely.
It is not really important if it is slightly to tightly close. In fact you could have them on a tray or a bucket that would be fine to. One caveat is that it might depend on the equipment, the rules regarding the usage of the equipment etc. You would need to check these questions with a Senior person on the site.
The longer the better. If everyone operate at 35-40 min either there is a good reason to do so (often the case) or not. To be safe, I would suggest to be conservative there. Often what might happen is you want to make sure that you have the sample autoclaved at the highest temparature for at least 20 min. Because of leakages or other factors it might be best to leave it longer to make sure it is autoclaved at least 20 min.

Hope that helps!


Transmission of disease from mother to fetus Can  parasite, microbes be passed from mother to fetus through the placenta ?

I know some like HIV can be.

Pregnant mothers can indeed pass on various microbes to their fetuses but it is not always directly through the placenta, as the placenta can be protective.  Although the blood of the mother and fetus do not mix directly, the two can interact.  Maternal proteins can flow across to the fetus, as maternal antibodies are actually the source of a newborn's immune system for a few months, and maternal immune cells have even been found in fetuses, which of course means other cells or viruses can get across.

HIV is a good example for your question, actually.  HIV can infect newborns through the placenta, but the majority of infections occur during birth, not in utero.  Birth is a pretty bloody process, and the rupturing of the amniotic sac exposes the infant to anything in the mother's blood, which is when most infections occur.  For HIV specifically, physicians can all but prevent mother-to-infant transmission by administering anti-HIV drugs just before birth.

Here is a list from the CDC of some STDs which details how infections may be passed on to newborns; most clarify that it mainly happens during the birthing process.  That being said, plenty of diseases will cause transplacental infections.  Usually they are viruses, as viruses are simply smaller, but there are definitely bacterial and parasitic examples, such as Borrelia duttonii, Trypanosoma cruzi, and Toxoplasma gondii.  Here's a list of bacterial ones and here's a list of viral ones.


How necessary is human zygote cytoplasm for generating a human? I'm primarily questioning the roles of genetics and cytoplasmic factors of zygote in generating a human being with a natural embryological process.

For instance, is there an experiment where we check if we get a human when we replace the DNA of a mice zygote with human DNA?

The zygote itself is necessary because in the early embryo there is almost no transcription of its own genome, instead it uses mRNA deposited in the egg cell by the mother (see also maternal to zygotic transition).

That being said, I don't think any ethics committee would allow an experiment like this in the first place.


Can a cleaved plasmid "close" without exact matching "sticky ends"? Say if you have a multiple restriction site and use two restriction enzymes on it to cleave a plasmid, can it recombine with ligase?

My concern is that without the small sequence of nucleotides that were in between the two restriction sites, the two ends of the plasmid won't stick and anneal. Would it work if the two sticky ends are almost the same in sequence – two bp off instead of all five?

The plasmid won't religate efficiently if the ends are not compatible.  However, it's possible that very rarely your plasmids may re-ligate, perhaps because of a tiny level of contamination with exonuclease that trims back the ends to be blunt.  Or there may be spontaneous blunt breaks or other strange events.  This may happen in a tiny fraction of the plasmids, one in millions, but since your transformation step selects for circularized plasmid very efficiently you may end up detecting it.

Note that these rescued plasmids are often aberrant since they are unpredictably trimmed at the ends or otherwise followed a non-designed path to circularize; this is not something you want to count on for your cloning, it's an annoying byproduct that you want to avoid.


What's the difference between Cytoplasmic pool and Granular storage pool? What's the difference between Cytoplasmic pool and Granular storage pool when speaking about neurotransmitters and synaptic cleft. I encountered this here:

  Amphetamine’s mechanism of action
  thus depends on the cytoplasmic, newly synthesized, rapidly metabolized pool of dopamine.
  Methylphenidate’s mechanism of action depends
  on the granular storage pool (Brust, 2004)

Reference

Brust, J. C. M. (2004). Neurological aspects of substance abuse. Philadelphia, PA, Elsevier.

Neurotransmitters like dopamine are synthesized in the cytoplasm and then imported into synaptic vesicles.  When the neurotransmitters are released it is by a fusion of the synaptic vesicle with the neuron's cell membrane, emptying the contents into the synaptic cleft.  Re-uptake of the neurotransmitter back into the pre-synaptic neuron's cytoplasm is done by active transporters, in Dopamine's case by DAT.  The cytoplasmic pool refers to the dopamine in the cytoplasm, while the granular pool refers to the dopamine stored in the synaptic vesicles.


Are there bacteria that respire anaerobically in aerobic conditions? There are facultative anaerobic bacteria that switch to anaerobic respiration in an anaerobic state, but are there any organisms that would still perform anaerobic respiration even when shifted to aerobic conditions? Obligate anaerobes would die when introduced to an aerobic condition right? Are there any which can survive?

This doubt came into my mind while reading the Hugh-Leifson Oxidative Fermentative test. Such a bacterium would be read false positive for oxidisers in such a case because it would ferment glucose even in aerobic conditions.

Are there any organisms that would still perform anaerobic respiration even when shifted to aerobic conditions?

Yes, there are. They are called aerotolerant anaerobes as shown in this figure on tube 5. In the thioglycollate broth, growth is seen throughout the length of the tube

Legend

Obligate aerobe
Obligate anaerobe
Facultative anaerobe
Microaerophilic
Aerotolerant anaerobes

  Are there any which can survive?

Obligate anaerobes wouldn't survive in aerobic conditions. Hence they are named so.

  Such a bacterium would be read false positive for oxidizers in such a case because it would ferment glucose even in aerobic conditions.

The thioglycollate broth shown here is used to differentiate bacteria into the above said criteria. The Hugh-Liefson test does'nt do that. You can not conclude that a bacteria is aerobic or anaerobic using that test. The H-L test, is interpreted in two ways.

Fermentative - When both the closed tube and open tube show a colour change
Oxidative - Colour change only in the open tube

In short, the words aerobic/anaerobic are not used to interpret the H-L test. But we can draw parallels.

Obligate aerobe - Open tube (+), Closed tube (-) - Oxidative
Obligate anaerobe- Open tube (+ at bottom), Closed tube (+) - Fermentative
Facultative anaerobe- Open tube (+), Closed tube (+) - Fermentative
Microaerophilic- Open tube (+), Closed tube (-) - Oxidative
Aerotolerant anaerobes- Open tube (+), Closed tube (+) - Fermentative


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

One of the chief components of centrosome is γ-Tubulin.

In this study the authors have reported the effect of γ-Tubulin knockout in mice.

Quoting the abstract:

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

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

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

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


Will a nucleic acid sequence deduced from a protein sequence be expressed from a plasmid? I have a fasta file containing the amino acid sequence of glycogenin-1: https://www.rcsb.org/fasta/entry/6EQJ
I want to create a plasmid that produces glycogenin-1.
Is it possible to use the glycogenin-1 amino acid sequence to produce said plasmid? Or would one need the nucleic acid sequence to do so?

I lack the knowledge to fully answer your question but I can give some potentially useful pieces of information:

In theory you can easily in-silico reverse translate a peptide
sequence to an unambiguous nucleotide sequence using the GMOs
optimized codon usage. I can share a Python script for that.

Also you could easily search for the 'real' nucleotide sequence in
databases. For example use 'Blast' to find the gene of your peptide
sequence.

But attention! There are known cases of codon-optimized sequences
causing bad protein folding or even (paradoxically) worse expression
levels than the native sequence.

There is software that helps with the design of plasmids, also in
light of use of unique restriction sights, helping to decide which of
your restriction enzymes are applicable.


Rate of Evolution of population of long lived individuals Is it necessary that rate of evolution of longer lived trees will be lesser than that of annuals ? I understand that new individuals will come up faster in annuals  and it may adapt to varying conditions faster but does it necessarily imply that long lived trees will evolve slower ?

That is true to a certain extent in normal environments, where there is not an excess prevalence of mutagenic elements. The "Generation Time Hypothesis" explains why a smaller generation time and hence a higher reproductive rate ( as in annuals) corresponds to a higher rate of mutation (substitutions in DNA) and therefore have a faster evolutionary rate as compared to slow reproducing and longer generation time individuals(for example, long-lived trees).

Since "fitness"-increasing adaptations produced by somatic variations are very less, the formation of new offsprings giving rise to individuals carrying a DNA which has been subjected to processes (Repeated divisions, replications and translations, amphimixis, and different environment) making it more vulnerable to mutation, becomes mandatory, to propel evolution. This process is much faster in annuals than in long lived trees like Sequoia. Moreover Sexual selection (especially in animals) operates at a much slower rate in longer-generation time individuals. Next, smaller individuals, having higher metabolic rates usually have shorter generation time (more pronounced in case of animals). Higher metabolic activity is linked to greater mutation rate (Due to metabolic intermediates acting as mutagens) and hence faster evolutionary rate. Higher metabolic rate also is linked to higher temperature (faster mutation) and these individuals have a geographic distribution favouring the tropics.(Again increases evolutionary rate)

All these, imply faster evolution for short lived individuals(which usually have higher reproductive rate) as compared to long lived trees. But under "normal" environmental conditions (not drastic and fast changes), the evolutionary rate of large individuals is fast enough to preserve their existence (as the Sequoia prevalence indicates). However, in fast changing environment, larger and long-lived individuals are more likely to be wiped out (probably, this applied to Dinosaurs!).


Incestual Reproduction in Animals I'm quite curious on how animals view incestual pairings. Given there are enough mates around, i have quite observed that most females (subjects are dogs, cats, pigeons and chickens) would go choose another mate that is not a direct family member (parent, sibling, offspring). How does this work? Is it instinct to not favor family members or does it still revolve around who's the fittest mate?

Anecdotally I have never observed a preference in lab mice, but we have never made a detailed study of it. Males do not seem to favor non-incestuous over incestuous breeding. Though inbreeding does tend to produce smaller litter sizes over generations and inbred strains of lab mice do tend to be less hearty. Though lab mice are a bit removed from the situation in the wild.


Bistability vs bimodelity In a systematic viewpoint, bistability refers to the existence of two stable equilibriums for a biological system. But, I don't understand the difference between bistability and bimodality. In both cases, the system should have two different behaviors, so I guess bistability is a specific case of bimodality, in which either of the system's behaviors might not be stable. Is this a valid distinction between these terms?

Bistability referrers to two coexisting stable conditions (if you disrupt they will tend to restore to one of those two areas) and has a slightly broader application it can also involve chemical stability for instance. Bistability includes the element of stability (obvious in the name) if disrupted bistable condition tend to return to one of two stable configurations. Enzyme stable configurations could be another. Galapagos finch beak shape during wet years is the one I think of but that could also be argued as tri-stable. to go really simple you can even think of a clicky pen, fully clicked is stable and unclicked is stable but anything else immediately moves to one of the other states.

Bimodal just means the distribution has two peaks, they may or may not be stable, many are only temporary. It is a much simpler concept.

Another way to consider it is bimodal is purely descriptive while bistability has a predictive quality.


Long-term-potentiation and memory. Where do we stand? I was reading the answers to the question: How and where, in the human brain, are memories stored? and, as expected, LTP and LTD came out.

Every time I read about LTP/LTD there is always something that bugs me a lot.

When I read papers about LTP/LTD (OK, I should really say "when I browse", as I'm not exactly in that area of neurosciences, and that is probably the reason why I am confused by this) I always see these very neat experiments where stimulating a neuron in a certain way increases/decreases its further responses. Then, I look at the time axes on the graphs, or read the Methods, and I see that the LTP was induced and analysed few minutes after the stimulus.

So my questions are:

Is there clear evidence that LTP is involved in long-term memory (not counting 1 hour as long-term...)?
Has LTP/LTD been shown in vivo after long period of time (e.g. months).
For those who work in the field, is there a strong belief that LTP/LTD are the only phenomena underlying memory?

Is there clear evidence that LTP is involved in long-term memory (not
  counting 1 hour as long-term...)?  Has LTP/LTD been shown in vivo
  after long period of time (e.g. months).

This Journal of Neuroscience paper shows LTP in vivo measured out to one year:  Abraham WC, Logan B, Greenwood JM, Dragunow M. 2002. Induction and experience-dependent consolidation of stable long-term potentiation lasting months in the hippocampus. The Journal of neuroscience : the official journal of the Society for Neuroscience 22: 9626–34.


Are there examples of selection on males influencing female phenotypes? I've been studying selection on female body color in a sexually dimorphic species and am intrigued by the possibility that selection on males, whether it be through sexual or natural selection, may influence the color of females. I think pleiotropic interactions may lead to this, or maybe some sort of genetic linkage.

A hypothetical example may be that selection for red dewlap color in anoles results in more melanic females.

I'm having trouble finding examples of this but I think it's a real phenomenon. Does anybody know examples of this occurring in a sexually dimorphic species?

Selection in one sex can produce a correlated response in the other when there is pleiotropy (or linkage disequilibrium) (see Lynch & Walsh 1998, and Lande 1979 & 1980).

Genes can be considered pleiotropic when they affect more than one trait, for example; the male and female forms of equivalent traits, and this can be seen as covariance between the sexes. Cross-sex covariance is common (see Bonduriansky & Rowe 2005, Poissant et al. 2010, Lewis et al. 2011, Griffin et al. 2013, and Blows et al. 2015 for good examples). This means that selection in one sex will often lead to a response in the other.

The correlated response to selection is captured within Lande's multivariate breeders equation, where the change in a vector of traits ($\Delta \bar{z}$) is a result of the genetic variance-covariance matrix ("G-matrix", $G$) multiplied by a vector of selection on the traits ($\beta$).

$\Delta \bar{z} = G \times \beta$

If covariance is zero (i.e. genes have independent male and female effects) then selection does not produce a correlated response in the unselected sex. However, cross-sex covariance is generally present, so correlated responses to selection should impose constraint on the evolution of sexual dimorphism under sexually antagonistic selection. Note that the within-trait cross-sex covariance is in the diagonal elements of the B-submatrix.

One good example of selection on one sex producing a response in the other is this paper. The authors selected on male mandible size in replicate populations of broad horned flour beetles. The mandible is a male limited secondary sexual trait, but selection on the mandible in males produced changes in female fitness and female traits. Selection for larger (smaller) male mandibles resulted in significantly decreased (increased) female abdomen size, and reduced lifetime reproductive success.

  "We find that females from populations selected for larger male
  mandibles have lower fitness, whereas females in small-mandible
  populations have highest fitness, even though females never develop
  exaggerated mandibles."

One thing that is really quite cool about that experiment is that the response came in a non-equivalent trait, i.e. it was not female mandibles but other traits that evolved. There is generally less prior probability that there will be a cross-sex cross-trait covariance unless the traits have clear links.


Aside from cockroaches and other insects, which species (of all kinds) are 'immune' to ionizing radiation? I have just been reading this excellent question and answer about cockroaches ability to withstand ionizing radiation.  My question is an extension of that question: aside from insects, which other animals (if any) have an increased defence against ionizing radiation?

Are there species of plants, fungi, and bacteria also "immune"?

According to Paul Stamets, Gomphidius glutinosus is especially well suited to collecting Cesium-137:

  G. glutinosus has been reported to absorb – via the mycelium – and
  concentrate radioactive Cesium 137 more than 10,000-fold over ambient
  background levels.

That article and Stamets' book Mycelium Running have more details on other species.


What is the name of this yellow / orange fungus? I've seen this in October 2016 on Corsica (Island of France):

I would guess each one is about 5cm - 15cm in diameter. Obviously, they come in small groups.

Most fungi need to be studied under a microscope to determine a species. I think this belongs to the genus of Pholiota. I couldn't find an English name, if I translate the Dutch name, it would be 'Bundle mushroom'. This name refers to the fact that they always grow in groups, usually on (dead) trees or trunks.

At first look thought this was a Honey fungus, but these are parasitic so usually don't grow on dead wood.


Can scientists create totally synthetic life? This particular question has been of a great deal of interest to me, especially since it dives at the heart of abiogenesis.

In 2010, Dr. Craig Venter actually used a bacterial shell and wrote DNA for it.

Scientists have created the world's first synthetic life form in a landmark experiment that paves the way for designer organisms that are built rather than evolved.
(Snip)
The new organism is based on an existing bacterium that causes mastitis in goats, but at its core is an entirely synthetic genome that was constructed from chemicals in the laboratory.

Keep in mind, this is only a synthetic genome, not a truly unique organism created from scratch.  Although I am confident that the technology will become available in the future.  As has been pointed out, the entire genome wasn't built de novo, but rather most of it was copied from a baseline which was built up from the base chemicals with no biological processes, and then the watermarks were added (still damn impressive since they took inorganic matter and made a living cell function with it). But they are working at building a totally unique genome from scratch (PDF).
This is actually quite an emerging field, so much so that the MIT press has set up an entire series of journalsfor this.  As far as to the purpose of these artificial organisms, most research funded by companies are meant to be for specific purposes that biology hasn't solved yet (such as a bacteria that eats a toxic waste or something).  Although, a lot of people are concerned about scientists venturing into the domain of theology.
In terms of abiogenesis, there are many resources to learn more about this.  Here is a list of 88 papers that discuss the natural mechanisms of abiogenesis (this list is a little old, so I am sure that there are many, many more papers at this time).
I also found this list of links and resources for artificial life.  I cannot verify the usefulness of this since the field is a bit outside my area of expertise.  However, it does seem quite extensive.
EDIT TO ADD:  Now we have "XNA" (a totally synthetic genome) on the way.


How can I calculate Shannon-Wiener diversity index in caves with different kind of habitats and different sampling methods? I would like to start a monitoring in different caves, compare caves of different age and length, and find out if there are any correlations between these factors and their diversity.

I was thinking to use the Shannon-Wiener diversity index and to use both pitfall traps and timed area search sampling methods. Can I get a single index value for each cave even if the methods are different?

And what about that caves which have stream or pools where the fauna can be very abundant? Even if I collect a sample of water, the abundance of certain species can be very high (e.g. copepoda).

Sorry for the banal questions but I have not experience with indices and statistics.

Clarification after comments:

I have about 20 caves to sample, I want to compare the fauna of these caves (richness and abundance). As I told they have differents lenghts, ages and others environmental features. Some of the caves have also streams or little pools (where I will take water samples to identify the fauna).

I have read some articles where the diversity indices were calculated using just one single methodology (traps or timed area search), and also for only one kind of fauna (acquatic or terrestrial).

The question is: Is there any methodology to get one single value of diversity index for each cave? (which considers both terrestrial and aquatic fauna). Or maybe in these conditions I can just get the number of species for each cave, without being able to compare their abundance?

You could account for this in your statistical analysis. I'm assuming that  you will collect terrestrial fauna the same way in every cave, and if there is a stream in a cave aquatic fauna will be collected in some standardized way as well. I'll also assume you'll have some other explanatory variables that you think may explain diversity, richness, or abundance. These could include cave temperature, length, depth, etc.

Calculate the Shannon-Weiner index for each cave using all species and abundances, whether they came from an aquatic or terrestrial sample. Then for you statistical model include whether a stream was present in a cave or not using a binary variable along with your other explanatory variables.

index ~ f(temperature, length, depth, stream)

In this example temperature, length, and depth are all continuous variables. Stream will be a binary variable (either 0 or 1, 1 meaning a stream was present). This will give you a measure of how much a stream contributes to diversity.


Biological advantage of electric synapses Electric synapses are synapses that do not process information but simply foward one action potential from one neuron to the next. There are no neurotransmitters, no inhibitory and exitatory postsynaptic potentials that would cause different responses in the post-synapse.

So, I'm wondering: What are the biological advantages over just one long axon? My research has only told me the advantages over "normal" synapses (speed), but I couldn't find any advantage over just using one longer neuron which, I suppose, would be even faster.

Having just read this article (http://www.ncbi.nlm.nih.gov/books/NBK11164/) there are several advantages/functional reasons that seem apparent and important in having electrical synapses with gap junctions compared to just a very long neuron.

a) signals in electrical synapse can be bidirectional.
b) electrical synapse synchronize electrical activity among populations of neurons.
c) The large pores in gap junctions allows passage of ATP and other important intracellular metabolites, such as second messengers between neurons.

I'm sure there are plenty of other reasons but these should provide a better picture in terms of the functional significance of having electric synapses.

Hope this helps!


Book suggestion on computational molecular evolution I'm currently reading Computational Molecular Evolution by Yang. Can you recommend alternative books?

I am finding it to be lacking on conceptual discussion (it's more focussed on the mathematics and statistical intricacies). I'd like to find something which discusses why we do the things, and the strengths and weaknesses of the ideas, which are presented in the Yang book whilst not being overly specialist - more of an introductory text to the field.

Any introduction to phylogenetics books??

I would suggest the course of Coursera.org:

Computational Molecular Evolution

By Anders Gorm Pedersen

Technical University of Denmark (DTU)

PS: Do tell us if you found a better book!


SARS-CoV-2 proteome: is the SPIKE protein not an issue for a hospitalized patient? I am performing molecular docking of ligands using the modeled proteome of SARS-Cov-2. My question is, after a patient is hospitalized, is the SPIKE protein not really an issue anymore, since its role for binding with ACE2 has already been carried out?  Or, is SPIKE an ongoing issue that is not only an early event in the causal pathway?

Rationale is that SPIKE is quite large, and takes more than a minute of run-time per ligand -- thinking about excluding it to speed up runs.  NSP15 is also another "larger" protein, but I know NSPs are translated inside infected cells - so should be included in docking.

It is always a problem. "The virus" is not a single particle that only needs to enter a single cell, a single time. It is a population of millions of viral particles, that infect millions of cells. So, as long as there are more cells to infect, the viral population still needs a mechanism to enter the cell (i.e. it still needs all the proteins needed to function).


Biopython - Big Discrepancy Calculating RNA melting Temperature over Literature I experience big discrepancies when calculating melting temperature of RNA 7-mers with Biopython over values generated by a popular algorithm.

I tried the nearest neighbour algorithm with RNA and salt concentrations as described in a respective paper (thermodynamic table used as in paper below from: Freier et al 1986). Yet, the values largely differ (execute code below to see).
I tried all seven salt correction methods provided by Biopython, still I never get close to the values generated by siRNA design algorithm for the same 7-mers.

Can someone tell me how accurate Biopython's melting temperature nearest neighbour algorithm is? Especially for short oligomers like my 7-mers? Is there maybe something I am implementing wrong? Any suggestions?

Values derived from executing sample input:
http://sidirect2.rnai.jp/
Tm is given for the seed duplex of the guide strand: bases 2-7

Literature:
"Thermodynamic  stability  and  Watson–Crick
base  pairing  in  the  seed  duplex  are  major
determinants  of  the  efficiency  of  the
siRNA-based  off-target  effect"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2602766/pdf/gkn902.pdf

from Bio.Seq import Seq
from Bio.SeqUtils import MeltingTemp

test_list = [
('GGAUUUG', 21.5),
('CUCAUUG', 18.1),
('CAUAUUC', 8.7),
('UUUGAGU', 19.2),
('UUUUGAG', 12.2),
('GUUUCAA', 14.9),
('AGUUUCG', 19.7),
('GAAGUUU', 13.3)
]

for t in test_list:
    myseq = Seq(t[0])
    tm = MeltingTemp.Tm_NN(myseq, dnac1=100, Na=100,   nn_table=MeltingTemp.RNA_NN1, saltcorr=7)  # NN1 = Freier et al (1986)
    tm = round(tm, 1)  # round to one decimal
    print 'BioPython Tm: ' + str(tm) + '  siDirect Tm: ' + str(t[1])

# Output:
>>> BioPython Tm: 10.1  siDirect Tm: 21.5  # GGAUUUG
>>> BioPython Tm: 8.2  siDirect Tm: 18.1   # CUCAUUG
>>> BioPython Tm: -2.0  siDirect Tm: 8.7   # CAUAUUC
>>> BioPython Tm: 8.2  siDirect Tm: 19.2   # UUUGAGU
>>> BioPython Tm: 1.3  siDirect Tm: 12.2   # UUUUGAG
>>> BioPython Tm: 4.4  siDirect Tm: 14.9   # GUUUCAA
>>> BioPython Tm: 9.0  siDirect Tm: 19.7   # AGUUUCG
>>> BioPython Tm: 2.1  siDirect Tm: 13.3   # GAAGUUU

Question first asked at stack-exchange: https://stackoverflow.com/questions/30037939/biopython-big-discrepancy-calculating-rna-melting-temperature-over-literature

Comparing Biopython MetlingTemp to other calculators.

I have written the recent version of MeltingTemp in Biopython's SeqUtils.  I have extensively tested the Tm calculations against other programs like MELTING and Primer3Plus and other online Tm calculators with consistent results, thus I'm pretty confident that there is no gross error in the module. The simple answer in this case is: the calculation of siDirect is wrong.

Sources of discrepancy.

One minor thing: Many programs calculate k as k = total Oligo/4. MeltingTemp uses k = Oligo1 - (Oligo2/2). Thus to mimic this behaviour, you have to use

dnac1=50, dnac2=50

instead of

dnac1=100

And now the major thing: Oligo concentration is usually given in nanomolar. However, if you look at the calculation in the Perl script, siDirect seems to use micromolar!

my \$tm = ( 1000 * $dH / ( -10.8 + $dS + 1.987 * log(0.0001/4) ) - 273.15 + 16.6 * log(0.1)/log(10) )

The critical part here is:

log(0.0001/4)

which should be:

log(0.0000001/4)

Thus, you have to pass 1000-fold higher oligo concentrations to Biopython's MeltingTemp to get the same result as siDirect:

>>> from Bio.SeqUtils import MeltingTemp as mt
>>> print mt.Tm_NN('GGAUUUG', dnac1=50000, dnac2=50000, Na=100,
                  nn_table=mt.RNA_NN1, saltcorr=1)
20.1472140567
>>> print mt.Tm_NN('CUCAUUG', dnac1=50000, dnac2=50000, Na=100,
                   nn_table=mt.RNA_NN1, saltcorr=1)
18.1074422939

This is of course wrong if your primer concentration is 100 nM, but that's the result you get from siDirect.


What is the optimal sampling method for modeling of microalgae growth? Recently, I am performing microalgae (Chlorella sp.) cultivation experiments for the mathematical modeling of microalgae growth with respect to time.

The main issue is that an analysis of lipid contents in microalgae requires a large volume of culture media per data point. Especially, in the early stage of the cultivation, the density of the microalgae is very low, so almost 20% of the total culture media needs to be consumed for obtaining just a single data point. Due to this limitation, sometimes, I measured only three times (the beginning, middle, and last).

More data points are obviously desired for the accurate modeling but it ends up with huge loss of the media. This may affect the quality of the overall experimental results. This seems like a sort of trade-off. The problem is that I cannot increase the size of the reactor volume at the moment.

Could anybody recommend how to come up with the optimal sampling number in this situation?

Any experience, ideas or recommended papers are welcome.

Thank you.

For these kind of experiments, especially when you talk about modelling, it can be worth to set up a chemostat or at least a turbidostat. An example of such a study can be found in: Simultaneous growth and neutral lipid accumulation in microalgae by Klok et al. (Pubmed).

Alternatively you can use lipid dyes such as Bodipy but these are often very tricky to get to work and they might not penetrate in your Chlorella. Nile Red in any case is almost impossible to get working quantitatively despite it being used quite extensively, see details in this publication. Be very cautious when going down this route.


Are plants actual oxygen factories? Is the oxygen exhaled by plants during the day compensated by inhalation of carbon dioxide at night?

All green plants do Photosynthesis as well as Respiration.

Plants respire during the day and night, but they only photosynthesis during the day when it is light:
there is equations for aerobic respiration and photosynthesis:

C6H12O6 + 6O2 → 6CO2 + 6H2O (aerobic respiration)

6CO2 + 6H2O → C6H12O6 + 6O2 (photosynthesis)

In terms of reactants and products, they are the reverse of each other. In terms of gas exchange:

Process        -------Carbon dioxide    -----------------Oxygen

Respiration     -----------Out  ----------------------------    In

Photosynthesis  -------In         ----------------------------    Out

Photosynthesis is only in the presence of Sunlight . So it occurs only during the day .

For photosynthesis they require Carbon Dioxide gas ( CO2 gas )

This gas enters the leaves through tiny pores on them called stomata .

The byproduct of photosynthesis is Oxygen gas ( O2 gas )

It is either passes out through the same stomata OR used for respiration

For respiration they require O2 gas .
It enters the leaves through the same pores or stomata .

The by product of respiration is CO2 gas .

During day time it is immediately used for photosynthesis .

During night time the CO2 gas is released in the atmosphere

Net gas exchange

The net (overall) effect depends on the time of day and the light intensity. Photosynthesis doesn’t occur at night. When there is no photosynthesis, there is a net release of carbon dioxide and a net uptake of oxygen.

If there is enough light during the day, then:

the rate of photosynthesis is higher than the rate of respiration
there is a net release of oxygen and a net uptake of carbon dioxide

(consider CAM plants)

in a plant using full CAM, the stomata in the leaves remain shut during the day to reduce evapotranspiration, but open at night to collect carbon dioxide (CO2)

https://en.wikipedia.org/wiki/Crassulacean_acid_metabolism#During_the_night

this link help you understand the process better by simple language :

http://www.bbc.co.uk/education/guides/zxtcwmn/revision/1


Question about alternative polyadenylation I know that alternative polyadenylation creates different transcript isoforms. My question is whether alternative polyadenylation ever results in differences in the terminal/last exon? The only case I can think where it might be is if the terminal exon is alternatively spliced?

EDIT:
I think what I was trying to ask was for a given gene, what factors could cause the transcripts to end in different locations. I drew a picture and it helped me figure it out a little
Here are 4 transcripts for a given gene, each of which end at a different location. Exon's C and D end in different locations because D is completely different exon than C that is being spliced to exon B. Exon on C and E start at the same location, but exon E is shorter, due to a UTR-Alternative polyA event. Exon B and F start at the same location, but F is shorter due to a Coding APA change. So alternative polyadenylation drives the formation of transcripts 1,3,4 while alternative splicing drives the formation of transcript 2. So I guess to rephrase my question, are there any other biological process that can affect where a transcript ends

According to a 2011 review1 alterntive polyadenylation sites can be located upstream of the 3'UTR (i.e. within introns or exons).  When these sites are used it results in transcripts missing exons at the 3' end and can force alternative splicing.  This alters the final protein product.

This figure from that paper may help make this clearer.

  Figure 1. Schematic Representation of CR-APA and UTR-APA

  CR-APA produces mRNA isoforms with distinct C-terminal coding regions,
  resulting in distinct protein isoforms. UTR-APA produces distinct mRNA
  isoforms with different-length 3′ UTRs but encodes the same protein.
  Longer 3′ UTRs usually contain cis-regulatory elements, such as miRNA
  and/or protein binding sites, which often bring about mRNA instability
  or translational repression. CR-APA, coding region-alternative
  polyadenylation; UTR-APA, 3′ UTR-alternative polyadenylation. Light
  green boxes, untranslated regions; light blue boxes, shared coding
  regions; dark blue and yellow boxes, unshared coding regions; lines,
  introns.

Reference:
1: Di Giammartino, D. C., Nishida, K., & Manley, J. L. (2011). Mechanisms and consequences of alternative polyadenylation. Molecular cell, 43(6), 853-866.


Can radiation therapy cause cancer? Radiation therapy is a very popular cancer treatment method. But can it have any risk for make a different cancer? Because i think that radiation exposure can make DNA mutation and thus increase the risk to cause cancer, so why we still use radiation to treat cancer? That's so contradictory.

Yup. Radiation induced secondary cancers exist and vary in their site of incidence and risk of incidence based on the site of treatment. In breast cancers treated with radiation, for example , there is upto a 3 fold increase in relative risk relative to the general population for leukaemias within five years and 1.5 times the relative risk for secondary lung cancers within 15 years.

The literature also reports 1 in 10 malignancies as being of a secondary nature, and radiotherapy amongst others is probably responsible for a fraction of those.

Despite this risk, radiotherapy is very often worth using because without it the risk of dying from the primary cancer is vastly greater than the risk of a secondary malignancy from therapy, and secondly, unlike systemic chemotherapy, the side effect profiles of radiation are more tolerable and localised.

It is also possible to "shape" fields of irradiation to maximise the dose delivered to the tumour and to minimise exposure to normal tissue; this is called intensity modulated radiotherapy (IMRT).

Also, a lot of the cancers radiotherapy is used for occur in older people, and the benefits of saving someone from their primary tumour again outweighs the risk of secondary malignancies later on. It is especially of concern in paediatric patients because that brings with it the risk of secondary malignancies in middle-age, but advances in intensity modulation I think has the potential to minimise that risk.


Miscarriage in early humans Today, about 10 to 20 percent of known pregnancy end in miscarriage. Pregnancy is a biological process that has been very well studied by medicine. As a result, modern medicine helps a lot to prevent miscarriages and to prevent death of pregnant women.

What was the percentage of pregnancy ending in miscarriage before modern medicine? Typically, what was the percentage pregnancy ending in miscarriage in early Homo sapiens, during the paleolithic age?

Pregnancy is a biological process that has been very well studied by medicine. As a result, modern medicine helps a lot to prevent miscarriages and to prevent death of pregnant women.

While the latter clause is correct (maternal - and infant - mortality is reduced with medical care), the former is not.

Miscarriages have been a problem as far back as recorded history. The written record includes medicinal recipes to prevent miscarriages. The problem then, as now, is that it just can't be done very well.

From a 2000 Obstetrics journal article:

  Human reproduction is extraordinarily wasteful. The reasons for this have taxed all of the contributors to this book. As we move into the 21st century it is sobering to reflect on the fact that we have failed to harness the power of the evolving revolution in molecular medical biology to answer the fundamental question: why is the fate of a fertilized egg so hazardous and so unsuccessful? The following account summarizes our limited knowledge of the epidemiology of miscarriage and then moves on to consider some of the medical causes of miscarriage...

Miscarriage is difficult to study, and the causes difficult to establish, so the literature showing that any interventions help (antibiotics, bed rest, supplements, etc.) is not plentiful. Smoking seems to have a deleterious effect on pregnancy. How this relates to early populations is a matter of conjecture.

Some good studies do exist, however. One good study in the New England Journal of Medicine followed an ideal group: women who had no history of infertility, who were trying to become pregnant.

Of 221 couples followed for 6 months, a total of 199 pregnancies were detected, of which 126 ended in live birth (therefore a 37% miscarriage rate). Because of the methodology, failure of blastocysts to implant could not be measured. The findings of this study were supported by others (31%), etc.: early loss increased when implantation occurred later than 10 days after ovulation. While the authors were hopeful ("There may be opportunities to increase fertility by extending the time during which implantation can occur."), they were also realistic ("Such interventions should be approached cautiously, however, because they may have unintended consequences with respect to the quality of surviving embryos.") Basically, you can't fool around too much with Mother Nature in this realm.

Has modern medicine been able to change this rate? Not really. Even with IVF, where thousands of dollars are spent trying to preserve a single pregnancy (certainly not the norm), miscarriage is common. The best way to increase the viability of IVF pregnancy is to select better oocytes, embryos, etc. In other words, maternal factors remain refractory to manipulation.

Even things obstetricians long took for gospel (for example, bedrest with pre-eclampsia) have little evidence of benefit to the fetus.

The literature is vast in this area (reproduction is an important field to study). I can write a book on how little can be manipulated on average (I will consider spending thousands of dollars on one pregnancy not average), but it wouldn't sell. What does sell are false claims, this one being as good as any claimed today:

  To prevent miscarrying or if one that is apt to miscarrie goe a journey let her take this powder morning and evening whilst shee journeys: Take of Dragons Blood the weight of a silver two-pence, a dram of red corrall powdered, the weight of 2 barly corns of Ambergrease, Besar ye weight of 3 barly corns, mix all these together and keep them close stoped in little vial glasse when you use take as much of it as lie upon a penny in a little clary water at nighte when you goe to bed, and in ye morning fasting and sleep after it to use it till you are out of danger.


What is the name of this flower? A flower has grown on a leaf in our garden. What is the name of this flower? Give some description.

It appears to me to be a Night Blooming Cereus:

We had one in our greenhouse in Botany. It rarely bloomed, and the bloom was wilted by mid-morning.

  Night-blooming cereus is the common name referring to a large number of flowering ceroid cacti that bloom at night. The flowers are short lived, and some of these species, such as Selenicereus grandiflorus, bloom only once a year, for a single night. Wikipedia

Dave's garden lists it as "Dutchman's Pipe Cactus, Night blooming Cereus"
Epiphyllum oxypetalum.


Are retroviruses cytotoxic? There are typically hundreds of retroviruses found in healthy human beings.

Are retroviruses then cytotoxic? (In other words, are they able to kill or damage other cells).

As you point out human beings (and other organisms) have hundreds of retroviruses and many can be seen in the human genome, some of which appear to be the remains of deactivated viruses, others which may be active.   Most retroviruses are not pathogenic - they don't cause disease.

This is because many retroviruses replicate slowly, budding and secreting from the cell surface in small numbers without killing their host cell.

There are several disease-causing retroviruses.  Human T-cell Leukemia Virus (HTLV) can cause T-cells to replicate in an uncontrolled fashion, resulting in leukemia.  This is not a necessary result for HTLV to replicate, but it is a result of viral infection as viral replication tweaks the cell machinery to replicate.

While it's not clear exactly how, Human Immunodeficiency Virus (HIV) kills its hosts cells.  Unfortunately HIV's hosts are CD4 immune cells.  The fact that sporadic replication of HIV can cause all host immune cells to die entirely makes HIV a pathogen.

Disease is usually thought of as a lack of adaptation of a pathogen and host: viruses do better if they do not kill their host.  Both these cases are possibly not the future for either virus: either could adapt to reproduce without causing a disease. Or they might have already , having spun off some strains into the pool of quiet retroviruses medical science does not concern itself with.


Can someone identify the species of this frog/ toad? Location: Tirupati, Andhra Pradesh, India

I found it at night time near a lake

It was quite small in size ( 5-6 cm Approx.) having dark brown spots all over its body and three prominent green stripes running along the length of its body and 2 stripes running across its upper body ( one crossing over its eyes).

Looks to me like an Indus Valley bullfrog (Hoplobatrachus tigerinus).
Your specimen would be a bit small, but the species is nocturnal, the area fits and the patterning looks like a decent match as well:

(taken from the Wikipedia page)


Why do flies leave dirty spots on shiny/glossy surfaces? I've seen flies leave dark spots on lacquered wood, mirrors, glass and monitors. Why do they do that? Is it some food stash or are they dumping waste in a single spot? Why pick a smooth surface?

House flies (Musca domestica) prefer to rest on light colored surfaces, and what is lighter than windows, windowframes, glossy surfaces that reflect light, etc.? Where they rest (not eat) is where they defecate (or regurgitate), leaving marks politely called "fly specks".

  House flies also leave dark fecal and regurgitation spots on wall surfaces where they rest, and with a preference for resting on light colored surfaces, these spots can be quite noticeable when fly numbers are high.

If you ever visit an "open" barn, you'll notice the phenomenon is quite remarkable. If the number of flies is high, there will be specks everywhere, but the windows and other shiny surfaces will be more densely covered.


Can mitochondria be regenerated by the cell? In the cell, division of mitochondria takes place on a regular basis, but what if there are no mitochondria present in cell (suppose all of them died), then can the cell make new mitochondria on its own?

If we were to suppose, as in the question, that all the mitochondria in a cell 'died' ('were irreparably damaged' would be better, as they are not independently alive) without any other consequences the cell would have no way of regenerating them. Even if the cell had another source of ATP (see @another 'Homo sapien' comment) such as anaerobic glycolysis, one very clear reason is that the mitochondrial DNA could not be replaced (there are no copies of it in the nucleus). If the mitochondrial DNA were not replaced, then there would be no way of making the mitochondrial proteins it encodes.
The cell would die for a more immediate reason than suggested in the comment, and one that should be of interest in relation to a less well-known function of mitochondria. Mitochondria play a key role in the process of programmed cell death — apoptosis. In this process signals cause the mitochondrial membrane to become permeable and allow the efflux of cytochrome c, which is a signal for activating the apoptopic pathway. Presumably if mitochondria were damaged by other means the leaching out of cytochrome c would have the same effect, causing the death of the cell.
If you think of the overall economy of an organism, it's often easier to make new cells rather than trying to repair ones that are beyond redemption.
Further Information

Mitochondrial DNA: http://www.ncbi.nlm.nih.gov/books/NBK26924/
Apoptosis and mitochondria: https://en.wikipedia.org/wiki/Apoptosis#Activation_mechanisms


What causes the human body to “jump” when we get a shock? At a Remembrance parade today, a cannon was set off to mark the beginning of a two minute silence. As it went off, the crowds quite comically jumped in sync, from the shock it gave them. I’ve seen very similar reactions in other scenarios, such as a jump-scare in a horror film.

Seeing the in-sync crowd jump today made me wonder.. what is it, in the human body, that make us jump when we get a shock?

This is similar to many other reactions humans have when scared, such as freezing, feeling like as if your heart is beating out of your chest, shaky legs, or the feeling that hair stands up on the back of your neck.

Fear starts with a trigger, and in your example, it is the sudden loud sound of the cannon. That stimulus signals to your brain that you might be in danger. Whether the stimulus is touch, sight, or sound, the scary signal quickly reaches the thalamus at the center of the brain and travels down to the amygdala, at the base of the brain.

From here a neurotransmitter called glutamate then carries the signal even deeper into the brain. This is what causes us to freeze, or involuntarily jump, and put humans through what is know as the "fight or flight" response.

These two reactions are automatic and involuntary because the deep brain is ancient in terms of evolution. We have little control over it. The reason is because a fight-or-flight response unleashes powerful hormones that affect the entire body.

When frightened, your body floods with the hormone adrenaline, skyrocketing your heart rate and blood pressure. The hormonal surge also causes your heart to pump blood more forcefully to the muscles. That's why you might feel a little shaky or unsteady when you're scared — the extra blood is getting your body ready to sprint away from the danger or stand and fight if you need to; hence the name fight or flight response.

Our bodies can reverse the fear response fairly quickly, though. If it turns out we aren't in a life-threatening situation, the parasympathetic nervous system (PSNS) kicks in to counter the fight-or-flight instinct, primarily by stopping the flood of adrenaline and lowering our heart rate back to normal. That's why every time we jump during a scary movie, or in your case a cannon sound, we don't run out of the theater/parade screaming; after the initial reaction, our PSNS helps us recognize the threat is not real and calms us down.

On a side note, part of the reason the PSNS exists is because adrenaline can actually be toxic in large amounts. If too much adrenaline floods into the heart, it can lead to the failure of that organ and death. You cannot control the fight or flight response, however you can limit it through meditation.

Hope that helps <3,

Jess


What is the functional significance of the difference in cardiolipin/cholesterol ratio in different membranes? I have read somewhere that the plasma membrane has little cardiolipin but excess cholesterol whereas the inner mitochondrial membrane is rich in cardiolipin and has little cholesterol.I just wanted to know why there is this difference.

According to wikipedia, cardiolipin is found in two places, the inner mitochondrial membrane, and bacterial membranes. Given the endosymbiotic origin of mitochondria, it makes sense that they would retain some remnant of their bacterial ancestry. But more importantly, cardiolipin plays a role in the enzymatic functions of mitchondrial membranes. Cardiolipin forms a bicyclic resonance structure that allows it to trap a proton, which helps oxidative phosphorylation.

Because this structure also responds to pH and divalent cations, it can change it's conformation and aggregation behavior as cellular conditions change.
Cardiolipin also plays a role in holding enzyme complex quaternary structures together. Mitochondrial Complex III requires 1 cardiolipin, Complex IV requires 2 cardiolipin, and Complex V binds 4 cardiolipins.
Cardiolipin also plays a role in apoptosis, where it is oxidized and undergoes conformational changes that cause it to move from inner to outer mitochondrial membranes and generate pores that cytochrome C can escape through and trigger apoptosis.
Cholesterol can be easily oxidized into oxysterols, which are thought to perform a variety of functions, but are not fully understood. If cholesterol levels in the mitochondria were high, I think it would be oxidized and cause trouble.
http://en.wikipedia.org/wiki/Oxysterol


Seed Dormancy and Seed Transportation My textbook says "As the seed matures it loses water and enter dormancy". I am confused as to whether this happens before the seeds are transported or after, and as to how seeds know to become dormant when required and then become active again.

I presume what the author is trying to convey is that as a seed ages, it enters a quiescent phase as a result of natural desiccation. Without more context, I'd guess that the quote you've provided here is referring to secondary dormancy, which is a response to unfavorable germination conditions. By definition, secondary dormancy occurs after the seed is released from the plant.

The mechanisms of secondary dormancy are not well understood, and resumption of embryonic function could be dependent on any number of factors. Generally, dormancy continues until such time as favorable conditions are observed by the dormant seed. For Avena sativa, seeds become dormant if temperatures in excess of the maximum for germination are observed. Other seeds become dormant in response to over- or dehydration, temperature variability, age, other factors, and combinations ad nauseum.

Some of the more common environmental causes of exiting dormancy include afterripening, chilling and lighting.


Can viruses be toxic? Bacteria can produce toxins like endotoxins and exotoxins. In diseases like cholera or tetanus they can harm infected people due to these toxins.
Now, although viruses are much smaller and are dependent on the host cell for their production, are there DNA sequences in viruses which can produce similar toxins, or are viruses made of something that is toxic?

If not, can viruses be seen as causing an allergic reaction because like common allergies they don't harm directly, only our immune system generates the problems?

In general, DNA that encodes toxins can be incorporated in a viral genome and thus it can be expressed in the infected host inducing toxicity.
Here an example: http://www.sciencedirect.com/science/article/pii/S1438422104000542

Also, viruses can trigger allergic reactions (http://www.ncbi.nlm.nih.gov/pubmed/21980825) or promote them (http://erj.ersjournals.com/content/19/2/341).

Finally, there are some reports about viruses causing "with symptoms that mimic allergies" (https://www.youtube.com/watch?v=iDF07R1XHSk)


Why did the sensitive plant (Mimosa pudica) evolve its leaf-closing mechanism? Why did the sensitive plant, Mimosa pudica, evolve its leaf closing mechanism? Does it help in a heavy storm? Does it scare off whatever animals might think it a good meal?

There are many reasons why Mimosa pudica (More commonly now referred to as the TickleMe Plant) may have evolved it's leave- closing mechanism. I have observed the movement when insects have landed on my plants. The insects apprear to be frightened by the movement as they do move on rather quickly when the plant collapses. The movement of the TickleMe Plant also occurs when the sun sets or if I place the plant in a dark room. This may be a way to reduce water loss by transpiration as the leaves fold down upon each other. Another reason for the leave movement may be to expose the few thorns found on adult plants. This could be another warning for herbivores to stay away. In cold weather TickleMe Plants will close their leaves as well, could this be a way to maintain its body temperature. All in all, this is the most amazing house plant and I am always learning new things about this plant and its beautiful cotton candy like TickleMe Plant pink flowers.


Do saltwater fish need to drink? In my biology class we got the question if saltwater fish need to drink. We need to use the term osmosis, but I cannot think of a valid answer and we were allowed to ask help.

Short answer, yes. The fresh water concentration inside saltwater fish is higher than the surrounding sea water, and the salt concentration inside the fish is lower.  This means that fresh water continuously flows out of the fish through their gills via osmosis.  To combat this loss of fresh water, fish must constantly be drinking sea water to replenish the lost fresh water. This also requires that they pump out the excess salt in the sea water they drink using their kidneys and specialized chloride cells in their gills.

Some more information can be found here, or you can watch a short video on the subject here.


What is the exact concept of "Repulsion" and "Coupling" (Genetics)? From all sorts of books including standard books (like those by Tamarin, Griffith etc) as well as internet; I could not clear-up many things about "Repulsion" and "Coupling". Such as:-

Is "Coupling" an exact synonym of "Linkage" ? and is "repulsion" an exact synonym of "recombinant"? No-where I could yet found mention of it.
What are they telling as coupling-"phase" and repulsion-"phase"? Are there 2 different "step"s or "time-frames" or "generations"?
Coupling and repulsion- are they indicating to a "phenomenon"? or the Genotypic "state"?
according to Griffith's introduction to genetic analysis (7th Ed)

  Now let us consider what may be learned by repeating the crossing experiments but changing the combinations of alleles contributed as gametes by the homozygous parents in the first cross. In this cross, each parent was homozygous for one dominant allele and for one recessive allele. Again F1 females were testcrossed:

  The following progeny were obtained from the testcross:

  Again, these results are not even close to a 1:1:1:1 Mendelian ratio. Now, however, the largest classes are those that have one dominant allele or the other rather than, as before, two dominant alleles or two recessives. But notice that once again the allelic combinations that were originally contributed to the F1 by the parental flies provide the most frequent classes in the testcross progeny. In the early work on coupling, Bateson and Punnett coined the term repulsion to describe this situation, because it seemed to them that, in this case, the nonallelic dominant alleles “repelled” each other—the opposite of the situation in coupling, where the dominant alleles seemed to “stick together.”

From this paragraph; it strongly seems to me; repulsion is not opposite word of coupling; rather it is synonym of coupling; where we started the breeding experiment with such parents those contained Dominant allele on one locus and recessive allele in the other locus for all the chromosomes.  As a result; parental combination  Pr+ and vg trended to stay together "coupled" (965 progenies at testcross output) and similarly parental combination pr and Vg+ stayed "coupled". Have I understood it correctly? or I'm missing certain significance of the concept of repulsion?

I guess the confusion is stemming from trying to fit the phenotypic terms coupling and repulsion to their genotypic basis.

Coupling and Repulsion are both used considering the phenotypic profile of the progeny, and hence, takes into consideration only the distribution of the dominant allele. If, in the progeny of the test cross, the percentage of double dominant is less than that the average percentage of single dominant, that would be what we call repulsion, as in the two dominant traits tend to be separated. The opposite, percentage of double dominant being greater than the average of individual dominant, is coupling.

This said, it is clear what would be the corresponding genotypic states. If the chromosomal states are $Pr^+/Vg^+.. pr/vg$, coupling would be observed if the $pr$ and the $vg$ loci are linked, since for individual dominant phenotypes to appear, recombination is necessary which is rendered less probable due to linkage. A genotype of $Pr^+/vg..pr/Vg^+$ would result in the phenomenon of repulsion in a test cross. The case you cite, has the latter, and hence, we observe repulsion.

Now to your questions.

  Is "Coupling" an exact synonym of "Linkage" ? and is "repulsion" an exact synonym of "recombinant"? No-where I could yet found mention of it.

Neither. More accurate would be to consider both coupling and repulsion as consequences of linkage, differing in the configuration of the linked gene (see above).

  What are they telling as coupling-"phase" and repulsion-"phase"? Are there 2 different "step"s or "time-frames" or "generations"?

Although this is difficult to answer without knowing the context, I belive that the author here might be referring to the variable possible configuration of the alleles, as in, if they are in a coupling-phase, they are so oriented that the resultant progeny will show the coupling phenomenon. The phase may change to repulsion if a recombination event occurs. (again, see above.)

  Coupling and repulsion- are they indicating to a "phenomenon"? or the Genotypic "state"?

Not to argue much in this semantic mashup, they are best viewed as differing phenomenon (as in the different obtained progeny phenotypic ratios) resulting from varied genotypic states.


Will I grow taller? How can i tell? I'm 17 and I'm about 160 cm and my weight is 47 kg . I just want to know if I will still grow taller ?

Simpler answer (although I like Remi.b's):

Probably.

If you want to know for sure go to a doctor and have them look at your Epiphyseal Plates in your long bones (Femur, Tibula, Fibula). If they've fused, you won't grow anymore. If they're still distinct then you'll continue to grow until they fuse.

For males that can happen as late as early-20's. However, depending on genetics, you might not gain that much height.

Here's a graph you might be interested in:

You're at the tail-end of probably your last growth spurt. You have probably 2-3 years' worth of growing left, but don't expect miracles. You've got maybe another 1-2cm.


Why do veins look blue? I know that veins carry oxygen.

Veins look blue because the oxygen-depleted blood in them is blue.

Is this true??

Well, even though most people presume that it appears blue (reference) is due to the blood being deoxygenated, it is actually not the truth because blood is never blue whether it is deoxygenated or not. In a paper by Dr Alwin Kienle titled Why do veins appear blue? A new look at an old question, the authors measured how much light of various wavelengths was reflected from both real blood vessels in skin and imitation vessels in a skin-like environment. The synthetic vessel (which was a capillary tube filled with blood and placed in a milky substance with optical properties similar to skin) allowed the authors to experiment with a variety of parameters (particularly vessel depth and diameter), and they were then able to validate their results by taking measurements on actual vessels in skin. They eventually came to the conclusion that the optical properties of skin and blood is what makes the veins appear blue.

I quote from the paper as to the reason of blood appearing blue.

  "Blue light does not penetrate as deeply into tissue as red light.
  Therefore, if the vessel is sufficiently deep, the reflectance in the
  blue will be affected to a lesser extent. Deoxygenated venous blood
  has a greater absorption coefficient than oxygenated arterial blood in
  the red spectral region, and this difference of two, rather small,
  values is amplified because of the long path length of red light in
  scattering tissue. As a result, veins are more likely to look blue
  than arteries at the same diameter and depth. Often arteries are not
  seen at all because they are generally smaller than veins and have
  thicker vessel walls. It has been shown that a small vessel will look
  red when close to the surface. However, if a superficial vessel is
  large it can still look bluish, particularly in the case of the vein.
  On the other hand, if the depth of a vessel is large, even red
  remitted light will not be influenced by the vessel, and it will not
  be seen."

So in short, the blue appearance could be attributed more to the location of the vein than just the deoxygenation.


Why would hawk moths evolve long tongues for Darwin's Star Orchid when there are other flowers around? Why would hawk moth evolve long tongues for Darwin's Star Orchid when there are other flowers around? Also isn't it counter productive for some flower to evolve a long nectar tube as this would shift the pollinators to other plants?
This coevolution makes sense if the only source of food for the moth is this star orchid and the only pollinator for the flower is the hawk moth. But if we consider other species to also exist in the picture, this coevolution seems counterproductive to me. For example most flower evolve mechanisms to attract pollinators as their is competition for pollinators as well.

I think the key terms are niche and co-evolution;

Why would hawk moths evolve long tongues for Darwin's Star Orchid when
there are other flowers around [?]

Because the moths have grown a long proboscis as an adaptation to a certain niche. As you say, not much other species can feast on the flower's nectar, so it makes perfect sense to narrow your niche by elongating your proboscis, and reap the benefits of this little visited flower.
A niche is

[T]he range of environmental conditions in which a species can exist.

As the University of South Africa explains:

One important part of the idea of the niche is that it is controlled
by how the species exploits resources in its environment.  If there
are two species living together and exploiting the same resources,
then one will usually be worse than the other at doing this –
eventually, that species will disappear because the other species will
outcompete it. However, species can live together because they
exploit different resources or because they exploit the same resources
in different ways.  These species then have different niches, even
though they occur in the same place.

Then how would the flower benefit? Now I'm going a bit more into a hypothetical explanation, but flowers need cross-pollination to reproduce and genetic mixing. If a plant species can bind a certain pollinating species to itself, it can make sure that that pollinating species only forages on that particular species of plant. Hence, that plant species can ascertain that the pollinating species carries only the right pollen and therefore make sure the transferred pollen is from the same plant species. This is beneficial, as pollen from other species won't pollinate them.
It's all a matter of co-evolution, in this case of two mutualistic species, nicely and succinctly explained by the University of California, Berkeley:

The term coevolution is used to describe cases where two (or more) species reciprocally affect each other's evolution. So for example, an evolutionary change in the morphology of a plant, might affect the morphology of an herbivore that eats the plant, which in turn might affect the evolution of the plant, which might affect the evolution of the herbivore...and so on.
Coevolution is likely to happen when different species have close
ecological interactions with one another. These ecological
relationships include:

Predator/prey and parasite/host
Competitive species
Mutualistic species

The hawk moth Xanthopan morganii praedicta pollinates the Madagascar star orchid (Angraecum sesquipedale) with its long proboscis. source: Encyclopedia Briattanica


What would happen if you combined the world's deadliest diseases & viruses? What would happen if you took the deadliest diseases/viruses in the world and combined them in a single medium (a solution of water or a test subject)? Would the strongest virus defeat the rest or would a  new deadly virus be created?

Viruses in the same cell can recombine (although they don't always do). This can happen by crossing-over of the genomic strands or reassortment of genomic segments. Therefore, you can get a new virus out of the fist two. The new one is not necessarily deadlier than the first two. If there's no recombination, the test subject will enjoy both diseases until the deadliest one kills him.


How many calories do gut bacteria burn? It has become well-accepted that microbiota of the gut (a.k.a. gut bacteria) consume calories that are ingested and can have significant effects on energy metabolism in humans. For example, if you take the feces from mice that have had a gastric bypass and transplant those into the colon/GI tract of obese mice, then the obese mice lose weight (See here for article about this study).

Are there any known estimates on how many calories the typical gut microbiota in an adult human consumes? That is, about how many calories your gut microbiota use per day?

For more information there is a freely available source on Pubmed, "The Human Microbiome, Diet and Health Workshop Summary."

A recent study by Bahr et al. found that "healthy" gut microbes increased non-aerobic resting metabolism by 16%, compared to gut microbes being treated by risperidone. Risperidone is an antipsychotic drug that causes weight gain and Bahr et al. were trying to determine why. In addition to to the article, their university issued a non-technical press release on the article.

This article doesn't exactly answer your question but does provide a good staring place.


How can I isolate live Wolbachia endosymbionts from Drosophila I am interested to culture Wolbachia bacteria in cell line.

You can see this protocol for Wolbachia isolation:

See this protocol for infecting cell lines with Wolbachia.

In this study the authors have established a cell line from a Wolbachia infected tissue of Aedes albopictus. You can have a look at that too.


Sexing spotted doves I recently took pictures of Spotted doves (Spilopelia chinensis) during their courtship. The one on the right, is large with a off-white breast and the one on the left is comparatively small with dingy reddish white breast.

My professor and I presumed that the one on the right is the male and the other is the female. The larger one mounted the other during cloacal kiss.

I've checked Wikipedia and other sites which seem to copy Wikipedia, they say that the species does not show sexual dimorphism. On the other hand, this website claims that there is a difference.

Does it show sexual dimorphism?

Location: West Bengal, India

First I think that is a Western Spotted Dove (Spilopelia suratensis), now splitted from the Eastern spotted Dove (Spilopelia chinensis). In your area there should be both species but the red iris and eye-ring should indicate the Western. Sexes are alike so there are no signs you characteristics you can check (source, handbook of the bird of the world, which is the most updated and reliable source in many occasions). Males sing much more often than females (so you can observe this behaviour) and in many species, but I dunno about this one, is the male providing food to the female...so I think your guess is right!

All the best,

Have fun


What species is this bug that appears in my bathroom? I'm trying to identify the attached. A few of them appear every day in my bathroom, never more than that, but new ones are there every day. Length is 2-3 mm, and location is the United Kingdom.

Based on my knowledge of species found in Sweden, I think this is a species of Ptinus (Spider beetles), for instance Ptinus sexpunctatus. The general appearance, along with long antenna and long legs fits well. Species in this genus are often also found indoors. Some of the other species in the same genus can also have white/light markings on the elytra, so I'm not absolutely sure about the species. Typical of P. sexpunctatus is that is has six white marking on the wings, but the two hind ones on each wing can sometimes merge into one.

(picture of Ptinus sexpunctatus, from http://www.coleoptera.org.uk/)

(side view, from Wikipedia)


What kind of tree is this (Seattle, WA)? This tree is a volunteer and I am hoping to find out what kind of tree it is.

Young tree

Leaf sample

Below is a more recent photo showing flowering.

It looks like a Laburnum. Probably a Common Laburnum Laburnum anagyroides, also known as a Golden Chain Tree. It is from central and southern Europe.

The seeds are poisonous.

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

Here is a photo of the leaves

From http://www.saps.org.uk/trees/laburnum.htm

And the flower

http://wildflowerfinder.org.uk/Flowers/L/Laburnum/Laburnum.htm


Can a protein falling below a threshold trigger another response? Is it possible that the falling of the concentration of a protein below a threshold triggers the release or production of another protein?

Of course, that is possible. I'll give a simple example. If your protein (X) is an inhibitor of the other protein (Y), then when X falls, Y will rise. This would not really be "thresholded".

There are many mechanisms that can lead to thresholding which include co-operativity (in the action of X) and positive feedbacks. How these mechanisms work would be a different question altogether. (A quick read would be this wikipedia article).


What instances are there in which two species share the same binomial name? Since binomials are required to be unique only within a kingdom, two species can share the same binomial name if they are in different kingdoms. I know of one instance of this, Orestias elegans: this name denotes a species of fish (kingdom Animalia) as well as a species of orchid (kingdom Plantae).

Are there other instances where one binomial name validly refers to two (or more!) species?

There are four other instances of species-level hemihomonyms I can find:

Agathis montana can be either a critically endangered species of conifer or a parasitic insect.
Centropogon australis can be either a fish or a plant with a long red flower.
Asterina gibbosa can be either a sea star or a type of fungus
Baileya australis can be a moth or a yellow flowering plant


Why is PEG important for efficient yeast transformation? One way to do an yeast transformation is by using lithium acetate, a single-stranded carrier DNA, and PEG (1). I was wondering why is the polyethylene glycol important for the efficient transformation. How does it affect the take-up of the foreign DNA? Yamakawa et al (2) showed that PEG is essential for the recovery of the cells but I couldn't access that paper to read more about it.

1. R Daniel Gietz & Robert H Schiest (2007). High-efficiency yeast transformation using the LiAc/SS carrier DNA/PEG method

2. Yamakawa, M., Hishinuma, F. and Gunge, N. (1985). Intact cell transformation of Saccharomyces cerevisiae by polyethylene glycol. Agric. Biol. Chem. 43, 869-
871.

http://www.protocol-online.org/biology-forums/posts/26634.html

I found this link - it says 'we don't really know'.  It says PEG binds DNA, I assume shielding the membrane from its negative charge and allowing internalization to happen.

I would guess that the amphipathic nature of PEG, being partly hydrophobic, also helps soften up the membrane.  Interestingly, if you increase the PEG concentration beyond the limits, it decreases the efficiency of the procedure.


Isoprenoid Diphosphate Concentration in Yeast saccharomyces cerevisiae Isoprenoid  Diphosphate(IPP) is an important metabolites which is precursor in lot of secondary metabolites like Dolichol diphosphate, ubiquinone, prenylated proteins and carotenoid (not synthesized in s cerevisiae).

What is the average concentration of IPP present in yeast per gm ?

Although this information doesn't provide a direct answer to your question, I hope that it sets the scene for what is achievable in metabolic engineering from IPP. It should also provide a jumping off point for further literature research.

This is a fairly recent review of metabolic engineering of relevant pathways in various microbial systems, including Saccaharmoyes:

  Ajikumar  PK et al. (2008)  Terpenoids: Opportunities for Biosynthesis of Natural Product Drugs Using Engineered Microorganisms. Molecular Pharmaceutics 5:167–190

The review refers to:

  Ro, D. et al. (2006) Production of the antimalarial drug precursor artemisinic acid in engineered yeast. Nature 440, 940–943.

In this work, the introduction of a pathway-specific gene led to the production of 4.4 mg L-1 of product. This was increased to 153 mg L-1 by several manipulations including:

Increasing flux through the pathway by expressing a modified HMG CoA reductase

Decreasing flux into sterol synthesis by downregulation of the ERG9 gene combined with expression of a dominant negative allele of the transcription factor Upc2.

UPDATE

After posting my answer I found this paper:

  Huang, B. et al. (2011) Metabolite target analysis of isoprenoid pathway in Saccharomyces cerevisiae in response to genetic modification by GC-SIM-MS coupled with chemometrics. Metabolomics 7:134–146

The paper includes a detailed discussion of methodologies, which I won't go into here.

Although there are no measurements of IPP, in Table 7 they present this result: geranyl pyrophosphate 32 ng ml-1 in a 48 h culture, A600 ~ 2.3. ERG9 disruption increased this to 56 ng ml-1

As far as I can tell these values are presented as ng ml-1 original culture. Using 1 U of OD600 corresponds to 0.41 g of dry cells liter−1 taken from here I calculate a value for GPP of 34 µg g-1 dry weight in the wild-type strain.


Does evolution only give rise to traits that confer fitness? Does evolution only give rise to traits that confer fitness? In other words, does the existence of a trait imply it's conferring of fitness? If not, what are some counter examples?

I'll try to beat @Remi.b to the suggestion that you review Understanding Evolution as a general overview of evolutionary topics.

For a quick answer: no.

Sometimes people confuse the great importance of natural selection in evolution with an equivalency between natural selection and evolution. However, there are many many contributors to evolution, many of which do not involve fitness.

I'll list just a couple examples:

Genetic drift is random change in allele frequency because of random sampling of reproductive organisms.

Founder effect is a somewhat related concept, referring to the change in allele frequency in a population that becomes isolated from the rest of the individuals of a species: that population has a selection of traits that might differ from the species as a whole, and lead to future speciation.

There are many more.


Why is wind cold for humans? Coming out of the pool the other day, I felt very cold because I was wet and the wind picked up. My idea is that a "cold" feeling should be associated with low temperatures, but it's indeed wrong.

Why do we perceive wind at a farely normal temperature as cold?

One important point that you might not be considering is the heat of vaporization.

You may be aware that while it normally takes 4.18 J (1 calorie) of heat to raise 1 gram of water 1 °C, it takes around 2250 J of heat to raise 1 g of water from liquid at 99.5 °C to gas at 100.5 °C, due to the energy needed to go from a liquid to a gas. - What you may not know is that the enthalpy of vaporization isn't limited to vaporization at the boiling point. Any conversion of water to water vapor requires heat of vaporization, though exactly how much is temperature dependant.

So when water evaporates, it cools things much more than one might expect from the "average" energy (or even statistically above average energy) a water molecule may have in the liquid state - several hundred times more. All this is driven by the entropic benefits of having water molecules in the gaseous state rather than the liquid state.

Wind makes the process more efficient because it removes the water-vapor laden air, unbalancing the equilibrium of the process in favor of further evaporation. More water makes it more efficient (to a point), because there's more water to evaporate and the rate of evaporation increases, increasing the removal of heat.

This is not just a physiological perception effect - one can actually measure the temperature drop when water evaporates. Evaporative coolers make use of this effect, and traditional wet-bulb hygrometers (psychrometers) use exactly this effect to measure the humidity -- in some cases you can get a temperature differential of 20 °C or more between a dry bulb thermometer and a wet bulb thermometer.

There is a small perceptual effect in that the evaporative cooling is happening on your skin, where a large number of temperature receptors are located. Therefore, your skin (and temperature receptors) feel a cooling effect even if your core temperature doesn't change detectably. Local cooling produces a larger temperature change than might be expected if you calculated for a whole-body heat change.


Why does Penicillin only affect bacterial cell walls I was quite fascinated by the feature Should Science Pull the Trigger on Antiviral Drugs—That Can Blast the Common Cold? in this month's Wired magazine.

They explain that Penicillin is effective at killing bacteria because it interferes with the growth of bacterial cell walls.

How does Penicillin do that exactly? And why does it not dissolve human cells as well?

Bacteria have a mesh-like structure surrounding their plasma membrane called a cell wall.  The cell wall is made up of peptidoglycan polymers that form a rigid crystalline structure that helps protect the osmotic pressure of the bacterial cytoplasm.

Penicillin and other β-lactams work by inhibiting the final step of peptidoglycan synthesis, which prevents transpeptidation (crosslinking) of the peptidoglycan molecules. This leads to the death of the bacterium by osmotic pressure due to the loss of the cell wall.

This drug doesn't affect human cells because they lack a cell wall surrounding their plasma membrane.


Skin Colour in "Northern" Regions of The earth Question: Netflix has recently produced a two-part miniseries, The Evolution of US, that examines the evolution of "man". The topic of of human skin colour was covered and it was stated that 'lighter skin pigmentation was a preferred natural selection for early humans living in the "northern" regions'. The idea being that lighter skin could "absorb" sun-rays; which apparently is necessary for activating vitamin-D. Is this a true statement ? And where might I find good sources of literature to read on this topic ?

Now this particular series does not define "northern" and to be fair neither was the term "lighter skin" . My motivation in asking the question is driven by my own travels in far eastern Russia, Mongolia, Alaska, and parts of Peru and Ecuador. In each of those locations I observed numerous groups of indigenous people with dark brown skin and pitch black straight hair; which seems to contradict the statement in the series.

Melanin reduces the skin's ability to make Vit D due to reduced UV penetration. This is a disadvantage in northern areas where people get less sun light, and also need to wear heavy cloths to keep warm which adds to the problem. People in Sunny regions have the opposite need as there is more than enough UV light exposure, but they run the risk of developing skin cancer, which is why having melanin provides an evolutionary advantage in these regions.

Interestingly, in the Arabian Gulf region, there is currently an epidemic of Vit D deficiency especially among those with dark skin. Although there is plenty of sun light, people tend to avoid the harsh sun almost completely by commuting strictly in cars and avoiding walking outdoors during the day. Car windows (and glass in general) are opaque to UV rays, therefor reducing the skin's ability to produce Vit D, and forcing many locals who adopt such lifestyle to take oral Vit D supplements.

Here is a link with some references to confirm the medical link between Vit D deficiency and lack of sunlight exposure:

https://www.webmd.com/food-recipes/qa/how-can-dark-skin-lead-to-vitamin-d-deficiency


Understanding DNA supercoiling While trying to understand DNA supercoiling, I came across these lines in the book Genetics by Ursula Goodenough :

  All natural DNA is superhelical. The axis of the duplex itself follows
  a helical path in space. For virtually all DNA, the sense of the
  superhelical turns is opposite to that of duplex, thereofer, they are
  negative supertwists.

I am unable to understand these lines. Specially, the second one.

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

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

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


Why do insects (flies) put their legs together when they die (as if they're praying)? Other animals don't seem to have an organized pose to die in. Or do they?

A good working theory is that this is caused by Rigor Mortis and the anatomy of insect legs.

In most cases, the muscles that pull the leg down (or closer together) are larger than the ones that pull the leg up.  This is because those muscles (flexors) must support the insect's weight:

(Click for larger view)

When the muscles contract after death, the larger muscles win out, causing the legs to move together.

From Why Do Insects Cross Their Legs When They Die?:

  I suspect this is rigor mortis -- that post-death stiffening that occurs due to a chemical transformation of muscle tissue -- contracting legs as much as possible in the directions of least resistance, says Brian Farrell, an entomologist at Harvard University.


Is it possible to dock multiple ligands with the target? Is it possible to dock multiple ligands with a target? If so, what is the suitable software used for? -- Is it possible to fix specific docking region for the target (or) automatic?

Huameng Li and Chenglong Li have done multiple ligand docking in two (AFAIK) of their works:

Multiple ligand simultaneous docking: Orchestrated dancing of ligands in binding sites of protein
Drug Design Targeting Protein–Protein Interactions (PPIs) Using Multiple Ligand Simultaneous Docking (MLSD).....

The method is called Multiple Ligand Simultaneous Docking (MLSD). I am not at all an expert in this field and you should read the first paper for details on how they implemented this. This algorithm was implemented on AutoDock.


Should I help this young Magpie? I found this young Eurasian Magpie in my garden:

He is just standing there, not doing anything. I believe he fell from a tree and can't fly yet and is just waiting for the feeding from his parents until he can fly, but I wonder if that’s true and if I should do anything to help.

There’s another young one on a branch of a nearby tree, also:

It's best to leave the bird alone. The parents are likely still in the area and tending to the young, including feeding and chasing away would-be predators. You're better off staying away so as to not intimidate or upset the parents. If you have outdoor pets, relocate them indoors or to an enclosed area for a few days.

Failing this, the advice given in comments to call your local animal rescue is best.


Are Bovine serum albumin, Avidin, Ficoll-70 and Dextran-70 positively charged or negatively charged? Bovine serum albumin, Avidin, Ficoll-70 and Dextran-70,are they
positively charged or negatively charged ? And which other solvents can be used as a substitute to water for preparing solutions in each case ?

For charge, you could check this one by sequence level, for example for Bovine Albumin (Uniprot: P02769) you can get the theoretical pI of 5.82, as the mean of pKa aminoacid values, to do this can use protparm, so when the pH > pI, the protein has a net negative charge and when the pH < pI, the protein has a net positive charge.

And there are only two organic polar solvents I known to work proteins, DMSO (pKa = 35) and
Dimethylformamide (DMF, pKa=-0.01 (20ºC))