Sparking during electroporation of plasmid DNA into bacterial cells During electroporation of bacterial cells (I work with Mycobacterium tuberculosis, but I think this applies to E. coli as well), sometimes I get sparking. I've read this is due to salts present, either in the DNA sample or the bacteria.

I use the Qiagen plasmid prep kit, which includes EB (Elution Buffer). This contains Tris-Cl. Could this be contributing to the sparking? Can you explain how this works? Does eluting with water instead of EB reduce chances of sparking?

In my experience the elution buffer does not matter (both for E.coli and Mycobacteria). I have heard this before from co-workers, but it usually is based on superstition or anecdotal evidence. I have compared water/EB elution and never saw a difference in sparking (in fact, I usually get slightly more colonies with EB).

When I get arcing (sparks), it's usually because I did not wash enough, have bubbles or have to many bacteria. Arcing is a collapse of resistance.


How did the first life form on Earth reproduce without DNA? How did the earliest life forms exist without DNA? The most likely scenario I can think of for life happening from nothing is that, over billions of years, with trillions of water molecules and dust particles and chemicals moving around, eventually a small clump of this murky stuff formed a pattern. Or maybe, under some lucky conditions, a whole mud pit of such a inorganic system started forming into structures which had a pattern of motion, and one of those structures became the first sub-cell, like a primitive ribosome or something. I remember learning some parts of cells were once separate entities, but there are massive gaps in that idea.

The primary gap being: How did reproduction occur in that incredibly lucky, freak incident of a tiny dust clump or whatever? How did reproduction occur without DNA? Do scientists have a theory on how the first reproduction occurred?

So earth is estimated to be around 4.5 billion years old, and life has existed for about 3.4-3.9 billion years of that, around >75% the time. For a little perspective, Homo sapiens have been around for up to ~250,000 years, just 0.00005% of the time earth has existed. In that time the earth has changed massively, early earth was pretty hostile, but that could have made it a good place to develop early life.

What was the pre-cursors to self-replicating DNA like?

Well one popular theory is the RNA world hypothesis, which suggests that precursors to life as we know it were RNA molecules that could self replicate (reproduce). These RNA molecules supposedly evolved in to life in the DNA/RNA/Protein world via an intermediate stage of ribonucleoproteins. The reason why RNA could have preceeded DNA based life is because it has the potential to carry information and to be the catalyst of its own synthesis.

  "The unique potential of RNA molecules to act both as information carrier and as catalyst forms the basis of the RNA world hypothesis.

  "RNA therefore has all the properties required of a molecule that could catalyze its own synthesis (Figure 6-92). Although self-replicating systems of RNA molecules have not been found in nature, scientists are hopeful that they can be constructed in the laboratory." in Molecular Biology of the Cell

However, the RNA world probably wasn't the first step on the road to self-replicating life, but other polymers with characteristics similar to RNA that could have acted as the template and catalyst required for RNA synthesis.

  "Although RNA seems well suited to form the basis for a self-replicating set of biochemical catalysts, it is unlikely that RNA was the first kind of molecule to do so. From a purely chemical standpoint, it is difficult to imagine how long RNA molecules could be formed initially by purely nonenzymatic means. For one thing, the precursors of RNA, the ribonucleotides, are difficult to form nonenzymatically." in Molecular Biology of the Cell

-

  "Shapiro doesn't think it's necessary to invoke multiple universes or life-laden comets crashing into ancient Earth. Instead, he thinks life started with molecules that were smaller and less complex than RNA, which performed simple chemical reactions that eventually led to a self-sustaining system involving the formation of more complex molecules." on LiveScience.com

This means that the first self-replicating RNA molecules were preceded by other molecules that were important in the progression from simple atoms, through non-biotic molecules, to large self replicating polymers which can be considered life. Copley et al suggest a progression in detail, with monomers being an early step in the progression (see figure 4 in the paper, and section 4 for extensive detail) where monomers precede multimers, which precede micro-RNA.

  "Our model describes a continuous path for emergence of this sophisticated system
  from a simpler reaction network fueled by geochemical processes. The processes involved in metabolism and replication were intertwined from the very beginning, a concept that neatly eliminates the chicken/egg problem. Further, this model suggests that many features of the RNA World, and indeed modern life, arose long before the RNA World and were retained as pre-biotic systems became more sophisticated." - Copley et al

An alternative and slightly different theory suggests that viruses were the precursors to modern life, a so called Virus world. Similarly it supposes that early replicators were RNA based, but that viruses evolved in to the earliest forms of self replicating DNA carriers.

  "The Virus World Theory is closely related to the RNA World Theory, which says life first evolved as small pieces of RNA that slowly developed into complex DNA-carrying organisms. The Virus World Theory agrees that life's genetic material began as RNA. But it differs by arguing that the ancestors of viruses evolved before cells." from NationalGeographic.com.

Further good reading here, here, and here. I also recommend the book The Story of Life as an interesting related read.


What's the name of this colorful tiny spider? Found this colorful spider yesterday in my study. Couldn't find exact match over internet. Does anyone know what spider is this? Is it harmful?

It seems a lot like the 'jade jumping spider'.
The jade jumping spider scientifically known as Siler semiglaucus has been observed primarily in Asia. I notice that the legs and abdomen have similar patterns to this species. As for the feelers and head I'm not so sure, but the dark hair on the front legs makes me more convinced of my guess. Perhaps look at different species that share the same genus to see if there is any other species that looks more similar to your observation.

If you're still not convinced, as a last resort, perhaps take a look at the peacock spider also known as Maratus volans. It's a long shot but maybe you see connections that I couldn't catch from the photo :).


Are both B and Y ions required to determine the sequence of a protein by mass spectrometry? I was wondering if both all b and y ions are required to determine to order of the amio acids in a peptide.

In my opinion knowing only ALL B ions or ALL y-ions is enough to determine the sequence of the amino acids in a peptide. I was also wondering how these b and y ions are differentiated in a spectrum?

In an MS/MS spectrum, difference between the successive peaks of a b or y ion series allows one to determine the amino acids making the series/peptide. Either one of them should be enough to give you the sequence. However, an MS/MS spectrum obtained from the mass spec instrument doesnt tell fragment types. Therefore it takes some expertise and tricks to spot y or b ion series. For example: if you are analysing a sample digested by trypsin, your C-term residue will either be K or R. So you can look for a Y1 ion if there is 147 indicating K or 175 indicating R. Also, Y ions tend to be highest intensity peaks in a spectrum. For more helpful tips on this there is an excellent tutorial :
http://www.ionsource.com/tutorial/DeNovo/DeNovoTOC.htm.

Also, in practice you seldom get all of the b or y ion peaks and there are often missing peaks. For this reason it is useful to have both b and y ions series so that gaps in one can be filled by the other. This is not only useful when you are dealing with denovo sequencing but also in a more typical shotgun proteomics experiment. In a typical shotgun proteomics experiment one searches their mass spec data with peptide search engines. These are software which use a protein sequence database which is in silico digested, based on the specificity of the protease used in the experiment, and from the resulting peptide sequences search engines make a library of predicted MS/MS spectra (this is done by fragmenting along the peptide backbone and listing all possible b and y ions). Then these predicted spectra are matched with the observed spectra to predict the peptide sequences that could result in the observed spectra. Again, not all of the peaks present in a predicted spectra will be found in an observed spectra. So it is best to have ions from both b and y ion series. More ions matched between the observed and predicted spectra, better is the score and confidence in identification.


Why don't we see new diseases more often? Or, ever? It seems like every disease we ever hear about is something that's been around since ancient times, since thousands of years ago. Of course new diseases were catalogued over the course of the past couple hundred years, but they weren't actually new diseases-- they just hadn't been previously classified/identified.

Given that (in my understanding) viruses and microbial lifeforms can evolve and change considerably more rapidly than higher order organisms, why don't we often/ever hear about completely new diseases that have never been seen before? Diseases that may have only just been born.

The first thing to note is that nothing is truly new, everything is a slightly different version of what existed previously, it's only on the very long term that you can see major change. Mutations occur continuously and new variants arise often. For example you need a new flu shot every year due to the high mutation rate of the influenza virus but we still call it flu because it's only a little different.

While disease causing organisms evolve at a relatively slow rate new diseases can appear suddenly when the effect on humans suddenly changes; the most obvious example of which is when a disease changes host species. For example the sudden appearance of HIV when Simian immunodeficiency virus (SIV) "jumped species" to infect human, most likely through the consumption and processing of Primate meat. While HIV appears new it is again ancient in the sense that it has caused a similar condition to HIV/AIDS in many African non-human primates for a significant period.


Why do snakes not have eyelids? Why is it that snakes do not have eyelids?

Is it due to that fact that they are not as evolved as we humans and other organisms that have eye lids, or is there any other significance behind it if any?

Snakes have no eyelids. Each eye is covered with a single, transparent scale. These eye scales protect the eyes from mechanical damage, and prevent the eyes from drying out, just as an eye lid would do. In effect, snakes developed another solution to protect their eyes.

As a result, snakes cannot blink and they sleep with their eyes open.

A snake’s eye scales are part of its skin. This means that when a snake sheds its skin, it must also shed its eye scales. When it is time for shedding, the eye scale turns opaque, reducing vision (Fig. 1).

Fig. 1. Opaque snake eye before skin shedding. Figure source: Snakes are long blogspot

Source: Museum of Victoria


Why do mountain gorilla eat just 1.7% fruit, while lowland gorillas eat 25%? Eastern lowland gorillas have more diverse diets, which vary
seasonally. Leaves and pith are commonly eaten, but fruits can make up
as much as 25% of their diets. https://en.wikipedia.org/wiki/Gorilla#Food_and_foraging

The mountain gorilla is primarily a herbivore; the majority of its
diet is composed of the leaves, shoots and stems (85.8%) of 142 plant
species. It also feeds on bark (6.9%), roots (3.3%), flowers (2.3%),
and fruit (1.7%) https://en.wikipedia.org/wiki/Mountain_gorilla#Habitat_and_ecology

Mountain plants have to be hardy, especially if they grow above the frost line. They are more likely to be tough vegetation (leaves, shoots, and stems) as mentioned in the mountain gorilla diet.

The lowlands have much more plant diversity (and generally better food). Sweet fruits have better calories for the effort required to forage and digest them, so you would expect the lowland gorillas to prefer fruit.


Why do larger diameter myelinated axons have greater conduction velocities than small diameter myelinated axons? A canonical statement I have frequently read is that "large diameter axons conduct action potentials at faster velocities than small diameter axons". After recently learning the effect of increased capacitance on the cell membrane (namely, that more charge is required for depolarization to occur...Are large cell bodies of neurons harder to depolarize than small cell bodies of neurons?), I find this canon to be rather confusing.

I have attached a picture to make my question clearer:

In the above picture, both neurons have the same myelin spacing. So, my question is why should the action potential in Axon B traverse the distance X1 to X2 more quickly than in Axon A. Shouldn't the increased capacitance of Axon B (due to its increased diameter) increase the time it takes for the action potential to travel between the two points?

Why should the action potential in Axon B traverse the distance X1 to X2 more quickly than in Axon A?

The larger the diameter of the axon, the less the longitudinal resistance, so the current can propagate along the axon more easily.

Shouldn't the increased capacitance of Axon B (due to its increased diameter) increase the time it takes for the action potential to travel between the two points?

Both, the capacitance and the number of ion channels increase quadratically whit the diameter. So the increase in capacitance is compensated by an increase in total ionic current.

Wiki cable therory


Initial population when i count backwards? My question is dealing with how many ancestors it took to produce me:

--> to produce me it took 2 people (my parents) = ($2^1$) people = 2
--> one generation further included = ($2^1 + 2^2$) people = 6
--> in the past 500 years my pedigree chart contains 15 generations, so $2^{16}$ people = 65.532 people to produce me (-2 to be completely correct)
--> when i calculate back to 35.000 year ago I get a larger number *)
--> when i calculate to all humans 2.400.000 ago I get a ridiculous large number *)
--> when i include up to all mammal grandfathers and grandmothers 60.000.000 years ago the total number takes pages to scroll *)

*) see: http://ed.je/2L6 for the actual numbers did not want to clutter here.

*) I took 3 generations per 100 years to let the numbers be small as possible.

So, I think I'm making a mistake somewhere. Only I don't know where: to create a child you need 2 parents. And to create a parent you need 2 further parents. But somehow calculating back to "all mammals" just related directly to me would mean $2^{1.800.001}$ mammals walking around 60 millions years ago being my direct predecessor back then.

So where am I going wrong? Somehow I can't figure out where my error lies (I've not studied Biology though).

I visualize a pedigree tree (reverse pyramid) starting with me and then logically each parent needs to be born out of 2 other parents just calculating my way up.

Your calculations are the following. Assuming non-overlapping generations, the number of ancestors you have in the last $t$ generation is given by:

$$\sum_{i=1}^t 2^t$$

This sounds correct. But there are some very strong assumptions:

Generations are non-overlapping. A more realistic model would need to consider $t$ as a continuous variable a give a probability of reproducing which depend on the age of the individual.
Never two related individuals mate together. Otherwise, you paternal grandfather might be your maternal grandfather. In reality we are all somehow related, we have a common ancestor (Hey Bro). For example if you consider that your parents are siblings and that their parents are siblings and so forth… then you don't need more than 2 great-great-great-great-grandparents. In order to keep track of such events (inbreeding), you need a stochastic model and you would need to know the population size $N(t)$ as a function of $t$.

Tracking the change of population size through time is part of a very big in biology which is called population biology. For example you will find in this post a model of population growth of two interacting species (prey-predator)


Do birds grieve and feel emotion? Crows are surprisingly clever with tool making/use and even understanding displacement water over sand! Clearly there's some relatively high level cognitive processes going on up in those avian brains.

When I stumbled across a video of what appears to be a bird grieving over its mate (shown in clip below), I wondered how far animal emotion and psychology goes.

Is that bird in the video grieving? (and shaking because of stress?)
What species of bird is this?

Your "grieving bird" is a video of a peregrine falcon (Falco peregrinus) and its (nearly?) dead chick on a hot summer day in Phoenix, Arizona (USA) in 2016.

 Photo credit: Arizona Game And Fish Department

The video is from a nest camera webcam set up in the Maricopa County building in Phoenix, Arizona by the Arizona Game and Fish Department.(See this video for more information). The camera was active in 2016, but according to here the falcons did not return to the nest in 2017. Your video shows one of the adult birds with the only chick that hatched (out of 4 eggs) in 2016. That chick died from a combination of heat and an 8-story fall in June 2016 [Source]. Your video is an edited and audioless version of a video capture of the live stream that can be seen on Youtube. The information for this video indicates that the adult bird in view is the father.

The adult falcon in the video is not wimpering, crying, or grieving. Instead, the bird is trying to cool down on a hot day. He is displaying a familiar temperature regulatory behavior: panting.

From Bartholomew et al. (1968):

  Most birds pant when subjected to heat stress...

In fact, in the more complete video I link to above (with audio), you can clearly hear the bird making panting sounds while breathing heavily.
The falcon also spreads out its wings to better help cool himself down toward the end of the video as it cares to its injured chick.

You can see another video of a panting falcon in New Hampshire (USA) here, and you can find more information about panting, gular fluttering, and other thermoregulatory behaviors in birds here, here, and here.


Why does hypertension occur in obstructive sleep apnea? What is the physiological mechanism behind systemic hypertension resulting from obstructive sleep apnea?

From Obstructive sleep apnea syndrome and hypertension: mechanism of the linkage and 24-h blood pressure control:

  OSAS directly induces negative intrathoracic pressure and decreases pulmonary stretch receptor stimulation, chemoreceptor stimulation, hypoxemia, hypercapnia and microarousal. These changes potentiate various risk factors, including the sympathetic nervous system, renin-angiotensin-aldosterone system and inflammation.

Summary:

Low oxygen levels at night increase oxidative stress to the body inducing inflammatory reactions and damage to the interior of blood vessels
Nitrogen monoxide production is decreased, decreasing flow-mediated dilation of blood vessels
Frequent night-time awakenings bring elevated sympathetic nervous system activity
During episodes of hypoxia, blood pressure and heart rate increase
"Increased sympathetic nervous activity may also cause coronary spasm and induce vasospastic angina pectoris."
"[P]eriodic negative intrathoracic pressure (−80 mm Hg, at most), together with a midnight surge of BP, exerts mechanical stress on the ventricular and atrial walls, resulting in the development of left ventricular hypertrophy and left atrial remodeling and, consequently, an elevated risk of heart failure and atrial fibrillation"


Can chitosan affect the absorption of unsaturated fatty acid? I know chitosan will decrease the absorption of fat. However unsaturated fatty acid, such as DHA, is beneficial. Does chitosan effect the absorption of unsaturated fatty acid?

It seems that there is no difference in the effects of chitosan on the uptake of saturated and unsaturated fatty acids. The study cited below (which has been done on guinea pigs) fed the animals a diet which contained different digestion-resistant fibers (maltodextrin, cellulose and chitosan) and also fats. Then the fatty acid content of the feces was measured afterwards.

Only for the group which got additional feeding of chitosan showed a significant increase in the excreted fatty acids. This was true for the saturated (lauric, myristic and palmitic acid) but also for the unsaturated fatty acids (Oleic, linoleic and α-linolenic acid). This effect is specific for fatty acids, The uptake of neutral sterols and bile acids was not affected in any of the experimental groups.

The second paper suggests that chitosan forms an emulsion with fatty acids under the acidic conditions of the stomach. This emulsion is stable and later excreted with the feces.

References:

Selective in vivo effect of chitosan on fatty acid, neutral sterol
and bile acid excretion: a longitudinal study.
Interaction between chitosan and oil under stomach and duodenal
digestive chemical conditions.


Clarification in the name "white cheeked barbet" Everyday I was listening sound of the birs "white cheeked barbet". Then I was wondering how this name came to it? It should be by certain properties of them. In wikipedia it says

  Barbets are named for the bristles at the bases of their stout, sharp bills.

But this statement I couldn't believe from picture, since I couldn't see bristles. The words "white cheeked" can be understood from photo clearly.  I then thought this may be due to some change during the migration, or anything else.

Can one help how this bird gates named "white cheeked barbet"?

It seems as though it is named for feathers below the beak that have a barblike appearance, rather than actual barbs. It may be clearer from these images:

India Nature Watch

Or in this photo: SivamDesign - Flickr


Is there a bacterium that became a virus? Is it possible for a virus to be a descendant of a bacterium that was not through horizontal gene transfer?

How I think this could happen:

Suppose a species of bacteria lives in an environment where it gets all the resources it needs to reproduce (and let's assume that there will be no major changes in the environment).  That is, if it loses a gene that synthesizes some substance (or regulates some process), it will not be at an evolutionary disadvantage.  Because it can achieve this from the environment.  Even depending on the gene, it can even be an evolutionary advantage, as it can become more efficient when it comes to reproducing.  And I have seen that an experiment was carried out related to this question, it was shown that viruses can lose some genes in an environment where it can naturally find the protein that is associated with those genes.  Thus, there is a chance that this species will become so simple, that it will end up becoming a virus.

This virology site has a post about a 2017 paper about membrane-vesicled plasmids that act in ways that are theorized to be precursors to how viruses work:

It is likely that the plasmid-containing membrane vesicles are precursors of what we know today as virus particles. It is thought that viruses originated from selfish genetic elements such as plasmids and transposons when these nucleic acids acquired structural proteins (pictured; image credit). Phylogenetic analyses of the structural proteins of many enveloped and naked viruses reveal that they likely originated from cell proteins on multiple occasions (link to paper).
The membrane-encased Archaeal plasmid seems well on its way to becoming a virus, pending acquisition of viral structural proteins.

Though plasmids are not viruses and are not bacteria, bacteria are hosts for plasmids, and plasmids add indirectly to the genetic constitution of bacteria. Expression of plasmid genes can help bacteria survive hostile or extreme environments, and they reproduce along with bacterial chromosomes. Via the Wikipedia link:

Unlike viruses, which encase their genetic material in a protective protein coat called a capsid, plasmids are "naked" DNA and do not encode genes necessary to encase the genetic material for transfer to a new host; however, some classes of plasmids encode the conjugative "sex" pilus necessary for their own transfer.


Do the phage repressors CI and Mnt exhibit crosstalk? I am interested in using the CI and Mnt proteins as well as their respective promoters (pR and Pmnt) within the same synthetic system, but am concerned as to their similarity and potential crosstalk. A quick search of the literature yielded no results and a Multalin did show some significant sequence homology (although Mnt forms a homodimer while CI does not).

Sequences: CI and pR, Mnt repressor and Mnt promoter

Has it ever been reported that the CI or Mnt repressor exhibit crosstalk on the pR and Pmnt promoters?

There are no reports for it yet. I don't think just because they show overall homology, they would exhibit crosstalk. Just see the alignment of the DNA binding domains of these proteins first ~70 residues from N-terminal. Moreover their DBDs belong to different PFAM families.

Similarly with the promoter sequences.
As reported in iGEM website:

Mnt promoter: tagatctcctatagtgagtcgtattaattt
cI promoter: gtgttgactattttacctctggcggtgata

They are quite different.
Moreover, if iGEM has a reported standard part such as a bistable system component: Mnt/cI promoter (BBa_K228003) then it would have been pretty much standardized. iGEM parts are usually reliable.


Are there macrophages in the blood vessels and within the blood stream? Monocytes are phagocytes that "evolve" or "differentiate" into macrophages. I read that there are monocytes in the blood stream and vessels and that macrophages are found mainly in other tissues and in the lymphatic system.

My question: are there macrophages (and not merely monocytes) in the blood vessels and within the blood stream? And if there are, are they numerous there or sparse?

Usually, monocytes and neutrophils are present(there are other cells like Lymphocytes and other leukocytes), the only time a macrophage will be present is when inflammation occurs, I suspect this is due to the large size of the macrophage, it would be difficult for it to travel in the bloodstream, as it is quite big, compared to the small size of a monocyte. During inflammation, vascular dilation and permeability increase, which makes it easier for cells and proteins to diffuse across the endothelium.

A source that macrophages are present in all tissues: https://www.researchgate.net/publication/227897252_Macrophages_in_the_embryo_and_beyond_Much_more_than_just_giant_phagocytes

A source that talks about all the leukocytes and lymphocytes present in the blood normally: http://www.histology.leeds.ac.uk/blood/blood_wbc.php


Why and how does complexity usually tend to increase through time? The question of complexity is classic in the very first lectures of evolutionary biology where the teacher usually tries to tell the students that complexity does not necessarily increase and that humans are not more complex than other organisms.

My questions are:

Why does complexity tend to increase through evolutionary time?
What are the different hypotheses to explain this pattern?

When writing "Mass extinction" on google image, we find many graphs displaying the number of families (or other taxa) through evolutionary times with the five mass extinctions. What would it look like to draw such graph replacing the family richness in the y-axis by :

Mean complexity among all living things?
Complexity of the most complex taxon?

I suppose that anyone who wishes to answer to this post will necessarily need to define the words "complexity". He or she might define it in terms of number of genes, number of metabolic pathways, length of DNA sequence, number of cell types, some kind of index taken from information theory. When asking my questions I had in mind a definition close to "number of genes" or "number of metabolic pathways".

This is actually a very interesting yet difficult question to give a single precise answer to. I will try and summarize for you a "meta answer":

Complexity Science Some consider complexity not to be a Biological topic as such, since it is a property that accumulates in non-biological systems e.g. economics, technology, music, language - in fact anything that "evolves" through time. This new field of science is called "Complexity Science" or "Complex Systems" and is primarily a field of mathematics or information theory: Complex systems

Complexity in Biology What I can say is that these kinds of questions have started an almost new field in Biology, called "diversity evolution", here is a very interesting paper: Diversity Evolution.

Defining Complexity You were right to mention Complexity first needs to be defined, and as an early field of science this is where much focus has been recently. There are quite a few definitions but it is perhaps too controversial to list any particulars... HERE is a whole UCL lecture dedicated to defining Complexity!

Topics of Complexity Science I have written enough, so perhaps this lovely diagram of the topics of Complexity Science will be of some help:


What is meant by 73 hour birth I was reading an article, when I read a sentence saying, His mother ... nearly died less than three years later during Mathers' 73-hour birth.

What does mean by 73-hour birth?

I could find that topic related to Eminem's mother, Debbie Mathers-Briggs, who almost died delivering her first son(Eminem) at the end of a 73-hour labor or 73-hour birth. That "73 hour birth" means she was in labor(to undergo the efforts of childbirth) for "73 hours".


Can we detect the origin of a 1000 year old dead body after grave excavation? I recently read an article saying DNA analysis has shown some of the people buried in Viking graves in Scandinavia originated from places like Persia and it is talking about something around 1000 years ago.

How accurate could this analysis be based on our DNA and the fact that we have 99.9%  DNA similarity?

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

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

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


What does C. Elegans sense when touched? I'm reading up on C. Elegans' touch responses.  Once touched, what is it that the neurons are sensing, specifically?  Presumably, touch deforms the body cells, and that deformation is sensed by the sensory neurons. Is that correct?  Alternately, are the neurons themselves directly stimulated due to the organism's small size? (Or am I way off?)

In short, you are correct. You touch the skin, and that compresses mechanoreceptors, which then generate a cascading neuronal response.

As far as the actual neurons, it really depends on the type of touch. For example, a well characterized type is gentle mechanical stimuli, which can involve ALM, AVM, PLMs, and PVM, depending on the response (Will Schafer's review doi:  10.1007/s00424-014-1574-3).

Those gentle touch receptors (TRNs) are in the hypodermis, and they have specialized mechanotransduction (MeT) channels along their neurites. It's the altering of those channels that causes receptor activation and the whole downstream behavioral response (summarized from the scientific reports paper below).

So, in summary: mechanoreceptor neurons are activated, and those produce a response. By "response" I mean that those mechanoreceptor neurons activate some interneuron pathways, which in turn activate motor neurons, which make the worm do stuff.

There are many other mechanosensation mechanisms, and WormBook is the place to see a ~comprehensive review of those.

The actual mechanical mechanism/way that MeT channels are activated is a great enough question that a recent paper was published in Scientific Reports to address it. That paper is DOI:10.1038/s41598-017-12190-0 (Elmi et al. Determining the biomechanics of touch sensation in C elegans).

They introduce the paper reiterating what I summarized above.

  [...] touch sensation can be considered as a chain of events initiated
  by the spatiotemporal distribution of mechanical loads applied to the
  skin, which result in stresses that deform the skin’s surface,
  sub-layers and underlying mechanoreceptors. In response to the
  transmitted mechanical energy, the mechanoreceptors activate a
  neuronal signaling network that encodes the physical contact as
  information which we perceive as ‘touch’.

Elmi et al. set up a clever assay to look at how the worm's body changes. The body is pretty elastic (up to 16 micrometers) and there's some imperfect skin displacement because the body isn't perfectly cylindrical.

They used that data to build a preliminary model of the different layers of a worm body, and then they validated and tuned the model. It's a cool paper (with some math/physics, which from your profile it looks like you might appreciate).


Is there any difference in terms of personal healthcare between complete DNA sequencing and SNPs genotyping? There are several companies (most notably 23andMe) providing SNP genotyping for individuals claiming that there is no sense for individual in obtaining full genome sequence since only small part of it could be interpreted.

While this agrees with my understanding of the subject, I wonder whether there could be any use to perform full sequence of one's genome for means of personal health care?

The only effect I recall which affects individual's health and could not be caught by SNP genotyping is DNA methylation, but complete sequencing procedure does not detect it either, as far as I know.

This difference would have the greatest impact on treatment for cancer, in which a treatment protocol is based on genes deleted, amplified, altered in the tumor vs the reference genome for that patient.

In terms of health risks based on SNP genotypes, the data are far from complete. Sure, some level of risk can be assigned to a variant (SNP), say at certain markers within the FTO gene and risk of obesity. However, the complete list of risk alleles for this and numerous other complex traits is not fully described. Furthermore, the impact of environmental factors (EF), or lifestyle choices, on those genetic variants is only beginning to gain wider attention. For example, a risk allele may not show itself as risk until the EF, such as amount of physical activity or percent energy from dietary polyunsaturated fat, passes a certain threshold. Such gene-environment interactions are thought to contribute to the variance in traits (phenotypes), but to what degree is not known.

Added in edit 15 May 2012: Epistasis, or gene-gene interactions, also are important but far from being cataloged for humans. A situation could arise where one allele elevates risk for a certain condition, but compensatory alleles elsewhere in the genome decrease that risk. We don't know the full extent of epistasis in humans.

Thus, in terms of personal healthcare outside of something like cancer and monogenetic disorders, there may be little that is gained from genotyping or complete genome sequencing, little that is compared to other advice you already know. I carry risk alleles for certain conditions, but there is not really any advice one can give me that is specific for those alleles that I have, where that advice is different than or goes beyond general advice health care providers already have dispensed.


Questions about what a productive cough actually is and where it comes from When I'm sick with a productive cough, what is the stuff I'm coughing up, is it coming from my lungs, and if so how come it doesn't hurt a lot and trigger a violent cough like if I got even a single drop of water down the wrong hole.

When I'm sick with a productive cough, what is the stuff I'm coughing up (?)

If we're talking about a productive cough, you're most likely coughing up mucus, which is a thick (highly viscous) liquid that functions as both a lubricant to the internal behaviors of the body, as well as a defense against foreign particulates from getting too far within the body (e.g., breathing in dust through the nose and preventing it from traveling into the lungs).

  is it coming from my lungs (?)

Mucus is produced all throughout the respiratory tract by mucosae. However, since you're talking about coughing up mucus (as apposed to it running from your nose), it's probably originating from the lower respiratory tract. So, yes!, it's quite possible that the mucus is coming from your lungs.

  how come it doesn't hurt a lot and trigger a violent cough like if I got even a single drop of water down the wrong hole (?)

Hmm.. I think this is a bit more difficult to address. First off, as previously mentioned, mucus has a much higher viscosity than water does. Because of this, it could be that water more violently moves around while being coughed up, whereas mucus may remain more intact, thus causing less (increased) agitation.

It could also be that, because the trachea (the "wrong hole") isn't as accustomed to coughing as the esophagus is, then increased sensativity is experienced (relative to what's felt when coughing within the esophagus).


Horizontal gene transfer versus convergent evolution There are several often noted examples of convergent evolution (eyes, bat/bird wing evolution etc.)  How do we rule out horizontal gene transfer in these cases?

Without any molecular evidence you could infer convergent evolution if the species being compared shared a common ancestor that lacked the trait in question.

With genomic and developmental data you would measure the degree of similarity shared between the relative factors in each species. Little or no similarity indicates convergent evolution.

Horizontal gene transfer is predominantly found in bacteria. Although there are examples of limited gene transfer in eukaryotes, the donor is almost always bacteria. And there are currently no known cases of multi-gene transmission of complex networks.

It is interesting to contemplate how a full network might be transmitted horizontally. Horizontal Network Transfer would first require a mechanism for segregating the relevant genes from the rest of the genome. It would also require invasive machinery that allows the large amount of foreign genetic material to bypass the host's defense systems. Furthermore, integration of a foreign network is increasingly more difficult with the more genes you transmit due to positional and regulatory effects of the host genome. And on top of that, it is highly unlikely that a full complement of genes involved in a complex developmental process would function in any way resembling eye or wing development. These networks have been coevolving within massively complex genomic environments for hundreds of millions of years. Expressing a large network in a foreign cell would likely prove toxic.

A looser definition of HGT might include bioengineering, specifically stable transgene integration.


Genotype-Phenotype evolution distinction I understand the difference between the genotype of an organism and the phenotype of an organism, (genotype being the genetic code, phenotype being the physical expression), however I am unsure about what this figure mean when it says "Selection that takes place in the environment is based on the specific phenotype of an organism-its traits, not the underlying genotype".

(misconceptions about evolution)

I thought the genotype controlled the phenotype, so what does the figure mean exactly when its saying that natural selection isn't based on the genotype?

Thank you!

The difficulty is in the semantic. In the sentence

  Selection acts on the genotype because that is what is inherited

it is unclear what is meant by "acts on". The point that the author(s) of this misconception were probably trying to make is that what define the reproductive success of an individual is the phenotype of an individual. In other words, it is the expression of those genes that affect the probability of the genes to be passed on but it is not the actual genetic sequence itself (or at least less directly so).

Let's assume a haploid case where at a given gene, allele A means 'tall' and allele B means 'short' and let's assume that size matters in defining fitness. It is ultimately not whether an individual carry the allele A or B that matters but whether the individual is tall or short. If by some fantastically random event there is an individual with allele B that is tall then this individual will rather have the same fitness as the tall individuals and not the same fitness as the B carrier individuals.


Do males of all sexual species have Y chromosomes? I know for instance some cells are sexual, so, this got me wondering, do the males of all species that have distinct sexes have Y chromosomes?

Very short answer
No, not all males of all sexual species have Y chromosomes. You might want to have a look to the Wikipedia page on sex-determination systems.
Long answer
Diversity among the species that reproduce sexually
Not all species that have sexual reproduction have sexes. Yeasts, for example, have mating types but no sex.
Diversity among the species that have sexes
Sex is determined by both genetic and environmental factors. In some species, genetic factors are more important than environmental factors in other species it is the reverse. Species which sex is mostly determined by the genetics are said to have GSD (Genetic Sex Determination). For example, humans are GSD, as the female is XX and the male is XY. The species where sex is mostly determined by the environment are called ESD (Environmental Sex Determination). For examples, crocodiles are ESD as sex is determined by temperature. It is important to understand however that there is a whole continuum between these two extremes.
Diversity among the species that are GSD
Among the species that are GSD, some have sexual chromosomes some don't. Some have one locus  (locus=position on a chromosome) that determines the sex, some have many loci (loci=plural of locus). Humans, for example, have sexual chromosomes (X and Y) and have only one locus which determines the sex. This locus is called SRY and it codes for a protein called TDF.
Now you can split GSD with sexual chromosomes into two more categories (it is a bit more complex in reality): XY and ZW. XY are those species where the male is heterogametic (XY), while the female is homogametic (XX). In ZW systems, the male is homogametic (ZZ) and the female is heterogametic (ZW). Birds and some plants have ZW systems for example, while mammals (except "basal" mammals) and Drosophila have XY system.
See also the post What determines sex in birds?
Extra Information
Dosage Compensation
In species that have sex chromosomes, there is a difference in the number of copy of genes between the sexes. In eutherian mammals, for example, females have two copies of all the genes on the X chromosomes, while males only have one copy of most of these genes (plus a few Y chromosome genes). The set of methods to deal with this issue is called Dosage Compensation and there is also an impressive diversity dosage compensations.
Comments on this diversity of sexual systems
The diversity in a sex-determination system, dosage compensation and other things related to sex are impressive. It is even more impressive when we look at how many independent origins there are. Below are some other examples.
The Amazon molly (a fish) is a species that have sexual reproduction but there are no males. The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used. (see this article)
There are also hermaphrodites including sequential hermaphrodites (first male, then females or the opposite) in plants and animals. There are also species where populations are made of hermaphrodites and females and others where there are hermaphrodites and males (very uncommon).
In some species, the sex is determined by social factors. In clownfish, the sex is determined by comparing its own size with the size of the other fishers living in the same anemone.
In an ant species (or two species actually), males and females can both reproduce by parthenogenesis (some kind of cloning but with meiosis and cross-over) but they the meet they reproduce together and their offsprings are sterile workers. So males and females are just like two sister species that reproduce sexually to create an army to protect and feed them. See more information in this paper

Here is a nice figure from Bachtrog et al. 2014 that offers an idea of the diversity of sex determination system (thank to @rg225 for pointing out this figure).

Book suggestion
The Evolution of Sex-Determination is a great book that may interest you.


does order of genes in a chromosome matter? does the order of genes within a chromosome matter? or is the main thing that the genes are there.

so for example, our DNA is very similar to that of apes not only by the genes themselves but also by the arrangement of those genes in the chromosomes.

is the order of this arrangement significant? Or if it were shuffled around, then the functional impact would be more or less the same?

Another example, an international study in the mouse genome has revealed that virtually all mouse genes have direct counterparts in humans, i.e. humans and mice contain virtually the same set of genes. is the difference between humans and mice due primarily to the different order of the genes or to the slight differences in the genes themselves?

This question was raised from a claim here which seems to imply it does not matter.

  The chances are infinitesimal that human chr 2 were to resemble those
  of other primates at random. This is what you say in science when you
  mean 'impossible'. One simply doesn't see a segment of DNA the size of
  Chr 2A and 2B being so similar for such a length when we look at rats,
  dogs, worms or any more distantly related living thing.

is the difference between humans and mice due primarily to the
  different order of the genes or to the slight differences in the genes
  themselves?

The latter.

  This question was raised from a claim here which seems to imply it
  does not matter.

You are talking about two different things.  Gene expression is often controlled by nearby DNA sequences that don't code for protein.  Moving a gene away from the DNA that controls it can change its expression a lot, and have huge consequences on the organism.  But in many cases, you can move a whole gene, including its controlling sequences, to another place, and nothing much will happen.

People were bringing up synteny as evidence of evolutionary relatedness, not as the cause for all primates looking similar.


How are light sheet microscopy 3D images and their computed sections built up from stacks of 2D images? The iBiology Techniques video Microscopy: Dual-View Inverted Selective Plane Illumination (diSPIM) (Hari Shroff) describes light sheet microscopy and the improvement in resolution by introducing dual-view (two cameras) capability.

What's happening is that the object is moving randomly in 3D, and so for each frame, the stacks are used to generate a 3D image, and then it is de-rotated to synthesize a view in a plane fixed to the object, rather than the microscope.

Is there a simple way to understand how these image stacks are processed to obtain a smooth 3D reconstruction that can then be sectioned computationally? Is there some kind of interpolation or modeling of structure at the limit of the depth resolution?

Rather than a complete explanation, which would likely be fairly mathematical and in depth, a simpler explanation plus a reference or link to a more in-depth description might be a better way to help me get on the right track.

According to their website dispim.org they are using registration software like the ImageJ Multiview-Reconstruction Plugin. Judging from the descriptions, this plugin uses the alignment of multiple points in the different angle images (like fluorescent beads that have been introduced to the medium or the cell nuclei) by rigid transformation and then deconvolves the 3D information using the point spread functions.

Knowing your optical system (microscope lenses etc.) you can calculate how the image of a point light source would look like in the image. This can be used to reversely calculate the actual position of your light source from the image and reconstruct an image without the distortions.

From that they get a volumetric image that can be projected into any coordinate system. I recommend watching the videos on the plugin page to get an idea how this works.


Interplay of neuritic and synaptic growth Let me try to give a picture of my understanding of neuritic and synaptic growth and their interplay.

Pick two neurons in corresponding areas of opposite hemispheres which are connected by a synapse (and a rather long axon).

Both neurons were originally born at approximately the same time t during brain development in a given distance d, without already having neurites.

They necessarily have a latest common ancestor (stem cell), which doesn't have to be the same parent cell, but maybe the same grandmother or great-grandmother cell.

Now several processes start with different delays and at different speeds:

the two neurons wander away from each other
they specialize thus expressing specific "markers" on their membranes
their axons grow
their dendritic trees grow

Case 1: If neuritic growth is fast enough, the two neurons can meet and build a synapse early (recognizing each other by markers they have in common due to their common ancestor). While wandering away from each other, the neurites have to grow accordingly.

Case 2: If neuritic growth is too slow, and the neurons wander away from each other too fast, the growth of axons and dendrites at least has to be guided somehow (by glia cells or by molecule gradients?) such that later they have a chance to find each other. Finally they recognize each other by markers expressed eventually during specialization.

I could imagine that both cases do occur purely, but even that they can be somehow intermingled.

Question: Is this picture essentially correct or flawed? (A yes/no answer would suffice!)

  Furthermore, I am looking for a concise presentation of (resp. gentle
  introduction to) these processes (and maybe others?) and their
  interplay that lead to specific synaptogenesis.

Short answer
Both short and long-distance synapse formation can occur.

Background
Short-distance connections can be made between adjacent cells (Van den Pol et al, 1988). Your 'common ancestor part' is a bit obscure to me. In the end, every cell is born out of a single one :)

Long-distance connections can also be made. For example after neuroneogenesis either during development or even in the adult brain, whole neurons can migrate from their origin to a new part (Kaneko et al., 2017), or axons can grow to find a new target distally, for example after neural injury (Purves et al., 2001).

References
- Kaneko et al., J Neurochem (2017); 141(6): 835-47
- Purves et al. (eds), Neuroscience (2001), 2nd ed. Sunderland (MA): Sinauer Associates
- Van den Pol et al., J Comp Neurol (1998); 399(4): 541-60


How extensive was interbreeding among human species? I have read this article about non-Africans interbreeding with Neanderthals, Neanderthals interbreeding with Denisovans, and Asians interbreeding with Denisovans as well.

Now, I'm wondering what that even entailed.

Were populations of these species cohabitating a piece of land and completely mixing up? Would the humans of that time and place be 50/50?

Or would that just be a single act of interbreeding where an adventurous person had children with another species and those children became a part of the sapiens population?

Do the genetics suggest how much interbreeding happened or can they only say that some interbreeding happened?

Bonus, unrelated question. Does natural selection in any way suggest that mixed species offspring was better adapted to the environment and thus spread so far or can it just be a random event with little effect one way or the other that just spread regardless.

Interbreeding between H. sapiens and neandertalis was quite limited.

  Our results indicate that the amount of Neanderthal DNA in living non-Africans can be explained with maximum probability by the exchange of a single pair of individuals between the subpopulations at each 77 generations, but larger exchange frequencies are also allowed with sizeable probability.

--Extremely Rare Interbreeding Events Can Explain Neanderthal DNA in Living Humans

  ... the interbreeding success rate between humans and Neanderthals was found to be below 2% (Fig. 2, Table 1, Fig. S1, and Table S1). Under demographic scenario A (Table 1), which is based on the most realistic demographic parameters, we estimate this interbreeding success to be even well below 1% (0.51%, mode of black curve in Fig. 2; 95% confidence interval: 0.33–0.89%). ...  If we assume that both species interacted for 10,000 y during the range expansion of modern humans (11), successful admixtures between Neanderthals and humans would have occurred, on average, only once every 23–50 y over the whole hybrid zone to produce introgression levels of 1–3%, which shows that they were extremely rare events.

--Strong reproductive isolation between humans and Neanderthals inferred from observed patterns of introgression

Note that this technically doesn't touch on "interbreeding" but rather addresses successful interbreeding; sterile individuals won't be detected in this approach, and even sub-fertile individuals (whose lineages died out) will be underrepresented.

We have strong evidence that male progeny of sapiens/neandertalis crosses were either sterile or extremely sub-fertile:

  These results suggest that part of the reduction in Neandertal ancestry near genes is due to Neandertal alleles that reduced fertility in males when moved to a modern human genetic background.

--The landscape of Neandertal ancestry in present-day humans

And even apart from that, there's good evidence that hybrids were less "fit" (in evolutionary terms) than either parent:

  After hybridization, on average, selection appears to have removed Neanderthal alleles from the human population. ...  We find that the bulk of purifying selection against Neanderthal ancestry is best understood as acting on many weakly deleterious alleles. We propose that the majority of these alleles were effectively neutral-and segregating at high frequency-in Neanderthals, but became selected against after entering human populations of much larger effective size. While individually of small effect, these alleles potentially imposed a heavy genetic load on the early-generation human-Neanderthal hybrids.

--The Strength of Selection against Neanderthal Introgression

So it's very likely that the rate of interbreeding, per se, must have been higher than the roughly once-per-generation rate that can be inferred from genome analysis, but most of the hybrids were sterile, or poorly adapted.  Of course, this is exactly what you'd expect from interspecies hybridization; the number of successful sapiens/neandertal hybrids through the millennia of their interactions was probably lower than the number of fertile mules in the past few hundred years.


(Web)app to search metabolic/signalling pathways I'm looking for an application where you can find pathways by selecting a chemical occurring in it.

So, for example,
selecting 6-phosphogluconolactone brings up the pentose phosphate pathway or any other where it occurs as an intermediate or product.

Same could be possible for endocrine or any other signalling. The target organism is human.

Is there anything like this in existence?

KEGG  http://www.genome.jp/kegg/kegg2.html

GLAMM http://glamm.lbl.gov/

I had to truncate to gluconolactone to make the search work in both cases.


Average masses of atoms / amino acids I recognized that there is some controversy about the average mass of amino acid masses in different online sources.
Expasy and Wikipedia report the same masses, but UWPR and Mascot report different ones. However, the monoisotopic masses are always the same.
Does anyone know where these differences come from or where to find a definite source for the masses?
In the end, the question boils down to the average masses of single atoms. The UWPR names UniMod as a source for their calculation. What different ways of calculation for average mass exist and who defined them?

I guess confusion comes from either:

Inclusion vs exclusion of H2O (free AA vs in chain)

Averaging with
equal weight between all AA vs weight of their relative
occurrence

Does this help?


Could plants do photosynthesis at moonlight? Related to this and this but not exactly same; could plants do photosynthesis at moonlight or more dim-intensity light?

Of course they can and do, except in total darkness (spectroscopically, only bands in the far red and in the blue spectra matter - blanking these affects 'total darkness').

In photosynhesis a photon is adsorbed by Photosystem II to break down water into oxygen and protons in solution. Another photon must be adsorbed by Photosystem ! to power the enzymatic machinery that make NADPH and ATP that power the Calvin cycle.

We know the sun powers photosynthesis effectively. The sun produces somewhat less than 100,000 lux (lumen per square meter). Moonlight is one one millionth of this or about 0.1 lux. One lux is something like 10^15 photons per second (per square meter); so moonlight provides something approaching 10^14 photons per second to drive photosynthesis. The spectrum of moonlight is not markedly different from that of sunlight. So, moonlight provides an ample number of photons per second per square meter to power photosynthesis.

The trouble, though, is that the rate of photosynthesis is low compared to the rate of metabolism in the rest of the plant. So, in effect, the plant gives off carbon dioxide by night and oxygen by day even though both gasses are being emitted all the time.

EDIT (per request) some references:

Photosynthesis
Respiration
Moonlight lux versus sunlight
Photons per second in a lumen


Is it firmly established, that mutations are sufficient for cancer? It is evident for scientists, that all cancer cells have some mutated genes. Say mutations in general.

But this evidence means necessary condition.

But what about sufficient conditions?

Is it possible, that mutations are necessary but insufficient for cancer?

I.e. may be other factors exist, which are probably more important?

Acquiring mutations (more than one) are the necessary (and sufficient) steps on the way to cancer. The current opinion is that cells need "multiple hits" to fully transform into a cancer cell. It is also called the Knudson hypothesis, the original paper is here.

For example melanocytes (the pigment cells in the body) which acquire the activating BRAF V600E mutation (which is an important step in getting a melanoma cell, this mutation is found in about 70% of all melanoma) is not enough to transform the cell. Other mutations are necessary to do this.

Among the things important for cells to become malignant are to escape the apoptosis mechanisms of the cells and also the immune system. Both are linked to the mutation, inactivation or epigenetic silencing of genes, so I would say genes are the key to cancer.

For further readings these two articles should be interesting:

Are oncogenes sufficient to cause human cancer?
Significance of multiple mutations in cancer


Consequences of abnormal blood pressure unrelated to cardiac output? A question from Kaplan's MCAT Biology Review asks:

In bacterial sepsis (overwhelming bloodstream infection), a number of capillary beds throughout the body open simultaneously. What effect would this have on the blood pressure? Besides the risk of infection, why might sepsis be dangerous for the heart?

The answer is:

Opening up more capillary beds (which are in parallel) will decrease the overall resistance of the circuit. The cardiac output will therefore increase in an attempt to maintain constant blood pressure. This is a risk to the heart because the increased demand on the heart can eventually tire it, leading to a heart attack or a precipitous drop in blood pressure.

I had always viewed blood pressure as a means to achieve appropriate blood flow, and a system with lower resistance would simply operate with lower pressure (via Ohm's Law). However, the answer implies that maintaining normal blood pressure is a goal in itself, such that the body would naturally raise cardiac output to dangerous levels in order to maintain it.
Can someone help explain:

Does blood pressure play a role in blood circulation that makes it more important than just a means towards appropriate cardiac output?

What are health consequences of abnormal blood pressure unrelated to cardiac output from a biochemical perspective? If I search for "abnormal blood pressure" I'll get broad symptoms like "dizziness" that don't explain its effect on different tissues that cause the symptoms.

Blood pressure, as you noted, is just a means to an end: the flow of blood through tissues. The trouble is, many of the body's regulatory systems use blood pressure (rather than flow) as an index of cardiovascular status. A key example is the baroreceptor system, which senses changes in blood pressure and tries to correct them by effects on the heart, blood vessels and kidneys.
In sepsis with decreased blood pressure, baroreceptor firing increases in an attempt to increase cardiac output $^1$. This increased demand on the heart can be counterproductive and cause the heart to fail. But this phenomenon is not unique to sepsis. There are many other conditions where a hyperdynamic circulation leads to heart failure: such as anaemia, thyrotoxicosis and thiamine deficiency $^2$.
All of these examples highlight a basic principle in pathophysiology: adaptations can sometimes turn maladaptive.
Note: The effects of sepsis on the cardiovascular system are complex and go beyond vasodilation. For more details, you could read a textbook of pathophysiology/medicine. Or go through any of the review articles on this topic, such as the one by Lelubre & Vincent $^3$.

References:

Gattinoni L, Carlesso E. Supporting hemodynamics: what should we target? What treatments should we use? Crit Care [Internet]. 2013 Mar 12 [cited 2020 Aug 24]:17(Suppl 1):Article S4 [8 p.]. Available from: https://ccforum.biomedcentral.com/articles/10.1186/cc11502
Mehta PA, Dubrey SW. High output heart failure. QJM. 2009 Apr;102(4):235–41. https://doi.org/10.1093/qjmed/hcn147
Lelubre C, Vincent J. Mechanisms and treatment of organ failure in sepsis. Nat Rev Nephrol. 2018;147(7):417–27. https://doi.org/10.1038/s41581-018-0005-7


At small axon diameters (<1 µm), why does myelination not increase neuronal conduction velocity? As per the diagram below (and other graphs available online), why do unmyelinated fibres have a higher conduction velocity than myelinated fibres when the axon diameter is less than around 1 µm?

Graphs like these are based on a complete cross-sectional area. Myelination adds thickness, so if you want to add myelin outside and keep the same diameter, you have to have a smaller lumen inside the axon.
As you can see in the "unmyelinated" plot versus diameter, smaller fibers have lower conduction velocity. Since the benefits of cross-sectional area are most important at small diameters (because the velocity changes with the squart root of diameter), for small diameter axons you end up losing more from losing internal area than you gain from adding external insulation.
If you keep the internal diameter the same and just add myelin, you will always increase the conduction velocity, but the total diameter including the myelin won't be the same anymore.


The drawing of genetic crosses I'm preparing myself for the GRE. The quantitative stuff has all been going well. I'm aiming for a geology grad scheme. In the event of having to take subject specific tests, I'm teaching myself a few "out there" things in science.

I'm going through biology and looking at genetics for the first time since high school(!)

I just had a question here really to do with genetic crosses. I've been looking at Mendel and the experiments he carried out. One specifically looking at short pea plants. I'm looking at an example where all F1 plants are tall (F1 being the generation of plants). In the example the F2 generation are created in selfing the F1 plants.

Now, I've got my head around the science involved, but I just basically wondered if any biologists here could show me how to make a genetic cross of F2 in order that I could show the genotypes and phenotypes of the offspring.

This isn't necessary but I feel as though it would help my understanding.

At the moment I'm drawing a two by two grid. I suppose I need to fill it with the appropriate alleles?

Thanks.

The cross you're studying is Mendel's monohybrid cross. Which looks something like this.

Now here, the genotype of F1 gen plants is Tt.

To draw this cross, proceed exactly like you decided. Draw the 2/2 grid and cross the alleles Tt x Tt

Your cross should look like this (ignore the plant drawings):

(Source: classes.midlandstech.com)


Is it possible to live without health problems sleeping one day and not the other? Basically, I want to know if it would be humanely possible to sleep one day, skip the next, sleep, skip, sleep, skip, etc, with a 8 hour sleep time.

If you need any extra information, let me know.

I'm not aware of any study testing this hypothesis. I would surmise that adverse health effects are likely because the circadian clock operates on a 24-hour time frame, and because lack of sleep for ~40 hours every second day will alter hormone, cytokine and other measures to levels not normally seen in 8-hour sleep/16-hour wake cycle.


How Do Acid and Base Loving Plants Get Enough PO4? Acidic and Basic soils experience phosphate sequestration through binding with either calcium, aluminum, or iron. How do plant that thrive in acidic and basic soils obtain the necessary phosphate? Blueberries are an example that I particularly enjoy.

Thanks to the University of Hawaii for posting this picture.

Fixation of phosphorous occurs when the chemical equations tip in favour of less soluble compounds. Plants are able to absorb Orthophosphate ions, such as H2PO4- and HPO42-.

Orthophosphate is most available to plants at pH values near neutrality. It is believed that in relatively acidic soils, orthophosphate ions are precipitated or sorbed by species of Al(III) and Fe(III). In alkaline soils, orthophosphate may react with calcium carbonate to form relatively insoluble hydroxyapatite:

3HPO42- + 5CaCo3(s) + 2H2O -> Ca5(PO4)3(OH)(s) +5HCO3- + OH-

Environmental Chemistry, Seventh Edition -Stanley E. Manahan
This does tend to make it more difficult for plants to obtain their phosphorous when it is stuck to something that they cannot absorb, but it is not hopeless. These equations are equilibria, so they can be made to go both directions by adding or removing reagents from each side.

The plants will pull from the left side of the equations by removing the orthophosphate ions. More will be released to maintain the equilibrium.
In acidic or basic environments, rainwater will serve as a base or acid to push the equations from the right.
Decaying organic matter releases orthophosphates that the plant can absorb.

In this way, plants living in acidic or basic environments would still obtain enough phosphorous.


Reasons for a flower type to consume water faster than another? This is an easy experiment where you put a white flower into a recipient filled with water and liquid watercolor, so that the flower gets dyed.

While doing this experiment for different types of flowers, and assuming equal ambient conditions, what would be the most important characteristics  (e.g. flower size, petal length, stem thickness, number of petals...) and the biological reasons for certain flower type to consume water (and get itself dyed) faster than another? (e.g., does a thicker stem mean the xylem is stronger?)

More specifically, I'm interested in comparing a rose like this and a carnation (like the one shown in comments) as an example to the answer.

(Note: I couldn't show a carnation sample image due to my reputation being lower than 10, but I'll update it as soon as I can).

Don't forget to consider the 'engineering' of the plant, as brought about by evolutionary history. Some plants will build fewer openings in their leaves ('stomata'); others use a strategy that allows them to only open these at night (see 'C4 photosynthesis') or CAM (Crassulacean Acid Metabolism) photosynthesis.


Why does uniprot sometimes not label single-pass transmembrane proteins as "anchors"? Currently, section 3a) of unitprot TRANSMEM reference page divides single-pass transmembrane proteins into 4 types: I, II, III, IV. I is not explicitly labelled as an "anchor" whereas the others are. What criteria need to be made for a single-pass protein not to be classed as an anchor?

A membrane anchor is close to the end (N-terminus or C-terminus) of a protein. For "Single-pass type I membrane proteins" the transmembrane region is not necessarily close to N- or C-terminus, which is why single-pass type I membrane domain are not labeled as anchors.

Instead, relevant entries usually have a signal peptide annotated.

Note that we have replaced the example for single-pass type I membrane protein by http://www.uniprot.org/uniprot/P14778#subcellular_location which is more relevant (the modified version of the documentation will be available with release 2016_01).


What triggers the migration of robins? I live in central Massachusetts, and have begun seeing robins, as we generally do in early March. The temperature is well below normal, though, and three feet of snow are covering the still-frozen ground from which they usually feed. We were expecting them to arrive late, when conditions would seem more conducive to survival.

What triggers their migration process?

I don't know about the specific cues that American robins use for migration. This species is also both a short range (e.g. between states or to lower altitudes) and long range migrant (e.g. Florida & Mexico), so the cues that they use can probably differ between overwintering populations. There are also year-round populations of robins in the US, but probably not many (if any) in Massachusetts. There are however at least two papers that show that American robins are arriving earlier and earlier, at least in Wisconsin and Colorado (Inouye et al, 2000 and Jones et al, 2012). The studies find that arrivals dates have shifted ~13 days earlier between 1990 and 2010 in Wisconsin and 14 days earlier between 1981 and 2000 in Colorado. The study from Colorado also shows that the first date of bare ground has not changed, so snow melt has not changed over the time period. As a consequence, the interval between arrival and bare ground has grown by 18 days. This could indicate a phenological mismatch between spring arrival and the resources used by robins, and your observations seems to agree with this pattern.

This are at least some comments and a couple of papers that could be useful for your question. Sorry I cannot say more about the actual cues used for their migration.


Modern Whales with Vestigial legs Myth? Is it a myth that modern whales have been found with hind legs sticking out of their sides and full formed tibias, fibias, and toe bones? I keep finding assertions, but no citations. For example, the wikipedia page has no citation for it.

http://en.wikipedia.org/wiki/Whales#Appendages

The link you give doesn't mention limbs sticking out of the body wall, but only vestigial hind limb elements. Many whales do retain pelves and femora, as this page at the Bergen Museum shows. Given the variation in limb development across vertebrates, it would not be surprising to find more distal elements (but I would be very surprised if they extended past the body wall).


Can elements of one's environment act directly as hormones? Can pollution and things in an organism's environment serve as hormones?

A hormone is defined as "a chemical released by a cell or a gland in one part of the body that sends out messages that affect cells in other parts of the organism" (I'm just taking Wikipedia definition).

Hormones work by binding to specific receptors present on their target cells so, if there is something in the environment that mimics the hormone, by binding to the same receptor they can act as hormones: these substances are called xenohormones and can often act as endocrine disruptors compounds (EDC), by acting on various organs in the body.

Probably the most known xenohormones are xenoestrogens that are been studied as possibly harmful for human health (e.g. linked to breast cancer), and as an environmental hazards, as they can, for instance, cause reproductive problems in fish.

Xenohormones are not necessarily bad, though. Some analogs of human hormones are used in therapy, having being synthesised specifically, for instance, to have higher potency then their natural counterparts.


How to get the average number of pairwise differences among populations? I have genetic data in .structure and .vcf format (and can easily reach other formats with PGDSpider). The population of interest is structured and I would like to calculate the average number of pairwise differences (over a given window) between any pair of populations.

Is there an existing tool that would do it?

With relation to the other bioconductor question I would point you towards these packages;

VariantAnnotation: Provides functionality for reading and manipulating vcf files.
GenomicRanges: Provides functionality for creating genome intervals. Also provides overlap functions for calculating overlaps between various ranges.
rtracklayer: Allows you to easily change formats between different biological file formats.
AnnotationHub: Makes many common and uncommon annotation files available in the R terminal in various formats such as TxDb, OrgDb etc. etc.

Here's a tutorial very similar to what you are asking for. It utilises some of the packages mentioned above. Principally, AnnotationHub, GenomicRanges and VariantAnnotation.

If you want the manual of these packages, they are available on the linked pages.


Sperm formation - Frequent Ejaculations I have visited various authenticated websites and other materials and learnt that a complete sperm development takes approximately 64 days.

My doubts :

If sperm truly takes 64 days to develop, how can a man ejaculate multiple times (e.g., 4-5) in a day and still have sperm come out each time? Why don't all the sperm come out at once? And each time he ejaculates, the sperm are complete (i.e., the "head" and "tail" portions are always included), right?
Does frequent ejaculation, then, reduce the sperm count of each subsequent ejaculation? If so, do the sperms remain depleted for extended periods (i.e., 64 days), or are they replaced more regularly? At what rate are they replaced?

The arithmetic of human sperm
A young, healthy man produces about 1000 sperms every second, which comes to about 90 million per day [1]. These sperms are stored in the epididymis and ductus deferens until ejaculation. With several days of storage, the number can easily become big enough to allow for multiple ejaculations on the same day.
The maturation period of 64 days does not matter here, because sperms form and mature asynchronously [1]. While one spermatogonium is on day 1 of its life, another is on day 2, another on day 3 and so on. Only those sperms that are mature are released from the testes (NOT directly in semen, but into the epididymis for storage).
Does semen normally contain sperm with abnormal morphology?
Yes. Even men in whom 96% of the ejaculated sperms have abnormal morphology can successfully conceive [2].
What happens on ejaculating repeatedly?
This has already been assessed in several studies [3–5]. Overall, the results have been that with repeated ejaculation in quick succession,

Semen volume decreases.
Sperm count decreases (pointing to sperm depletion) but not to zero.
The percentage of sperms with abnormal morphology remains unchanged.

Hope that answers your questions.
References

Mesiano S, Jones EE. The male reproductive system. In: Boron WF, Boulpaep EF, editors. Medical physiology. 3rd ed. Philadelphia: Elsevier; c2017. p 1092–1107.
Cooper TG, Noonan E, von Eckardstein S, et al. World Health Organization reference values for human semen characteristics. Human Reproduction Update. 2010 May–Jun;16(3):231–45. doi: 10.1093/humupd/dmp048
Oldereid NB, Gordeladze JO, Kirkhus B, Purvis K. Human sperm characteristics during frequent ejaculation. J Reprod Fertil. 1984 May;71(1):135–140. doi: 10.1530/jrf.0.0710135
Zvĕrina J, Pondĕlícková J. Changes in seminal parameters of ejaculates after repeated ejaculation. Andrologia. 1988 Jan–Feb;20(1):52–4. doi: 10.1111/j.1439-0272.1988.tb02363.x
Mayorga-Torres JM, Agarwal A, Roychoudhury S, et al. Can a short term of repeated ejaculations affect seminal parameters? J Reprod Infertil. 2016 Jul-Sep;17(3):177-83. http://www.jri.ir/article/674


Are "sympathetic nerves" the same as "cardiopulmonary splanchnic" nerves? I've gathered from a number of sources (e.g., Patel (2015), Wikipedia, and here) that the sympathetic nerves leaving the sympathetic trunk to innervate the heart and lungs are called "cardiopulmonary splanchnic nerves".
However, I've noticed that both the 14th and 15th edition of Tortora & Derrickson's A&P textbook seem to suggest that these nerves are simply called "sympathetic nerves," even though they make reference to abdominopelvic and adrenal splanchnic nerves more specifically.  See below from Tortora & Derrickson (2013):

...Then, the axons of the postganglionic neurons leave the trunk by forming sympathetic nerves that extend to visceral effectors in the thoracic cavity (Figure 15.4). Sympathetic nerves provide sympathetic innervation to the heart and lungs.

Here are subsets of images from Patel (2015) [LEFT] vs Tortora & Derrickson (2013) [RIGHT] (my emphasis):

My question: Are "Sympathetic nerves" the same as "cardiopulmonary splanchnic" nerves?

Are these names interchangeable? I can't find further evidence supporting Tortora and Derrickson's usage of this phrase in such a specific manner to refer to postganglionic neurons leaving the trunk to innervate the heart and lungs. Are they acting rogue? Are they simplifying? Any insight would be appreciated.

Cited works:
Patel, T. R. 2015. "Chapter 36 - Anatomy of the Sympathetic Nervous System." Pages 495-506 in Tubbs, R.S., Rizk, E., Shoja, M.M., Loukas, M., Barbaro, N. and Spinner, R.J. eds. Nerves and Nerve Injuries: Vol 1: History, Embryology, Anatomy, Imaging, and Diagnostics. Academic Press.
 Tortora, G. J. and B. Derrickson. 2013. Principles of anatomy and physiology, 14th edition. John Wiley & sons, Inc.

You might consider cross-posting to SE Medical sciences who know more about this stuff.

I think that they are simply using a more general term than other authors. In the same way, most people call crabs crabs, but some people might occasionally refer to them as crustaceans.

Based on wikipedia, it seems that cardiopulmonary splanchnic nerves are a subset of sympathetic nerves. The sympathetic nervous system innervates a large number of organ systems of the body (see image), such that the cardiopulmonary splanchnic nerves are simply the sympathetic nerves that innervate the heart and lungs.

Looking further at the wikipedia for splanchnic nerves, it seems that this is a technical term relating to the fashion in which organs are innervated by the sympathetic nervous system; e.g. in my crude understanding they are organ hookups to the sympathetic nervous system.

In other words, all cardiopulmonary splanchnic nerves are sympathetic nerves, but most sympathetic nerves are not cardiopulmonary splanchnic nerves.


awakening effects of light I tried reading by light from a neighbouring room and felt sleepier than if my own lights were on.

Is there a formula for the intensity of light vs physiological preparation for sleep(calcium, melatonin)? Or is there a threshold intensity below which the body goes to "sleepy mode"?

I don't believe either is the reason. Back in the day of early man, the different intensity levels of light was used as a signal to our body's "master clock" to tell us when it was time to go to sleep. So to simply put it, when exposed to less intense light, such as artificial light, its picked up as the dimmer, less intense, light akin to when historically we would be getting ready to go to sleep.


Why is ATP produced in photosynthesis used to synthesize glucose? In photosynthesis ATP is produced in light-dependent reactions only to go to the Calvin cycle to be turned into glucose to make ATP during respiration:

Why isn't this ATP just directly released into the cell? Is there a benefit to using the ATP to make glucose? Also, ATP can be made in the chloroplasts with cellular respiration? What happens to this ATP?

As far as I can understand your question, you wish to know why a plant cell consumes ATP to produce glucose when it can directly use the ATP as an energy molecule.

ATP is an energy currency and is required in different biochemical pathways. However, it is not a good energy storage molecule. Following are the reasons why production of an energy molecule such as glucose is essential:

Not all parts of the plant are photosynthetic. These non-photosynthetic pzrts need an alternate source of energy. Since ATP is unstable, it cannot be transported to different parts of the plant without degradation.
Since photosynthesis cannot happen in the dark, the plants would require some energy molecule that can be utilized later on, in the dark conditions.
Chloroplasts themselves require ATP in the dark conditions. They express an ATP-ADP translocase that actually imports ATP from the cytosol while pumping out ADP+Pi (See this review).
Plants also need energy storage for seeds. This storage is usually in the form of starch (a polymer of glucose).
Glucose is required for synthesis of cellulose which makes the cell wall of plants.
The glycolytic pathway (including pentose phosphate pathway) produces important metabolites such as ribose (in the form of PRPP, which is important for nucleotide synthesis), pyruvate (which is used to synthesize alanine) etc.
Glucose and some glycolytic metabolites (such as glycerol) also serve as osmolytes i.e. they maintain osmotic pressure in the cell.

Basically, points 4-7 convey that Calvin-Benson cycle not only produces sugar but what it actually does is fix inorganic carbon (as CO2) to organic form (in the form of sugar). So, most (practically all) of the carbon that a photosynthetic plant has, comes from this carbon fixation process and that's how plants are photoautotrophic.


amount of tRNA and its extra arm How much of the total RNAs is tRNA? Some say 15% and some 20%. Those percentages came from my different teachers. Which is correct? And what are the functions of the extra arm (variable loop) of tRNA? My teacher said it was just for classification but an international textbook says its function is unknown.

With respect to at least two sources I could find, tRNA is commonly reported as encompassing 15% total RNA in both rapidly-dividing mammalian cells such as HeLa, and in S. cerevisiae (1, 2). To give you an interesting tool to look it up in the same way I did, I used Harvards' Bionumbers webpage to search tRNA.

As for the function of the variable loop, it would seem that it serves to stabilize the tRNA overall structure through three-base interactions, and somehow interfaces with the type II tRNA synthetase (3). I'll try to find more on this interaction.


Are there knots in DNA? This question may sound silly.
How does it come that the DNA molecules are not totally entangled with time in the cell ? If I take long strings in a box and shake it, that would create knots, and I wouldn't be able to easily isolate each string apart.

But during mitoses, the chromosomes are totally isolated from each others while otherwise, the DNA is freely floating in the nucleus.

I think a key factor is that DNA molecules are not passive bits of string that are left to move freely (which is what causes knots in string-like things that are left alone too long).
For one thing the DNA molecule is an active part of the cell metabolism, as it is constantly being transcribed (to generate RNA and proteins) or copied or corrected and so on. And as part of its role in metabolism the DNA molecule is closely associated with RNA molecules, proteins and specifically proteins that the DNA is wrapped around called "histones". The Wikipedia page for "Chromatin" (what chromosomes are made of, basically) describes various aspects of this organization, including:

That DNA which codes genes that are actively transcribed ("turned on") is more loosely packaged and associated with RNA polymerases (referred to as euchromatin) while that DNA which codes inactive genes ("turned off") is more condensed and associated with structural proteins (heterochromatin).

So DNA is constantly being manipulated by all kinds of proteins and enzymes that affect its shape and position in space; it isn't just lying there. And insofar as it might get into knots, that would likely be part of the manipulations of the enzymes and proteins, or would fairly easily be dealt with by them. This doesn't mean DNA doesn't have knots however, in fact it appears it very much can:
DNA AND KNOT THEORY (from The Institute for Environmental Modelling at the University of Tennessee)

Conclusions: Principles of topology give cell biologists a quantitative, powerful, and invariant way to measure properties of DNA. Principles of knot theory have helped elucidate the mechanisms by which enzymes unpack DNA. Additionally, topological methods have been influential in determining the left handed winding of DNA around histones. Measuring changes in crossing number have also been instrumental in understanding the termination of DNA replication and the role of enzymes in recombination.

(note this paper looks at DNA in E.coli, which does not organize its DNA in chromatin the way Eukaryotes do).
Untangling DNA (from the Nature blog CreatureCast, 2013)
This link includes a video about topoisomerases, enzymes also referred to in the previous link that unentangle DNA.
A Monte Carlo Study of Knots in Long Double-Stranded DNA Chains (PLOS Computational Biology, 2016)
Quote from the abstract:

Even though our coarse-grained model is only based on experimental knotting probabilities of short DNA strands, it reproduces the correct persistence length of DNA. This indicates that knots are not only a fine gauge for structural properties, but a promising tool for the design of polymer models.

The active site of the SET domain is constructed on a knot (Nature Structural Biology, 200)
A knot or not a knot? SETting the record ‘straight’ on proteins (Computational Biology and Chemistry, 2003)
These papers discuss potential knots within a histone protein, not DNA, but illustrates that topology and knots can be important in macromolecules:

A knot within the SET domain helps form the methyltransferase active site, where AdoHcy binds and lysine methylation is likely to occur.
A novel knot found in the SET domain is examined in the light of five recent crystal structures and their descriptions in the literature. Using the algorithm of Taylor it was established that the backbone chain does not form a true knot.

Discovery of a predicted DNA knot substantiates a model for site-specific recombination (Science, 1985)
This link is a bit painful to read (and from 1985 so I don't know if it was superseded, but it has over 200 citations) so I will leave it at the title.
And finally this article, which I looked at last but probably should have looked at first because the first sentence of the abstract literally answers your question :
Direct observation of DNA knots using a solid-state nanopore (Nature Nanotechnology, 2016)

Long DNA molecules can self-entangle into knots. Experimental techniques for observing such DNA knots (primarily gel electrophoresis) are limited to bulk methods and circular molecules below 10 kilobase pairs in length. Here, we show that solid-state nanopores can be used to directly observe individual knots in both linear and circular single DNA molecules of arbitrary length.


Is pulse rate measurable in the capillary bed and venous vasculature? Pulse rate is easily felt when gently pressing the arteries in the wrist or neck region (Fig. 1).

Fig. 1. Feeling the pulse at the radial artery. Source: Wikipedia

Arteries supply the thin vasculature in the capillary bed where the blood flow encounters a large increase in resistance due to the narrow vasculature and blood flow is reduced, albeit the pressure may still be relatively high. The capillary bed, in turn, feeds the venous system (Fig. 2), characterized by a low blood pressure and relatively slow and continuous blood flow. This steady, slow blood flow is apparent during blood sampling procedures from the veins in the arm, where I have never noticed any pulsatile flow by visual observation (anecdotal evidence, but quite representative I'm sure).

Fig. 2. Blood vessels. Source: Aruba trial.

Is there an observable/measurable pulse in the capillaries and veins, or is blood flow continuous in these vessels?

PS. This question was re-formulated based on a deleted question posted by @laggingreflex and credits go to OP.

In the capillary bed? Absolutely! In the venous return? Depends!

I had to build one of these for class. In short: you can tell how oxygenated the blood is by its color, but you have to correct for how much blood there is: The dilation of the arterioles and capillaries with the heartbeat increases the size of the area being measured, and changes all sorts of properties including conductance. There's a neat heartbeat monitoring method method that involves putting two electrodes on your arm, one at the wrist and one at the elbow, and measuring the increase in conductivity every time your heart beats and your arm swells.

Depending on heart rate and all sorts of other things, there's not usually a detectable heartbeat in the veins right outside the heart (see the CVP, which is pretty much flat). However, the jugular venous pressure is the pressure of the internal jugular vein that drains the head, and that has heartbeat oscillations (not one-to-one, there are "echoes" and other weirdnesses because it's almost connected to the heart. See here for more).

In sum: The capillary bed absolutely swells and contracts with each heartbeat, but in the veins blood usually just oozes along. There are a couple exceptions but mostly they're silent.

(The Korotkoff sounds you're talking about are a fluid dynamics thing. When the veins are regular-sized they're wide enough to permit laminar flow(where all the blood moves in a straight line), which is smooth but still pulsatile. Like these guys the blood flow starts and stops but is in sync with itself. When you compress them you increase the Reynolds number and you get turbulent flow, which you can hear because it's making noise.)


Plasmid specific DNA degradation I'm interested if there is a way to degrade the plasmid DNA inside an E.Coli cell specifically so that the method does no harm to the chromosomal DNA. First I was thinking about restriction endonucleases but I'm afraid that;

it isn't specific enough and kills the cell
or it does nothing, because the E.Coli methylates the plasmid DNA too

My second thought was the CRISPR/Cas9 system but it sounds like an overcomplication of the problem. Any simpler ideas? (For eg. specific enzymes)

EDIT: the main idea is to create more competent E.Coli cells with directed evolution. Currently this is just a thought experiment, so there is no specific plasmid sequence. In details; I would transform the plasmid into the cells, then do the selection part with an antibiotic and let them grow, then transfer the cells into a medium where there is no antibiotic and add IPTG to induce the plasmid-DNA-hydrolase enzyme, then maybe an other selection part could be performed to remove the cells which still contain the plasmid (for example with FACS if there is a GFP gene on the plasmid), then make the cells competent again with CaCl2 and do this whole process over and over again.

traditional method to remove a plasmid from E. Coli is to grow the cells with Etidium bromide.

http://vlab.amrita.edu/?sub=3&brch=186&sim=1097&cnt=1


What is a lethal dose of THC? With the oil form of THC being stronger then ever. What would happen if one was to take a stomach full of THC oil?

According to the abstract from this paper, the intragastric LD50 of $\Delta^9THC$ (tetrahydrocannabinol) in sesame oil using Fischer rats was 1270 mg/kg. Assuming rats and humans are identical (they're not), for an average-sized adult human weighing 70 kg (~155 lb.), the median lethal dose would be 88.9 grams, or about 3.1 oz.

Keep in mind that's 3.1 oz. of pure THC. That's a lot of weed.


How does vitamin A deficiency arise? How does vitamin A deficiency arise?

I am living in a "developed" country, so excuse me if I miss some facts
that are real, and threatening, in other parts of our world.

I heard about https://en.wikipedia.org/wiki/Vitamin_A_deficiency ,
but looking at what foodstuff contains vitamin A or precursors,
I'm at loss how anyone can suffer from vitamin A deficiency.

Obviously, I'm lacking some information here.

One thing that looks particularly misleading is when you are
presented with vitamin A contents of foods, neglecting precursors
like carotenoids that can be easily converted to vitamin A as needed.

As a (sometimes misleading) rule of thumb, I was thinking that most
yellow or orange looking food was prone to contain vitamin A or some
of its precursors.

The WHO report "Global
 prevalence of
vitamin A deficiency
in populations
 at risk
1995–2005" (page 12 of 68) puts it like this:

  Where animal source or fortified foods are minimally consumed, dietary
  adequacy must rely heavily on foods providing beta-carotene. However,
  while nutritious in many ways, a diet with modest amounts of
  vegetables and fruits as the sole source of vitamin A may not deliver
  adequate amounts, based on an intestinal carotenoid-to-retinol
  conversion ratio of 12:1 (2)  This ratio reflects a conversion
  efficiency that is about half that previously thought, leading to
  greater appreciation for why VAD may coexist in cultures that heavily
  depend on vegetables and fruits as their sole or main dietary source
  of vitamin A.

  Usually, VAD develops in an environment of ecological, social and
  economical deprivation, in which a chronically deficient dietary
  intake of vitamin A coexists with severe infections, such as measles,
  and frequent infections causing diarrhoea and respiratory diseases
  that can lower intake through depressed appetite and absorption, and
  deplete body stores of vitamin A through excessive metabolism and
  excretion (3, 4). The consequent “synergism” can result in the body’s
  liver stores becoming depleted and peripheral tissue and serum retinol
  concentrations decreasing to deficient levels, raising the risks of
  xerophthalmia, further infection, other VADD and mortality.

Just as a side note: green leaves contain heaps of beta-carotenes as well!


How can an albatross stay airborne for months? Albatrosses, of the biological family Diomedeidae, are large seabirds allied to the procellariids, storm-petrels and diving-petrels in the order Procellariiformes. They range widely in the Southern Ocean and the North Pacific.

  Short tailed Albatross , Source: Wikipedia, DOR 16/09/2012

I read that albatrosses can stay airborne for up to a decade and that they can cycle brain activity between hemispheres. How do they do this feat, and how did they evolve this ability?

Possible points to consider:
immune system, predation, cycling solar output, weather, seasons...

I'm not really inside the field but few weeks ago I noticed a Plos One article that was dealing with this. Indeed albatross can fly for thousands of miles and this is possible at no mechanical cost, because they use a dynamic way of flight that takes the energy from wind (dynamic soaring) (ref-1). Their muscle-skeletal system further evolved so that no energy is required to keep open the wing.

In addition, when foraging, they minimize diving and landing activities because they follow Killer Whales, so that food is always in proximity. (ref-2) Very smart birds.

ref-1 Sachs et al., Plos One 2012

ref-2 Sakamato et al., Plos One 2009 both references are open access.