Trauma, blood loss and thirst Back story.

Watched an episode of Arctic Air, (season three episode six), where they are practicing and hoping to become a licensed search and rescue airline.

Anyhow; two hikers gets attacked by a grizzly bear and whilst one get killed the other manages to throw himself off a cliff and ending up with his leg pinched under a rock. He also has big lacerations on his chest from the grizzly. Finally he manages to send a distress signal.

Though not licensed a team travels out to asses the situation. As they find the wounded climber they start to help. First they clean the lacerations by pouring alcohol over them, and then lay some bandages on top. After a while the injured man complains he is thirsty, and they give him water.

TLDR;/Question If I recall correctly one should not give water to a trauma patient. They can have internal bleeding and/or, as in this case big external wounds which likely has caused quite some blood loss.

Liquid will, IIRC, cause some bad effect on the re-production on blood, and might also affect existing blood.

Am I correct in this? If so; what happens and why should one not give liquid to the patient?

Guess there could be some situations where liquid is proper. E.g. patient has been laying in exposure to sun for N hours and dehydration might also cause ill effects... ? (Kidneys, blood-pressure, plasma?) But that might be a negative in any case if one suspect internal bleeding?

After some general research there are specifically 3 arguments that I came across that people give for supporting this particular theory.

1) somebody seriously injured might be given an anesthesia shot by the doctor or whoever that treats him first up for relief from the pain and distress. This would lead to relaxation of the stomach muscles and the contents of your stomach can travel up to your throat and into your lungs which would be fatal. Read about pulmonary aspiration.

2) the second case is if there is an injury to the gut or the GI tract, then providing water would be counter productive. A layman might not be able to assess the level of injury to someone just by sight.

3) the third is that giving water would increase blood pressure and (sometimes) apparently dilute the scars. This could also lead to chances where sutured wounds might reopen.

There are no real guidelines as to how much water can be given to an injured person. Depends on the situation or how much time he has been bleeding for and the kind of environment that he is subjected to like you pointed out. Some medics have recommended sucking on citrus fruits to prevent dehydration. Also, swabbing the patient all over the body with a cold compress can provide some relief and delay dehydration.

Guidelines for bleeding victims are here.


Which organism can point us to the evolution of sight? I'm trying to identify the basic biological mechanisms for sight.

Could you help me with identifying any organism that has the most basic ability to see objects?

Most importantly, creatures like dogs, cats, insects are able to not just see light, but are also able to identify objects and other living beings. I feel that an organism could be classified as "being able to see" if it can identify objects and movement and use its "visual sensory organ" to help it move around, locate food, identify species of animals, differentiate between living and non-living and escape predators if any.

Even if an organism can see just black and white or the most basic perception of sight, it would qualify for what I'm searching for. Is there any such known organism that has such a basic visual perception and has the way its eye+brain perceives images, been studied?

I'm not referring to the kind of "photosensitivity" that plants have. Detecting the presence and direction of light is not sufficient.

Which is the least evolved organism that can see?

The term less evolved does not mean anything. Instead one can ask

  Which lineage was the first to evolve the ability to see?

And by "see" of course, I mean detect electromagnetic waves. Seeing does not imply color vision and does not imply accurate vision.

It will be hard to tell really which lineage came up with vision first. But I am sure you'll be interested to know that some cyanobacteria are able to detect electromagnetic waves (reviewed in Nilsson and Colley 2016).


To what extent is eating and nutrition important in recovery from minor illness like viral fever? I'm guessing it is important,  but just to be a little more precise,

What would be the maximum amount of calories above which it is just a waste (or even harmful)
How much does the metabolism raise during the illness?
More carbs or more proteins? (or less?)

During infection a body has to produce absolute masses of immune cells, raise your temperature via increased metabolism, repair tissue damage, migrate components of the immune system including proteins and cells, produce masses of antibodies and probably lot's more.

A lot of protein components need to be made which require protein synthesis and energy. Metabolism of fats and carbs goes up too. Also, importantly, vitamins are a key part of the immune system serving to migrate the immune system  such as vitamin D aids migration of cells to the skin. Vitamin C is required for collagen synthesis in repair. Minerals are required for the metalloenzymes. However your dependency on each component depends on the type of infection, your immune response, your natural state including your reserves of everything.

How important is it? Very. I've listed what the things are needed for which gives an indication of how important they are. If starved, the body will do the best it can by focussing its resources on the thing it deems most important.


Can the basement membrane of blood capillaries expand? I have been doing some rudimentary research into the basement membrane and found the it contains collagen fibers which are known for their elasticity.  Does this mean that the basement membrane can expand in capillaries?

It's a good question.
Though there is hardly some evidence to answer your question.
However I will share what all I found.
So in capillary basement membrane, mostly collagen type 1 and 4 are  present.
Now collagen type 4 aids in elongation of the new capillaries-

in the ex vivo rat aortic model of angiogenesis using a type I collagen matrix, type IV collagen promoted new vessel elongation and survival in a dose-dependent manner compared with controls (no type IV collagen), which grew until day 9 and then regressed during the second and third week of culture (treatment with 3, 30, 300 g/ml of type IV collagen in 43, 57, 119% increase in microvascular length) [139]. In all then, type IV collagen seems important for stability of blood vessel formation.

The collagen in capillary basement membrane impart mechanical stability to the vessel.
Also elastin is a component of the basement membrane. Reference
Now though I couldn't find that it's the elastin of basement membrane only, but-

Comprising 50% of the dry weight of major arteries, elastin is the most prominent ECM protein in arteries [43]. In vessels, elastic lamina alternate with rings of smooth muscle forming a strong, flexible part of the arterial wall [43, 44].

Here is the article


Rhizosphere vs. Endorhiza? In relation to microbiology and the naming of the various areas of the plant as it relates to microbial inhabitance, I am confused as to the difference between the terms endorhiza and rhizosphere.

In this case I see rhizosphere referred simply to as the 'roots', but in this case I also see endorhiza explained simply as 'roots' also.

However in this case, I see a further explanation for endorhiza (which does make sense etymologically): 'internal root tissues'.

Does this mean endorhiza is be a sub-term for the area inside the roots, and the larger area of the rhizome in general represented by rhizosphere, and that is the difference?

Healthy plant growth depends on a microbial community that lives around and inside the roots of plants (Bais et al. 2001). Roots secrete from the roots a number of chemical compounds that influences the microbial community around but outside of the roots. The microbial community can include bacteria, fungi, and single-celled parasites, as well as larger organisms like insect larvae and even roots from other plants. Some chemicals attract certain organisms while other chemicals repel organisms. This community of organisms around the roots is called the rhizosphere (Walker et al. 2003). The paper by Walker (open access) describes some of the many types of symbiotic relationships that occur in the rhizosphere.
Endorhiza refers to the internal environment of the root system. The endorhiza contains another microbial community of bacteria and fungi (Backman and Sikora 2008). The organisms of this endorhizal community are collectively called endophytes. Like the rhizosphere, the organisms in the endorhiza are important symbiotic species that benefit the health of the plant.
Similar communities have been identified for other regions of the plant, such as the phyllosphere, the organisms that live on the leaves, stems and other plant parts above the ground (Backman and Sikora 2008).

Citations
Backman, P.A. and R.A. Sikora. 2008. Endophytes: An emerging tool for biological control. Biological Control 46: 1-3.
Bais, H.P. et al. 2001. Root specific metabolism: The biology and biochemistry of underground organs. In Vitro Cellular & Developmental Biology - Plant 37: 730-741.
Walker, T.S. et al. 2003. Root exudation and rhizosphere biology. Plant Physiology 132: 44-51.


What are the factors that contribute to genetically identical individuals behaving differently? If you run the same task on a pair of identical computers, you will end up getting the same results, even with the same response time.

But let's say you line two different person, and ask them the exact same question. Each will answer totally different, even if they are twins, raised in the same family, went to the same school and shared the same roof, and probably had the same experience in life. One of them may love carrots, one may not.

The question is, what is generating such different behaviour and way of thinking? Aren't they sharing the same genes?

If yes, the question is still standing.

If no, then we'll have another question:

If we create 2 identical clones of a person, raise them in the same situation, will they think identical too? If not, why? And what's the reason of this?

Your question has actually more to do with developmental biology and the origin of phenotypic variance in populations than with neuroscience.
Here is a list of factors which variance explain observed phenotypic variance in a population:

Genetics (incl. additive, dominance and epistatic variances)
Environment (incl. macro and micro environments)
Developmental noise (incl. cellular noise)
Epigenetic
All the covariances among above factors

Of course, when you consider a pair of monozygotic twin as your population, there is little to no genetic variance. They will also likely experience little epigenetic variance. Assuming they live together, practice the same sport, eat the same type of food, etc... then they will also experience little macro-environmental variance. Micro-envrionmental variance and developmental noise are probably the main factors causing these two hypothetical twins to differ.
You might want to read the post Why is a heritability coefficient not an index of how “genetic” something is? to better understand the current post.


Analysing the ERP (Event-Related Potential from EEG recordings) in terms of the P-300 wave I am trying to understand how to analyze ERP (Event-Related Potentials) from EEG recordings in focus on P-300 waves.

I have come up with a few questions which I hope you might be able to help with:

I assume that the number of repetitions af the stimulus should give better results, but I am not sure why. On one hand, it should help because avaraged results are usually better in neurosciences. On the other hand, maybe there is an unwanted adaptation effect of the subject?
So, are repetitions wanted in this kind of experiment?
There are time points in which I didn't expect P300 but the brain activity was not 0. I understand that there is always a background activity in the brain, but maybe there is more to it? And if so, are there certain frequenciess that are more likely to happen under these conditions?
When I analyze the data using an avarage response, should I assume anything on the P300 response?
What is the recommended Sample Rate I should use. I guess there should be an advantage for high sample rate for more resolution bur I am not sure about that. Am I right, or maybe a lower sample rate has advantages thst I am not aware of?

So, are repetitions wanted in this kind of experiment?

Yes: repetitions reduce random noise and increase the chance to tell artifact from response. Adaptation is a serious issue, typically becoming apparent by decreasing amplitudes, or even skipped responses. Reading the existing literature and/or performing experiments with various stimulus intervals may help to identify adaptation effects, if any.

  ...there is allways a background activity in the brain...

Correct - if not, you are either not recording properly, or subject is brain dead.

  are there certain frequencys that are more likey to happen under these conditions

If you repeat your recordings and average them out, this is not an issue. Otherwise, yes, FFT analysis shows several frequency bands, dependent on the state of the subject. For example, awake subjects show primarily fast beta activity (13-30 Hz), drowsy or sleeping subjects much slow-wave alpha (1-4 Hz).

  should I assume anything on the P300 response?

In short: The P300 response is most commonly elicited in an "oddball" paradigm when a subject detects an occasional "target" stimulus in a regular train of standard stimuli. The P300 wave only occurs if the subject is actively engaged in the task of detecting targets (Picton, 1992).

  What is the recommended sample Rate I should use. I guess there should be an advantage for high sample rate for more resolution bu[t] I am not sure about that. Am I right, or maybe a lower samp[le] rate has advantages th[a]t I am not aware of?

The higher the sample rate, the better. Downsampling can always be done later. Typically 1000 Hz is sufficient for fast responses. For a P300 this should already be kind of an overkill.

Reference
- Picton, J Clin Neurophysiol (1992); 9(4): 456-79


How much divergence would be needed for classifications as astrobiology? It is possible that life has invaded mars or the moon by way of probes rovers and other man made tech. How many years or generations of sequential and phenotypical diverge would be  necessary to establish the organism as astrobiology?

I think if life was transferred to either body on a probe, it would not count as alien yet because it could not have had time to develop very far on its own, since all probes are recent evolution wise. These would be offshoots from earth life. Truly alien life would most likely use different biochemistry because it originated in a different planet, it would be a totally different tree of life. However, the presence of life on the moon or mars, even if just contaminating earth bacteria, would be incredibly important for astrobiologists, as it would provide direct evidence that life can survive in these harsh environments. Life on the moon would most likely be dormant bacteria, because there is no air or water or food. However, if bacteria could survive prolonged exposure to space and be revived upon entering a suitable environment, that would provide evidence for panspermia. Read this: https://en.wikipedia.org/wiki/Surveyor_3

If panspermia is true, then those aliens might not be that unrelated after all. But until we find one, we can't make any conclusions.


What is the role of gills in terrestrial Crustaceans? Why do Crustaceans that live on land have maintained their gills? In aquatic species, the gills play a pivotal role in respiration, but terrestrial crustaceans have tracheal lungs. So why do they have gills?

Short answer
Gills in terrestrial crabs serve a role in water storage and ion homeostasis.

Background
Crustaceans are a huge group of species within the phylum of arthropods, including crabs, lobsters, crayfish, shrimp, krill and barnacles. Because of the huge variety of species within the crustaceans, I'll focus this answer on terrestrial crabs.

Air-breathing crabs have universally retained gills, but have also developed accessory breathing organs, usually lungs formed from the inner lining of the gill chamber. Aquatic crabs generally have large gills with very thin closely packed lamellae. Land crabs feature lungs that are well vascularized, have short blood-gas diffusion distances and often have adaptations to increase surface area, all of which greatly increase the diffusing capacity of the respiratory
system (Farreley & Greenaway, 1994).

In contrast, the gills in land crabs  are reduced in size and in surface area. The epithelium is usually modified for ion transport as indicated by the presence of densely packed mitochondria and relatively long blood/gas diffusion distances. Hence, the gills in land crabs are thought to primarily serve an osmoregulatory role, rather than a gas-exchange function (Farreley & Greenaway, 1994). The gills are thought to be involved in salt and water uptake. Their spongy structure is thought to aid in their function as water storage areas in periods of molting (Edney, 1977).  However, the gills in many species are still capable of gas exchange, although less efficiently than the lungs (Farreley & Greenaway, 1994).

References
- Edney, Water Balance in Land Arthropods, Zoophys & Ecology, Springer, New York (1977); 9
- Farreley & Greenaway, J Exp Biol (1994); 187: 113–30


Simulating Drug Entry in Protein and binding? Is there any simulation protocol or paper which can simulate the dynamics of drug entry and  interaction with the target protein?

This is a tough topic, have a look at the following references and see, if they can help you:

Structural modelling and dynamics of proteins for insights into drug
interactions.
Ligand entry pathways in the ligand binding domain of PPARγ receptor
Pathway and mechanism of drug binding to G-protein-coupled receptors
Molecular Dynamic Simulation and Inhibitor Prediction of Cysteine
Synthase Structured Model as a Potential Drug Target for
Trichomoniasis


Is it a coincidence that the sensory systems for smell, vision, taste, and hearing are all near each other in the head? I was wondering if it's an evolutionary advantage to have many sensory systems in a small place of the body, the head. This applies to mammals, reptiles, synapsid, dinosaurs... and many more.

My theories:

The distance to the brain is short and thus smaller time delay to
respond faster to the outside world,have more reflexes, hunt faster
prey and fight more accurately.
The short distance makes the "wire" (signal carrying) shorter and
thus less vulnerable to be cut from a injury, because for a organism
losing an eye reduces possibilities of survival dramatically.
In humans at least the head is the upper part, then vision organs
see more with less obstacles such as vegetation or terrain irregularities, or anything that obstacles vision, normally higher
means seeing more things. This I'm not sure applies so strongly to
smell. To taste, certainly not. To hearing, possibly a little,
thought nor much as vision.

We evolved from a common ancestor that was like that but that doesn't explain why it's not common to get out of that coincidence.

No it's not a coincidence that eyes, nose, mouth, and ears are all near each other in the head. As you note the layout is inherited from an ancestor, that's your answer.

A study of vertebrate head sensory systems shows that the

  The olfactory, vestibular auditory, and lateral line sensory organs displayed a strong link with the urochordate-vertebrate ancestor.

So this paper highlights that these structures go back earlier than the animals in your list. The development of vertebrates is very complicated so major departures from this developmental program which are successful are going to be rare events. This is reflected by blind cave dwelling animals that have vestigial non-functional eyes. The lack of selection pressure means the eyes don't work but they are still there because building an eye is part of a deep developmental programme. The image below shows (in orange) the key drivers of differentiation for various cell types. It makes it obvious that the program that produces olfaction also produces vision (otic) so modifications to the developmental program will have wide-ranging effects.

The theories that you've listed are interesting and there is work going into developing new senses. Udo Wachter wore a belt that vibrated to north 24/7, "north" became part of his dreams, he always knew where home was, and he mourned the loss of the the sense. So proximity to the brain is not a critical factor for the senses.


What makes an animal/species suitable for domestication/training? Humans have domesticated all manner of creatures during the course of their civilization - dogs, horses, several types of cattle, varieties of birds, and perhaps others too.

A prerequisite for an animal to be domesticated, obviously, is that there be some return from the animal voluntarily, or otherwise. For instance, milk from cows/buffalos.

What I'm looking for is an answer to the question what ... characteristics must an animal fulfil to be domesticated/trained. Docile is, perhaps, one characterstic. Amenable to training may be another. What other characteristics must be fulfilled before one would venture to consider training/domestication of another species?

The ability of an animal to be trained or domesticated appears to be genetic. A quick Google search revealed this Review: http://rspb.royalsocietypublishing.org/content/278/1722/3161.full.pdf


Are cells really the basic unit of all life? Please see comments as to the appropriateness of this question on biology SE.

All known life on Earth is made up of cells. It is thus safe to say that all known life is characterized by the presence of cells. But is having cells as a basic unit a requirement for life?

I'm thus asking if life is currently existent and/or possible without biomembranes, and to what degree cells actually matter in our present understanding of life.

An all-encompassing, comprehensive and cited answer would be very much appreciated.

According to Gerry Joyce: "Life is a self-sustained chemical system capable of undergoing Darwinian evolution."

From a meta-analysis of 123 definitions of life: "Life is metabolizing material informational system with ability of self-reproduction with changes (evolution), which requires energy and suitable environment."

According to Alexander Oparin: “Any system capable of replication and mutation is alive”.

At hand are some key elements in order to match these criteria. Maintaining a Darwinian cycle requires replication, mutation, and selection. Thus, we can break down the above into 5 criteria (personal communication with Gerry Joyce).

Life stores information
Life reproduces its information
Life alters that information
Life does something with that information (uses energy)
Life does all of this in a self-sustained manner

I would point out that the above criteria is quite different from what is currently on wikipedia described by metabolism and homeostasis. There are certainly additional criteria that certainly raise the threshold for what may be considered life. The common discussion revolves around viruses which do many of these things but not in a self-sustained way.

The question at hand then asks if cells are the minimum unit of life? What makes a cell a cell is that there is compartmentalization. The underlying reason behind this compartment is due to the necessity of tying the phenotype to the genotype. Paraphrasing using our definition of life, it links the information with the function that the information carries out. In the modern biological scheme, it keeps the proteins (phenotype) with the DNA (genotype).

The necessity of compartmentalization is negated when the phenotype is already linked with the genotype. The most frequent example is RNA where the material that carries the information is also the material that carries out its function. It tend, is reasonable to hypothesize that life can be made entirely with RNA without the need for compartmentalization (although compartmentalization certainly helps see Paegal and Joyce and Chen and Szostak).

Recent experiments by Gerry Joyce and others have been able to satisfy several of the requirements of life. The have self-replicating RNAs, that store information, that reproduce their information, that introduce alterations to their information, and do it in a self-sustained manner. What Gerry and his colleagues agree on is that their current self-replication Ribozyme system doesn't do anything particularly novel. However, by introducing a larger variety of functional elements to their ribozymes perhaps they will.


Atomic force microscopy: depth penetration? What depth penetration can  one typically get with atomic force microscopes? (i.e. how far into the tissue can one image?). I have found numbers on acquisition times (minutes) and spatial resolutions (~nm), but what about depth?

Also, what is the sensitivity of AFM? (e.g. in moles)

Taken right from the Wiki page you linked to:

AFM only images the surface of a specimen, to a maximum depth of 10-20 µm and a maximum scan area of 150 µm x 150 µm. Compared with scanning electron microscopy, SEM has a much larger depth of penetration and scanning area (~1 order of magnitude greater). AFM is also a much slower scanning method.


use of adjuvants and peptides in modern vaccines? when preparation of modern vaccines we generally use a part of the microbe or the antigen such as polysaccharides to create an effective vaccine against the vaccine. so when the preparation of sub unit and conjugate vaccine we use adjuvant? so what is the use of using an peptide in case of babies having week immune system?

Basically my question is What is the use of peptides when we are using adjuvants to enhance the immunogenic response?

In many vaccines, there are two components: One immunogenic substance, these can be parts or complete (inactivated) pathogens (for example the small pox vaccination), peptides or proteins (like the tetanus vaccination) or polysacceride components from the capsule of bacteria (for example against MenC). Against these components the actual immune response is directed. See references 1 to 3 for some more details.

Then they can (depending on the vaccine) contain adjuvants, which enhance the immunologic reaction of the body. This is done either to enhance the reaction and to get a proper immune reaction but also to be able to reduce the amount of injected antigen. So the adjuvant simply causes a general inflammatory reaction. Classically Alum (aluminium hydroxide is used here), newer adjuvants are squalen based oil-in water preparations or CpG olinucleotides (see references 4 and 5 for numerous examples on adjuvants and literature).

So what you basically do is to identify (more or less) a part of the pathogen which can serve as a vaccine and use this part for the vaccine.

Making Vaccines: How Are Vaccines Made
Designing Tomorrow's Vaccines
Strategies for designing and optimizing new generation vaccines
Dose Optimization Strategies for Vaccines: The Role of Adjuvants and
New Technologies
Vaccine Adjuvants Review


Inhibitory functional connectivity Functional connectivity may be defined as

  »the temporal correlation between spatially remote neurophysiological events, expressed as deviation from statistical independence across these events in distributed neuronal groups and areas«

or alternatively as

  »the presence of statistical dependencies between two sets of neurophysiological data«.

Images of large-scale brain networks typically show highlighted regions of interest that - in my humble understanding - are supposed to be functionally connected. But being highlighted means being active (at least more active than other regions), and thus functional connectivity seems to be mainly excitatory (even though only virtually).

But what about inhibitory functional connectivity? Can it be found by equal statistical means as excitatory functional connectivity - and how would it be "highlighted" in brain images?

On Neuroimaging Analysis

  But being highlighted means being active (at least more active than other regions)

This is not the case in functional connectivity analysis, or indeed not necessarily the case in any sort of functional neuroimaging analysis. The colormap highlighting in such images as you referred to (see the primary reference for that particular image) reflect statistic scores, commonly z- or t-statistics. Correlation simply means that time-courses behave similarly over time, and the color coding tells you how strongly they correlate with the “common profile” of the cluster. This makes no direct statement regarding the total “activation level“ over time, as represented by e.g. the area under the curve of the timecourse. In fact, such a metric would be meaningless, since fMRI signals are de-meaned so that they fluctuate around zero (as seen e.g. in the timecourses depicted here). Functional connectivity networks thus do not imply in whatever fashion a higher level of activity in highlighted networks. For further visual clarification you can consult Figure 1. of this article showing that functional connectivity networks can be and often are active at the same amplitudes and have similar levels of “total activity“ as visually inferred from the integral of the power spectra. This integral analysis is not presented, however, as it is meaningless.

On Inhibitory Functional Networks

Whether functional connectivity networks are implied to be excitatory depends on the exact mode of analysis. If the analysis is truly based only on detecting large correlation scores, identified networks will not resolve inhibitory projections, as such connections would cause anticorrelation rather than correlation. It could still be that a functional connectivity network is based on multiple areas receiving strong inhibitory input from an upstream node, yet that node would not be part of the network. Consequently, proficient functional connectivity analysis will identify networks via methods such as independent component analysis (ICA), which are able to group both strong correlation and anticorrelation together, as seen here.

TL;DR

Yes it can, it often is, and it's generally highlighted in blue.


How non-invasive blood glucose concentration measurement work? Diabetes patients need to conduct the “fingerstick” a few times a day. One of the mechanisms of "fingerstick" is to take small amount of blood sample and put it onto a test strip. The enzyme on the test strip reduces the glucose and the electronics of the glucose meter detect the redox species produced. However, this method is painful and increase the risk of infection.

Photonic sensing technology opens up a new method for non-invasive blood glucose concentration. According to an article of medGadget in 2013 (The link follows http://www.medgadget.com/2013/10/non-invasive-measurement-of-blood-glucose-levels-using-glucotrack-interview.html ), the non-invasive kind was invented. By simply clipping the earlobe (without puncturing the skin), the blood glucose concentration could be measured. Does anybody knows the working principle for that? Or, suggest a paper describing that?

I'm not exactly sure how it is done non-invasively in the manner you describe but suspect that it has to do with IR absorption spectroscopy. Glucose has distinct bands in the near-IR frequency range. So by illuminating the ear lobe and the capillaries in the surface, picking off the refracted light, and spectrally analyzing you should be able to determine the amount of glucose relative to some reference calibration.

I worked for a start-up company that did this semi-invasively for glucose measurements in the ICU. We drew a small blood sample and optically analyzed it in a glass cell using a scanning interferometer - then returned the blood to the patient.

The optical method that draws blood probably is the best approach with regards to accuracy - where you would like to get within 10 mg/dL - but it also has its problems including response to 'interferents' in the blood that can pose as glucose not to mention high cost for the interferometer and fouling of the blood access system.


How does human life expectancy change with age? Human life expectancy tends to be given as a single number reflecting age at death from birth.

But life expectancy should really grow the longer you live, because, for example, once you hit your fifth birthday your chances of dying before age five drop to zero, so the contribution to the average life expectancy of all the people who died before age five shouldn't apply.

To put it another way, once you hit age ninety, your life expectancy calculated then and there should be at least ninety years even though that exceeds the life expectancy in every country on the planet, simply because you've clearly already made it that far.

Does life expectancy as a function of current age have a name, and what shape does this function typically take? Perhaps more interestingly, does this function take a significantly different shape in humans than in other animals (I'd expect infant mortality to significantly affect this for example)?

I think you might be looking for period life tables

  A period life table is based on the mortality experience of a population during a relatively short period of time. Here we present the 2014 period life table for the Social Security area population. For this table, the period life expectancy at a given age is the average remaining number of years expected prior to death for a person at that exact age, born on January 1, using the mortality rates for 2014 over the course of his or her remaining life.


Why does resting potential not become continually more negative? (Firstly, I know this is similar to other questions, but I have read those answers and they do not really cover this topic).

My understanding of resting potential: action potential is not being transmitted; by way of action potentials via Na+ and K+ pumps, for every 2K+ pumped in, 3Na+ is pumped out of the cell. This process is termed "resting potential" and the transmembrane pd roughly = -65mV.

If more Na+ are pumped out than K+ in, why does the resting potential difference remain at -65, why does it not continue to decrease (until an action potential is triggered)?

The resting membrane potential is due to internal/external differences in ion concentrations and very importantly differences in permeability to those ions.
The fact that the sodium/potassium pump does not move an equal number of ions in each direction hardly matters at all for resting membrane potential; the resting membrane potential would be almost the same if that wasn't true. What is important is just the overall concentration of the two ion species, and the permeability of the membrane to different ions (almost all of this permeability is through specialized ion channels, because ions don't otherwise flow easily through a lipid bilayer).
You can calculate the resting potential/equilibrium potential using the Goldman equation - note that nothing in this equation involves the sodium/potassium pump moving different numbers of sodium and potassium ions.
The reason the membrane potential is negative is because the membrane at rest is most permeable to potassium, and because there is more potassium inside the cell than outside. Therefore, there will be a net flow of positive ions out of the cell, until enough ions have left that there is some negative charge inside the cell to counteract that net flow.


Evolutionary advantages of wet nose of cats and dogs? Everyone knows that some animals, at least cats and dogs, keep their noses wet and cool. But why did they evolve it? What evolutionary advantages does it provide? Smell-sensing cells need cooling for precision, may be? Or the liquid dissolves smellful gases into itself, simplifying analysis this way? Or may be it just simplifies cleaning the nose from the previous sniffing act?

Why did it evolve ?

  Mammals with rhinaria tend to have more acute olfaction, and the loss of the rhinarium in the haplorrhine primates is related to their decreased reliance on olfaction, being associated with other derived characteristics such as a reduced number of turbinates.

  The rhinarium is very useful to animals with good sense of smell because it acts as a wind direction detector. The cold receptors in the skin respond to the place where evaporation is the highest. Thus the detection of a particular smell is associated with the direction it came from.
  The rhinarium is adapted for different purposes in different mammals according to ecological niche.

  In aquatic mammals, development of lobes next to the nostrils allow them to be closed for diving. In mammals that root, the rhinarium often develops into a hard pad, with the nostrils off to the side. In the elephants it has become a tactile organ. In the walrus, it is covered with stiff bristles to protect it during foraging for shellfish. In many animals the form and purpose of the rhinarium remains to be elucidated.

Essentially it is the case of having a better sense of smell provided by the extended surface area, which has evolved to fit whatever the organism in question needs. I'll update this when I find this in a few more papers.

I took this from the wiki:
http://en.wikipedia.org/wiki/Rhinarium

How does it work ?

  A model of the canine nasal airway, developed from a 3-D
  reconstruction of high-resolution magnetic resonance imaging (MRI)
  scans, was used to study the aerodynamics of canine olfaction.
  Simulation results reveal that a unique olfactory airflow pattern
  exists within the canine nasal cavity during sniffing that is critical
  for efficient olfaction.

  Calculations show that this novel olfactory airflow pattern provides a
  crucial residence time for odorant absorption in the sensory region
  and promotes spatiotemporal fractionation of odorant mixtures along
  the olfactory epithelium.

  The canine nose functions similar to a chromatograph that imposes
  odorant-specific deposition patterns upon the thin mucus layer
  covering the nasal cavity....The results show that deposition patterns
  are primarily influenced by the intricate olfactory flowfield and the
  odorant solubility in the mucus layer.

  Highly-soluble odorants are quickly absorbed near the entrance to the
  olfactory region, and thus do not reach the periphery with significant
  concentrations. In contrast, insoluble odorants are deposited more
  evenly and may even exit the olfactory region without being completely
  absorbed. Predicted odorant deposition patterns correspond with the
  anatomical organization of olfactory receptors known to occur in
  keen-scented (macrosmatic) mammals, providing a mechanism that helps
  explain the excellent olfactory acuity of the dog.

In short the mucus on a dog's nose 'pre-sorts' smells by trapping the passage of some odour particles more than others along the nose, with different types of molecules being picked up at different "depths" in the nasal cavity.

You can read about it here:

Craven, Brent, Gary Settles, and Eric Paterson. "The Aerodynamics and Transport Phenomena of Canine Olfaction." APS Division of Fluid Dynamics Meeting Abstracts. Vol. 1. 2008.

Lawson, Michael, et al. "Odorant Transport and Deposition in the Canine Nasal Airways." APS Division of Fluid Dynamics Meeting Abstracts. Vol. 1. 2009.

Craven, Brent A. A fundamental study of the anatomy, aerodynamics, and transport phenomena of canine olfaction. ProQuest, 2008.


correction of read counts for spikes I have 4 RNA-seq samples (1st is control and the other 3 are treatments) and 5 spikes. I used different concentrations for 5 spikes but over different samples, I used similar concentration. for example I used similar concentration for spike1 in 4 samples. and this is the case for the rest of spikes. I am trying to normalize the read counts for the spike. do you guys know how to do that?

this is what I have done so far:
I counted the spikes in different samples and and got the ration of them (treatments compared to the control for all spikes). the ratio is as expected (looking at the concentration of spikes).
one thing that I can do to correct the read counts for spikes is to multiply by the ratio between samples. but I am not sure if that is the right way.

The most common and simplest normalization method for spikes is the Total Count Normalization. It's actually what you're doing here, so what you're doing here is correct. TCM is a useful algorithm for normalizing sequencing depth, that includes your spike amounts.

  https://academic.oup.com/bib/article-lookup/doi/10.1093/bib/bbs046

has reference on the TCM normalization.

  Gene counts are divided by the total number of mapped reads (or library size) associated with their lane and multiplied by the mean total count across all the samples of the dataset.

The paper doesn't talk about spike-in controls, but the idea is the same. We'd use the spike-in controls for estimating the difference in sequence depth (instead of the whole data set).


Is plastic just as good for you as corn? To specify, I mean plain corn-on-the-cob, not anything processed like corn flakes.

Since one of the main important functions of corn is that it's not digestible, and therefore helps with digestion by loosening feces, would that make it just as beneficial as chopping up and eating a plastic bag?

The part of the corn kernel that is visible in human feces is the outer coat of bran called the pericarp (see this image). This is a common structure in cereal grains like corn and wheat.  However, the bulk of the corn kernal is starchy endosperm, which is readily digestible by humans and provides carbohydrates and vitamins A and C.  The non-digestible (by humans) pericarp does help to keep fecal material soft.

Plastic bags do not provide those same benefits. Studies on human consumption of plastic bags are lacking, for obvious reasons.  However, marine organisms like sea turtles unfortunately consume large amounts of plastic debris (Derraik 2002). Bugoni et al. (2001) found that plastic debris caused mortality for 13% of the green turtles in their study. A review of 408 leatherback sea turtle autopsy records by Mrosovsky et al. (2009) found plastic inside 34% of turtles. The mortality in the sea turtles may be due to the accumulation of plastics in the gut which can block movement of food, alter feeding behaviors, and prevent absorbtion of nutrients.

If humans were to consume chopped up plastic bags, the evidence suggests that instead of receiving the same benefits as we do from whole kernal corn we are much more likely to be harmed. Eat your corn, recycle your plastic.

Literature Cited

Bugoni, L. et al., 2001. Marine debris and human impacts on sea turtles in southern Brazil. Marine Pollution Bulletin 42: 1330-1334.

Derraik, J.G.B. 2002. The pollution of the marine environment by plastic debris: A review. Marine Pollution Bulletin 44: 842-852.

Mrosovsky, N. et al. 2009. Leatherback turtles: The menance of plastic. Marine Pollution Bulletin 58: 287-289.


Learning tensors for evolutionary or developmental biology I'm looking for book recommendations on tensor algebra for use in biology.

Tensors are being used increasingly in evolutionary biology and developmental biology, it seems.  For example, here is an example of an empirical study that makes use of tensors in its analysis of data: http://rspb.royalsocietypublishing.org/content/282/1819/20151119

There are lots of books on the mathematics of tensors, and many introductions online.  So far, what I have found is that either (a) the presentation is heavily oriented toward physics applications, or (b) the presentation begins from an abstract algebra (or category theory?) point of view.

I'm willing to work through physics-style or abstract algebra presentations of tensor concepts and methods, but I am wondering whether there are any textbooks or other introductions that someone would recommend for biological applications.

(I have read the brief appendix on tensors in Sean Rice's book Evolutionary Theory.  Although I've found his other mathematical appendices and most of the mathematics in the book accessible, the tensor material in the book is too brief for me--I need more.)

The field of tensor decompositons has been discovered in many fields simultaneously, each with their own notation. Many modern notation in fields like CS or STAT have originated from the work of Tamara Kolda
http://www.kolda.net/publication/koba09/
However, this is restricted to the CP and Tucker decomposition, and we have many others now. See
https://arxiv.org/pdf/1609.00893.pdf
and
https://arxiv.org/abs/1708.09165


Resting and action membrane potential..? In the resting membrane potential of neurons the inside of membrane is kept negative and outside of membrane is kept positive by the utilization of energy through Na-K Atpase pump, While during action membrane potential through the opening of specific gated ion channels inside of membrane is made positive while outside is made negative, What is the significance of specific charges across the membrane, does these specific charges across the membrane play any role in the passage of neurotransmitters ? or these charges are just arbitrary ?does this can happen that during resting membrane potential the inside will become positive and outside will become negative and vice versa, I want to know that what is the significance of these specific charges across the membrane ..?

Answering the question: "Why is a negative membrane potential important?"

I don't think cells have strong feelings about being slightly negative inside its membrane. I'm guessing these are the driving factors:

the cell membrane is nonpolar, so charged particles can only pass via transport proteins. This makes ion gradients an easy way to maintain a source of (literally, in the physics sense) potential energy.
the cell needs to control its environment and send signals to other cells. The particle gradient (sodium, for example), allows it to accomplish these tasks: bring in glucose by co-transporting with sodium, send an action potential by triggering voltage-gated ion channels.
Therefore, the Na/K pump is a way to "charge" the ability of the cell to perform various types of work in the future.

To risk an analogy, a cell having a membrane potential is like you charging your cell in the morning. You aren't quite sure what exactly you'll be doing with your phone all day, but it will be many different tasks and all will be doable because you've got a controlled energy source.


What if target DNA doesn’t have restriction sites All the examples on DNA cloning I have encountered have assumed that the target gene and vector both have compatible restriction sites at just the right locations (probably for ease of explanation). Instead suppose I have a vector that has restriction sites for multiple restriction enzymes, but my target DNA sequence doesn’t have a restriction site for any of them, how would I go about creating a recombinant DNA from these?

If you're synthesizing the insert then you just design it with restriction sites that are compatible to the vector. Otherwise, you can design PCR primers that have restriction sites in them. That way when you amplify your insert you'll attach the restriction sites to it. EMBL, Addgene, and NEB all offer somewhat more detailed explanations of this on their sites.


Why a striped baby is not the result of a white and a black parent? Someone asked me:

  If a striped cat is the result of a white and a black cat, why the result of a white woman and a black man is not a striped child?

I know the answer. I also know that the result of a black cat and a white one is not a striped cat. But I'm looking for a simple answer. I'm looking for an explanation without a genetics background required. I'm looking for a metaphor or something similar.

The reason that there are no stripes when black and white people get babies is the fact that the number of pigment cells is the same for black and white people. What is different is the amount of pigment produced, and it will be different in the kids as well (lighter than the dark parent, darker than the light parent) See references 1 and 2 for details on the melanocyte density. Skin color is a multigenic trait, so the genetic background of both parents and their effects on pigmentation come into full play here.

Besides this effect, humans do have stripes, although they are mostly not visible. They are called Blaschko's lines and look like below:

These develop from the migration pattern of the melanocytes (and their precursor cells) in the developing embryo. They can get visible in some rare genetic conditions or by diseases. See reference 3 for a more popular explanation and reference 4 for a review on this field.

References:

The Regional Anatomy of the Human Integument with Special Reference
to the Distribution of Hair Follicles, Sweat Glands and Melanocytes
General Biology of Mammalian Pigmentation
Blaschko’s Lines
Lines of Blaschko.


Health effect of worm in Guava I ate a ripe guava, rife enough to be broken with hand, i later saw that it has white worms with one black end crawling inside it, are these worm harmful, i had unripe guava of same batch though most of them had small black spot inside, but no worm crawling, what are these crawling worms, were they present in guava from unripe stage or infected only after ripening ?

It is a safe bet that a "worm" as you describe in a ripe guava or any other ripe sweet fruit is a fruit fly.

from http://www.greenharvest.com.au/PestControlOrganic/Information/FruitFlyControl.html

Fruit flies are attracted to any ripe sweet fruit.  They are also attracted to vinegar and alcohol - both produced by yeast in and on the fruit, which is the high protein food that the fruit flies are really after in the fruit.

from
http://homeguides.sfgate.com/treat-fruit-flies-guavas-30550.html

  When ripe, guavas emit a pungent, musky odor that attracts fruit
  flies. Fruit flies lay their eggs beneath the fruit's skin, and the
  maggots feed on the flesh. The damage causes guavas to rot. Fruit fly
  infestations often spread quickly, but prompt treatment can get
  populations under control.

The fly large actually speed the rotting of the fruit by moving yeast around on their bodies.


Does biotin affect downstream experiments, such as RT-qPCR? I have two biotins--one of which is binding my RNA with cleavable bonds, and the other with irreversible bonds. Does biotin have an effect if it keeps its bonds with RNA? If it does, why is this the case?

Having looked into this question, I came across this paper, where they mixed biotin labelled EGFR-mutant-specific oligonucleotide and isolated the target using streptavidin beads followed by real-time TaqMan PCR allowing a 40 fold increase in detection sensitivity of the mutant allele, suggesting that biotin does not effect nucleotides in PCR based experiments.

The life technologies webpage claims that Streptavidin-Coupled Dynabeads M-270 can be used in a PCR reaction as stated below although certain streptavidin-coupled beads can have an effect on the PCR reaction. Hence I do not think biotin itself would be a problem for an amplification reaction.

  beads can be used directly in PCR, as they do not inhibit enzymatic reaction. Slight PCR-inhibition has been seen when 75–100 µg of Dynabeads® M-280 Streptavidin was used in 50 µL PCR reaction, and a concentration over 100 µg per 50 µL reaction seems to inhibit PCR completely. Dynabeads® M-270 Streptavidin do not show any inhibitory effect on PCR at these concentrations.

In fact you can buy kits such as this where you can generate/incorporate biotin into your RNA of interest for any purpose. The use of biotin and its incorporation into nucleotides seems prevalent in the literature and there are even kits for this purpose hence you should be on the safe side with your biotin labelled RNA experiments. I think the biggest challenge in RNA work is to keep it from degradation, which as far as I know is achieved through maintenance at -80 oC.


What is the difference between alarmones and riboswitches An Alarmone is an intracellular signal molecule that is produced due to harsh environmental factors. They regulate the gene expression at transcription level. A riboswitch is a regulatory segment of a messenger RNA molecule that binds a small molecule, resulting in a change in production of the proteins encoded by the mRNA, it works as a way to sense eviromental changes.

I've been reading some papers ("ZTP 5-Amino 4-lmidazole Carboxamide Riboside
S-Triphosphate): A Proposed Alarmone for 1O-Formyl-Tetrahydrofolate  Deficiency" , Bochner 1982; "An Ancient Riboswitch Class in Bacteria Regulates Purine Biosynthesis and One-Carbon Metabolism" Kim 2015) which study how ZTP can bring changes upon 10f-THF deficiency. Bochner (1982) through several experiments proposes ZTP as an alarmone for 10f-THF; some assumptions of Bochner might not have been entirely correct and a later paper fails to replicate some experiments. Later Kim (2015) propose ZTP as a riboswitch.

I'm not fully aware of the differences between the concept of "alarmone" and "riboswitch". Seems to me that both Bochner and Kim propose virtually the same thesis.

First time I actually hear the word alarmone so bear with me okay?

"An Alarmone is an intracellular signal molecule that is produced due to harsh environmental factors. They regulate the gene expression at transcription level" <- this probably refers to activating/inhibiting transcription factors and stuff like that. Looking at bit further into the wikipedia article from whence you copied the description, we see that ppGpp is considered an alarmone.

According to the wikipedia article on ppGpp (https://en.wikipedia.org/wiki/Guanosine_pentaphosphate) we see e.g. this line "When (p)ppGpp associates with the promoter it affects the RNA polymerase enzyme's ability to bind and initiate transcription", so this alarmone can act by inhibiting RNA polymerase's ability to bind to the promoter.

A riboswitch on the other hand is a structural element INSIDE an RNA molecule that causes a conformational change upon binding a ligand. This conformational change then has an effect on transcription or translation etc. Thus, an alarmone could probably bind to a riboswitch to exert its effect, but a riboswitch is a quite specific thing.
You can read about some of the mechanisms in the wikipedia article https://en.wikipedia.org/wiki/Riboswitch

So basically, think of alarmones as signalling molecules and riboswitches as structural elements in transcripts that regulate gene expression upon ligand binding.


Where is DNA during the process of RNA extraction using Trisure? Where is DNA during the process of RNA extraction using Trisure described here? Given that DNA is also a nucleic acid, should I expect the isolated RNA to also contain DNA? However, Bioline claims RNA 'with
virtually no genomic DNA contamination'.

Expectedly, they don’t really want to tell you what TRIsure is. What they do say is that DNA is found in the organic or interphase after extraction whereas RNA partitions to the aqueous phase. This is almost certainly some variant of acid phenol extraction. As confirmation, the MSDS lists phenol, ammonium thiocyanate, guanidinium thiocyanate, glycerol and citric acid as its components.


What sort of fish is this? Just saw a meme online with this fish on it. Is this a real fish? Can some aquatic expert identify this for us?

That is a blue parrotfish (Scarus coeruleus):

(photo: Marc Tarlock via Wikimedia Commons)


What is this pink angiosperm from Morocco? What is this pink angiosperm photographed in Morocco in spring? The diameter of the flower is about 2 cm. The petals are fused. The plant is crawling and did not have any erect parts.

This is a species of morning glory (fairly obvious from the flower). It is a member of the angiosperm family Convolvulaceae. The flower and the leaves together identify it as Convolvulus althaeoides. It is a Mediterranean native.  Links provided.

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

https://www.google.com/search?q=convolvulus+althaeoides&source=lnms&tbm=isch&sa=X&ved=0ahUKEwit1P3t7L7aAhVPmVkKHZIJD_gQ_AUICigB&biw=1097&bih=642


Use of restriction endonucleases to analyse Variable Number Tandem Repeats (VNTRs) The textbook I’m using states that “Ends of VNTR have conserved sequences. These can easily be cut by restriction endonucleases.”
But restriction endonucleases cleave palindromic sequences. Does this mean that the repeated DNA and conserved sequences together form a palindromic sequence?

The general situation regarding using restriction endonucleases to analyse Variable Number Tandem Repeats can be explained with (as well as without) reference to the illustration below.

The original region of DNA in which the insertion occurs will in general be complex (rather than repeated) and conserved to a reasonable extent among H. sapiens. The complex conserved sequence is represented by a gradient of colour in the upper part of the diagram so that the point at which the original copy of the repeat inserted can be identified in different individuals (or alleles), A, B and C, where, for the sake of argument, two, three and four copies have been generated.
The individual repeat unit is relatively short (typically 10–100 bp), so it is relatively easy to find conserved sites for at least one commercially-available restriction endonuclease on either side of the original insertion, but not within the repeat.
The mathematics of this reasoning are quite simple, and I provide exercises on my University website. However, as an example, consider a 4-base pair sequence that is the target for a restriction enzyme. It need not be palindromic, but as most Type I restriction endonucleases are, let’s choose GGCC. The chance of finding this in any tetra-nucleotide is 1 in 256 (4x4x4x4), or, in other words, it should occur in any 256 bp stretch of DNA. (Of course this is just an average of what may be a normal distribution, and overall base composition will affect the actual frequency.)
The net result will be that it will be possible to generate fragments of an overall size such that the flanking regions are not so large that they make it difficult to distinguish differences reflecting different numbers of repeats.
And today?
The polymerase chain reaction (PCR) might well be used instead of restriction endonuclease digestion as, given that the DNA sequence of the region has been determined, one could choose appropriate positions in the flanking regions to generate DNA fragments for analysis. See, e.g. Richie et al. (1999).


How does body fat leave your body? So I know that it’s not from tears or sweat because they are composed of mainly water and sodium, it’s not from going poo or pee as poo and pee are made of the parts of food that supply your body with no nutrients and your body also doesn’t “burn body fat” because there is a theory that no matter is ever destroyed so it’s none of those but another thing is it’s not your hair, ear wax, finger nails or anything of that sort because people can lose over 17 pounds in 3 months but you can’t build up that amount of hair , ear wax or whatever else in three months so how does body fat leave your body

Many of the statements in your question are false, including your ideas about waste products.

Ultimately, fats, just like carbohydrates, end up as water and carbon dioxide if they are used in cellular respiration for energy. The reaction path is different, but the ultimate reaction products are the same as you would get from burning fat in a fire: reaction with atmospheric oxygen oxidizes the reactants to carbon dioxide and water.

This is the reverse process of photosynthesis, where carbon dioxide and water react to form sugars, with oxygen as a byproduct.

The mass leaves the body as exhaled carbon dioxide and as metabolic water through the urine, vapor in exhaled air, etc.


How are chromatids correctly segregated during mitosis? In my book this is described as happening by kinetochores depolymerising from their attached microtubule spindle, then being dragged towards the spindle's centrosome by a dynein protein. I can understand this, but what it does not seem to answer is how different copies of chomatids beome attached to the correct spindles in the first place (i.e. spindles connected to opposing centrosomes). How does this work?

It's a spatial constraint.  As the DNA is replicated, the two resulting chromatids are kept stuck together by cohesin proteins.  The DNA sequence that corresponds to the centromere then coalesces the kinetochore.  It seems that the DNA-protein interactions at the centromeres creates a particular structure along the chromosome.  Since the two chromatids have their kinetochores pointing in opposite directions, when a spindle microtubule attaches to the kinetochore, it is nearly impossible for another microtubule from the same spindle to attach to the opposing kinetochore.


Is the Amazon forest O2 and CO2 neutral? In these days, we receive a lot of concerning news about the Amazon burning. Recently, I came across widespread claims about the production of O2   and the absorption of CO2 by the Amazon forest, something known as "carbon dioxide in, oxygen out". However, I also found claims that the Amazon ecosystem uses up all the oxygen it produces, and that it is a stable carbon sink, i.e. it acts like a carbon storage system, not as a sponge for carbon.

What are the real facts about oxygen and carbon dioxyde dynamics in the Amazon forest? I'd intuitively say that the second hypothesis is stronger, but I'd like to have a confirmation backed by some papers.

tl;dr We don't really know. A reasonable guess is that it's a weak sink, gradually turning into a source via increased drought frequency, but it's extremely hard to measure; carbon flux is highly variable both spatially and temporally (so it matters both when and where you measure), and it's difficult to make sure that you're accurately measuring all the different components of carbon flux.

Dolman and Janssen 2018 say:

  Ground observations suggest that, through tree growth, the Amazon forest acts as a net carbon sink to the atmosphere (Brienen et al 2015), which is confirmed by atmospheric studies (Gatti et al 2015). However, the sink strength appears to have been declining since the 1990s and recent drought events in 2005, 2010 and 2015 might have temporarily reversed the Amazon carbon sink into a source (Feldpausch et al 2016, Gatti et al 2015)

They go on to discuss the great difficulties in constructing an accurate model of Amazonian carbon dynamics (for the purpose of predicting future source/sink relationships).

Rice et al. 2004

summary based on measuring living trees and coarse woody debris [CWD], it looks like a particular patch of forest was a small net source, but this may be a transient effect.

  Amazon forests could be globally significant sinks or sources for atmospheric carbon dioxide, but carbon balance of these forests remains poorly quantified.

In other words, "it's still unclear [as of 2004], so we did another study."

  We surveyed 19.75 ha along four 1‐km transects of well‐drained old‐growth upland forest in the Tapajós National Forest near Santarém, Pará, Brazil (2°51′ S, 54°58′ W) in order to assess carbon pool sizes, fluxes, and climatic controls on carbon balance.

So they took a very small sample of a particular forest type.

  The gain in live wood biomass was exceeded by respiration losses from CWD [coarse woody debris], resulting in an overall estimated net loss from total aboveground biomass ...

So this particular patch of forest was a carbon source at this particular time ...

  ... a period of high mortality [probably] preceded the initiation of this study ... transfer of carbon between live and dead biomass pools appears to have led to substantial increases in the pool of CWD, causing the observed net carbon release.

... but that may be due mostly to a recent die-off - maybe not true over a longer time scale ...

  ... the hypothesized sequestration flux from CO2 fertilization ... would be comparatively small and masked for considerable periods by climate‐driven shifts in forest structure and associated carbon balance in tropical forests.

... it will probably bounce around a lot (i.e., it's not wise to extrapolate this result either in space or time).

Miller et al. 2004

  We used two independent approaches, biometry and micrometeorology, to determine the net ecosystem production (NEP) of an old growth forest in Pará, Brazil. ... Biometric inventories indicated that the forest was either a source or, at most, a modest sink of carbon from 1984 to 2000 ... biometric and micrometeorological measurements in tandem provide strong evidence that the forest was not a strong, persistent carbon sink during the study interval.

and a more recent reference ...

Antonucci et al. 2018

  The objective this paper was to quantify the hourly variability of CO2 fluxes in the year of the El Niño, in 2015, in a tropical rain forest in the Western Amazon ... The average daily behavior of CO2 fluxes showed higher concentrations of absorption during the day than emissions overnight, behaving as a carbon sink, corroborating the importance of the forest in assimilation of the atmospheric carbon.

references

Miller et al, "Biometric and micrometeorological measurements of tropical forest carbon balance". Ecological Applications 2004, https://doi.org/10.1890/02-6005
Rice et al., "Carbon balance and vegetation dynamics in an old-growth Amazonian forest". Ecological Applications 2004, https://doi.org/10.1890/02-6006
Antonucci et al, "CO2 fluxes in a wet tropical forest area in Western Amazon in year of El Niño". Ciência e Natura, v. 40, 2018. https://periodicos.ufsm.br/cienciaenatura/article/view/30718
Dolman and Janssen, "The enigma of the Amazonian carbon balance", Environmental Research Letters 2018. https://iopscience.iop.org/article/10.1088/1748-9326/aac78e/meta


Use of pigs for obtaining transplant organs It is being said that organs can be obtained for transplant from the pigs. What is special about pigs that we are using them? Why can't we use monkeys or chimpanzees with whom we share a more recent common ancestor?

Monkeys and many other primates are too small to provide organs that will provide the needs of a human host. The fact that primates are so close to humans physiologically is not always a win as transplanted organs will bring diseases into the host that can be quite dangerous.

Besides, because even human human transplants induce immune rejection of organs. Its typical that immune suppressants will be a lifetime treatment for the patient.

Finally, the cost of a pig organ is negligible and their organs are about the right size, and I would bet that activists don't protest pig transplants nearly as much as primate donors.


How does Haloxyfop control young grassy weeds in fields of broadleaved crops? Haloxyfop (haloxyfop-P-methyl) is a selective herbicide used to control grassy weeds in young stages. The mode of action (iirc) is basically inhibition of acetyl CoA carboxylase (ACCase). Why does this affect the monocots, while not harming the dicots?

On the Botany department website of Purdue University (http://www.btny.purdue.edu/weedscience/moa/ACCase_Inhibitors/text.html) I found the following information on Acetyl-CoA carboxylase (ACCase) inhibitors:

  [...] (ACCase inhibitors) inhibit the enzyme carboxyltransferase, an [...] Acetyl-CoAesterase which speeds the formation of malonyl-CoA from acetyl-CoA and CO2.
  Malonyl-CoA and acetyl-CoA are the building blocks of phospholipids and triacylglycerols [...] (that) combine to form lipid bilayers that serve as the cellular membranes. Affected plants cannot produce new cell membranes. This takes place in the grass’s meristematic tissue, which explains the mushy and disintegrated growing point. [...]

  Selectivity [...] Monocots (grasses) [and] dicots (broadleaves) [...] both possess ACCase enzymes in their cytoplasm and chloroplasts. Dicots have a prokaryotic form of the enzyme in the chloroplast and the eukaryotic form in the cytoplasm. Monocots have the eukaryotic form in both their cytoplasm and chloroplasts. Only production of the eukaryotic form is inhibited.

So to sum up, ACCase inhibitors act on eukaryotic ACCase, not the prokaryotic type. ACCase is essential for cell membrane formation. Blocking ACCase results in a depletion of its product, namely malonyl-CoA. Malonyl-CoA is essential for the synthesis of long fatty acids used in the cell membrane. Without cell membranes, cells lose integrity and turn to mush. Tissue growth is impossible without ACCase activity. Since monocots only have the eukaryotic ACC in both cytoplasm and chloroplasts, they die. Dicots, on the other hand, express prokaryotic ACC in their chloroplasts, making them resistant to ACCase inhibitors.

After some literature search I also found that blocking (knocking out) acetyl-CoA carboxylase in Arabidopsis (a dicotyledon) results in dead plant embryos and, hence, non-viable seeds (Baud et al., 2003).


Does transcription terminate at the end of antibiotic resistance genes on the Duet expression plasmids? I am working with the pETDuet and pRSFDuet plasmids to express RNAs under control of the T7 promoter. On these plasmids the antibiotic resistance genes (Amp for pET, and Kan for pRSF) are downstream of the T7 promoter site where I cloned in my genes. The Amp and Kan genes are transcribed in the opposite orientation of the T7 promoter and since these genes are downstream from where I inserted my genes, readthrough transcription from the resistance genes would result in a sequence complementary to the RNA sequence I wish to produce. My question is: do the antibiotic resistance genes in these plasmids have a built in transcription termination mechanism?
I have used the ARNold tool: http://rssf.i2bc.paris-saclay.fr/toolbox/arnold/index.php to look for Rho-independent terminators at the 3' end of the antibiotic resistance genes and in the region downstream. There was one hit for the pETDuet plasmid but nothing for the pRSFDuet plasmid. There were no hits for the  pCDFDuet or pCOLADuet plasmids either. My sense is hairpin terminators were not specifically incorporated to stop transcription downstream of the antibiotic resistance genes. The other possibility is the antibiotic resistance genes terminate in a Rho-dependent manner, is this known to occur for the Amp and Kan genes?

Generally they do, however this is often doesn't completely stop transcription run-through.
Note that in a T-7 reaction there shouldn't be any transcription of the Amp or Kan genes as these are run off promoters that  the T7 phage RNA polymerase won't be able to transcribe off as it is extremely specific for the T7 promoter.
The solution if you are really worried is to linearize your plasmid immediately downstream of your terminator but before the AMPR gene using a restriction enzyme with a single cut. This will also give you a specific size sequence being transcribed, which is very useful if you are determining copy number in say a qPCR.


How do I read an RNA expression pattern? When reading about diseases one can find links to proteins and their associated genes, an example of which is here.

I'm wondering how to decode/read the following graph as a non-specialist in this area:

What does it all mean?

This image shows the expression of a gene (in your case Lamin A/C) in various tissues. A picture with a higher resultion for mouse looks like this (from here):

You can see the median expression (calculated from all samples) and can also see, in which tissues this gene is highly expressed and in which there is less or no expression.

This is important if you want to analyze the function of a gene. The tissue specific expression pattern can vary strongly between different tissues (as you can see in the figure) which can give information about the function of the gene. The same is true if you look on the time distribution of gene expression, you can identify genes which are important for different steps of differentiation.


Biggest change in size from birth Which mammal has the largest change in size from birth to fully grown percentage wise?

@JM97 is correct.

According to National Geographic >>

The gestation period of a Red Kangaroo is 33 days and it's baby at birth weighs a mere 0.03 oz. To put it into a more precise perspective, on birth, the baby weighs 1/100,000 of an adult red kangaroo's weight.

Second place goes to the baby of a Giant Panda; at birth it weighs 3.2oz which is 1/900 of an adult giant panda's weight.


How is (Insect) population control through male sterilization effective This is no doubt a simple question.

I was reading about Sterile Insect Technique where sterile males out-compete non-sterile ones to mate with females and thus reduce the population.

My question is - why don't the females just re-mate after they don't reproduce?

I'm assuming that the number of sterile males will be much less than the existing male population.

Is it because my assumption is incorrect and there are more sterile males?  Or my assumption is correct and given the life-cycle of the organism, the females have only once chance to mate?  Or something else?

Sterile insects are typically produced by radiation. A sufficient dose is used to cause substantial DNA damage in the gametes of the males. However, this doesn't mean the sperm are completely non-functional.

In fact, it is important that the sperm are functional and simply contain dominant-lethal mutations at a sufficient probability (Robinson, 2005 describes this in detail as well as the dosing strategies to optimize the desired outcome).

The males still mate and fertilize the eggs of the female; it is only later that the eggs will eventually fail to develop, but there is no way for the females to be aware of this (nor much that can be done even if they were - once the eggs are fertilized they cannot be fertilized again).

It is also important to release a sufficient population of sterile males to impact the population. Depending on the species, it may or may not be necessary to completely overwhelm the existing population, but a typical goal seems to be 10-100x the native population. By raising males in laboratory conditions, it may be possible to produce a larger population than would typically survive to mating age in the wild.

References:

Cockburn, A. F., Howells, A. J., & Whitten, M. J. (1984). Recombinant DNA technology and genetic control of pest insects. Biotechnology and genetic engineering reviews, 2(1), 68-99.

Klassen, W., & Curtis, C. F. (2005). History of the sterile insect technique. In Sterile insect technique (pp. 3-36). Springer Netherlands.

Robinson, A. S. (2005). Genetic basis of the sterile insect technique. In Sterile Insect Technique (pp. 95-114). Springer, Dordrecht.


What kind of salamander is this? This guy was found in central Virginia, under a flower pot. He's about 3 inches long, because part of his tail is either missing or it's just short. He looked dried out, so of course I wet my hand, scooped him into a small container, and moved him to our birdbath (which is on the ground and had been recently rinsed so the ground was plenty moist). I ran my hand (still wet) over his back and he seemed happier and started moving around.
However, I can't seem to find on Google just what kind of salamander he is. The VA Herpetological Society has an entry for a Jefferson Salamander, but those are only found in North/West VA. Attached is a picture of him (blurry, sorry) when I found him. I have a video of him coming out of the container and going under the leaves next to the birdbath, but it's too big of a file to put on here. Instead, here is a link to the file in my Google Drive: Salamander
Edit: I checked some pictures I had of him, and he has five toes on his hind legs. He is a dark gray-brown with faint mottling and a semi-light underbelly. Sorry that I didn't say this earlier. Hope this helps!
Can anyone identify him?

Maybe it's a Mabee's Salamander, Ambystoma mabeei.  Unfortunately, I can't really see the underside in your video, but I have the sense that it is a lighter color.  The clubbed tail, with an apparent break, seems like it may have been autotomized or otherwise injured, making it harder to compare.  I had the impression your example had dark spots dorsally and lightening ventrally, as can be seen in the image above.  Some other images are a bit different.  However, Mabee's Salamander is only found in "six localities in the coastal plain in extreme southeastern Virginia: the cities of Hampton and Suffolk and the counties of York, Southampton, Gloucester, and Isle of Wight. It is also found in Newport News." and is considered threatened, so unless your location matches what you read there it is still not likely to be the answer.


How does bonding between non-complementary bases occur? My teacher told me that when DNA polymerase makes an error (roughly every 10 million nucleotides?) that if, for example, it matches an A with a G that the error remains and is the main cause of point mutations. How do the two bases that aren't complementary remain bonded?

How do the two bases that aren't complementary remain bonded?

Non complementary bases can only form non-Watson-Crick bonds, which are very unstable and noticeably different.
Therefore any mismatch in the DNA of the genome will form a recognisable disruption of the DNA helix. This disruption is usually removed very quickly by the cells, since it makes DNA much more unstable.

Most cells have multiple mechanisms to detect and repair these sites, with one system specifically dedicated to DNA mismatch repair.
This system acts on mismatches directly after DNA replication, since at this point specific markers (sometimes DNA methylation, sometimes not fully understood) can differentiate between the newly synthesised DNA strand (which may contain an error) and the old one.

The repair mechanism will remove the mismatch and replace it with a properly bonded base pair, so that mismatches in the DNA are always short term issues - it is still possible though that 'wrong' mismatching base is replaced, which then (finally) leads to a mutation.

The error rate of DNA polymerase (1 in 10^7 sounds about right, this is the combination of the initial error rate and the DNA polymerase proof-reading mechansim) therefore has to multiplied with the error rate of this repair mechansim, which is around 10^3 (I can't find a source for this right now), to get a final error rate of DNA replication in cells.


Interpretation of genetic results Result of genetic testing indicated: c.341del, p.Thr114Lysfs*37.
The c.341del probably means:deletion at the cDNA 341 nucleotide.
Buy what does the second part:p.Thr114Lysfs*37 ?

You are right about the cDNA 341 nucleotide deletion.
It is an exon deletion, meaning that the deletion is part of a gene that encodes to a protein.
This corresponds to the second part - the protein level (annotated with p.).
The mutation that is caused on the protein level is a frameshift mutation (corresponds to the fs).
A frameshift mutation changes the reading frame of the protein.
You can find more information on frameshift mutations annotations on the HGVS nomenclature website.

In your case (p.Thr114Lysfs*37) the annotation indicates that the cDNA 341 nucleotide deletion led to a frameshift mutation of the protein with a Thr amino acid residue being replaced by a Lys amino acid residue. Furthermore, this also altered when the protein terminates: there is a new translation termination (stop) codon after 37 amino acid residues instead of terminating at the end of the protein where it normally does.


Do birds have quadriceps and thighs fused into their hips? I'm looking at 3D modeling a large bird like an emu or ostrich, but I don't know how the muscles surrounding the femur connect to the hips/back. It seems weird that the entire thigh and quadriceps would be fused into the hip because that would greatly reduce the range of motion of the femur which affects how I animate it, but I can't find any reference that shows it either way.

This is probably WAAAAY to late to be of any use to you but hey...
So the simple answer is:
Kinda.
You were actually correct to intuit that the femora of birds have a limited range of motion, with most of the limb motion being provided from the "knee"-down.
So you shouldn't animate bird legs the same way that you would the legs of other non-bird animals.
That's not to say that the femur doesn't move - it does but not my much (it typically doesn't extend posteriorly beyond the vertical). Much of the thicc thigh musculature is there for support.


Why do the neuron pathways decussate? I learn about the brain right now, and there are crossing of neuron pathways everywhere; in the thalamus, the medulla oblongata, the pyramidal tract... And I don't understand why? What is the reason to connect - for example - the right foot to the left part of your brain?

Crossing or decussation is a lot more robust against wiring errors than their seemingly simpler same-sided wiring counterparts. See here for the research carried out to establish this and for more detail.


Do ants really dispose of their own dead, and how/why? I just read this from Wikipedia's Swarm Behavior article:

  Despite the lack of centralized decision making, ant colonies exhibit complex behaviour and have even been able to demonstrate the ability to solve geometric problems. For example, colonies routinely find the maximum distance from all colony entrances to dispose of dead bodies.

There was no citation.

Is it true that ants dispose of their own dead? If so, how and why? I would've though it would be much better to just eat their own dead, which would be a "free" food source allowing the colony to reclaim some protein and nutrients. It would cost much more energy (and risk) to transport dead ant carcasses away from the hive.

Eating the dead makes far more likely you will catch whatever killed them. They transport and dispose of the dead for the same reasons we do, to reduce disease vectors. They dispose of their garbage for much the same reason, in fact they often dispose of both in the same place even if they separate the two in distinct piles. Hygiene is very important is colonial insects because you are constantly surrounded by other ants which makes disease transfer very easy. Fungal infections are particularly problematic. They also have specialized toilet sites for the same reason.

Note only some ants transport the dead outside, other put them is special chambers far from normal traffic and reserved for that purpose and refuse disposal. In either case they are moving them away from casual contact.

Source

Source 2


What is the difference between differentially expressed genes and deregulated genes? Can anyone explain clearly what is the difference between differentially expressed genes and deregulated genes?

Any gene whose gene expression differs significantly from some reference is considered to be differentially expressed. I think the most common representation of differential expression is the volcano plot, where you're plotting the fold change or log2 fold change against the -log10 p value assigned that gene.

This means a couple of things: One, you need a sufficently large sample size that you can actually get statistics, and two, you need a sufficient reference sample which will act as your baseline.

If a gene is degregulated, however, the expression is aberrant. In order to characterize aberrant expression you need a normal sample or accepted reference sample, and the sample of interest. This might be as simple as tumor vs normal tissue from the same patient.


Fuel from photosynthesis I was reading how plants make use of sunlight, CO2 and some other stuff to make energy. So why can't we create artificially engineered bio solar panels which will take sunlight, C02, water and other things and give us energy (maybe electricity or heat etc). So basically instead of solar panels which are made of silicon or something we can have bio panels made of organic materials. Then we need to supply it with water and it will convert sunlight into electricity.

I googled this on the internet and I don't find anything relevant in this regard. So I am assuming there must be a very good reason we are not trying to do this. I want to know if there is any research going on in this regard and if not why this idea is not feasible.

What you are suggesting is an organic photosynthesizer,but that's not necessary when you already have plants that have genetically adapted for millions of years just to be suitable for this very purpose.
 Of course,artifical photosynthesis already exists,essentially using the same process;photons,chloroplasts,calvin cycle,photosystems 1 & 2,etc.It utilizes the general concept with photoelectrochemistry,so basically just replacing the organic tools with artificial photoelectric cells,which also uses h20 and light.What you are asking is why we have not developed genetically engineered organic matter to produce higher efficiency.As a matter of fact,GMO plant's already exist with immunity,though I have not heard of GMO that catalyzes photosynthetic reactions,and best not,because genetic engineering is still at it's best a new field that is too complex,for example,the general GMO is to incorporate the bacterial enzyme cas9 to cleave away specified DNA to alter an organism's genome,such as inhibiting receptors to cannabinoids,or to fight pests with substances that are not harmful to humans,etc.But it has consequences,such as permanence of that edited genome,so if the organism/plant reproduces,the progeny would also exhibit the same GMO properties.
 Photosynthesis is a complicated series of reactions that uses complicated enzymes and such.For example,the enzyme rubisco that changes co2 to energy rich molecules such as glucose,from highly unstable phosphoglycerates.Artifical photosynthesis is quite new,but it also uses the same fuel;co2,h20,and light,not sure if it uses biological nutrients like soil,but the process also uses Nicotinamide adenine dinucleotide phosphate,or NADP+.It is used for anabolic reactions,so it builds up molecules,vice versa are catabolic reactions,which is when enyzmes break down lipids and molecules in metabolism.Albeit I do not know for sure if this molecule has the same purpose in artifical photosynthesis,but for general photosythesis,yes.NADP+ also absorbs electrons for independent and dependent reactions to generate ATP and NADPH,etc.
 I hope this simplifies some things.CONCLUSION:we do have artifical photosynthesis,but gmoed photosynthesis may be harmful to a plant's heredity if we damaged it's genome,causing potential harm.
  Artifical is quite similar to organic,so I guess you say they are biopanels,using h20,co2,and light.


Does Sirtuin protein family Sir2 work in low-calorie diet mostly? I am reading about the protein family in relation to the prolongation of cell life.
It is known that

  Sirtuins have been implicated in influencing a wide range of cellular
  processes like ageing, transcription, apoptosis, inflammation and
  stress resistance, as well as energy efficiency and alertness during
  low-calorie situations.

However, I am not sure if these physiologic processes are only during low-calorie situations.
Alertness is at least.

It says in the original paper only that

  Our results suggest that in the hypothalamus, SIRT1 functions as a key
  mediator of the central response to low nutritional availability,
  providing insight into the role of the hypothalamus in the regulation
  of metabolism and aging in mammals.

However, it does not specify how the Sir2 works to high-calorie diet.
Therefore, I asked mostly.
When is the protein family active?

Does the Sirtuin protein family work mostly during low-calorie diet?

Does sirtuin 1 (SIRT1/SIR1) function to mediate the effects of a low calorie diet? Perhaps, but its really not clear.  Is the function of SIRT1 primarily to mediate low calorie response? Absolutely not.  What does that mean for SIRT2/SIR2 - its probably not more closely associated with calorie restriction signals, though it might be connected in a similar ambiguous way... but see below.

Firstly SIRT1 has also been shown to have many influences in many studies of conditions such as Alzheimers, anxiety and other neuro-functions.  SIRT1 modifies p53 - a bottleneck in cellular reproduction and a key regulator in cancer prevention, but which also an important aspect as to why it is active in calorie restriction conditions.

When reading reference like the one you have here its important to remember that correlation is not causality.  Very few genes in animals function only when specific behavior or conditions are experienced, especially signaling genes.

Examining the OMIM report (see link above) there has been a close examination of the possible role of SIRT1 in calorie restriction since the early 2000s in knockout mice.

SIRT1 would seem to play an important role in embryonic development for instance - cell growth is so important at that point and 80% of mice who are homozygous SIRT1 (-/-) knockouts die before they are born and even more die in the early natal period.  The mice who do survive have problems generating red blood cells which is another important case of cellular reproduction.

Yet the relationship of the knockout mice to calorie restriction has been debated - its been difficult to interpret the activity and the weight loss or gain of the knockout mice compared to wild type mice since the SIRT1 knockouts are smaller.  They may also have genetic traits that compensate for the absence SIRT1 in order to have survived.

More recently mice where SIRT1 expression in the brain have been produced, but the result has been anxiety or anxiousness as opposed to specific calorie restriction diet.

This reminds me of the story of leptin, in the early 90s they found that leptin deficient mice became quite fat, but despite this obvious linkage to obesity, leptin turned out to mediate a lot of other psychological factors as well - it only caused obesity when its function was blocked.  It did not turn out to be an appetite signal.

SIRT2 seems to have similar roles in calorie restriction.

  Rogina et al (2002) found that under 2 life-extending conditions, Rpd3 (601241) mutants fed normal food and wildtype flies fed low calorie food, Sir2 expression was increased 2-fold.

But also has similar relationships to Alzheimers.  SIRT2 has not been followed up on as much as SIRT1.  This correlation might not be causal or should be nuanced in a similar way.


Found an unknown species, whom should I contact? My father has found a very queer looking insect. He'd been watching it for over half a year on the tree right next to our house  and in all this time hasn't been able to find anything like it on the internet. Yesterday it died, and we found it on our porch, dad's put it in an air-isolated box for identification, please let me know if you are interested. We can send a picture of it for you via email or any other provided way, or please let us know what we should do it and whom we should contact. We live in Sydney.

Thank you, best of luck in everything!

Natural History Museum; UK, is a good resource.

http://www.nhm.ac.uk/take-part/identify-nature.html

  According to their webpage;

  Have you found a strange bug or a new plant in your garden, or stumbled across an intriguing animal bone or fossil while out on a country walk? Let us help you find out about it.

  Four ways to identify your specimens and sightings

  Check our selection of ID guides and apps below to see if one is relevant.
  Upload your photos and descriptions to our online identification forums for help from our scientists and other naturalists. Please tell us as much about your specimen as possible, including a detailed description, where and when you saw it, and its approximate size.
  Post your specimen or photographs to:
  Identification and Advisory Service
  Natural History Museum
  Cromwell Road
  London SW7 5BD
  Visit the Centre for UK Biodiversity at the Museum and show your wildlife or geology specimen to a member of our ID team. Drop in between 10.00-12.00 and 14.00-16.00:
  Monday to Friday (except bank holidays)
  the first Saturday of the month (or the second Saturday after a bank holiday weekend)
  If you need to discuss the best way for us to help with your enquiry, call our Identification and Advisory Service team on +44 (0)20 7942 5045 or email us.

  See more at: http://www.nhm.ac.uk/take-part/identify-nature.html#sthash.UGsoIYvE.dpuf

They also have provided some downloadable apps and pdf document resources in their webpage.


What is the length of tunnels puffins dig in the Farne Islands? I was watching this video and the host said that the puffins dig over 80km of tunnels in the Farne Islands. Is that true? I couldn't find a source to confirm that number.

If that's the current number of tunnels at any one time, it can be right, it depends if they dig a new nest every year.

Farne islands has mostly horned puffins with rainbow beaks as opposed to tufted puffins which have an different beak, the former makes nest around 1 meter and the latter up to 2.75 meters,

Puffins lay one egg per year, there are 30-50,000 pairs of them on Farne islands, that's about 40km of new tunnels every year.

Every five years the trust carries out a larger audit, the last being in 2013, when puffin numbers on the islands were strong, at just under 40,000 pairs.

That was an increase on the 2008 figure when a stormy summer hit numbers hard from a high of more than 50,000 down to 36,000 breeding pairs.


How might IVF (and related technologies) alter epigenetic marks? I was reading up on KCNQ1, which encodes a voltage-gated potassium channel, and I discovered that it happens to be only maternally expressed. This is regulated by KCNQ1OT1, a non-coding RNA, which is also epigenetically regulated (expressed only paternally). Mutations in KCNQ1OT1 are associated with Beckwith-Wiedemann Syndrome (BWS).

Further reading led to the discovery that there are ART-related (assisted reproductive technology) cases of BWS due to loss of methylation at KCNQ1.

However, this article found epigenetic stability of KCNQ1OT1 methylation in cultured human embryonic stem cells, which leads me to think that KCNQ1 might also have been properly methylated.

So what exactly are assisted reproductive technologies doing that can disrupt inheritance of epigenetic marks (that culturing hESCs doesn't do)? (Is this understood for any gene?)

I was at a talk last year where some geneticists were starting to look at the effect of IVF techniques on genetic issues.  Because of the work being done and the inclinations of the clients involved, this has not been studied very much.  One presumes that since zygotes are still used, there will not be much epigenetic effects due to methylation patterns - its the same cell stocks being used in vitro and in vivo.

There may be an effect on genetics because the natural selection process.  Spermatogenesis and oogenesis is a highly selective process; only a small fraction of the ova generated by the ovaries ever mature and a large percentage of sperm generated are not motile or have other irregularities.  During fertilization, sperm competition obviously throws out all but one in 250 million.  It also appears that there are processes in the fallopian tubes that can store the sperm for several (up to 5) days before fertilization.

So while its not strongly established one can see how various IVF processes vary from in vivo fertilization.  This could have an impact on epigenetic factors, although different sperm vary genetically due to Meiosis and this would be a big source of genetic variation in the outcome.


Can proteins from different viruses be gathered in one virus? There is a biology project I must do with some of my classmates and we're facing a problem.
We would like to choose proteins from different viruses that seem interesting to us (for example one protein from a negative-strand ARN virus and the other one from a DNA virus) and gather them (theory) together through this process called "directed mutagenesis". Is it possible ? If no, isn't there another mechanism that allows the gathering ?

Thank you !
(PS: Sorry for the english)

If I understand your question, you're asking if you can take a protein from Virus A, and make Virus B produce that protein. The answer is yes, you certainly can do that, although depending on the proteins and viruses there may be some constraints. There are many examples of this being done, and even more examples of making a virus produce proteins from humans or other species.

The actual process of inserting a new gene can be pretty trivial; you can pick up handy kits of viruses specifically designed to have new genes inserted into them.  If you're putting the gene into a virus of your interest, the design process can be a little trickier; you need to be sure that the inserted protein doesn't disrupt something essential for the recipient, isn't too large for its genome, and so on.

But in principle, it's pretty simple.


How to estimate a genome's size? The genome size of human is 3.000.000.000 bp and for Arabidopsis it is 255.000.000 bp. I know these numbers because their genomes have been published. Which methods are used by scientists to estimate the genome size before they sequence that genome?

Gel electrophoresis is a basic lab method to get size info about nucleotide fragments, although one might need to chop up larger DNA to be able to apply this method. The wikipedia page covers the topic well, thus I'd suggest reading it. I'll just give a short outline:

Nucleotide fragments are loaded into a gel (agarose or acrylamide).
The gel is put into a static electric field
Nucleotide fragment move to the positive end, because they have negative charge
larger fragments migrate slower than smaller fragments
standardized DNA ladder can be used to get approx size.

UV fluorescent dye is used to stain the fragments.

Another way, is to check closely related species. Among closely related species it is a fair assumption that they have similar genome size. You can also hybridize the unknown DNA to a DNA of such close relative to see how much of them are similar and you can also make estimates based on the size of the hybridized regions.