Can pathogens enter the bloodstream if the epidermis has been scraped off?

Our epidermis is the first line defence against natural infections; it is also a part of the innate immune system. This is due to

it contains a layer of dead cells that separates the living cells of the deeper layers of epidermis and dermis from the environment.
This part of the epidermis is avascular and so pathogens can not easily enter into the bloodstream through it.
It contains natural bacterial flora (like in our gut) that kills a large number of pathogenic microorganisms with their toxins.
secretion of sebaceous gland contains some antimicrobial substances.

There are lots of other protective features of epidermis.

Dermis is richly supplied by blood vessels. So even if all the layers of dermis remain intact its high vascular nature will act as an open entrance of microorganisms. By definition abrasion involves only the epidermis or some parts of the dermis but still we need to take tetanus vaccine after getting an injury contaminated with soil. In diseases like Stevens-Johnson Syndrome (where epidermis separates from dermis) or in burn patients the skin is covered with antibiotics and dressings. The patient is also given high dose of antibiotics to fight those bacteria that still entered into the bloodstream.


Great question! A lot of things affect how quickly a population or species can adapt to a new environment, including population size, mutation rate, generation time, standing genetic diversity, and selective pressure.

The diversity of life encompasses practically all combinations of those variables. A bacterial population might very well contain enough diversity to allow a portion of the population to overcome a rapid change. In fact, applying antibiotics to a bacterial population and counting the survivors is a common measure of mutation rates.

On the other hand, organisms with small populations and long generation times will be much less likely to overcome a rapid environmental change. This is why there is so much concern over anthropogenic changes to the environment, including climate change.

It's hard to provide a definitive answer, since "rapid change" is a relative term, and the difficulty of adapting isn't known. Some striking adaptations can be caused by a single base pair mutation, such as in beetles and Monarch butterflies that are insensitive to toxic plant compounds.

It's important to point out that natural selection is based on relative fitness. Therefore, an adaptive mutation will spread because it's likely that carriers will be more fit than all of their neighbors. This does not necessarily mean that individuals without the mutation will die or fail to reproduce, only that those with the mutation will do it better.

Likewise, adaptation is not necessarily caused by the environment changing and wiping out all but a few lucky mutants like in the bacteria example. Instead, the environmental change might make things more difficult, but as long as the population can persist, then mutations will continue to enter the population which could confer a selective advantage against the change. So, no, a population does not (cannot) carry all possible adaptations. A population cannot adapt to an environment it hasn't encountered.

Finally, it's worth pointing out that a species can expand its range through migration. A new, unsuitable environment can act as a migration sink (that is, migrants make it there but fail to establish) for a nearby population. If this happens for long enough, some of the migrants may have a mutation allowing them to establish in the new environment.


How to decide which is the correct scientific name for a particular species

When it comes to plants and animals, common names clearly differ from region to region.

A first effort to univocally classify them was done in the 16th century by Carl Linnæus (see my answer to this question for some historical background).

The nomenclature of plants is governed by the International Code of Nomenclature for algae, fungi, and plants (ICN), and for animals from the International Code of Zoological Nomenclature (ICZN).

The fact that there are rules, however, does not imply that names are conserved over time, nor that there is a rule for everything!

As time goes by rules change, certain species may be assimilated by others, or a certain subspecies will separate and become its own, and at times name changing proposals even raise havoc in the scientific community.

In summary, it is important to remember that taxonomy poses rules that are there to facilitate talking about science. Those are not absolute rules, sometimes they are arbitrary, and therefore for certain species there is no univocal name (and surely there is no correct name).


Does one need to have all the genes for bipolar disorder in order to have the disease?

No. In genome-wide association studies (GWAS) of psychiatric conditions, it is a constant finding that the associated variants each influence the probability/risk. The effects of all known variants can then be summed up to a polygenic score (PGS). A person with higher PGS is more likely than someone with a low PGS. But some people with low PGS (i.e. people who don't have "all the genes") still get the condition, it is just not as frequent as people with high PGS.

Another reason why we can say 'no' to this question is through findings of quantitative genetics studies. These estimate the heritability of certain traits. For the answer to be 'yes', the heritability would have to be one ($h^2 = 1$). However, as far as I know, there are no known psychiatric conditions that have heritabilities of one. Some high (e.g. $h^2\approx 0.8$), yes, but not one.

It's also worth mentioning that there is probably no sharp line between having bipolar disorder and not having it. It's a medical diagnosis that is useful but rough. Most likely, all of us have a little "bipolar" in us. I think it's probably most useful to view it as a spectrum.

  Is it possible for a person to have all the genes for bipolar disorder and still not have the disease?

This is not known and it may not even be a well-defined question. We don't know all the variants that affect the risk of bipolar disorder (or most other polygenic disorders). So we cannot say for sure.

Some 'omnigenetic' hypotheses propose that all genetic variants have some effect on all traits. Some effects are just smaller and some larger. In this case, the expression 'all the genes for X' may be technically meaningless.


Why doesn't Diabetes cause death by starvation?

Not all cells depend on insulin to take in glucose from blood (e.g. vascular endothelial cells). But the majority do (muscle tissue and fat tissue).

The lack of insulin causes the cell to use auxiliary metabolic pathways to generate its energy [1]:

in muscle, the protein breakdown is stimulated
liver gluconeogenesis is stimulated by low insulin levels and high amino acid levels in blood and using substrate from muscle and fat tissue
glucocorticoids stimulate lipolysis
liver starts ketone body synthesis, which along with medium chain fatty acids prove to be quite a good alternative energy source for the brain

Energy from nutritional principles is as follows:

Lipids = 9 kcal/g
Proteins = 4 kcal/g
Carbohydrates = 4 kcal/g - the most important because they are used as is. Lipids and proteins require energy from other sources to start chemical reactions which yield energy.

References:

Mark Brandt, Ph.D. Endocrine Notes Supplement from Rose Hulman Institute of Technology, pages 78-80
Wikipedia (links)


The theory is staggeringly improbable. However, so is life. The probability of life emerging from non-life is the basis of the misguided idea of intelligent design (a thinly veiled repackaging of creationism). Bear with me: the probability of life on Earth is 1. It is here, and this is the only observation of Earth we have. But the thought of complex life appearing out of some molecular soup by chance (abiogenesis) is also staggeringly improbable. But as I said, life is here. How did it get here? There are only three possibilities: Abiogenesis, divine creation, or from panspermia (which kicks the can down the road, because it had to have begun somewhere). God is no explanation at all, because even a mystical imaginary creator would have needed some mechanism besides waving a finger. So in terms of probability, both abiogenesis and panspermia would be astronomically improbable, but since life is here (probability of life is 1), then one of these two is the source of it. We have no hard evidence to choose between them.


Why doesn't Sanger (fluorescent) DNA sequencing double count nucleotides?

In chain-termination sequencing, a population of molecules is detected as opposed to a single one. The readout looks like this:

[ http://seqcore.brcf.med.umich.edu/doc/dnaseq/trouble/badseq.html ]

The peaks represent intensity of the four different fluorophores at the detector. Every fragment that is terminated at the same spot will have the same fluorophore and the same length. Because capillary gel electrophoresis separates molecules by size, these fragments will pass through at approximately the same time. "Approximately the same time" is why you see broad-ish and overlapping peaks on the readout as opposed to sharp and distinct lines.

Ideally, the readout will appear like the left half of the image, where there's minimal overlap between peaks. However, often you will see overlapping peaks, as in the right half of the image. The link above explains many reasons for why this occurs. Whether or not a peak is correctly assigned is determined by Phred scores, which is a statistical analysis of the shape and resolution of each peak.


Are viruses ever manufactured directly from viral DNA embedded in the genome?

It sounds like you're referring to the transition from the lysogenic cycle to the lytic cycle. The lysogenic cycle involves the viruses' DNA being integrated into the host's genome, such that the host has a dormant infection, the lytic cycle involves the virus' DNA being transcribed and translated to make the components of viruses, like capsid proteins, which then self-assemble to form many viruses which then leave the cell. The fact that this transition can occur means someone can experience an active viral infection, with proliferating virus particles, without exposure to additional viral contaminants. If it couldn't, then would there be much point (from a virus' perspective) to the storage of viral DNA in the genome which, as you've noted, retroviruses can do?

Transitioning from integrated DNA to phage particles:

To use the lambda phage (which is a bacteriophage and thus infects bacteria, not humans, but the underlying principles are the same) as an example, the expression of the viral DNA is controlled. But, the viral DNA is not a monolith - parts of the viral DNA of a prophage (the genetic material of the bacteriophage integrated into the bacterial host genome) are expressed but their expression prevents the expression of those parts of the viral DNA which would cause a transition from prophage an active infection, i.e a switch from lysogeny to the lytic cycle.

The lambda phage genome is shown below:

But an easier to deal with version which focuses more on the elements required for regulation would be:

There's lots of stuff going on here, but the key point is that lambda repressor, a protein coded for by the yellow cI gene, represses any transition to the lytic cycle. Aside: cI stands for clear I, because virus mutants which don't have c1 go straight into the lytic cycle and so produce clear spots on agar plates of bacteria since the bacteria are straight out killed rather than hosting the virus in the prophage form.
The lambda repressor prevents the transcription of the genes under those arrows in the top part of the diagram, and it's those genes which code for the things required for active virus particles, such as enzymes required to rupture the host cell's wall, and the proteins required to form the virus' coat.

So, to sum up, yes. Viruses existing as viral DNA embedded in the genome can cause infections, even in individuals not exposed to additional contaminants (but contaminants which cause damage to the host's DNA, like mutagens, will trigger the transition from lysogeny to lytic), and some of the viral DNA is always expressed (repressor genes) in order to prevent the expression of the parts of the viral DNA which would cause an active infection, were they to be expressed.


I agree that iPSCs will continue to be developed and will probably be used to make brains at some point in the future. Whilst it's obviously not possible right now, feasibility isn't the issue here. A lot of my answer will be somewhat opinion based as a result of the nature of such an ethical question.

As to the ethics of experimenting on such living brains, It's undeniably a tricky question - and, as with all ethical dilemmas, suffers from the inherent variability of ethics and morals (you will struggle to find two people with exactly identical ideas about right and wrong, and from a purely logical and scientific perspective there's no reason to believe that moral objectives exist at all).

An interesting phrase that you use in your question is "we are mostly our brain". I suppose it depends on what characteristics you're looking at: a brain alone would be incapable of surviving and by mass the brain only accounts for around 2% of the human body. we are mostly water; simple, lifeless and unconscious.

Therefore we are evidently ranging into territory of consciousness, and by "we" you are referring to our seemingly conscious 'mind' as conjured by the complexities of the brain. As for this, I think perhaps the philosophy stack exchange is the place to go...

Ultimately it depends on whether we look at a brain as simply a collection of atoms which form molecules, cells, tissues and then organs or as something more - this is the whole idea of emergence (for example, an individual ant is unconscious and negligible, but many thousands of ants communicating using chemicals and simple commands forms a highly complex and adaptable ant colony - the ant colony is greater than the sum of its parts). if the former is true, then there should be no difference in manufacturing a brain and experimenting on it to making muscle tissue and performing experiments on that (or even creating a crystal from chemicals and using that for experiments). If we look at the brain as something greater than the simple sum of its parts - as a living, conscious being - then I suppose we'd need to go through the proper channels that we have now when dealing with something that's alive.

From here an infinite variety of problems crop up: would the brain be given the full rights of a human, or treated more like animal test subjects? Would consent from the brain be required? Could a brain even be conscious if unattached to the rest of a body? Would killing the brain be murder as it would be with a human?

So far I've just been stating issues: my personal opinion is that we ought to find a balance somewhere between treating the potentially conscious brain as merely an impressively complex collection of lifeless components and giving it the full rights of a human being. where that line should be drawn? I don't really know. Personally, I'd rather test drugs and treatments on a mere brain than on a fully formed and functional human being, but someone else might not agree.

These questions are always difficult, and science can't really give any reasonable answers (scientists can't even agree on what makes something alive, let alone conscious). there is an entire field called bioethics devoted to things like this.
my advice would be to ask this on the philosophy stack exchange as you will get some interesting answers there.


Why are fatty acids consisting of even number of carbons predominant?

In short, it's because fatty acids are made from two-carbon blocks.

The way that most organisms make fatty acids is by the successive addition of two-carbon units (acetyl-CoA). So we usually get even-numbered fatty acids just because the building blocks are also even.

In plants and in synthetic contexts, we can have some reactions that can produce odd-numbered fatty acids (by building with two-carbon units three times to get six, and then breaking that six in half to get three, for example). Such odd fatty acids are seen in some organisms, but humans are usually thought to get them from other sources (e.g. microbiota, diet).

EDIT:

Point 1: Fatty acids are generally built two-carbons at a time.

The European Bioinformatics Institute has a really good explanation of fatty acid synthesis. The quote below is from that (https://www.ebi.ac.uk/interpro/potm/2007_6/Page2.htm):

  "Whether existing as one complex or as independent enzymes, the
  reactions catalysed by types I and II fatty acid synthases are the
  same.  Both systems are primed with acetyl-CoA, and then add 2-carbon
  units to the growing chain using malonyl-CoA as substrate."

Point 2: Odd-numbered fatty acids can be produced by various organisms, and can be linked to dysfunction in humans.

doi:10.1038/srep44845 talks about the importance of odd chain fatty acids in disease as a preface to its findings about the sources of such fatty acids. They try to narrow down where odd-chain fatty acids come from, but they definitely seem to be building their case on the pretense that odd chain fatty acids are not great in humans.

  "According to the literature, the origin of C15:0 and C17:0 has long
  been attributed to the diet, specifically from ruminant fat as the
  main contributor in a typical Western diet. This has been explained by
  the fact that these two OC-FAs are produced by the rumen microbiome
  and then incorporated into the fat deposits of the host animal
  destined for human consumption."

Point 3: Plants produce odd-chain fatty acids

An established/old paper (doi:10.1006/abbi.1994.1110) mentions this, and there's a Wikipedia article (https://en.wikipedia.org/wiki/Odd-chain_fatty_acid) that paraphrases in a nice way:

  Some plant-based fatty acids, however, have an odd number of carbon
  atoms, and Phytanic fatty acid absorbed from plant chlorophyll has
  multiple methyl branch points. As a result, it breaks down into three
  odd numbered 3C Propionyl segments as well as three even numbered 2C
  Acetyl segments and one even numbered 4C Isobutynoyl segment.


Book recomendation: cell cycle regulation

Robust texts covering such 4 listed points with rigour include the following selection:

Molecular Biology of the Cell
Molecular Cell Biology
Cell Cycle Regulation
The Cell Cycle Principles of Control.

& even a review of the latter here.

HTH


As far as I was able to find there exists two models of the action potential by using RC circuits. Do note that there is no flow of electrons per se across a tube, but rather a migration of potential. See this.

The Hodgkins Huxley model :

  The Hodgkin–Huxley model, or conductance-based model, is a mathematical model that describes how action potentials in neurons are initiated and propagated. It is a set of nonlinear differential equations that approximates the electrical characteristics of excitable cells such as neurons and cardiac myocytes, and hence it is a continuous time model

http://en.wikipedia.org/wiki/Hodgkin%E2%80%93Huxley_model

The Fitzhugh-Nagumo model:

  The FitzHugh–Nagumo model is a simplified version of the Hodgkin–Huxley model which models in a detailed manner activation and deactivation dynamics of a spiking neuron. In the original papers of FitzHugh, this model was called Bonhoeffer–van der Pol oscillator...

http://en.wikipedia.org/wiki/FitzHugh%E2%80%93Nagumo_model

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

Hodgkin, Allan L., and Andrew F. Huxley. "Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo." The Journal of physiology 116.4 (1952): 449-472.

Now, I have not dealt with differential equations in quite a while, and hence may not be the best source for explaining the model itself, but I'll try and update the post with what (if anything) I understand.


What is SDS PAGE gel polymerization time?

There is nothing like a general polymerization time, as this is a chemical reaction which depends on many factors. The most important are:

APS: Concentration and and the age of the chemical are important. APS decomposes over time when it is not stored completely dry (which it is not on most benches) and also with freezing thawing cycles in storage. APS provides the free radicals necessary for the reaction; without it no polymerization will happen. In my experience APS is the most critical part of the reaction, with old solutions making the polymerization really slow. I would make a stock solution, freeze it in aliquots. For making gels I thaw on aliquot and keep it in the fridge afterwards for a week and then discard it.

TEMED: Is the catalyst for the reaction, too much of it will start the reaction very fast.

Temperature: The warmer it is, the faster the polymerization will be. In the cold room you will not get complete reaction, if any.

What you can do is to store the remaining acrylamide in the beaker and wait until it is polymerized. Then your gel should also be ok to use. A longer polymerization time (assuming that your gel was completely polymerized before) will not change the resolving capacity of your gel.


As already pointed it out, there is no scientific consensus on the answer to this question. This is because it is hard to test proposed explanations and it's likely that several factors interacted.

All of these have been claimed to be the explanation for the evolution of bipedalism:

Freed hands for increased tool use. (Encyclopedia Britannica)
Freed hands for the use of weapons in hunting or the use of containers to transport plant foods obtained by gathering.
There are three variants: the “man the hunter” version which sees male hunting as the key stimulus (Washburn 1967 in Haraway 2013); the “woman the gatherer” version which sees women needing their hands free to carry gathered vegetable foods as the stimulus; and the “man the provisioner” version, which stresses males carrying food (either meat or plants) to provision females and offspring.
All of these explanations are probably flawed because they invoke present utility to explain the origins of bipedalism.
Bipedalism was created by female sexual selection of males with large, visible genitals.
Although unlikely, this may be correct, but it is impossible to test. (Encyclopedia Britannica)
Bipedalism evolved to aid in avoiding predators. Higher head allows you to see longer distances over the grass. (Encyclopedia Britannica)
Bipedalism evolves because it allows energy efficient locomotion between forest patches in an increasingly open environment.
“Radiator theory”: Natural selection favored bipedalism in open environments because it decreases exposure to the sun and helps keep the brain cool. (Wheeler, discussed in Haviland 2007 and Encyclopedia Britannica)
Brain is highly sensitive to heat stress.
This allowed hominins to be active in mid-day, when competing predators are less active. (Essentials of Physical Anthropology, p. 165). Since the same carnivorous animals with which hominins were in competition (both would scavenge dead game) could attack hominins, hominins were probably safer from predator attacks during midday as well.
Terrestrial bipedalism may be a continuation of an upright body posture inherent in a tree-climbing/brachiating adaptation.
Gibbons, the most arboreal of the apes and the best brachiators, walk bipedally on the rare occasions they come to the ground. (Encyclopedia Britannica)

The earliest hominin fossils appear to have been bipedal, with no clear evidence of a transition through a knuckle-walking stage, the principal mode of locomotion of modern African ape. (Kivell and Schmitt 2009, here's a secondary source, and here's a primary source that disagrees, Richmond and Strait 2000)

If this is true, then the modern African ape mode of locomotion (knuckle-walking) is a derived trait, and vertical body posture may be the ancestral trait in the African hominoid evolutionary lineages. In other words, if this is true, the ancestor of all great apes including humans was already bipedal, and modern African apes have evolved to knuckle-walk since then.
Also if this is true, the previously mentioned factors would reinforce and refine bipedal locomotion in the hominin lineage.

It is likely that explanations 4, 5, 6 and 7 all interacted to select for bipedalism. They correspond best to the paleontological and ecological data. Numbers 1 and 2 are unlikely, because bipedalism appears long before evidence of tool use.


In order to assemble your TAG oligos by PCR you will need to redesign your primers so they are complementary to the TAG oligos as DNA polymerases work by adding nucleotides to the 3' end of a DNA strand.
Your design would look like this :

Now with this design you won't be able to assemble everything together as TAG-3 complementarity to primer 2 only presents 5' ends to be extended, which your DNA polymerase can't do. So you can either order the entire reverse complement of your TAG-3 oligo or design a primer 3 that would anneal at the 3' end of TAG-3 to amplify TAG-3.
With all these parts, you should be able to assemble everything in a single reaction, but depending on your downstream process you may have to purify the product of interest as the single reaction will generate intermediates (1, 2, 3, 1+2, 2+3).


TL;DR answer: Regression to the mean doesn't always occur (children can be taller than either parent, as can be easily observed at any high-school basketball game), so it doesn't affect the theory of evolution through natural selection.

The observation of regression to the mean was of great concern to Darwin and early thoughts on natural selection (don't confuse "evolution", which is the observed phenomenon, and "natural selection", which is one of the theories proposed to explain evolution).  The problem has been effectively resolved since the rediscovery of Mendel's genetic work at the end of the 19th century.

"Regression to the mean" is inevitable if inheritance works through blending of features.  That was how everyone believed inheritance to work in the mid-1800s, and Darwin understood that it presented an insuperable obstacle to his theory.  That is, if blending inheritance was true, then natural selection could not be true.  Darwin puzzled over this quite a bit, and came up with some unsatisfying suggestions to overcome it, but at the end of the day, one of the predictions that his theory of evolution through natural selection made, was that blending inheritance could not be true.

Of course, blending inheritance is not true.  Mendel showed that in fact inheritance is quantal, not blending.  We now know that many traits of interest look, superficially, as if they're blending (which leads to regression to the mean), but are actually the result of multiple traits interacting.

With blending inheritance, the variation that is required for natural selection to work is lost, generation after generation; regression to the mean in an inevitable consequence.  With gene-based inheritance, variation (can be) preserved generation after generation; regression to the mean is a common but not inevitable consequence, because the variation in the original population is still present and can be re-created given appropriate selection pressure.


DNA degradation half-lifetime within fossilized/frozen species is ~ 500 years., even when the conditions are perfect for preservation.

Thus, in theory, if we could sequence anything that is less then 13 000 years old (expected length of preserved nucleotide sequences ~30 bp, which is just enough to stitch together two unique regions). If we have several copies of DNA (several cells), we can go a little bit further by sequencing same reads several times. If we assume an average cell is 30 um in diameter, we have ~40 000 cells in a cubic mm of tissue samle. this will allow us to extend the sequencing horizon by another 8000 years. With a cubic sample of intact, perfectly preserved tissue (this is REALLY A LOT and REALLY RARE) we could get an additional 5000 years, limiting our possibility to know the genome, let alone reproduce it to 26-30 000 years.

By using a couple of sequence assembly tricks, such as existence of reference genomes of closely related species, we could either decrease the amount of tissue sames or allow the DNA to get a little bit more degraded. However, even with a cubic centimeter of tissue we won't be able to go beyond 50-100 000 years.

The furthest we have gotten now is a Neanderthal sequence (~30 000 years) and it was already tough. It would be impossible to get a hand on dinasaurus DNA sequence, let alone trying to clone it. Mammoth, Saber-tooth Tiger and Dodo should be ok, provided we can find their remainders.

Now, Once you get the raw DNA sequence, you have to get the epigenetic code right, find a compatible egg of a related spicies (that is quite hard), inject your DNA into it, and hopefully, with lots of ifs you can get your clone and hope it survives. However the part about getting the epigenetic code right and finding a compatible egg is really not easy. Personally, I won't parry on anything that doesn't have close related species still living.

UPDATE: as of June 2013 a genome of a wild horse 700 000 years old have been sequenced, which is the furthers we could get so far.


Which animal dug this 5 cm diameter hole deep into mud and build a large mound around it?

A crustacean (land crayfish). There are a lot to choose from.

http://web.nchu.edu.tw/~htshih/crab_fw/fw-crabe.htm


Can someone who cannot talk still whistle?

Sounds such as certain phonemes are made merely with the use of air flow and movement of the lips or tongue, without the need for action of the vocal chords. Think of 'f', 's', 't', k in the English language. These are called unvoiced phonemes in phoniatrics (see the phonemic chart). Also, clicking sounds and whistling can be made without use of the vocal chords.


Can genetics be an answer to our human flaws?

Here are three elements you want to consider

we are not able to make genetic manipulation of all the cells in a grown-up individual. There exist a whole bunch of treatment making use of genetic engineering in adult humans but they are typically quite costly.
The phenotypic traits that you mention are extremely complex. There is no simple gene that will allow a lizard to regenerate a lost limb. You will have to learn more about cell specialization in order to understand why lizards have a power of regeneration that we don't. Similarly, you can't just transfer a few genes and expect a human to be able to photosynthetize. Photosynthesis is a very complex process which require the ability to perform a whole bunch of reaction, which require organelles we don't have for the reactions to take place, which requires the ability to gather and concentrate lots of $CO_2$, etc... It is really really not that easy. You should learn more about the specific traits you are mentioning to get a notion for why it is not that easy.
Genetic manipulation on human is vastly illegal for ethical reasons. But these ethical reasons are to be discussed on philosophy.SE.


Aesculapian snake (Zamenis longissimus). Common european species, non venomous, rodent/egg eater.

edit1: they can swim and can be found next to water bodies but are terrestrial.


Could bacteria and phages be found in tissues?

Per my comment to the question, here is an answer to the same question asked on ResearchGate:

Whole genome sequencing of human tissue samples often results in reads aligning to bacterial references, and this is actually a method used in the diagnoses of infectious diseases.
Understanding the Promises and Hurdles of Metagenomic Next-Generation Sequencing as a Diagnostic Tool for Infectious Diseases
Identification of low abundance microbiome in clinical samples using whole genome sequencing
However, because pathogen DNA may be present at a much lower abundance than host DNA, it may be difficult to distinguish true infections from contamination and false positives. Steven Salzberg addresses these concerns and offers a computational solution in a recent publication:
KrakenUniq: confident and fast metagenomics classification using unique k-mer counts
"Usually, the vast majority of the reads match (typically 95–99%) the host, and sometimes fewer than 100 reads out of many millions of reads are matched to the target species. Common skin bacteria from the patient or lab personnel and other contamination from sample collection or preparation can easily generate a similar number of reads, and thus mask the signal from the pathogen."

To expand on this answer, it is important to realize that accurate identification of low-abundance organisms in metagenomic reads requires very good reference genomes.  A separate paper from the Salzberg group discusses a startling discovery:  many high-copy repeats in the human genome have been incorrectly annotated as bacterial proteins in the NCBI RefSeq database.
Human contamination in bacterial genomes has created thousands of spurious proteins
This suggests that researchers should be careful when attempting to infer the presence of low-abundance bacteria or phage in human tissue sequencing data, particularly when the presence of those organisms is not corroborated by other analyses.


Usage of the taxonomic classification "Pinnipedia"

The Comments section of that page has the explanation:

  Wilson & Reeder (eds., 1993) note that "the pinnipeds (otariids,
  odobenids, and phocids) are included within the suborder Caniformia;
  placing them in a separate Order would make the Carnivora
  paraphyletic." This arrangement continues to be followed in Wilson &
  Reeder (eds., 2005)

If both Carnivora (Bowdich, 1821) and Pinnipedia (Illiger, 1811) are orders in the traditional Linnean taxonomic sense, then one cannot be nested within the other. If this were to happen, then Carnivora would be paraphyletic because it would exclude some of its members. The same argument is made when discussion birds as dinosaurs (you can't talk about Dinosauria that doesn't include Aves).

The problem arises when phylogenetic systematics (clade names) meets traditional Linnean systematics (orders, suborders, etc.). Phylogenetic systematics does not distinguish these higher taxonomic groups. Clades are just nested groups of monophyletic taxa.

So then to answer your last question, Pinnipedia does appear to be in common usage (Google Scholar reports several hundred citations in the past few years). The key is to distinguish Pinnipedia as a traditional Linnean order (not valid) and Pinnipedia as a monophyletic clade that includes seals, walrus, and sea lions (perfectly fine). Seals, walrus, and sea lions are all more closely related to each other than to other Carnivora, so they are monophyletic, and the name for that grouping is Pinnipedia.

Here's the Tree of Life page that has all the clade names.


Do adult mosquitoes have color preferences?

"Mosquito" is a quite broad term, since it englobes several Genera and more than 3500 species. But, at least for some Genera, there are indeed colour preferences.

For instance, Aedes seems to have colour preferences. Have a look at this table from Gjullin (1947), from a research in which the effect of different coloured clothing on the biting rate was investigated:

As you can see, black is the new black for Aedes mosquitoes. At least in the shirt of their victims.

Also, in his paper from 1903, Alpheus Packard describes an interesting experience, this time with Anopheles:

  Color-preference in the Mosquito

  In continuation of their researches on the structure and biology of Anopheles maculipennis, the commonest British mosquito and one known to convey malaria, Dr. Nuttall and Mr. A. E. Shipley observed some interesting facts on the preference this species exhibits for different colors and for different shades of color. The experiments were conducted as follows : In a spacious  photographic studio a large muslin tent was set up with one end against the glass window through which the sunlight poured. At the bottom of the tent were some large pans for the Anopheles to breed in, and these were from time to time renewed.

  The mosquitoes were fed on bananas, which, it may be noted, must be kept fairly fresh, otherwise dates or figs are preferable. On one side of the tent seventeen boxes without lids were piled one upon the other, the order being changed each day so as to eliminate any preference due to position or exposure to light. Each box was lined with a cloth having a slightly rough surface — not a shiny or smooth one — to which a mosquito could easily cling. The experiment consisted in counting the number of mosquitoes found in each box on seventeen different days.

  The results obtained are striking. During the seventeen days on which the count was made, 108 mosquitoes were found in the navy-blue box, 90 in the dark-red box, 81 in a reddish-brown box, 59 in the scarlet box, and 49 in the black box. There was at this point a sharp drop to 31 in a slate-gray box and 24 in an olive-green box. Violet, leaf-green, and full-blue boxes had respectively 18, 17 and 14. Pearl-gray had 9, pale green 4, light-blue 2, ochre and white 2 each, orange I, and pale yellow about the color of khaki none at all.

  It is thus evident that color has a marked power of attracting this species of
   mosquito, and that the color which is by far the most attractive is navy-blue. In both services and equally amongst civilians this is a very common, perhaps the commonest, color for male attire. The experiments just quoted show that it is at least equally popular with malaria-carrying mosquitoes. Light colors were avoided, especially those with a tinge of yellow. Khaki-colored garments would seem to have other advantages besides that of invisibility on a light soil.

Sources:

C. M. Gjullin; Effect of Clothing Color on the Rate of Attack of Aëdes Mosquitoes, Journal of Economic Entomology, Volume 40, Issue 3, 1 June 1947, Pages 326–327.
Packard, A. S. “Color-Preference in Insects.” Journal of the New York Entomological Society, vol. 11, no. 3, 1903, pp. 132–137. JSTOR, JSTOR, www.jstor.org/stable/25003044.


According to This paper and most biology textbooks, S-phase or synthesis phase is literally defined by the beginning and ending of DNA replication.  The first picture does not accurately represent the nature of DNA replication and is instead a model to help people track DNA copies during stages of cell division.  DNA is replicated as chromatin and condenses to "double" chromosome form.  You can see some micrographs of DNA condensation in this paper.  You'll see that they don't condense as single chromatids, but they are already replicated.


Trees need:

Deep roots to get more water and anchor their growth.
Strong trunks to support themselves against gravity.
A vascular system to move water and nutrients throughout the tree.
Small leaves that can be supported high by the trunk to compete for sunlight.

Water plants need:

Just enough root to anchor its location.
No vascular system. Water is everywhere.
Leaves that are more substantial than the stems to gather as much sunlight as possible through the cover of water.

So the kind of body that has to develop under water to thrive is in many ways the opposite of the kind of body needed to thrive on land.

Water plants would have to waste energy on

Vast roots.
A strong trunk.
A vascular system.

...Things it wouldn't need till later while receiving little sunlight on small leaves. It would have to shed its thirsty skin like a snake on the above water parts. Too complex and little or no demand for it.

If water plants had evolved a way to turn oxygen into helium and keep much of it trapped within its leaves, then we'd have tall ocean forests. The plants could grow just like they do now  but with slightly fluffy leaves. As soon as it broke water surface, the abundance of oxygen would ramp up helium production and really fluff them leaves. The slight stems would have to be scrappy instead of massive.

There would be Greek mythology that Gaia was married to Helios but left him for Poseidon the Gaia-Shaker. Poseidon and Gaia were cursed with children (the vast ocean forests) who rebel against them and adopt a lifestyle where they are always reaching out to Helios and later in life shedd their bodies to be closer to him in spirit. Some early humans tried to rob the Helium spirits of the ocean forests by inhailing them out of their plant bodies. They were cursed and turned into chipmunks with only their hands to remind them of their past humanity.

Edit to add reference: A piece by Mickey Walburg on eHow.com

Though I would call mangroves amphibian trees, I wouldn't call them large and I was trying to ascertain the spirit of what @kai teorn was asking rather than let the question sit unanswered when I believe I can answer it.
You learn something new often if you're looking and today @MattDMo introduced mangroves into my awareness. If he thought it was the answer to the spirit of the question post, he might have elaborated on it as an answer instead of a comment. I could be wrong about that.

Mangroves are mostly coastal. They are usually at the edges of the water. The ones that are a few meters in the water are usually more like shrubs than majestic boreal forest trees. They end up shooting roots everywhere and kinda lounge around compared to the typical tree standing straight reaching for the sun. Also the incidences of Mangroves in the ocean away from the shoreline are of maybe a handful bunched up, hardly a species wide return to the the oceans. Seen from aerial photos, Mangrove concentrations look like boreal forests surrounding lakes, not swamp lands.

  Why are there no tree-like plants that grow in lakes?

  Looking at aerial photos of boreal forests, with dense woods clear-cut
  by quiet lakes, I wondered why exactly are the woods so clear-cut at
  the edge of water?

I think the spirit of the next question is about trees in general in lakes. Not the few instances peppered around the world. Also some lakes grow and shrink throughout time, sometimes long enough for trees to gain a little ground and survive lake growth. But I don't think those trees as a species have developed adaptations to grow from shallow lake bottoms.

  Why won't trees develop adaptations that will let them grow from a
  shallow lake bottom, with the lower part of the trunk in the water and
  the crown above the water?

... and from the end of the post ...

  Of course there are aquatic and semi-aquatic plants like water lilies,
  Scirpus or Typha, but they are a far cry from the nearby terrestrial
  forests, in terms of biomass. Why don't they develop into large
  amphibian trees, or why don't terrestrial trees try to re-colonize
  lakes?

... I eliminated mangroves from qualification. Interesting but I still don't think it's what @kai teorn had in mind. I think @MattDMo introduced mangroves as a comment to enhance our knowledge.


No. of meiotic divisions to produce specific no. of seeds

Assuming that you have studied megasporogenesis and microsporogenesis. To produce a seed, you require the production of pollen(n) and egg(n) and their fusion.

Let's start with pollen grain(n):

  4 pollen grains are produced after 1 meiotic division in the pollen sacs.

$$4~\text{pollen grains} = 1~\text{meiotic division}$$

  To produce 1 pollen grain.

$$ 1~\text{pollen grain} = 1/4~\text{meiotic division} $$

  For production of $x$ pollen grains.

$$ x~\text{pollen grains}=x/4~ \text{meiotic divisions}\quad(1) $$

Now coming to egg(n):

  Only 1 egg is produced after 1 meiotic division in the megasporangium.

$$ 1~\text{egg}= 1~\text{meiotic division}$$

  For production of $x$ no. of eggs.

$$ x~\text{eggs}=x~\text{meiotic divisions}\quad(2)  $$

For production of $x$ no of seeds(2n):

  $x$ pollen grains and eggs are required. No. of meiotic divisions to produce $x$ pollen grains and eggs.

$$x~\text{seeds}=x + x/4~\text{meiotic divisions} \quad\text{From}~(1)~\text{and}~(2) $$


What are the exceptions to Mendel's laws?

You are right but the list is certainly not exhaustive. Here are a few more concepts you may want to consider.

Exception of law of dominance:

epistasis

Allelic effect at a given locus depend on the variants at other loci
environment dependence and specific case of frequency dependence

The concept of dominance can be used for any quantitative trait. Typically, when the quantitative trait of interest is fitness, then the trait often depend on the environment. A typical and interesting case is when the fitness depends on the frequency of alleles in the population. Depending of the frequency of the allele at a given locus, the relationship might be a relationship of dominance, additivity or dominance for the other allele.

Exception of law of segregation:

meiotic drive

from wiki: "Meiotic drive is a type of intragenomic conflict, whereby one or more loci within a genome will affect a manipulation of the meiotic process in such a way as to favor the transmission of one or more alleles over another, regardless of its phenotypic expression. More simply, meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time."

Exception of law of Independent assortment:

epistasis for fitness

Imagine a case where a given combination of allele is lethal at very young age, then you would never see these two alleles together in an individual. It is per se, not a case of exception to independent assortment but it gives the feeling of such exception. A case more extreme when a given combination of alleles prevents fecundation could however be considered as an exception to independent assortment.


Are females more flexible than males in all mammals?

Try birthing a child for once. You need to be flexible to accommodate the growth of another organism inside you.

Take a look at some pictures of the mothers spine during the course of a pregnancy, you will have no further questions. Same with belly size, breast size and vagina size upon birth.

This video is a nice explanation of this. Also includes the different centers of gravity for males and females (human).

http://www.youtube.com/watch?v=WO8DtsZO1nA


How can Southern blotting be used to establish gene copy number?

This method is commonly practiced. Atleast I see the people working with zebrafish transgenics using it.

When you shear the genomic DNA or do a restriction digestion, you are likely to get fragments of different sizes.
It is highly probable that the two (or more) locations harboring a copy of the DNA element are a part of fragments with different sizes. So on the blot you'll get two bands.

But as I said this test relies on probability that the two fragments are dissimilar in length. Therefore, southern blot should not be considered as an absolute test to determine copy number. Inverse PCR, FISH, etc can be used to determine copy number.


Multiplication to formalize Microbiological Processes

Here's the quick answer you asked for, too big for comments so sorry if this is not a full answer either.

This paper is an example of cytoskeletal modelling.  the equations are not simple products (that is to say they have exponentials, derivatives and other non- multiplication operations in them).

This example reference is a simple axonal growth model.  You will see derivatives being modeled as products.  Not sure if this is what you are looking for.


Is it necessary to calculate lane normalisation factor when doing western blot data analysis?

Generally speaking, the proper way to quantify a western blot is to normalize to a loading control such as Actin or GAPDH. In this case it would be (pGSK3/Actin)/(GSK3/Actin) as total GSK3 is not a loading control. A loading control is to protein that is accepted as unvarying in concentration across multiple samples if the same protein amoun is used, and to my knowledge GSK3 would show more biological variability than accepted loading controls. This would be considered the best practice to compare protein concentrations across samples.
That being said, if all you care about is the ratio of active to total, pGSK3/Total GSK3 is probably sufficient to assess if your manipulation changed active/inactive:total ratios. For example, in autophagy assays you can measure autophagic flux by measuring LC3-I to LC3-II, and I've never seen them normalized to a loading control since its a ratiometric readout contained within a single sample.


I work for MRC-Holland, the developer of MLPA, and what Kacper explains is indeed the case. Any RPO (right probe oligo) that is not ligated is also amplified in the MLPA reaction, as the reverse primer can bind to the primer binding site of the RPO. HOWEVER, since this unligated RPO oligo LACKS the binding site for the (fluoresently labelled) forward primer, the amplification ends here. LIGATED probes, in contrast, contain the binding site for BOTH primers, and hence are amplified exponentially. Furthermore, the fluorescent label is only incorporated in the amplicons that results from ligated probes.


What happens to snakes that swallow rodents as a whole?

Almost everything the snake eats is completely digested. They have a very efficient digestive system. Things that wouldn't be digested would be the rodent's claws and hair and feathers of birds. And during digestion, the snake's intestines go into overdrive mode and expand when necessary. When the snake isn't eating, the intestines are usually dormant.

If something goes wrong though, or if the snake is threatened, the snake regurgitates everything in order to increase its mobility.


I want to present another (possibly more practical) approach towards this phenomenon. Lets begin with amino acids as alternatives.

Amino acids, apart from being a source of toxic ammonia, are also harmful to the brain in another way. The two (concerned) types of amino acids, aromatic and acidic ones, are a lot more than just energy sources for the brain. Aromatic amino acids: tyrosine, phenylalanine and tryptophan, are precursors for the biosynthesis of neurotransmitters like serotonin, melatonin, norepinephrine, dopamine, etc. The greater the amount of precursors, more the product formed. Talking about acidic amino acids, glutamate and aspartate are themselves neurotransmitters. So, same case could apply to them too. So, it might have been that neurons, in evolution, decided to just get rid of such sensitive and powerful energy sources which can disrupt their basic function. You can see Fernstrom, 1994 for a study on this.
Fatty acids are definitely a nice candidate. But they have some side effects too. For a long time, it was thought that since fatty acids (or lipids in general) are attached to albumin while in blood, they cannot cross the blood-brain barrier (see Stryer for example). But, this is not the case, as now proven. Then why are fatty acids not a preferred energy source for brain? There might be quite a few reasons for this.

First, $\beta$-oxidation of fatty acids demands more oxygen as compared to glucose, making neurons more vulnerable to hypoxia. For example, the reaction for complete oxidation of glucose is (from Molecular Cell Biology):

$\ce{C_6H_{12}O_6 + 6 O_2 + 36 ADP^{3-} + 36 P_i^{2-} + 36 H^+ \rightarrow 6 CO_2 + 36 ATP^{4-} + 42 H_2O}$

On the other hand, the reaction for $\beta$-oxidation of palmitic acid is (from pharmaxchange):

$\ce{C_{37}H_{66}N_7O_{17}P_3S (Palmitoyl-coA) + 23 O_2 + 108 P_i^{2-} + 108 ADP^{3-} \rightarrow C_{21}H_{36}N_7O_{16}P_3S (coenzyme-A) + 108 ATP^{4-} + 16 CO_2 + 23 H_2O}$

where palmitic acid is $\ce{C_{16}H_{32}O_2}$. This clearly shows that glucose oxidation requires less oxygen (1 molecule per carbon) as compared to fatty acids (almost 3 molecules per 2 carbon).

Second, nonesterified fatty acids (NEFA) decrease membrane potential at inner mitochondrial membrane, causing collapse of electrochemical proton gradient.
NEFA also interfere with electron transport chain, stimulating generation of reactive oxygen species like superoxide ions (see Zhang et al, 2006 for example).
Apart from this, the rate of ATP generation from fatty acids is slower as compared to glucose, which makes glucose a better option for neurons (see Stryer).

All these factors might have a played a role in making neurons choosy for glucose. This is also supported by the fact that one of the enzymes of $\beta$-oxidation, 3-ketoacyl coenzyme-A thiolase, has significantly lower activity in neurons as compared to other tissues (Yang et al, 1987). You can see Reiser et al, 2013 for a study on this.

PS: It has been shown that the brain can also use lactate along with ketone bodies as an energy source. See Wyss et al, 2011 to know more about this.


Distinction between primary and secondary tumor

The difference is pretty easy to understand. The secondary tumors is metastiesed tumor sped to enother parts of body. On the other hand the primary tumor is the source of the metastiesed.

I give you one example of this. On of the most common tumor of testicles is seminoma metastiesed to the peritonium, lungs, brain.

The secondary tumor is usually hard to distinguised with primary. But usually if there is specific antigen which can be recognised by antibody. The antibody is usually cultivated in mice. But this antibody have to be recognised by enother antibody. The second antibody to mice antibody is cultivated usually in rats. After that the secondary antibody is usually modified by fluorescent chemical. This is indirect immunohistochemistry. Direct is usually only the first antibody modifided by some fluorescent.

So first of all you have to do biopsy of that potential tumor. After that the sample is usually fixated by freazing and sliced by cryomicrotom. Than samples is usually put in to petry dish and poor with izotonic solution. Then the primary antibody is add. It take some time to react (find the antigen), thereafter is add the secondary antibody. To view the antibody you have to activated fluorescent by laser in fluorescent microscope. So if the fluorescent is in the sample, the tumor should be secondary.

Nevertheless is still hard to distinguish secondary tumor from the primery. Usually is up to experiencies with the tumors and how they are behave in body of patient. This is one of the reasons why is hard to treat the cancer.


if mother is O-

That means:

group O in ABO system: anti-A and anti-B antibodies
group Rh- in Rh system: no D antigen and no ant-D antibodies unless previously senzitized

  baby is any +ve blood group other than O+

ABO system: A, B or both antigens present
Rh system: D antigen present

So, the mother has anti-A and anti-B antibodies and her immune response will be directed towards the fetal RBCs containing A, B and D antigens. But, in theory, the immune system should also produce anti-D antibodies because of antigen presenting cells which will expose D antigens to T lymphocytes.

What is known is that if the mother already has anti-D antibodies, no other are secreted from fetal D antigens. This is how passive immunization vaccines work:

  This is done so that the fetal Rhesus D positive erythrocytes are destroyed before her immune system can discover them. This is passive immunity and the effect of the immunity will wear off after about 4 to 6 weeks (or longer depending on injected dose) as the anti-Rh antibodies gradually decline to zero in the maternal blood [1].

But the mechanism is not clearly understood:

  The most fascinating aspect of the story scientifically is that we still do not have a complete, mechanistic understanding of how this therapy works. The original hypothesis that Rh-immune globulin functions by clearing fetal Rh(D)-positive red blood cells from the maternal circulation, thereby hiding this foreign antigen from the maternal immune system, is inconsistent with the fact that passive immunization with Rh-immune globulin guides the fetal red blood cells directly to antigen presenting cells, the same cells responsible for initiating an immune response to foreign antigens [2].

References:

Wikipedia contributors, "Rh disease," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Rh_disease&oldid=615938189 (accessed July 28, 2014).
Eldad Hod. A Treatment for RH Disease. Available from http://pathology.columbia.edu/rh_disease.html (accessed 28.07.2014)


Human can't digest cellulose.....but the length of small intestine is approximately same in humans and herbivores

Depends on what you mean by "digest". Herbivores aren't able to digest grass on their own, they keep bacteria in their guts to do that. Grass-eating herbivores also tend to have long digestive cycles and some have several stomach chambers.

In short, cellulose is a pain to digest.


Why structures of many proteins are still unknown?

The gold standard for determining protein structures is x-ray crystallography. However, in order to perform x-ray crystallography you have to obtain your protein in crystalline form. Many proteins are not soluble in water, so crystallization is difficult or impossible. See this answer for information about the difficulty of crystallizing trans-membrane proteins.


Can oxytocin travel from one cell to another via gap junctions?

Synaptic vesicles are on the order of tens of nanometers (for example Zhang et al give a mean diameter around 40 nm).
Gap junctions are much smaller, on the order of 1-2 nm. Maeda et al measure one at 1.4 nm.
Peptides the size of oxytocin present in the cytosol could theoretically travel through gap junctions. Vesicle-packaged peptides or molecules of any size cannot.

Maeda, S., Nakagawa, S., Suga, M., Yamashita, E., Oshima, A., Fujiyoshi, Y., & Tsukihara, T. (2009). Structure of the connexin 26 gap junction channel at 3.5 Å resolution. Nature, 458(7238), 597-602.
Zhang, B., Koh, Y. H., Beckstead, R. B., Budnik, V., Ganetzky, B., & Bellen, H. J. (1998). Synaptic vesicle size and number are regulated by a clathrin adaptor protein required for endocytosis. neuron, 21(6), 1465-1475.


Why don't phospholipid bilayers dissolve?

We should first understand what happens when a substance dissolves. During dissolution water interacts with the solute molecule; if the strength of interaction between the molecule and water is higher than the strength of interaction among the solute molecules then the solute dissolves.
(Also have a look at this post).

Phospholipid is an amphipathic molecule — it has both hydrophobic and hydrophilic parts (this you understand very well). The hydrophobic part is a long chain of hydrocarbon (hence tail) whereas the hydrophilic part is a small but highly polar region (hence head). You should note that these parts are not disjoint but are covalently bonded.

Even though the hydrophilic part interacts with water (which helps the cell survive in an aqueous environment), the strength of covalent bond (between hydrophilic and hydrophobic regions) is very strong and cannot be broken by physical interaction with water.
The lipid bilayer (even a monolayer) stays together because the water cannot interact with hydrophobic parts but they interact with each other via a pseudo-interaction called hydrophobic interaction.

I call it a pseudo-interaction (not a standard usage) because there is not actual molecular interaction that stabilizes the system. Hydrophobic interaction happens via increase in entropy of the system. Read the wikipedia page for details.


Can plants yield two more molecules of ATP from glycolysis?

Plants produce ATP in the ‘light reaction’ of photosynthesis.
The purpose of the Calvin cycle (the ‘dark reactions’) is to produce glucose, for which it uses some of this ATP to provide the energy to make carbon–carbon bonds.
Glycolyis in plants functions to produce ATP from reserve carbohydrate etc. when ATP is not available from photosynthesis, or in tissues, that do not have sufficient ATP from photosynthesis.

So this question makes no physiological sense†, as it is based on a misunderstanding of the purposes of the differ metabolic reactions in plants. The answer is not that it cannot happen, but that it would not happen — the regulatory mechanisms that prevent futile cycling of pathways would come into operation.

† It is analogous to saying that the liver can perform gluconeogenesis, and so can produce glyceraldehyde 3-phosphate. So can the liver bypass this step...


It could be Anthrenus verbasci.

These insects are not dangerous, but they can damage carpets, clothing and furniture.


How can you develop a bacterial infection when taking antibiotics for another area of the body with a bacterial infection?

Your first assumption is mostly correct

  Bacteria in the toe is a different type and didn't respond to the
  [antibiotic taken for the throat infection].

the reason being because it outlines some essential characteristics of "antibiotics" and antimicrobial drugs in general.

Selective Toxicity and Mode of Action

A very important characteristic of an antibiotic is its selective toxicity. An ideal antibiotic has a high level of selective toxicity meaning that it will only target the bacteria that is causing an infection while not damaging the host tissue (cells) and the person's biota (resident microorganisms). This characteristic generalizes antibiotics into two categories; broad-spectrum (low selectiveness) and narrow-spectrum (high selectiveness). For example, a broad-spectrum antibiotic will target both gram-positive and gram-negative bacteria while a narrow-spectrum antibiotic will either target gram-positive or gram-negative not both.

Another characteristic of an antibiotic is its mode of action or in other words the area of a bacterium that it targets to inhibit/kill it. Most commonly antibiotics target one or more of the following areas/processes:

Cell wall synthesis,
Cell membrane function,
Protein synthesis, and
Nucleic acid synthesis

It is important to know this because mode of action goes hand in hand with selective toxicity, for example an antibiotic that targets membrane function might prove ineffective against bacteria that form capsules another themselves.

So to answer your question

  why [did] the antibiotics taken for the throat not prevent the growth of
  the bacteria in the toe?

We can reason that the selective toxicity of the antibiotic taken for the throat was narrow or that its mode of action only targets the bacteria causing the throat infection but not the bacteria causing the toe infection.


Pathogenesis of Chronic Venous Congestion in Lungs?

I think CVC lead to Pulmonary congestion and edema.
They produce heavy, wet lungs.

Pulmonary changes include

perivascular and interstitial edema, particularly in the interlobular septa;
progessive edematous widening of alveolar septa; and
accumulation of edema fluid in alveolar spaces which contain Hemosiderin and microhemorrhages

Now, the progression of the disease to heart should be discussed.
I am not sure if hemosiderin can go directly from lungs to heart or if it has to travel through circulation and then to left-side of lung.


How many genes do we share with our mother?

There is a distinct difference between the 'genes' that we share, and the genome (the DNA) that the genes are made of.

All humans (excluding genetic disorders) have the same genes, but the same gene in different individuals may have a slightly different DNA sequence, and this may be manifested in the different traits you can observe between people (eye colour, height, etc) or be ’silent’ (have no observable effect).

So you therefore have 100% of the genes that your mother has.

However, as stated in another answer, you inherit the different 'alleles', or versions, of the genes from your parents, and end up with ~50% of the alleles from each parents (but all the genes).

With regard to species differences; many of the genes we inherit have evolved over millions (in fact billions) of years, and thus many of our genes are present in most other organisms (but in very different forms - the DNA). Chimpanzees are our closest relatives in evolutionary terms, and thus their genes are very similar to ours in the genome (~98% the same). But this only applies to the coding regions! Less than 2% of your genome actually codes for genes - the rest is mostly regulatory (not junk, as it used to be called), and this is where the true inter-species variation lies. So whilst we have ~98% homology in the protein-coding regions, this is MUCH less if you count the whole genome.


Is it possible to suffer from hyperthermia by spending too much of time in the hot springs?

You betcha!

  We report a case of acute hepatic failure combined with disseminated
  intravascular coagulopathy, acute renal failure, and neurological
  deficit caused by heat stroke after bathing in a hot spring.

Generically, the term you're looking for is non-exertional heat stroke.


Selection (whether natural or artificial) is one of the force causing evolution. So yes, artificial selection is one way to 'force' evolution to happen in a specific way. One could select trees for bigger fruits or dogs for longer fur for example. One cannot force "Natural Selection", as "forced natural selection" is defined as "artificial selection".

You might want to have a look at an intro to evolutionary biology such as Understanding Evolution by UC Berkeley for example


TCGA gene expression data are missing matched normal

The TCGA Project has been collecting primary tumors and matched normals per patient per cancer indication and has been exome (WXS) profiling those samples, and genome (WGS) profiling a subset of them. In those cases, the primary tumor is tissue collected from the primary tumor and the matched normal is usually a blood samples, but could be derived from a buccal swab or some other source. As you can imagine, it would make less sense in terms of expression to assay matched control that derives from another tissue type such as blood.

For the expression data, the majority of the data comes from RNA-Seq and array-based profiling of the primary tumor data, and in some cases where adjacent normal tissue was collected and submitted, the TCGA has also profiled those samples. These are probably what you are seeing with your TN filter, and generally why you are having trouble finding equivalent amounts of matched normals as compared to primary tumor samples for the expression projects.

Incidentally, the company I work for has recently launched a free genomics data portal for the research community called GeenPool Reference. As part of it, we have deposited all of the publicly available TCGA RNA-Seq. The data along with all the associated clinical metadata is readily available for navigating and data mining. You'll easily be able to figure out the quantity of samples, and their matched pairs. If you're interested, you can take a look at the data projects available in GenePool Reference here: http://www.stationxinc.com/reference-library

~Sandeep


This is most likely a member of the genus Amanita, judging by the vellum traces on the cap, remains of a ring (2nd photo, under your thumb), free white gills.

What we are missing for a better id is the base: is there a volva, a bulbous end...? Please dig out your mushrooms instead of cutting them off.

Also, the colour is significant: are there pinkish tinges (-> A. rubescens?) or is it just brown?


There are actually a few, the problem with these websites is that they usually cover only a part of all birds on this planet. I use:

Bird identifier: Usefull website for a lot of European birds.
Backyard Bird Identifier: Useful for some European birds but
mostly for North American and Canadian birds.
All about Birds: Useful, but needs more knowledge for the identification

What I also do is using Google with a description of the bird, which sometimes works surprisingly well.


Is there a significant difference in sedentary calorie-burn between a thinker and non-thinker?

Is there a significant difference in calorie burn?

No.

The brain, while only making up 2% of our body weight, accounts for ~20% of our energy use at rest. That's because the brain, being critical for survival, is a very high-maintenance organ. At rest, the membrane potentials of all neurons - firing or at "rest" - need to be controlled/maintained.

Of all the energy used by the brain, about 25% of it is needed for signal-independent function (protein synthesis, phospholipid turnover, etc.) Furthermore, there are two types of cells in the brain: neurons and glial cells. The glial cells (about 30%) use from 17 to 40% of the energy depending on whose estimates you use. The rest is needed (by neurons) for signal-related processes - maintaining/restoring cell membrane potential, etc. - only a fraction of which is used for thinking.

The brain never rests - it is highly active even in sleep, with both excitatory and inhibitory activities needing energy. Higher mental functions (e.g. doing math problems) only shifts the areas of highest activity a little bit compared to all the activity that occurs without our awareness of it.

Finally, if we could measure glucose consumption of the entire brain while daydreaming vs. doing math, we might be able to answer that question, but the truth is, brain activity doesn't occur in isolation. Someone doing challenging math problems is using more energy in other areas of the body as well; respiration rate, heart rate, muscle tension, etc. varies with the stress of the challenge, so glucose levels alone can't be relied upon (in fact, stress would increase our body's production of glucose) to indicate energy expenditure.

The end result is that in isolation, rigorous mental activity (which can be maintained only for a relatively short duration without fatigue, so it occurs in bursts) expends very little of the total energy the brain uses.

  A common view equates concentrated mental effort with mental work, and it is fashionable to attribute a high demand for mental effort to the process of problem solving in mathematics. Nevertheless, there appears to be no increased energy utilization by the brain during such processes. From resting levels, total cerebral blood flow and oxygen consumption remain unchanged during the exertion of the mental effort required to solve complex arithmetical problems.

Cerebral Metabolic Rate in Various Physiological States
Does Thinking Really Hard Burn More Calories?


What are some characteristics of venules and arterioles?

I think this question is a bit too broad to write a comprehensive answer to, and there will certainly be some variation between tissues.

However, here is one reference that might give you what you are looking for.

I used to make acrylic arterial casts, mostly of coronary arteries but also some dabbling in the pulmonary, renal, and hepatic systems. My experience with the coronary system is that most of the arterioles come off in a tree-like branching pattern from quite small arteries, but there are always exceptions. I think the "fuzziness" you refer to definitely depends on the scale of observation: the further away you are, the more "fuzzy" arterioles look: of course they will never be as "fuzzy" as capillaries, but certainly once you enter the muscles themselves there is a lot of branching, but that branching isn't necessarily uniform. That is, there may be larger branches running in one dimension, and smaller branches in another dimension.

In larger vessels you also have the vasa vasorum: arteries that feed the large arteries and veins themselves. Some of those vessels are certainly the same size as arterioles, and some branch directly off the main vessel, but I am not sure whether anatomists always consider those to be arterioles or if they are considered separate.

From the perspective of interventions such as surgery, etc, smaller arterioles aren't really any different from capillaries, and larger arterioles might need to be clamped off or cauterized, but there isn't really any way to avoid them if you are cutting into a vascularized tissue. One wouldn't avoid these vessels they way they might avoid larger vessels.


Does digestion require hydrochloric acid?

Parietal cells use ion pumps to expel protons and chlorine ions into the lumen, which create the necessary acidic environment to denature pepsinogen into pepsin.

It is the low pH environment that reconfigures or denatures pepsinogen into pepsin. The acid used does not matter. For example, one experiment in classifying properties of pepsinogen used a 3.5 pH solution of 0.5 N sulfuric acid to activate pepsin.

We evolved stomachs with parietal cells that use an energetically expensive process to maintain the acidic gradient necessary for digestion and protection from pathogens.

It may be that biochemical pathways to generate other acids did not evolve, because it is either energetically cheaper for these cells to make HCl, compared with other pathways that would generate other acids of sufficient strength; or the relevant chemical components involved are more abundant than others in what we eat and drink, and thus easier to make in quantities needed for digestion and defense. Chloride ions also serve a role in maintaining intra- and extracellular fluid pressure and thus play a larger part as electrolytes in the normal function of the body — they are available and cells use them.

But to answer your main question, an acidic environment activates pepsin, and it is not chemically necessary for this to be created by hydrochloric acid.


Statistical genetics: Allele frequencies that follow a Dirichlet distribution

Largely an informed guess based on properties of distributions rather than specific knowledge of statistical genetics: a beta distribution is useful for modeling the frequencies of two alleles at one locus. A Dirichelet distribution, which is a multivariate generalization of a beta distribution, would thus be useful for modeling a set of loci.

The flip side is to think of beta as just a special case of Dirichelet: if you only have one locus, beta works. If you have multiple loci, then Dirichelet.


How do transplanted stem cells find their way to bone marrow?

The transplantation is an equivalent of a process that naturally occurs in human body, homing of the hematopoietic stem cells.

Immature hematopoietic stem cells have the ability to pass the bone marrow barrier, and therefore is able to migrate between bones and other organs within an individual. (e.g. thymus, which is how it can produce T cells.) Williams et al. believe that the process, homing, is a complex interaction and is similar to the migration of leukocytes to inflammatory sites. 1

Peripheral stem cell transplantation makes use of this ability. The donor first will be administered with certain drugs to proliferate stem cells in bone marrow and hereby raising the concretion of hematopoietic stem cells in blood. Those stem cells in blood then will be collected and transfused into the recipient. Eventually those cells will find their way home.


What is a good Microbiology atlas for Bacteriology as online version?

Not sure what you are exactly looking for? If you change the question or comment I can update my answer...

NCBI's taxonomy site has a listing of bacteria.  Encyclopedia of life is also great.

Then there's UCSC's microbial genome browser.

Biocyc is  great reference for bacterial genes.  to get into E coli, which is the model bacterium there's Port Eco featuring 130 E coli genomes.

Am Soc Micro has an excellent E coli/ Salmonella site based on their classic reference - you have to pay for access though.


There are always exceptions but you can consider some general rules.

A is 1 i.e the sequence that is perfectly complementary (2 is complementary but direction is parallel — cannot base-pair), then B would be 1 (siRNA). Reasons (some are just based on general rules of siRNA design):

siRNAs have to be perfectly complementary
The size is also perfect for a siRNA (21nt)
U/A (2-3 residues) at the 5' of the siRNA
U at 10th position
GC content 43% (ideal 30-50%)

See here for guidelines for siRNA design.


Why do humans have irregular teeth and impacting wisdom teeth?

Teeth first:

The vast majority of people have no problems with their wisdom teeth, whether they emerge or not. Impacted wisdom teeth are very common and are usually painless. They do, however, sometimes mess around with other teeth and throw off our bites (which will always readjust, not necessarily in a cosmetically pleasing manner, but the bite will adjust). Today, because we value straight teeth, impacted wisdom teeth are often removed prophyllactically, even if we have no proof that it/they will cause any problems.

Since impacted wisdom teeth are not evident until well after reproductive ability is attained, there is no reason to believe that malocclusion from wisdom teeth should be evolutionarily selected against. If problem teeth are so bad as to cause disability for an individual, that individual is removed from the gene pool.

Given two equivalent males, there's no reason not to entertain the notion that a female did not choose the one with better occlusion. So, it is theoretically possible that what we have now is an improvement over what was the state of our occlusions long ago. But there is rarely only one reason for two individuals to choose each other as partners, so... the teeth are relatively unimportant evolutionarily.

Or, if impacted wisdom teeth hurt enough to interfere with reproduction ("Not tonight, Og, I have a killer toothache.") the individuals who don't reproduce because of it will be dropped from the gene pool.

There may have been selection against wisdom teeth, because there are populations who have a lower incidence of third molars.

80% of all people will have problems with their backs at some point in their lifetime, which is a direct result of bipedalism in humans. You might ask why we became bipedal with that painful trade off. But bipedalism gave us some distinct advantages in survival. So did the expansion of our brains. The greater advantage has precedence in evolution.

Impacted tooth
Ancient Mutation Explains Missing Wisdom Teeth


What is the most critical step of plasmid purification?

There are a few critical steps (which sounds horrible if written together, but the method per se is robust and usually without problems):

Resuspension of the pellet: Make sure it is really resuspended and not floating around as a big blob. If it is not resuspended properly your yields will go down dramatically.
NaOH/SDS-Lysis: Don't lyse for too long as you may end up with low quality DNA. This denatures the plasmid and makes it often useless for subsequent enzymatic reactions.
Mixing: Don't mix too harsh once you lyse the cells, otherwise you may break up genomic DNA of the bacteria which subsequently stays in solution and is not precipitated during neutralization.
Neutralization: Make sure you mix good here (by inverting the tubes 4-6 times) but not too harsh. It is critical to neutralize the whole lysate, otherwise proteins may stay in solution.
Drying: Overdrying of pellets can cause problems when you try to dissolve them again.


One option is to use biotin labelling. Most molecular biology supply companies do kits for this, and supply biotinylated nucleotides.


What is Genome wide analysis and Locus specific analysis

Welcome to Biology.SE!

A locus (plur. loci) is a region of arbitrary size on a chromosome. A locus can be a single nucleotide or it can much larger (like $10^7$ sites).

A genome-wide analysis is therefore an analysis using the whole genome at once while a locus-specific analysis is the same analysis performed at the level of individual loci.

To make an analogy, if a genome-wide analysis is like a country-wide analysis, then a locus specific analysis is like a city specific analysis.

Without more context, it will not be possible to say more than that!


TL;DR: it's a simplified measure of sustainability, but accurate enough to be useful for public engagement

EOD is hosted and calculated by Global Footprint Network (GFN), an international think tank. The GFN estimates national and global net supply and demand for renewable resources, specifically:

food and fiber products,
livestock and fish products,
timber and other forest products,
space for urban infrastructure, and
carbon sequestration.

From the website:

  Global Footprint Network measures a population’s demand for and
  ecosystems’ supply of resources and services. These calculations then
  serve as the foundation for calculating Earth Overshoot Day.

  On the supply side, a city, state, or nation’s biocapacity represents
  its biologically productive land and sea area, including forest lands,
  grazing lands, cropland, fishing grounds, and built-up land.

  On the demand side, the Ecological Footprint measures a population’s
  demand for plant-based food and fiber products, livestock and fish
  products, timber and other forest products, space for urban
  infrastructure, and forest to absorb its carbon dioxide emissions from
  fossil fuels.

The results are reported in 'global hectares', the area which would be required using global average productivity, to aid intercomparability.

The methodology was published in 2013 (Borucke &al 2013).

So, to answer the question in your title ("Earth overshoot day: is it a sound concept?"), data quality may be an issue (I haven't pored over the paper in detail) but the basic methodology is arguably appropriate for the question they're asking. The only issue I might have is that they effectively consider land and sea use to be interchangeable, but I'm not sure the alternative would be an improvement.

To answer the second part of your question ("what are we all living on then?"), it is possible to harvest more from a system than it can sustainably produce. Exceeding this harms the future productivity of the system. To take the specific examples named for EOD:

Overharvesting plant-based food and fibre products can result in soil acidification, soil erosion, and/or soil salinification;
Overharvesting livestock and fish products can result in overgrazing and/or overfishing;
Overharvesting timber and other forest products results in deforestation;
Using more space for urban infrastructure reduces the availability of land for the other examples on this list;
Producing more carbon emissions than can be absorbed by its forest leads to an increase in atmospheric carbon, resulting in climate change.

Ultimately, while 'Earth Overshoot Day' is a public engagement activity, there is a reasonably robust and transparent methodology behind it which is good enough for the job. Remember: all models are wrong, some models are useful.


EGFR, sialylation, and cancer progression

Wikipedia claims (without reference) that

  Metastatic cancer cells often express a high density of sialic
  acid-rich glycoproteins. This overexpression of sialic acid on
  surfaces creates a negative charge on cell membranes. This creates
  repulsion between cells (cell opposition)[5] and helps these
  late-stage cancer cells enter the blood stream.

so I assume this is a summary of the "50 or 60 years of cancer research" that you mentioned. I don't doubt you, I've just never read up on this particular aspect of cancer. Be that as it may, there is a difference between a cell's expressing high levels of sialoglycoproteins overall, and inducing high sialylation of one protein in particular, in this case EGFR.

As you may be aware, EGFR dimerization induced by multiple methods, including EGF binding, overexpression, mutation, chemical or antibody crosslinking, etc. activates tyrosine kinase domains in its intracellular region to auto-phosphorylate specific Tyr residues in its tail, which then recruit adapter and scaffolding proteins which support downstream signal transduction.

The paper you read shows how increasing sialylation of EGFR reduces its trans-affinity for itself and inhibits dimerization, and hence the downstream signaling cascade. This is a good thing in certain types of cancer which are driven by aberrant EGFR signaling, whether through overexpression of EGF and/or EGFR, mutations in the kinase domains, mutations in the dimerization domains, or otherwise.

This paper is also a great example of an apparent bad thing turning out to be good, when properly targeted and controlled. Excess sialylation of a cell may be bad, but specific over-sialylation of EGFR could turn out to be very useful, if we can learn how to modulate and target it. Another common example of this phenomenon is radiation therapy. Normally, high levels of radiation are bad for your body, and can actually cause cancer, among a range of other illnesses. But, there are many different ways of specifically targeting radiation to a tumor to kill it while sparing (to varying degrees) the surrounding tissue and the rest of the body.


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

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


Could somebody identify it?

Sure, I'd be glad to help you with that!

The fly in question is indeed a member of the Empididae family, and of the genus Empis. I couldn't quite decide on the species, but it's either Tessellata or Opaca (with me leaning more towards Tessellata). This fly (genus) is commonly referred to as a "Dance Fly".

Empis Tessellata

Empis Opaca


How do carbon 13:12 ratios confirm the biological origin of oldest microfossils?

Via: https://en.wikipedia.org/wiki/Carbon-13#Uses_in_science

  Due to differential uptake in plants as well as marine carbonates of 13C, it is possible to use these isotopic signatures in earth science. Biological processes preferentially take up the lower mass isotope through kinetic fractionation.

Via: https://en.wikipedia.org/wiki/Kinetic_fractionation

  All organisms preferentially use lighter isotopic species, because "energy costs" are lower, resulting in a significant fractionation between the substrate (heavier) and the biologically mediated product (lighter). As an example, photosynthesis preferentially takes up the light isotope of carbon 12C during assimilation of an atmospheric CO2 molecule. This kinetic isotope fractionation explains why plant material (and thus fossil fuels, which are derived from plants) is typically depleted in 13C by 25 per mil (2.5 per cent) relative to most inorganic carbon on Earth.


Which biological kingdom comprises the greatest biomass on Earth?

Probably Eukaryotes. Specifically, plants.

This is a very fundamental question of life that is often overlooked. It goes without saying that plants and animals are the strongest contenders. However bacteria may also rival them. Be aware though that this is a contentious claim given more thorough estimations that take into account fluctuations in bacterial presence. This EMBO Reports science and society article claims that plants account for 99% of Eukaryotic biomass.

For further reading the Wikipedia page on biomass doesn't seem too shabby for more details on tonnage and methods of calculation.

The most numerous organisms could possibly be viruses or bacteriophages depending on if you count viruses as "living".


What is the best argument for maximum parsimony method in phylogenetic tree construction?

The idea of parsimony is that when constructing phylogenetic trees a simple hypothesis (e.g., four evolutionary changes are necessary to connect two taxa) is more likely to be true than a more complex hypothesis (e.g., 15 evolutionary changes) (source: Berkeley University).

The reason is that for a certain taxon to evolve, there must be a certain number of evolutionary changes. In the end, this happens by more or less stochastic processes (Dingli & Pacheco, 2011) that randomly generate genetic changes (mutations). The characteristics of better fit individuals survive, while those of the least fit are terminated from the gene pool. Hence, every additional change that must be adopted to create a new taxon from another means that the chance that that happens decreases exponentially; it's all a matter of statistics. The less the number of changes needed, the higher the chance that that might have actually happened.

Reference
- Dingli & Pacheco, BMC Biology (2011);9:41


Solving a Pedigree Between Heterozygous Half-Cousins

From what I can tell, you are not including the probability of the grandfather being a carrier (it could be the grandmother who is the carrier). Calculation should go like:

P(Child is born with disorder) = P(II-2 is carrier) * P(I-2 is carrier) * P(II-3 is carrier) * P(III-2 is carrier) * P(Child is homozygous recessive)

P(Child is born with disorder) = (1/2) * (1/2) * (1/2) * (1/2) * (1/4)

P(Child is born with disorder) = 1/64


Is sequencing error a function of the nucleotide being read?

Unfortunately, it does depend on sequencing techniques.

For example, in Illumina sequencing, each sequence fragment is amplified (in order to get a stronger signal) and forms a cluster on the microarray. Each cluster is sequenced by cycles of:

Adding fluorescent terminator nucleotides. These nucleotides are modified to contain an inhibiting/terminating group and prevents more nucleotides from being added. Theoretically, only one nucleotide is incorporated into every DNA fragment in this step.
Washing off excess nucleotides.
Capturing the incorporated nucleotide using imaging techniques and determining which base was incorporated (based on the colour of fluorescence).
Cleaving the terminator from the added nucleotides, so that the reaction can continue.

Image from Metzker, 2010.

This way, each fragment is synthesized, one nucleotide at a time, and each nucleotide that is incorporated gets detected. However, the first step is not flawless: sometimes more than one nucleotide gets incorporated into a certain DNA fragment, or no nucleotides get incorporated. Eventually, the DNA fragments in a cluster (all containing the same sequence) will fall out of sync ("phasing") and the fluorescent signal will become less clear, with a mixture of different colours. This is the main cause of sequencing error for Illumina machines, and also the reason why Illumina reads are relatively short (~300bp).

So to answer your question, in this example, nucleotides may be erroneously read as nearby nucleotides in that sequence. Errors will vary using other sequencing methods and how those methods work.

The article I linked earlier explains various sequencing methods in more detail. (Unfortunately, it's behind a paywall so some may not be able to view it.)


How can DNA profiling be used to determine the number of organisms from a specific species that is within a certain area?

The general process of DNA profiling (I prefer calling it "DNA fingerprinting", but that's just me) generally involves developing PCR primers specific for a particular region surrounding some sort of highly polymorphic region. So in this case one would need primers surrounding VNTRs (or other polymorphic regions, have a look at the wikipedia article for an overview of some other methods). Presuming the PCR primers are specific for bears (one could blast them to get an idea of this), then regardless of what other animals were mixed in, the resulting bands would predominantly be from bears (after all, PCR results in an exponential amplification of favored species). This would be answer part (1).

For part 2, one needs to find a sufficient number of sufficiently variable regions for profiling to work. A single site might not be informative enough, but a couple of them together will be.

Part 3 is the logical outcome of parts 1 and 2. If you can amplify a bunch of mixed samples together and the repeats are of variable length (thus the use of VNTRs or similar repeats), then you'll see those as different sized bands on a gel.


Is a raised baseline between T and QRS normal in any ECG lead?

I am not sure if I understand your question correct. What I can see here is a clear ST depression, that might be indicative of myocardial ischemia/infarction. The underlying mechanism is the shortage of oxygen in myocytes leading to elevation of resting potential and slowing of the depolarization -- this accounts for the elevated baseline after T.

I am not at all an ECG expert, but I have seen the misplaces T-P segment many times while at medical school. It wasn't indicative for diagnosis, whereas all other segments were.

So, why are you worrying about this segment?


Identical twins occur when a single egg is fertilized to form one zygote, which then divides into two separate embryos. Thus, identical twins are always the same sex unless there has been a mutation during development.

However, two identical twins expressing different sexual phenotypes does happen in some extremely rare cases due to environmental factors, deactivation of different X chromosomes in females, or aneuploidy. This is normally because an XXY Klinefelter syndrome zygote has split unevenly.

You are correct though, in that identical twins usually have hundreds of genetic differences early in fetal development which can be attributed to mutations in the DNA. But usually these differences do not result in twins with different sexual phenotypes, though it is possible.


For histone methylation , whether the marks are activating or repressive is determined predominately by which histone tail is modified at which position. DNA methylation by itself however is position dependent; in regulatory regions such as enhancers and promoters methylation tends to be repressive (at enhancers this is mostly mediated by being anticorrelated with the activation mark H3k27Ac) whereas within gene bodies DNA methylation is associated with increased transcription (Ref - http://www.cell.com/cancer-cell/fulltext/S1535-6108(14)00316-X )


Plasticity between excitatory and inhibitory neurons?

Various forms of plasticity has been reported for inhibitory-excitatory synapses as well. See below figure from [Woodlin et al. 2003].

Holmgren CD, Zilberter Y (2001) Coincident spiking activity induces long-term changes in inhibition of neocortical pyramidal cells. J Neurosci 21: 8270–7
Woodin MA, Ganguly K, Poo MM (2003) Coincident pre- and postsynaptic activity modifies GABAergic synapses by postsynaptic changes in Cl- transporter activity. Neuron 39: 807–20


There are various mechanisms through which membrane proteins can remain localized in the membrane. See the below figure from MBOTC (book):

(A) They can aggregate together so that their relative positions are constant.
(B) They can be anchored to the Extracellular Matrix
(C) They can be anchored to the cytoskeleton
(D) They can be anchored via cell-cell interactions (adherens junctions, hemidesmosomes etc)
(E) Not mentioned in the figure; mentioned in the comments. Lipid rafts are membrane regions which are composed of rigid lipids like cholesterol and sphingolipids. Lipid rafts are thicker than regular membrane and do not diffuse into the latter. Some proteins are specifically anchored to/incorporated into the lipid rafts (T-Cell receptor, IgE receptor) and their relative position with adjacent proteins (co-receptors) remains constant.

  Why is the noncytosolic layer not able to do lateral movements between
  domains but cytosolic layer is able to do so?

Where did you read this. Both layers can do lateral movements; if proteins are specifically "anchored" to one side of the membrane then the concept of domain applies to that side only.