Mechanism by which hypokalemia reduces insulin secretion

tl;dr
Hypokalemia hyperpolarizes membranes by increasing the $K^+$ gradient, making $\mathcal{E}_K$ and consequently $\mathcal{E}_m$ more negative. This makes any signaling event controlled by depolarization less responsive.
It's complicated, but we can understand the effect by looking at $K^+$ alone
Good catch. Yes, the video (and diagram) are incorrect. The electrophysiology of pancreatic $\beta$-cells is still an area of active research. Your textbooks (e.g., Costanzo Chapter 9, under Regulation of Insulin Secretion) will tell you that an increase in the $\frac{[ATP]}{[ADP]}$ ratio closes ATP-sensitive $K^+$ channels, which depolarizes the membrane. This is, in large part, correct, but not thoroughly understood, and not only by decreasing the $K^+$ conductance of the membrane. Further work in the years since that linked article supports the importance of a $Cl^-$ gradient and anion current, but $K^+$ conductance is still involved, and probably still underlies the mechanism through which hypokalemia reduces insulin secretion.
Membrane potential is determined by the concentration gradients and permeabilities of ions
The membrane potential of the pancreatic $\beta$-cell, as with the neuron, is determined by both concentration gradients and permeabilities of the membrane to ions. I'm sure the OP understands this, but for the general reader, you can read about this basic principle in any neuroscience or physiology textbook. You can calculate the membrane potential using the Goldman equation or chord conductance equation. Both are representations of the same principle, but I think the chord conductance equation is more intuitive. We'll simplify for our purposes to.
$\mathcal{E}_m  = \frac{g_{i}}{g_T} \mathcal{E}_i + \frac{g_{j}}{g_T} \mathcal{E}_j + \frac{g_{k}}{g_T} \mathcal{E}_k + ... $
Here, for ions i, j, k, ..., the membrane potential is equal to the sum of a series of terms for each ion, with each ion term being a product of the equilibrium potential of that ion ($\mathcal{E}_i$) and the portion of the total conductance across the membrane that the conductance of that ion represents. Conductance can roughly be understood as permeability. More open ion channels means a greater permeability/conductance to that ion.
Short term changes in membrane potential used in signaling are accomplished by changing the conductance of the membrane to specific ions. If the $\frac{g_i}{g_T}$ increases for ion i, the membrane potential moves closer to the equilibrium potential for ion i.
The concentration gradient determines the equilbrium potential
Each ion has an equilibrium potential, a membrane potential at which the net current of an ion across the membrane is 0. From the Nernst equation, we can say:
$\mathcal{E}_i \propto log_{10}\frac{[I]_{out}}{[I]_{in}}$.
Here $[I]_{out}$ is the concentration of the ion outside the cell, and $[I]_{in}$
is the concentration inside the cell. We've eliminated the proportionality constant because, in physiological conditions, it's constant, it's different for pancreatic $\beta$-cells (vs. neurons), and it's not relevant to our discussion (since we're not going to make any calculations with real numbers. If you are very careful, you'll notice the log term has outside concentration on the top, inside concentration on the bottom. You may find the Nernst equation written with a negative proportionality constant and with the inside concentration on top. These are equivalent because of how logs work.
Changing conductance, or permeability, changes the membrane potential
When you increase the conductance of a membrane to a particular ion, the membrane potential moves closer to the equilibrium potential for that ion. This is why in the neuron, for example, increasing the conductance of the axon membrane to $Na^+$ causes depolarization. The equilibrium potential $\mathcal{E}_{Na}$, is positive. The resting membrane potential is negative. Higher permeability to $Na^+$ moves the membrane potential closer to $\mathcal{E}_Na$.  Similarly, increasing the conductance of the axon membrane to $K^+$ (after the membrane has depolarized) repolarizes and then hyperpolarizes the membrane. $\mathcal{E}_K$ is negative (more negative than resting membrane potential). Higher permeability to $K^+$ moves the membrane potential closer to that large negative $\mathcal{E}_K$.
Increasing the permeability of pancreatic $\beta$-cells to $K^+$ hyperpolarizes the membrane
I'm using examples of the neuron because this is typically where these concepts are most thoroughly taught, but lets try to apply our understanding to the pancreatic $\beta$-cell. Concentrations, permeabilities, and membrane potentials are a little different, but not that much. Resting membrane potential for a $\beta$-cell is about -60mV. Threshold potential for $Ca^{++}$ release (which leads to insulin secretion) is between -50 and -40 mV. (Refer to my earlier linked articles). I don't have an exact number for $\mathcal{E}_K$, the equilibrium potential of $K^+$ in $\beta$-cells, but it is more negative than the resting membrane potential of that cell. We know this because (as is demonstrated in the linked studies), the OP is correct, increasing the conductance of the membrane to $K^+$ causes a net $K^+$ current out of the cell, rather than in, moving the membrane potential to a more negative state (hyperpolarizing the membrane), similar to what we see in neurons.
Decreasing the permeability of pancreatic $\beta$-cells to $K^+$ DEPOLARIZES the membrane
As discussed in Constanzo Chapter 9, ATP-sensitive $K^+$ channels close (not open) in response to an increase in the $\frac{[ATP]}{[ADP]}$ ratio. This decreases the $K^+$ conductance of the membrane, allowing the membrane potential to move closer to other equilbrium potentials (e.g., $\mathcal{E}_{Na}$, which is positive). With $\mathcal{E}_K$, which is more negative than the prior membrane potential, contributing less, the membrane potential becomes less negative, or depolarizes.
You can use a less mathematical reasoning to work out what happens when the $K^+$ conductance decreases as well. Close a $K^+$ channel and positive ions that would have moved out of the cell stay inside the cell, making membrane potential less negative, depolarizing the membrane. This is effectively the same as bringing positive ions inside the cell.
When the membrane depolarizes, $Ca^{++}$ is released, which causes secretion of insulin.
Hypokalemia
In hypokalemia, outside concentrations of $K^+$ decrease. This has an effect on the equilibrium potential, $\mathcal{E}_K$. From the Nernst equation above, we can look at the log term to see how $\mathcal{E}_K$ changes when $[K^+]_{out}$ decreases. The fraction $\frac{[K^+]_{out}}{[K^+]_{in}}$ is less than 1 in all human cells (there is more $K^+$ inside the cell than out), so the log term is going to be log(some number between 0 and 1). You can work this out using a calculator, but in this domain (0-1), the log is negative. It is larger and negative the closer you get to 0, smaller (but still negative), the closer you get to 1. If this behavior is unfamiliar to you, I encourage you to explore it with a calculator.
If you decrease the numerator in the log term ($log_{10} \frac{out}{in}$), as we do in hypokalemia, you get a larger negative number. This doesn't change the net direction of flow, or current for $K^+$ at levels that occur in the cell. It's still net out. $\mathcal{E}_K$ is more negative than it would otherwise be, so why doesn't decreasing conductance/permeability by closing the ATP sensitive $K^+$ channels do the same thing and depolarize the membrane?
Closing ATP sensitive $K^+$ channels in the setting of hypokalemia does cause depolarization, but not enough. You have to go back to the chord conductance or Goldman equation and consider the effect of $\mathcal{E}_K$ on the membrane potential before the ATP sensitive $K^+$ channels are closed. With a more negative $\mathcal{E}_K$, the chord conductance term $\frac{g_{K}}{g_T} \mathcal{E}_K$ is more negative, and the overall $\mathcal{E}_m$ is more negative. Global hypokalemia effectively hyperpolarizes the membrane, not just in the pancreatic $\beta$-cell, but everywhere. This is an important principle for understanding the consequences of hypokalemia, not just in insulin secretion, but in all settings. As a rule, excitable membranes are sluggish in hypokalemia (except Purkinje fibers). This is why, for example, it causes muscle weakness.


It's definitely a species of Huntsman spider maybe of the genus "heteropoda" or "olios". Sorry I couldn't be more help.


What promoter is required for expression of a human protein Y in bacteria?

Canadianer has very deftly enabled me to arrive at the answer with knowledge I already had. I attempt to explain the same here.

We know that eukaryotes and prokaryotes have different RNA polymerase (enzyme responsible for transcription) enzymes. Eukaryotes have three different RNA polymerase, each responsible for synthesis of the three different types of RNAs. RNA Polymerase II is responsible for mRNA synthesis in eukaryotes. It recognises the eukaryotic (or say, human) promoter present in an eukaryotic cell. On the other hand, in prokaryotes, there's only one RNA polymerase responsible for synthesis of all the types of RNA.

Coming to the question, using a human promoter is probably logical since it would be ideal for initiation of transcription of the said human gene Y. But this is not true because a promoter is only responsible for recognition by RNA polymerase and allowing it to move further and transcribe the DNA sequence i.e. it doesn't matter what comes after a promoter. Also, prokaryotic RNA polymerase is unlikely to recognise the sequence of a human promoter. It is much more likely to recognise a bacterial promoter. Since a promoter's function is limited to allow recognition, it doesn't matter that it's a bacterial promoter as long as it can be recognised.

The two options about operators weren't a confusion for me since I already know that they don't have much to do with expression of gene as much as regulating it. Besides, any operator used would also require a promoter in any case, since that is how transcription is initiated.

Thus, the scientist should use a bacterial promoter.


How to decide if genes are linked in an unordered mapping problem?

I'd use a chi-squared test.  You calculate what you expect to see if your hypothesis is true, and you take what you do see, and the chi-squared result tells you how likely it is that your results are different enough from what's expected to indicate that your hypothesis is incorrect.


Why similarities among organisms led scientists to believe that organisms are evolved?

I will answer by explaining some misconceptions in your original question:

  Theory of evolution states that organisms are evolved into other more advanced ones over time

Nope that's not what the theory of evolution is stating, mainly because the expression "more advanced" does not mean much and also is a loaded expression. You might want to start with an intro course to evolutionary biology to understand what the theory of evolution says. Understanding Evolution is a very introductory course you might like

  @Remi.b Alright I will have a look at what theory of evolution states but the basic thing is humans are thought to have evolved from chimpanzees. What I want to know is chimpanzees might resemble to humans but why chimpanzees are considered ancestor of humans? It might be possible that humans and chimpanzees created individually?

No, the theory of evolution does not state that humans evolved from chimpanzees. It says that humans and chimpanzees / bonobos have a common ancestor (about 6 millions years ago) that was not a human, nor was it a chimpanzee or a bonobo.

You can find an introduction to phylogenetics in this post and you can find online tools to visualize the tree of life in this post.

Philosophical issue in your question

The theory of evolution makes predictions that have been tested and demonstrated correct. You are asking why would creationism would not lead to the same predictions. For this purpose, one need to know what predictions would creationism make but this is very much undefined. If you can point to specific predictions that creationism would make, then we could tell you whether we have a counter evidence. The issue is that there is always a way to say, everything has been designed so that it looks like evolution is at play even if species were created anew. But this is not falsifiable.

So, maybe you might want to make specific predictions, that in your opinion, would be congruent with creationism but not with the theory of evolution and then we can tell you if we have evidence to support this prediction.

Related posts

While it does not directly answer your question (because IMO, for semantic issue, the question is unanswerable), you might want to have a look at Is evolution a fact? and Demonstrable and repeatable examples of evolution


Red blood cells (RBCs) don't have nuclei in mammals, so they are usually considered to be pretty inert compared to other cells.

They do have some biochemical activity, and evidently there is some mechanism for cell death  in RBCs when they are induced to degrade or infected by pathogens.  I found this reference that shows caspases -8 and -3 are evident in mature RBCs.  Several other components of the cell death pathway are not evident.

At this time the authors speculate that they don't activate to induce cell death.

It seems that over the broad field of disease research 'apoptosis' and 'cell death' are used equivalently even when the well known apoptosis pathway is not involved.


Is SS clearly different from Natural Selection (NS)?
Is SS nested within NS or are NS and SS two different and (anti- or not) parallel processes?

Darwin, in The Descent of Man, and Selection in Relation to Sex defined sexual selection as a type of selection that "depends on the advantage which certain individuals have over other individuals of the same sex and species, in exclusive relation to reproduction." Throughout, he distinguishes between natural and sexual selection. This suggests to me that Darwin thought of them as different processes.  A spot check of various evolutionary texts show the authors all using some variation of Darwin's definition.
In my opinion, the two are are clearly different but not necessarily separate. Both NS and SS affect fitness, a major component of the evolutionary process.  I tend to think of SS as nested within NS. NS affects fitness indirectly. Beneficial traits increase survivorship.  The longer individuals survive, the more reproductive opportunities they will have and fitness will, on average, increase. But, survivorship does not guarantee reproduction. Thus, I think natural selection acts indirectly on reproductive success.
SS operates directly on reproductive success because males selected by females will reproduce, increasing their fitness. Sex is, after all, a natural process. In my view, female choice is the "environment" of the male (as far as reproduction) so variation of male traits in the female choice "environment" differentially affects the fitness of the males. That is natural selection.

Is the evolutionary processes due to sexual conflict are SS processes?

Absolutely. Sexual selection ultimately arises because of a difference between genders of energy investment in gametes. Males produce lots of gametes and relatively little energetic cost. Females produce relatively few gametes with lots of energetic cost (think of tiny sperm vs large, yolk-filled eggs). It benefits males to mate with as many females as possible because, even if a mating produces no offspring, he lost very little of his energy investment. Females will be choosier because they can't afford to waste gametes. Thus, there is an inherent conflict of interest between males and females.

Are the evolutionary processes of sexually antagonist genes SS processes?
Sexually antagonist genes are those genes where one allele is favored in females while another allele is favored in males (my own definition)

Are these genes related exclusively to reproduction?  If so, then that would be consistent with the original concept of SS. However, sexually antagonistic genes are not necessarily the result of or a cause of SS.  For example, Rice (1992) argued that sexually antagonistic genes may explain the evolutionary reduction of recombination between primitive sex chromosomes.
Rice, W.R. 1992. Sexually antagonistic genes: Experimental evidence. Science 256: 1436-1439.

Can SS be accurately defined or is there a continuum of kinds or processes from complete SS processes to complete NS processes?

I think SS is accurately defined, but whether is is a type of NS or not is (I think) open for debate. As I described above, I think of SS as a particular type of NS, one that operates directly on reproductive success rather than indirectly.

Below is a list of scenarios where you can answer by yes or no whether SS is involved in the evolution of some feature. In all of these scenarios, we'll consider cases where the males have to find a mate…
The males need good ears to find the females before other males. Is SS involved in the adaptation of ears abilities?

Depends. Do males and females also use their ears for other purposes, such as detecting prey or predators?  Is hearing ability much greater in males than in females? Darwin specifically addresses such a scenario. (Last sentence of page 256, first part of page 257.)
I think these ideas play out for most of your scenarios. It depends on if the traits differ between the sexes (not specified in your scenarios) and the traits lead directly to increased male reproductive success. But I will address one more.

The males need good camouflage because when they fly to find a mate they may get eaten by a predator and die before reproducing. Here the difference is that the predators are attracted to the spot if they can sense many males. So the presence of the other males influence the probability of finding a mate of a given male. Is SS is involved in the adaptation to good flying abilities?

In this case, I would say not SS. The camoflage is necessary for survival, not direct reproductive success. This is natural selection.  Increasing the probability of finding a mate is not the same as guaranteed reproduction.


What is (probably) the closest living relative of the trilobite?

There were so many species of trilobites for 300 million years, so perhaps some trilobites species are closer to horseshoe crabs whilst others are closer to woodlice, some trilobites were amphibious and could walk onto the seashore.

If you check this research about horseshoe crabs, there are a dozen fossils that are hybrids between a trilobite and a horseshoe crab, i.e. bellinatus trilobitoides.

 From the family tree you can see some early horseshoe crabs:

this is a harpetida trilobite:

The morphology of the fossils is mostly saved as dorsal morphology and ventral morphology. from the top the are similar to horseshoe crabs, and the different legs are similar to woodlice and bathynomus and horseshoe crabs in different fossils:

There are other living animals that resemble them like Serolina Delaria:

Tadpole Shrimps:

That's from this cool page with images of lots of things like trilobites.
Silverfish:

Bathynomus, similar to woodlice:

The videos of bathynomus are cool: https://www.youtube.com/watch?v=jfnHQPkta-Q


Why do retroviruses go through a DNA stage to replicate their RNA genome?

Interpreting the question

Initially I interpreted the question as little more than “Why one type of virus rather than another?” (dsDNA. ssDNA, ssRNA [+ve v. –ve] etc.), and this (which would be unanswerable) was the way @Taimur seems to have understood it. And I also felt that the poster’s reference to ‘complexity’ reflected more his familiarity with other viruses than any real appreciation of what is complex in a molecular manner.

However I now think I misunderstood the question because of not appreciating the erroneous assumption on which I believe it is based. If I am correct, it could be rephrased in the following manner to make that assumption clear:

  “If the only purpose of integrating a DNA copy of the retroviral RNA
  into the host genome is to replicate the RNA in the virion, why is an
  RNA-dependent RNA polymerase not used as in other RNA viruses?"

Answer

  This stage of the retroviral life cycle in which a DNA copy is
  integrated into the host genome is not an incidental stage in a
  mechanism to replicate the virion RNA — it is the key element of the
  modus operandi or strategy of existence of the virus.

Explanation

As explained in the first paragraph of the Wikipedia article on retroviruses, once integrated into the host genome it can persist there:

  “The host cell then treats the viral DNA as part of its own genome,
  translating and transcribing the viral genes along with the cell's own
  genes…”

One way of thinking of this is as a strategy the virus adopts for ‘hiding’ until circumstances are suitable for it to produce more infectious progeny. One might even regard the form that is integrated into the host DNA as the viral genome — rather than the form that is encapsulated by lipid and protein into virus particles.

This sort of lifestyle is similar in some ways to that of certain DNA bacteriophages that can produce either lytic or lysogenic infections. Such persistence of viral genomes in the host is also seen in some eukaryotic DNA viruses like herpes simplex virus, in which an individual may have what is called a latent infection, which produces occurrences of cold sores (in the case of HSV1) throughout the lifetime of the individual as the virus is activated from time to time by various stimuli.


What would happen if two different viruses penetrated one cell?

One infected cell may produce hundreds of new viruses. By the time the disease occurs, many thousands of cells may be infected and producing new viruses. These new viruses are released from the cell, often in bunches, and are almost identical. Sometimes the host cell makes mistakes in copying the virus nucleic acid, causing some genetic variation. However, the outsides of these new viruses tend to be pretty much all the same, and they will usually infect only some more of the same kind of cells that produce them ¯ either in the same host animal or, if they can get out, other animals. Viruses produced in the respiratory tract are usually shed in droplets from the mouth and nose; viruses produced in the digestive tract are usually shed in feces but sometimes also in vomitus.

One person or animal is usually infected with only one kind of virus at a time, so the bunches of virus they produce and shed are all the same. Then, if this virus infects another person, even if two of the same kind of virus bump into a single susceptible cell, the infection will still be all of one type. However (much less likely), if viruses from two different infections get mixed up in the air or in sewage and get into a single person, it is possible that two different viruses will attach to receptors on the same cell and infect that cell together. If the two viruses are closely related, their nucleic acids may "recombine" while they are being copied. When this happens, part of the genetic information from one virus is linked to the genetic information from another virus, and the new virus that is produced is a "hybrid."

If you read about influenza that is traveling about in populations you will see that the outside of the influenza virus has an H type and an N type. For example, you might read that this year's main influenza virus is type H3N2.A reason to get a new flu vaccination each year is that the vaccine has to be made to immunize us against this type. Somewhere out in the world, a double infection as described above may happen between two different types of influenza viruses and some of the new virus may be type H5N4. Once this new type is established, a new vaccine is needed, or people won't be protected. Development and production of vaccines are expensive, and distributing them and getting people to use them is difficult. So, here is at least one situation where your question about two viruses infecting one cell may have serious public health results. Of course, influenza viruses that develop in birds, and sometimes other animals, may also be transmitted to people. Not many other kinds of viruses can jump host species like this, but it is possible that Ebola was transmitted to people from apes, perhaps from eating "bush meat." Viruses and other infectious agents that are transmitted from animals to people are said to be "zoonotic"; once this happens, the virus can usually be transmitted from person to person after that. Obviously, this too is an important public health concern.

http://www.madsci.org/posts/archives/2007-12/1198562498.Vi.r.html


Trade-offs between phage and yeast displays?

According to Creative Biolabs, the primary differences are:

  In the screening/panning step, yeast display is suitable for Fluorescence Activated Cell Sorting (FACS), allowing to sort out antibodies with desired binding properties
  precisely. However, the affinity of antibodies to antigens in phage
  display can only be roughly stratified (sorted into categories of goodness) by adjusting the washing buffer
  compositions.
  Owing to its eukaryotic expression system, yeast displayed antibodies can be correctly folded and modified, such as [...] to be closer to their native structure in mammals
  compared to the antibodies expressed by E.coli in phage display.
  The diversity of yeast displayed antibodies may be lower than phage (107-109 for yeast, up to 1011 for phage), due to the low
  transformation efficiency of yeast.
  Due to the many more copies of antibody on yeast surface (104-105) than phage, it is possible to select out low affinity antibodies
  according to antibody avidity with yeast display system.


How can I resuspend a cell pellet without harming the bacteria?

Assuming that you are talking about E. coli: As long as you are resuspending the cells in a suitable liquid, e.g. fresh medium or buffer, then from my experience you don't have much to worry about - the cells are very robust. I've found that different strains and growth conditions give pellets with very different qualities - some will resuspend quite well with vortexing. If the pellet seems clumpy then trituration is something that I always found to work - pipette up and down until the pellet breaks up.

If you were going to do some kind of physiological measurement with the resuspended cells then it might require some checking, but if you only intend to regrow and induce expression I would say that giving the cells some time to recover in the new medium (check that absorbance is increasing) before inducing expression should be enough.


"Blood circulation". Why blood bleeds in atmosphere ?

That's actually the gauge pressure that we measure. Gauge pressure is the amount by which the pressure measured in a fluid exceeds that of the atmosphere. So, when we say that our blood pressure is 180mmhg, it's wrong. In reality, the blood pressure is (180+760)mmHg inside the blood vessel, and our blood pressure exceeds atmospheric pressure by 180mmhg.


Are added yogurt cultures harmful to the gut?

I'm not sure what you mean by 'synthetic' gut bacteria, so I can't address that. is yogurt harmful to the gut? I believe the answer is no.

Women (and their doctors) have long known that taking antibiotics can result in Candidia (a yeast infection). Physicians have been advising women taking antibiotics to eat yogurt with live cultures, including lactobacillus spp. and bifidus spp. In keeping with today's movement towards evidence based medicine, Natural Medicines Comprehensive Database rates effectiveness based on scientific evidence according to the following scale: Effective, Likely Effective, Possibly Effective, Possibly Ineffective, Likely Ineffective, Ineffective, and Insufficient Evidence to Rate.

The effectiveness ratings for (just) LACTOBACILLUS are as follows:

Likely effective for:

  Diarrhea in children caused by a certain virus (rotavirus). Children with rotaviral diarrhea who are being treated with lactobacillus seem to get over their diarrhea about a half day earlier than they would without this treatment. Larger doses of lactobacillus are more effective than smaller ones. At least 10 billion colony-forming units during the first 48 hours should be used.

Possibly effective for...

  Preventing diarrhea in children caused by antibiotics.
  Preventing diarrhea in hospitalized adults. Drinking a specific beverage containing Lactobacillus casei, Lactobacillus bulgaricus, and Streptococcus thermophilus (Actimel, Danone) twice daily during antibiotic treatment and for a week afterwards significantly decreases the risk of developing diarrhea.
  -Preventing diarrhea due to traveling. Taking a specific strain of Lactobacillus rhamnosus, Lactobacillus GG (Culturelle) seems to help prevent diarrhea in travelers.
  Preventing diarrhea due to cancer treatment (chemotherapy). There is some evidence that patients with cancer of the colon or rectum have less severe diarrhea, less stomach discomfort, shorter hospital care, and require fewer chemotherapy dose reductions due to GI side effects when they take a particular strain of Lactobacillus rhamnosus, Lactobacillus GG (Culturelle).
  Colic in babies. Taking a specific Lactobacillus reuteri product seems to be more effective than using the drug simethicone.
  Lung infections. Children ages 1 to 6 years who attend daycare centers seem to get fewer and less severe lung infections when given milk containing lactobacillus GG or a specific combination product containing both Lactobacillus acidophilus and Bifidobacterium (HOWARU Protect).
  Treating a bowel condition called ulcerative colitis. Some research suggests that taking a specific combination product containing lactobacillus, bifidobacteria, and streptococcus might improve symptoms.
  Treating irritable bowel syndrome (IBS). There is some research showing that certain strains of lactobacillus, but not others, can improve symptoms of IBS such as bloating, and stomach pain.
  Treating vaginal infections caused by bacteria (bacterial vaginosis).
  Treating and preventing eczema (atopic dermatitis) in infants and children who are allergic to cow’s milk.
  Helping prescription medications treat Helicobacter pylori (H pylori) infection, which causes stomach ulcers.
  Treating diarrhea caused by the bacterium Clostridium difficile.

Though some of the recommendations are for specific probiotic formulations, one can achieve similar results by reading yogurt packages and mixing types to assure coverage with the proper bacterial spp.

National Institutes of Health


What is the difference between [Clinical Trials as Topic] category and [Clinical Trial [Publication Type]] category in pubmed?

The actual definitions provided with the MeSH terms look essentially interchangeable:

Clinical Trial as Topic:
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.

Clinical Trial [Publication Type]:
A work that reports on the results of a clinical study in which participants are assigned to receive one or more interventions so that researchers can evaluate the interventions on biomedical or health-related outcomes. The assignments are determined by the study protocol. Participants may receive diagnostic, therapeutic, or other types of interventions. While most clinical trials concern humans, this publication type may be used for clinical veterinary articles meeting the requisites for humans.

But the difference is simple. CT as Topic refers to publications that talk about Clinical Trials in general, as a subject itself. But CT[Publication Type] refers to an article that is actually reporting the results/analysis of one or many clinical trials.

To show you what I mean, these are first PubMed results using the two MeSH heading, when you specifically tell the search engine to not include other branching MeSH terms:

Clinical Trial as Topic:

Clinical Trial[Publication type]:


It looks to me like beautyberry. Here is a link to a species page to judge for yourself. It's a very common cultivar and I've heard of people using it to control garden pests.

http://uswildflowers.com/detail.php?SName=Callicarpa%20americana

Here is an image of American Beautyberry from gardenknowhow.

It is often confused with Japanese Beautyberry which has smaller berries on stalks.


I think of E. coli being more white than yellow.  When you compare E. coli and S. aureus on an agar plate, the Staph colonies have a much more distinctive yellow tint.  The yellow tint in Staph colonies is due to staphyloxanthin, a carotenoid pigment.


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

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


Assembly of polypeptides expressed from different chromosomes to make a fully functional protein

They have complimentary interfaces on their surfaces and it is energetically favourable for them to stay together once they have found each other by Brownian motion. Often they are highly unstable alone. So it is simply thermodynamics and a decrease in Gibbs free energy.

This happens across life. Enzyme complexes in bacteria are on the same operon, especially in thermophiles, because they come together at a faster speed. In Eukaryotes it makes no difference as the mRNA needs to be processed etc.


I believe it is a type of fungus.

Yes, this is a kind of fungus. Specifically, I believe it's of the genus Laetiporus sp., and is commonly known as "chicken of the woods" and "sulfur shelf". Notice that in both images the mushroom is growing on an oak tree.

  Is this edible?

I strongly recommend that you watch this and this video. Collectively, they provide more than enough information on how to properly ID the fungus, how to harvest & cook, any potential look-alikes, and even possible medical applications.

IF my suggested identification of your posted organism is correct, then yes, it's edible.


Why is cancer not a communicable disease?

A cancer is not a pathogen

Cancer is a group of cells that (because of several specific mutations) start to duplicate abnormally. This group of cancerous cells are the own cells of the sick patient. It is not another species infecting the individual carrying the disease. It is the individual itself who developed the disease. Cancer is not a pathogen (but see below) that infect hosts and get transmitted from one host to another. It is more correct to picture cancer as an internal mistake of the body rather than as an external attack on our body. You might want to have a look to the wiki page for cancer for more information.

Transmissible agents that can cause cancer

Some cancers are caused by transmissible agents, such as oncoviruses. the transmissible agent may jump from one host to another and cause cancers giving the sensation that cancer is transmitted. It is just a sensation of course because in reality only the oncovirus gets transmitted and not cancer itself jumping from one host to another.

Cancers that become transmissible

Note however that it is not impossible to imagine a tumour jumping from one individual to another in cases where the immune response cannot detect cancer as 'non-self'. Some cancers are transmissible. Those cancers are called clonally transmissible cancer (As indicated by C Rags in the comments). Here is the list:

The Devil Facial Tumor Disease which occurs in Tasmanian Devils
The canine transmissible venereal tumour (article from Chris Stronks in the comments)
The Contagious reticulum cell sarcoma occurring in the hamster.


Why do our bodies maintain blood pressure but not the flow rate?

A constant blood-flow would not be advantageous to organisms with a varying activity level. The blood supplies (mainly) oxygen to the tissues and the supply of course needs to match the requirements. Organisms rely on a number of mechanisms to ensure this match, one of these is to increase the blood-flow (heart-beat). But flow through a (blood) vessel relates directly to the pressure and inversely to the cross-sectional area of the vessel, so if the flow is increased, the organism must accept either a higher blood pressure or expand  the blood-vessels. Of course, it is in reality a compromise of both mechanisms.


There are a number of main reasons for this: The main reason here is that there is more than one needed to transform a cell. This is usually the silencing of tumor suppressor genes like p53 and the activation of proto-oncogenes. Only one of these is not sufficient to transform a cell. This is also seen in melanoma, where nevi which carry the activating BRAF V600E mutation (which is the most often occuring activating mutation in this cancer) can stay silent for a lifetime. This is called the Knudson Hypothesis (a short overview can be found in reference 1)).

So the turn-off of the control system is not enough, the cell needs to be further pushed to become a cancer cell. More details can be found in reference 2

Then, our immune system is very good in catching cells, which have gone malignant. Most cells, which turned into cancer cells, are eliminated by the immune system. This idea has been first formulated by Paul Ehrlich in the late 19th century, see the references 3 and 4 for details. The figure from paper 4 shows this schematically:

References:

Two-hit hypothesis
Tumor Suppressor (TS) Genes and the Two-Hit Hypothesis
Cancer immunoediting: from immunosurveillance to tumor escape.
The Immunobiology of Cancer Immunosurveillance and Immunoediting


Can I kill bacteria with distilled water?

Indeed, bacteria are susceptible to osmotic stress from being in pure water. They are also susceptible to starvation in such an environment.

However, wild bacteria tend to have many mechanisms that protect against this and allow them to survive in spite of being exposed to water. Note, also, that freshwater can serve as a habitat for many species of bacteria: Consider ponds, streams, lakes, etc.

Thus bacteria which you encounter in everyday life will likely have been those that survived osmotic stress in the first place. And drying, and mild disinfectants, and sunlight, and temperature variation... So it is unlikely that water alone will kill them.

Here is a recent article on this topic: http://jgp.rupress.org/content/early/2015/04/07/jgp.201411296.short

And here's one about how osmotic stress affects susceptibility to other antibacterial effects: https://www.sciencedirect.com/science/article/pii/S0740002014001890


Your teacher is right, chloroplasts and vacuoles are not sufficient to define a plant cell.

Amoeba have both chloroplasts (McFadden et al, PNAS, 1994) and vacuoles (Day, J. Morphology, 1927) but they are not plants - and they do not have a cell wall.

Sea slugs eat algae and can "steal" their plastids and keep them working for weeks/months, effectively becoming photosynthetic animals for a while. This is called kleptoplastidy (Pillet, Mob. Genet. Elements, 2013).


Help identifying winged, moth-like creature

I'm quite certain that this is an owlet moth that belongs to the species Asota caricae. It has the nickname "Tiger Moth", and is commonly found in the tropics of India.

I would like to note though that your first picture is somewhat misleading, just from where the flash washes the color so much. Because of this, I decided to more heavily rely on the second image than the first, which exhibits orange instead of yellow.


How is yellow elastic cartilage a true cartilage?

True cartilage is something of a simplification or a misnomer, they are saying that it truly a form of cartilage and not another elastic tissue type. in fact
"true cartilage" is a term coined by your book. They could have also said it's part of the cartilage family of cell/tissue types.

It's similar to cartilage under a microscope, structurally and has similar consituents, although yellow cartilage also contains elastin. If you were to dissect humans, you would probably find that there are a lot of variations of cartilage of different elasticity, midway in between both forms.

this page is full of info and pics:

It's a good idea to check wikipedia and 2-3 pages to find results to that kind of query, you will find fabulous resources, whereas on stack it is really for studies that take more than 20 minutes via google.


Cats, dogs and other animals can suffer from epistaxis.  The causes differ depending on the animal.

  foreign things in the nose, abscess, cancerous growth, snake bite, some poisonings and diseases especially in the trachea and lungs and anthrax. Sometimes excessive sneezing or coughing can result in nose bleeding as well. All animals are susceptible to get nose bleeding.

They would need to see their vet or owner to get it treated.

https://www.thevillager.com.na/articles/7474/Dealing-With-an-Animal-Bleeding-From-the-Nose/


Does the testicle's temperature increases with the body temperature during a high fever?

The question is quite vague. Please specify for clear answer.
However, although testicles are out of the body, but a part for sure. Due to pyrogen attack when the body temperature increases, literally the temperature of the testicles should be increased but clear research has not been found yet.
Please specify your question.


Can Dpn1 digest hybrid PCR product with only one methylated strand?

According to the NEB website FAQ, yes, it can, but less efficiently.

"DpnI cleaves hemi-methylated dam sites 60X more slowly than fully methylated."


What is this bird of prey with white belly?

I think your identification is correct - this is a juvenile Common buzzard (Buteo buteo), which have a lighter coat than the grown-up birds. See this image (from here), which also shows a juvenile bird:


As you can simply find on Wikipedia, the cellular immunity, or Cell-mediated immunity,

  is an immune response that does not involve antibodies, but rather
  involves the activation of phagocytes, antigen-specific cytotoxic
  T-lymphocytes, and the release of various cytokines in response to an
  antigen.

The answer (c) (destroying the bacteria cell by enzyme) refers to the phagocytes, cells that contain many enzymes, like lysozymes. Those funny enzyme can destroy the bacteria cell's wall.

Actually, I think that the answer (d) could be right, but it's not complete. In fact not every enzymes works on the cell's wall!


What is the name of cellular respiration that Prokayotic cells use?

Prokayotic cells use anaerobic respiration.

Glycolysis is the only stage of cellular respiration that does not occur in mitochondria.

The glycolysis process does not need oxygen and uses anaerobic respiration. The other stages require oxygen and use aerobic respiration.


What gases are needed for humans to breathe?

Why not look at the existing space station as an example.  The International Space Station (ISS), a starting article is "Breathing easy on the space station" (NASA), while this article does not discuss the amounts of various chemicals, it looks at the process about how the chemical balance is maintained - an important point related to your question is that carbon dioxide is filtered away.

The second article "Breathing on the Space Station" (e-missions), discusses the actual percentages of each component.  It states that the chemical composition of the space station air is ideally similar to Earth's atmosphere.  With 78% nitrogen, 21% oxygen and 1% water vapour on the space station (Argon is in the Earth's atmosphere, but appears to be unnecessary on the space station).

I hope this helps.


In a protocol like this, a low centrifugation is typically used to separate DNA in solution from larger, heavier components of the mixture. By lightly pelleting the banana slurry at the bottom of the tube, the DNA in solution is less likely to stick to that fraction of the mix when you pour it through the gauze. That's where your increased yield will come from.


Why do neurons loose the potential to regenerate and reproduce in adult animals?

To answer the first part of your question: In order to regenerate, the neurons need to divide. In order to do that they need to round up so that they can form a mitotic spindle that sorts the chromosomes and makes sure that each daughter cell gets exactly one copy of the genome. For most animal cells this genome sorting only works in rounded cells, which is why neurons need to round up before they divide.

However for a Neuron, rounding up would mean that the neuron needs to retract its axon as well as all its dendrites. To do so is physically impossible for most neurons simply because of the length and complexity of the axon and dendrites (the axons of human motor neurons can be more than a meter long). See also the image below.

Even if retracting the axon and dendrite network was possible, this would mean that the neuron would lose its function completely because it would lose all connections to other neurons and with them all information it has stored. Thus, from an evolutionary standpoint it does not make sense to regenerate a neuron once it has matured and started to form connections with other neurons.

That being said, despite the fact that matured neurons cannot divide any more, our brain and our nervous system retain a lot of regenerative potential:

Provided that there is little scarring at the wound, a nerve fiber (consisting mainly of axons of neurons) can regrow because the neurons don't necessarily die when their axon is cut and they can regrow a new axon. The main difficulty for regeneration in this case is for the axon to find the path to its destination. Therefore it is important that there is minimal scar tissue (glial scar) because scar tissue prevents regrowing axons from finding their path.
The brain retains some neural progenitor (stem) cells that are able to differentiate into new neurons even at old age (but not as many stem cells as other tissue).
When parts of the brain are damaged, other regions can often take over that functionality (for example by by rewiring their axons and dendrites) a process called neuroplasticity. For example, people can often re-learn to speak after a stroke.

As to the second question: Using stem cell technology it is possible to grow fresh neurons in cell culture. In principle, these neurons (or rather their progenitor cells that mature into neurons) can be implanted in order to regenerate nervous tissue in the central nervous system. However, this cannot solve the problem that once the neurons are dead, even a new neuron that replaces the dead one cannot recreate all the connections that the old one had.
Replacing neurons is like replacing the hard disk of a computer. All information is lost. Therefore, current research on the therapy of spinal chord injury focuses on the prevention of scarring in order to help the existing neurons to regrow the axons and reconnect the body with the brain.

Edit: added references.


This is an interesting question.
Reading this two articles linked below, it seems very much that the connexins are turned over and degraded with the channel more or less staying at the same place (the figure is taken from the first paper, but the second has a similar):

Following this, the connexins are synthesized and then subjected into the ER and then the Golgi for proper protein maturation and oligomerization into hemichannels (misfold proteins are subjected to proteasomal degradation). They are then exported from the trans-Golgi in small vesicles to the cell membrane, transported to the sarcolemma where they form complete gap junction channes with hemichannels from another cell. Single channels aggregate into gap junction plaques.

The connexins are degraded in the proteasome and the lysosome. It is discussed that post-translational modifications as phosphorylation and ubiquitination play an important role here.

The degradation seems to take place at the formed channels. This was tested in two ways: When the export of new proteins to the membrane is inhibited, then the connexins in the membrane and the junctions get lost over time. If the proteasome is inhibited, the number is growing. And when both pathways are inhibited (export and degradation) the number is approximately constant. See paper 3 for more details.
This shows that the process of forming the junctions and degrading the connexins is a permanent and that cells, which form junction with each other stay in the same place.

References:

Connexin Expression and Turnover
Pathways for degradation of connexins and gap junctions
Degradation of connexin43 gap junctions involves both the proteasome
and the lysosome.


What is the evolutionary tradeoff against primates producing multiple offsprings (litter)?

There is a tradeoff between having multiple progeny, with relatively low parental investment in each, and few progeny, with high investment in each.  This used to be called "r" and "K" selection respectively, though the terms are now used less.  Very simplistically speaking, long-lived species within a fairly stable environment tend to produce few offspring and invest large amounts of care in each; this description fits primates very well, and so it's not surprising that they follow this paradigm.  The bottom line is that because of primate life history, having small litters is a more successful evolutionary strategy.

The Wikipedia article on r/K selection theory is reasonably good and points to updates and some further reading on the subject.


Are we evolving to age slower, or to live longer aging at the same rate?

The question has a more or less official scientific name - the grandmother effect (or hypothesis).   In the rational world of evolutionary biology, children love their parents for the same sort of reason - the parents give them resources to gather their strength and develop as adults so they can have their own children with the most advantage that they possibly can.

Humans are off the charts in the amount of resources we invest in our children - our lives are 1/4 to 1/3 over before we sometimes leave our parents household (in some societies of course they never leave the house, but step into an extended family).  This may be one of the reasons we are so successful as a species - we live in practically every place we possibly could and have no danger of competition from any other living thing excepting ourselves.

The grandmother effect is essentially the idea that if women, who are more attached to the offspring in more cases than fathers, continue to live and help support the grandchildren and make them more successful, then this will allow post menopausal women to have a longer lifespan (which they do).

The evolutionary biologist Sara Hrdy, emeritus UC Davis, has written quite a bit about the nuances of the evolution of the role of motherhood - reading some of her articles or books might give you a deeper sense of how profoundly filial love has shaped human beings.

--- more answer this stuff may or may not be worth reading depending on how broadly you want to understand this question...

Its important to say that many of the expansions of human average human lifespan have not been genetic.  Its commonly cited that sewer systems, clean water, antibiotics and plentiful food are the three most important factors in human lifespan - and before modern developed world nations, the average lifespan of human beings was somewhere in the 30s.  And there are significant lifespan differences in regions where these factors and others (education of women, access to prenatal and early care etc) are available.

Studies continue to be published that examine environmental and lifestyle factors compared to genetics and it seems that environment and lifestyle can make an astounding difference.

But genetics undoubtedly has a role to play here too.  There are probably some individual humans and animals which have evolved to live longer.  This has been found to be genetically related in some humans by demographics and family lines.

Still there are genetic factors that are being identified.  I think its a common misconception that evolution changes the entire species, but its not really true.  There are some who have that tendency and others who do not - at times there will be more of say shorter lived people and other times longer lived individuals will be more common.  It depends upon whether the living conditions of the population really favor one tendency over another.  Usually shorter lived individuals can assume to have other advantages, say the ability to store energy more efficiently.


Is the six-layer cortex model of the mammalian cortex still the most accepted model?

Short answer
The layers in the cortex are histologically and functionally defined. Both 3- and 6-layered cortices are found in the human brain. Hence, the different cortical layers are not models, but classifications based on empirical observations.

Background
The different cortical layers have been defined by histological staining and microscopy. The layered organization of the mammalian cortex is typically explained in textbooks by using the neocortex as an example, which has 6 layers (Fig. 1):

Fig. 1. Layered cortex. Source: What-When-How - Neuroscience.

As one can see in this picture, layer VI can be divided histologically into 2 sub-layers, namely VIa, containing mainly pyramidal cells, and VIb with mainly horizontal cells (Prieto & Weiner, 1999). Hence, a 7-layered cortex could be argued for as well - it is all kind of subjective.

The functions of the 6 layers are illustrated in Fig. 2.

Fig. 2. Functions of the 6 layers. Source: Free-Stock-Illustration.

However, the primary olfactory human cortex (the paleocortex) contains only 3 histological layers, as opposed to the 6 identified layers in the neocortex (Fig. 3). The primary olfactory cortex is part of the allocortex in man.

Fig. 3. Neocortex versus paleocortex. Source: Slideshare.

The primary olfactory cortex receives direct sensory input from mitral cells in the olfactory bulb in the outermost layer Ia. layers Ib, II, and III receive input via local and long-range intracortical connections. Sensory and intracortical inputs converge in layers II and III. The three-layered palaeocortex is different from the six-layered neocortex in sensory areas. In the neocortex, sensory and intracortical microcircuits are distributed to two different layers. Sensory inputs from the thalamus target layer 4. Layer 4 subsequently projects onto layer II/III, which distributes and receives intracortical associative fibers. Note that the olfactory system is exceptional in that it does not relay its information via the thalamus, explaining the absence of layer IV (Wiegand et al., 2011).

Reptilians and birds typically have a 3-layered cortex (Nauman et al., 2015).

References
- Nauman et al., Current Biology; 25(8): R317–R21
- Prieto & Weiner, J Comparative Neurology (1999); 404:332–58
- Wiegand et al., J Neurosci (2011); 31(34):12149 –58


How can we determine which chromosome came from which parent?

A straightforward way to identify which chromosome came from which parent would be to use sequences of known fragments of parental chromosomes or to use SNP arrays. I hope that I did not miss your question completely.
Regards,


PGDSpider will do the trick.

PGDSpider is able to parse 31 and to write 35 different file formats including STRUCTURE and .fstat.


How do veins's valve pocket sinus tend to become hypoxic?

As veins are not permeable to O2 thus O2 can't escape into surrounding cells.

Veins are not like impermeable rubber tubes, they are 'living' structures requiring, like all cells, Oxygen and glucose to survive. Smaller veins get the O2 from diffusion, while the larger veins need help from vasa vasorum, small blood bessels that bring blood to the walls of the veins.

The innermost cells lining veins are epithelial cells. They also line valves.

In the picture you posted, blood is not circulating well behind valves. The cause of hypoxia is that epithelial cells are continually removing O2 from the blood.

When enough O2 is removed to cause hypoxia, the endothelial cells may become damaged by the lack of O2, causing inflammation and (possibly) potentiating clot formation.

  Activation of endothelial cells by hypoxia or possibly inflammatory stimuli would lead to surface expression of adhesion receptors that facilitate the binding of circulating leukocytes and microvesicles. Subsequent activation of the leukocytes induces expression of the potent procoagulant protein tissue factor that triggers thrombosis.

Mackman N. (2012). New insights into the mechanisms of venous thrombosis. The Journal of clinical investigation, 122(7), 2331–2336. doi:10.1172/JCI60229


Does Darwin's Theory of Evolution refute Terence McKenna theory "Stoned Ape" theory of human evolution?

Briefly the "Stoned Ape theory" posits that psychoactive Psilocybin mushrooms in the diet of pre-Homo sapiens primates catalyzed the change Homo sapiens.  It suggests that the mushrooms conveyed selective benefits to consumers of the mushrooms, dissolving the 'egos' of our ancestors and allowing them to form communities.  It may also be sexual stimulant, goes the theory and so may have conveyed an advantage there.

I think this theory is not terribly popular now, but it is difficult to refute or to prove.  The only real proof would be to take a hominid or any other species and give them the fungus and see if they become intelligent.   Just because this has not happened does not disprove the theory.  the only other way to prove this really would be to have a time scope and look back and see what happened.  Its a similar question as to how life emerged on Earth.  We have some interesting evidence but conclusive proof is going to be hard to get.

I found a large collection of supporting evidence.  Even the definition of human intelligence and whether it is so unique is subject to debate.  Certainly there are other primates who appear to be as or more social than we.  I think other theories seem as or more likely.

Darwin's theory of evolution doesn't refute many theories of how something happens in evolutionary history.  The Panspermia hypothesis is taken quite seriously at this point - could it be that life originated elsewhere then was introduced here by meteorites.  The origin of Species doesn't have a lot to say about that.  I think the same is true for the emergence of human intelligence, which at this point we believe is unique on Earth.  Hard to make an irrefutable theory based upon a single example.


There is a useful diagram at this site.

During RNA synthesis in vivo the 3'-OH oxygen atom of the growing chain reacts with the α 5'-phosphate of the incoming ribonucleotide (nucleophilic attack), displacing the β + γ phosphates as a pyrophosphate group. This results in a 3'-5' bond between the prexisting oligoribonucleotide and the incoming ribonucleotide. In other words the loss of the pyrophosphate group is an inevitable consequence of the elongation reaction.

At initiation, however, the first ribonucleotide has not been the subject of a nucleophilic attack, because it is first in the chain. Its 3'-OH will carry out the nucleophilic attack descibed above when the next ribonucleotide is added to the chain.


First, ongoing inflammatory process/immune reaction in the gastrointestinal tract is not necessary associated with vomiting or diarrhoea. As an example we can consider infection with Helicobacter Pyroli, which may last for many years unnoticed.

Second, exposition to foreign antigens obtained form food or microflora and subsequent antigen presentation to the immune cells (which is indeed partially driven by locally released cytokines) occur in the GI tract all the time and again, is not usually manifested by vomiting or diarrhoea.

But moving to vaccines, attenuated oral vaccines (like Polio Sabin or Rotavirus) are developed in order to diminish the risk of pathological symptoms. Attenuation weaks the pathogen that is usually no longer able to proliferate and invade, but still poses antigens that may be presented to the immune cells and induce long-term immunological memory. Moreover, immune response (antigen presentation, production of the local IgA, B-cells affinity maturation) triggered by attenuated vaccines is the closest to the one induced by full infection (in comparison to inactivated/toxoid vaccines), but significantly weaker and localised. This we mean by "mimicking a natural infection".

Also, see: https://www.sciencedirect.com/science/article/pii/S0042682215001725


Clarify pre-column pressure vs. system pressure vs. backpressure for prepacked columns used with the äkta purification system

Is there a good article or webpage that goes through this theory at a basic level?

Yes, Chapter 7 of the manual linked to by Andreas Tosstorff is a good source, and is also the source of the images below. The manuals for your ÄKTA system and the HisTrap columns discuss pressure in some detail as well.

How can backpressure be created in a system that is not closed and goes one way?

This is a physics question and, not being a physicist, I can't go into detail. However, I also use the ÄKTA system for FPLC and may be able to provide some form of an answer. Any fluid moving through tubing experiences some resistance from, for example, friction between the fluid and the tubing walls, bends in the tubing and obstructions like filters, mixers, valves, etc. Even though the system is open at one end, there is resistance to the flow of fluid through it which creates backpressure. The largest sources of backpressure in the FPLC system at low flow rates are filters, flow restrictors (if installed) and the column itself.

How is the system pressure different from the pre-columns pressure?

The system pressure for the ÄKTA is measured at the pump. This measurement in itself is not very informative. The pressures that are important as far as keeping your column safe are the pre- and post-column pressures (the pressure measured immediately before and after the column, respectively), and the difference between these two (the pressure across the column). Your column has two pressure limits:

Hardware pressure limit: this is the maximum pressure the column itself will withstand before there is a risk of failure. I know this from experience after a malfunctioning valve gave 4 times the maximum hardware pressure to my column. In my case, failure meant the top of the column blowing. The pre-column pressure should not exceed the hardware pressure limit.
Resin pressure limit: this is the maximum pressure the resin within the column can withstand before collapsing. The pressure across the column should not exceed the resin pressure limit.

Should I calculate the pre-column pressure myself as an effect of the size and length of the tubing leading to the column?

Some ÄKTA systems are capable of measuring pre- and post-column pressures directly. Mine is not, and I don't know about yours. In the case where pressure is measured at the pump, the pre-column pressure is equal to backpressure between the pump and the column (caused by the tubing/filter/etc.) subtracted from the measured system pressure. To determine this, you essentially disconnect the top of the column, run the system under your intended conditions and record the measured pressure (this is the backpressure generated before the column). The manual for my columns (HiTrap Q) explains this step by step, and yours may as well.

The manual also explains how to determine pressure across the column in a similar manner. However, in my experience, the flow path after the column is relatively unrestrictive (unless a flow restrictor is installed), and its contribution to backpressure is relatively be negligible. Thus the pressure across the column is reasonably equal to the pre-column pressure, which is also reasonably equal to the measured system pressure. Furthermore, listed in every manual I read is some statement to the effect of:

  The maximum pressure over the packed bed (Δp) is an approximate limit. It is dependent on the characteristics of the chromatography medium and on sample/liquid viscosity. The measured value also includes the pressure generated by the column tubing. For many columns, the recommended flow rate is a better guideline for protecting the packed bed.

In fact, the manual for my columns doesn't even list the resin pressure limit and it took substantial digging to find out what it actually is. I always run at the recommended flow-rate and set the system pressure alarm at the resin pressure limit (0.3 mPa in my case versus 0.5 mPa hardware limit) without any of the corrections mentioned above. However, depending specifically on your system and usage, it may be necessary to make them.


How does a nerve cell adjust if O2 diffusion is interrupted?

If Oxygen diffusion is interrupted, there is a serious problem. Neurons inside of the brain slowly start to die, many other things like change in personality or the inability to process pain impulses occur if the brain is deprived of oxygen.If this is not fixed within 15 minutes it is impossible to survive.

The actual effects on the neurons are as follows:
Like in most cells the first solution to this kind of circumstance is anaerobic metabolism, the same happens in neurons but it does not last long and it is inefficient. As far as i'm concerned nerve conductance decreases in this kind of scenario and the receptors shrivel.

Well if the receptors are shriveling, they shouldn't be able to transfer impulses meaning that nerve conductance should stop.

This link to an article on the effects on the brain from oxygen deprivation.
https://www.livestrong.com/article/106179-effects-lack-oxygen-brain/


How much energy does human body fat contain?

I am not sure if I am able to answer your question, but I will give it a try and hope that someone tells us if I'm wrong.

Biologists talk about different kinds of energy depending on where you measure it. The first measurement is the gross energy (GE) which is measured through bomb calorimetry and is basically how much heat a substance gives off when completely burnt. I have recently read in a compendium that the GE value of fat is ~9,4 kcal/g.

The next stage is digestible energy (DE), which is how much of the forage you actually can digest, which would exclude for example fibres.

Next stage is the metabolizable energy (ME), the energy which can be used in actual metabolism (DE - energy losses from transporting nutrients etc). This are the value you reported. (I don't have a source, but I've heard the same values from multiple recognized sources.)

Now is the part where it gets a bit trickier, as the final measurement of energy is the net energy (NE). This is defined as the metabolic energy minus the heat increment, which could be simplified as the energy losses through the conversion between different types of energy (ie. from long carbohydrates into glucose etc.) within the body. Even more simplified it can be said to be the difference between the heat production in a fastened person and the heat production in a fed person, thus being the heat produced by eating, digesting, absorbing and transporting food.

I argue that because the fat already is incorporated in the body it has a very efficient value, and very little transportation within the body is needed. And because the energy (ie, the fat) is internal, it is not accounted for in the heat increment and therefore the NE of internal fat is the same as ME.

And according to the wikipedia-article you linked to United Nations recommendation of the average minimum energy consumption per person is 1800 kcal/day. Thus the amount of fat required to meet the minimum energy requirements of a person would be 1800/9=200g of fat per day.

If you want to read more about the different energy-measurements and the heat increment here is a good link. And don't forget that energy alone is not sufficient for a person as we need protein, vitamins, minerals etc...


Is it possible for a substance to be absorbed by the hair or the scalp?

As to the subject line, yes, lipid substances or any non-polar small molecule will enter the skin cells and the body below. The reason is because cell membranes simply consist of fatty substance that behaves like a solvent for other lipids.

As to the specific question about this product, Monovin A. This is a veterinary product and the producer, Laboratórios Bravet, intends it to be injected into animals in case of a vitamin A deficiency. The main ingredients is a retinol ester in the amount of 2,000,000 IU (which usually means retinol equivalents in this respect).[1]

Indeed, retinol is a lipid and long-chain esters like retinol esters are non-polar, too, and can readily be de-esterified by esterases, making vitamin A (=retinol, retinal, retinyl palmitate, retinoic acid) immediately available to the surrounding cells and, via transport in the blood stream, to the liver, which is the body's store for it. Daily doses of 25,000 IU are known to be toxic when administered over a long time. Doses of 50,000 IU can be dangerous over weeks. In general, it appears that single high doses are better tolerated than long over-exposure.[2][3] So, do the math and dilute the stuff such that you get at most one hundredth of an ampoule, else...

Now the effects. Indeed, hair loss is one of the symptoms of heavy vitamin A-deficiency, and logically, that symptom can be cured with vitamin A. That does not mean that more results in more. While retinoids are important therapeutic agents for the management of many skin diseases, notably acne vulgaris, psoriasis, ichthyosis, and palmoplantar keratoderma, there exists something like retinoid-induced effluvium which is a side effect of such medication with tretinoin (ATRA).

  Retinoid-induced hair loss (telogen effluvium) is among the most
  frequent and psychologically most distressing adverse effects of
  retinoid therapy, which results in premature termination of a
  clinically desired and often highly effective systemic therapy with
  retinoids.[4]

Since ATRA is readily produced from retinal, its concentration would be expected to be up, even if the original stuff was retinyl ester. In summary, I would expect no effect, or even hair loss, for you don't simply put such potent stuff on your head and elsewhere, and have no reaction from the body.

[1] http://www.bravet.com.br/pr-ceg-monovina.asp

[2] Vitamin A: Toxicity from Supplements In: Medical Sciences Bulletin 1995; Pharmaceutical Information Associates, Ltd.

[3] Hartmann S, Brørs O, Bock J, et al.: Exposure to retinyl esters, retinol, and retinoic acids in non-pregnant women following increasing single and repeated oral doses of vitamin A. In: Ann. Nutr. Metab.. 49, Nr. 3, 2005, p. 155–64. doi:10.1159/000086879. PMID 16006784

[4] K. Foitzik, T. Spexard u. a.: Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla. In: The Journal of investigative dermatology. Vol. 124, Nr 6, June 2005, p. 1119–1126. DOI:10.1111/j.0022-202X.2005.23686.x. PMID 15955085.


Lookup for transporter locations in humans

This site can help you locate RNA expression of a particular gene (if you know the gene for the protein in context) in various tissues. Its called biogps.
http://biogps.org/#goto=welcome

Hope it helps :)


if the load is removed from an eccentrically contracting muscle, will it start contracting concentrically?

Yes, because net force is the only thing that matters. To address @Chris's comment, in an eccentric contraction and a concentric contraction, the muscle is applying force in the same direction. However, in an eccentric contraction, the muscle is not applying enough force to actually lift the load. A biceps curl is a good model:

SportScience

In the second image, the muscle is contracting but not exerting enough force to lift the weight--the net force causes a slow lowering of the weight.

  Rather than working to pull a joint in the direction of the muscle contraction, the muscle acts to decelerate the joint at the end of a movement or otherwise control the repositioning of a load. - Muscle contraction (Wikipedia)

It may be clearer with an actual force diagram:

University of Guelph

The only factor influencing which way the lever (your arm) moves is the net force. So yes, if you change the load (force F in the above image), the muscle could begin pulling your arm in the opposite direction. The muscle isn't really "changing action", it's exerting the same force, but now there's less force resisting it and the overall movement changes direction.

The question in the title and in the body are not really the same question, but the force is still exerted in the same direction as the muscle. You don't "see" movement in that direction because the forearm on which the force is being exerted is fixed at the elbow joint.


What is range of the number of individual organelles in cells

BioNumbers is a database that contains exactly this sort of stuff.

For example, I took this from this site:

Number of mitochondria per cell:

Yeast Cryptococcus neoformans cell: ~34

Human HELA cell: ~6000

Mouse L cell: ~1000


Blast a sequence against multiple databases

To scan multiple databases:-

Download all the databases that you intend to match against (all databases will have a download option)
Download standalone BLAST executables from NCBI
Pool all the sequences from the different databases and make a BLAST database using the program makeblastdb (it is better to check for redundant sequences and remove them for improved performance)
Run blastp with desired parameters against this database
The first hit wont mean much. Use cutoffs on E-value or Bit-Scores or precentage identity

Now, if you vaccine targets a protein it is good to study the protein sequence conservation. BLAST isn't a really good option for studying conservation by comparing different orthologs. Use tools for multiple sequence alignment like ClustalW or T-COFFEE. In my opinion it is also better to use BLOSUM for scoring the alignments compared to PAM.

It might also be important to look at the protein structures. You can try VAST if possible.


Examples of creating a new animal species by humans

There are indeed many examples of new species created by humans, and observed to arise by humans. Many via deliberate experimentation. You can find examples googling "examples of speciation", looking at the Wikipedia page for speciation or the Talk Origins one:

http://www.talkorigins.org/faqs/faq-speciation.html

http://www.talkorigins.org/faqs/speciation.html

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

The issue is that there are two events of interest in "the origin of species" that are related but not the same thing: there is speciation, and then there is overall change. And as far as change itself goes you can have genetic change and phenotypic change which themselves aren't perfectly correlated.

Speciation is a very important evolutionary event, as it's the point at which genetic material is no longer exchanged between two groups and so they start evolving independently, meaning differences will accumulate over time (steadily and inevitably for genetic differences, more variably for phenotypic ones as that depends on the environment). But you can have differences accumulating without speciation (especially not with your "in vitro fertilization" criterion, which allows gene flow to be stopped for a long time without "speciation" by that definition happening), and you can have speciation happen without much genetic or phenotypic change.

And so on our human timescale we'll tend to see three categories of events:

1) large phenotypic change without speciation (especially by the in-vitro definition), because natural selection can cause large phenotypic change but random mutation cannot be rushed and that genetic drift is usually what will make groups no longer inter-fertile,

2) Speciation without large phenotypic change, again because speciation is just the beginning and all you need for "speciation" is just enough change to make interbreeding impossible or difficult, and so many examples of observed speciation involve just that, and

3) Speciation with large phenotypic change, which will usually be single-generation events with hybridization and polyploidy. Those are the most likely to fit your criteria that in-vitro fertilization shouldn't work. And they are legitimate and important evolutionary processes; polyploidy has happened many times in our lineage, it's an important source of genetic diversity, and hybridization and polyploidy are a major mechanism in the evolution of plants in particular. But they're not the major mechanism for the evolution of large vertebrates, so it's easy for Creationists to dismiss them.

Still, looking at the links I gave you I see a few examples that involve genetic change sufficient to block even in-vitro fertilization. The second Talk Origins link in particular refers to examples where speciation was determined by the offspring being sterile. There is also an article in the notes of the Wikipedia page about a recent discovery about the kind of genetic changes that can lead to speciation:

https://www.scientificamerican.com/article/wandering-fly-gene-suppor/

The general problem with giving Creationists examples though, is that the examples they want don't exist (and would usually contradict the theory of evolution anyway) and the ones that do exist they're not satisfied by (because the change involved isn't dramatic enough, or IS dramatic but as a result makes the dramatic look trivial because it happened via a small gradual underlying change - which, you know, is how evolution is thought to work).

I notice in fact that you are the one asking about the speciation with in-vitro fertilization, not your friend; your friend apparently just said that huskies and chihuahuas are not comparable to fish vs tetrapods. If this is personal curiosity from you then that's fine; if you are looking for arguments for your friend specifically then it looks like you're on the wrong track, since no amount of lack-of-interbreeding will make flies any less flies, which is usually the issue for people who focus on "fish to tetrapod" as a scale of change.

You might have better luck figuring out exactly what claims your friend makes, where they set the boundaries of what they think is possible and what they think it isn't, and then find an example that breaks that specific boundary. So they say "speciation can't happen !", you reply "speciation happened in fruit flies", and they answer "so what, fish haven't become tetrapods" - but, what is it they meant by "speciation can't happen" ? What mechanism do they think makes it impossible, what do they think this "speciation" is that's impossible, where do they set the boundary for themselves between "ordinary change that can happen" and "stuff that can't happen so evolution is false" ? They probably don't know clearly themselves, but figuring it out and addressing it is a better way of moving forward, and you both can learn things. And it makes it a bit easier for you too - you don't have to worry about finding proof that fish can become tetrapods, you can be like "OK fish can't become tetrapods whatever, but you said that new species cannot arise through genetic change, but here is a paper saying that a gene transposition makes it impossible for those two flies to interbreed, wouldn't that be an example of speciation via genetic change ? What do you think ?"


Understanding the use of English tenses in biological journal articles

I regard this is more of a question for SE English Language and Usage under the tag “technical”, and will vote to move it there. However, as the answer relates to reading papers in molecular biology, I provide an answer here.
Linguistic interpretation without context
The tense used in the phrase “X remains poorly understood”, taken in isolation, suggests that this is the situation now. Hence, it is the situation at the end of the study.
However…
Interpretation in context
This is the Introduction section of the paper. In the Introduction to papers reporting experimental biological research, it is usual (and helpful to the reader) to explain the background to the study and why it was undertaken. In this case to explain that the incomplete understanding of the subject justified further studies such as the one to be described.
This is made clear at the end  of the Introduction, where one often indicates in a sentence what the work to be described adds to knowledge: “Our results show that flagellum originated very early, before the diversification of contemporary bacterial phyla…”.
So the minimal implication is that as a result of the work described “X is now better understood”. And that is clearly the case here.
This is borne out by the final paragraph of the Results section in which the authors emphasize the contribution to knowledge that their work has made. You don’t get published in PNAS by saying that you have left the field still in the dark!
Why not use a different tense and say that you the problem has been solved?
An alternative would have been to write:
“Before this work was undertaken X was poorly understood”
The reason for not doing this could either be “scientific modesty” (also known as don’t antagonize the referees by appearing arrogant) or acknowledgement that, despite the significance of the work presented, there are still aspects of the problem that are not understood.


What are the criteria for determining the influence of epigenetic factors?

First of all, the nature of penetrance is almost entirely unknown.  Likely it's a combination of epistasis and gene interactions, induced gene regulatory pathways, developmental noise, and other factors.  Epigenetics (imprinting, etc) may have little to do with penetrance, while chromatin structure may be a consequence of other things (most now regard histone modifications, etc, as consequence of transcription rather than heritable regulatory mechanism).  Currently, the field of epigenetics is undergoing a (long-overdue) reassessment.  Until that happens, anyone who wants to make claims of "epigenetics" is free to, so spurious claims are rampant.


Detecting a Fasting State in the Body via Lasers

If by a fasting state, you mean blood glucose levels, researchers seem to think it is feasible. See for example Pleitez et al. (1) and Guo et al. (2). Their designs both utilize infrared IR laser light to measure glucose levels in the skin.


What is the importance of alkaline condition in biuret test?

In the Biuret reaction, copper forms a complex with the nitrogen of the peptide bond, that looks like this (Structure 61 from the paper below):

A strong base is necessary to provide the conditions for deprotonating these nitrogen atoms and have the conditions to form the complex. If you want to read this in detail, have a look at this publication:

Coordinating properties of the amide bond. Stability and structure of
metal ion complexes of peptides and related ligands


What is the biological potential for vision of wavelengths outside the human visual range?

There are some limits on what light can be detected biologically based on physics and chemistry. Although there are animals that can sense more UV or more infrared than humans, they are still subject to these limitations.

How Vision Works

The way most types of vision operate is by using photons to cause a conformational change in an opsin protein by influencing a chemical bond in a sensitive molecule (a chromophore, for example retinal, which changes from 11-cis to all-trans) bound to the opsin. To sense a particular wavelength of light using this mechanism, it is necessary that the energy of the light is sufficient to cause this chemical change in the opsin-chromophore, without being enough energy to destroy the molecule entirely by breaking a bond.

Sensing low-energy (long wavelength) light

Longer wavelength light ('infrared') is also known as heat. Detecting "heat" photons is difficult because they don't have much energy. Therefore, you need a molecule that is very sensitive. It turns out that the opsin-based vision strategies use chromophores that are too stable to sense long wavelength light.

Some snakes have particular sensitivity to infrared, for example the pit viper. However, these animals do not "see" infrared using their eyes: they have another specialized organ called the pit organ. The pit organ uses receptors that are much more like the heat receptors in your skin than the photoreceptors in your eye, but the pit organ uses a pinhole camera effect to organize the incoming light onto a very sensitive heat-sensitive membrane.

Humans of course are able to sense infrared, too, but the same way: through the skin rather than the eyes, and at low resolution. However, if you stand outside in the sun and close your eyes, you can probably still "see" the direction of the sun: one side of your body will feel warmer than the other! In a way, this is like a form of low-resolution "vision" if you want to define that term very broadly. The snake's infrared sensitivity is more like this sensation than eyesight.

When you get to very long wavelengths, for example radio waves, the wavelength is too long and too low-energy to even be relevant at a molecular level: these forms of light will travel right through cells, and individual photons don't carry enough energy to influence molecules in ways that can be sensed by biology.

Sensing high-energy (short wavelength) light

Very short wavelengths of light have the opposite problem: too much energy. Ionizing radiation (from the upper ultraviolet range and shorter) has enough energy to actually free electrons and create ions. This type of radiation damages biological molecules, including DNA, so organisms have a lot of good reasons to avoid these types of radiation. Exposure to short-wavelength radiation can also cause bleaching (permanent destruction) of photosensitive molecules and potentially damaging heating of tissue surrounding pigments, in addition to direct effects on other molecules in the cells.

Insects and other organisms that can see into the UV range see mostly in the near-UV range, >300nm, not too far from our own vision range (roughly corresponding to "UVA"). However, it isn't true that humans can't see these wavelengths due to some lack of sensitivity of our photoreceptors: instead, UV light is (at least partly) blocked by the cornea and lens, presumably to protect the retina from damage!

Humans and other organisms do have some sensitivity to damaging UV wavelengths, just not through vision. Instead, humans and other organisms sense UV based on the damage done within cells, which recruits repair mechanisms and apoptosis to prevent damage from leading to cancer.

Summary:

The chemical processes behind vision determine the range of potential wavelengths that can be sensed. Animals on earth are able to sample from this entire range. Mechanisms to sense wavelengths outside that range would require wholly different approaches, and maybe even a unique biochemistry. The mechanisms would have to be so different that we probably wouldn't refer to those mechanisms as "vision" (for example, even the infrared sensitivity of the pit viper isn't really though of as vision) but we would come up with a new term, such as "radio sensitivity" or "radiation sensitivity" just like we have different names for "hearing" relatively high-frequency pressure waves with the ears but we have "vibration sensitivity" for low-frequency pressure waves felt through the skin.


RNA migrating slower than DNA on Formaldehyde Gel?

The inclusion of formaldehyde in the gel and buffer is to keep the RNA denatured (ie after heating the sample to melt the double-stranded stem-loops, just prior to loading the gel), in the hope that the RNA will migrate through the gel with an Rf proportional to its molecular weight (approximated here by its length). Therefore the correct size markers would also be made of RNA (and prepared the same way, by heating).
It is difficult to predict, a priori, how a double-stranded DNA fragment would migrate under similar conditions, without also including a lane of ds DNA size markers.
In other words I would only use DNA markers for DNA and RNA markers for RNA. By repeating this experiment (1 lane of DNA MW vs 1 lane of RNA MW) at different voltage gradients and different concentrations of agarose, you might be able to plot two standard curves that would let you predict where your DNA fragment is expected to migrate relative to the RNA transcript, but without that data I would not assume that a larger DNA fragment would run slower than its RNA transcript.
Even if the dsDNA was exactly the same length as the ssRNA (and pretending that the MW of the dNTPs and NTPs are identical), the DNA's MW would be twice as much as the RNA, but the negative charge on the DNA would also be twice as much.


What errors can occur during DNA replication?

There are many way in which DNA can be damaged. As already pointed out in the comment by @skymninge, the Wikipedia page on DNA repair, as well as the mutation page detail some of the things that can go wrong.

You say:

  If G goes with C and A goes with T, I don't see how that part can mess up.

This, however, would imply that the four bases are completely different so that mispairing cannot exist. This is (may I add luckily?) not true.
Indeed the chemical structure of the bases is very similar, and changes between one base and another (transversions and transitions) are common.

These can result for instance from exposure to external agents such as ionizing radiation and alkylating agents, or from exposure to endogenous products such as reactive oxygen species.

Furthermore, the enzyme synthetizing DNA, called DNA polymerase, can insert the wrong base, although most of these errors can be corrected by its "proof-reading mechanisms". However, it is estimated that

  the frequency at which human DNA undergoes lasting, uncorrected errors range from $1 * 10^{-4}$ to $1 * 10^{-6}$ mutations per gamete for a given gene.

Source: Nature Scitable

So, in summary, the system is not perfect, and mutation can be introduced even endogenously. This may seem bad, but, at least for relatively small rates of mutation, is not, as it allows change in the population, which is the basis for evolution.


I see no reason why not. Just to make sure, I decided to test. I ran a search on all human proteins (using the UniProt flat file) for all possible dipeptide combinations of the 20 standard amino acids (selenocysteine is also present in humans but only in 22--or so, depending on how you count them--proteins, so I wouldn't expect all possible sec-containing dipeptides to be present) .

As expected, each of the 400 possible dipeptides were indeed present in at least one human protein. In case anyone wants to repeat this, the "protocol" is as follows:

Download the human flat file from Expassy.
Extract the peptide sequences

perl -ne 'if(s/^\s+//){s/\s+//g;print}' human.flat > human.pep

Generate the list of possible dipeptides:

AA
AC
AD
AE
AF
AG
AH
AI
AK
AL
AM
AN
AP
AQ
AR
AS
AT
AV
AW
AY
CA
CC
CD
CE
CF
CG
CH
CI
CK
CL
CM
CN
CP
CQ
CR
CS
CT
CV
CW
CY
DA
DC
DD
DE
DF
DG
DH
DI
DK
DL
DM
DN
DP
DQ
DR
DS
DT
DV
DW
DY
EA
EC
ED
EE
EF
EG
EH
EI
EK
EL
EM
EN
EP
EQ
ER
ES
ET
EV
EW
EY
FA
FC
FD
FE
FF
FG
FH
FI
FK
FL
FM
FN
FP
FQ
FR
FS
FT
FV
FW
FY
GA
GC
GD
GE
GF
GG
GH
GI
GK
GL
GM
GN
GP
GQ
GR
GS
GT
GV
GW
GY
HA
HC
HD
HE
HF
HG
HH
HI
HK
HL
HM
HN
HP
HQ
HR
HS
HT
HV
HW
HY
IA
IC
ID
IE
IF
IG
IH
II
IK
IL
IM
IN
IP
IQ
IR
IS
IT
IV
IW
IY
KA
KC
KD
KE
KF
KG
KH
KI
KK
KL
KM
KN
KP
KQ
KR
KS
KT
KV
KW
KY
LA
LC
LD
LE
LF
LG
LH
LI
LK
LL
LM
LN
LP
LQ
LR
LS
LT
LV
LW
LY
MA
MC
MD
ME
MF
MG
MH
MI
MK
ML
MM
MN
MP
MQ
MR
MS
MT
MV
MW
MY
NA
NC
ND
NE
NF
NG
NH
NI
NK
NL
NM
NN
NP
NQ
NR
NS
NT
NV
NW
NY
PA
PC
PD
PE
PF
PG
PH
PI
PK
PL
PM
PN
PP
PQ
PR
PS
PT
PV
PW
PY
QA
QC
QD
QE
QF
QG
QH
QI
QK
QL
QM
QN
QP
QQ
QR
QS
QT
QV
QW
QY
RA
RC
RD
RE
RF
RG
RH
RI
RK
RL
RM
RN
RP
RQ
RR
RS
RT
RV
RW
RY
SA
SC
SD
SE
SF
SG
SH
SI
SK
SL
SM
SN
SP
SQ
SR
SS
ST
SV
SW
SY
TA
TC
TD
TE
TF
TG
TH
TI
TK
TL
TM
TN
TP
TQ
TR
TS
TT
TV
TW
TY
VA
VC
VD
VE
VF
VG
VH
VI
VK
VL
VM
VN
VP
VQ
VR
VS
VT
VV
VW
VY
WA
WC
WD
WE
WF
WG
WH
WI
WK
WL
WM
WN
WP
WQ
WR
WS
WT
WV
WW
WY
YA
YC
YD
YE
YF
YG
YH
YI
YK
YL
YM
YN
YP
YQ
YR
YS
YT
YV
YW
YY

Save that list as dip.txt.
Use that file to search the protein sequences:

perl -ne 'BEGIN{open(A,"human.pep"); while(<A>){chomp; $k.=$_}}; chomp; print "$_\n" if $k=~/$_/  ' dip.txt

The script above will print each dipeptide that was found in at least one protein. Since all were printed, all dipeptides exist in the human proteome.


Is it possible for a child to grow taller than their tallest parent?

People can grow taller than their parents. Anecdotally: I'm 185 cm, my parents are 155 cm and 178 cm. Joakim Noah, an NBA basketball player is 211 cm, his dad was 193 cm and mother was 175 cm... how?

Genetics and environment play a role in determining height. First of all, a more nutritious environment during development can lead to increased height, this is one reason why more recent generations appear to be taller.

Height is also an example of a quantitative trait - this means many genes (or loci [singular is locus], locations in the DNA) affect the phenotype (the physical measurable result i.e. a persons height). It is infact how the vast majority of traits are determined. At each locus that affects height there may be polymorphism (when more than one allele, or variant of that gene, exists).

Example:

Suppose height entirely is determined by 2 additive loci, $A$ and $B$, and no environmental effect occurs, and there is diploidy (two of each locus, one from each parent, determines height in a person).

Each locus has two alleles denoted by $A_1$, $A_2$, $B_1 $ and $B_2$. Each copy of alleles $A_1$ and $B_1$ add 40 cm to a persons height, $A_2$ and $B_2$ add 50 cm to a persons height.

Now a man who is $A_1 A_1, B_1 B_2$ (remember, humans are diploid) and a woman who is $A_2 A_1, B_1 B_1$ have children. Both parents are 170 cm tall. The theoretical limits for the population would be 160 cm and 200 cm. The children will inherit one copy of $A_1$ from the father and $B_1$ from the mother, but they could inherit either $B_1$ or $B_2$ from the father and either $A_1$ or $A_2$ from the mother. If a child inherited both of the taller alleles then they would be taller than the parents ($A_1 A_2, B_1 B_2$ = 180 cm). Likewise some offspring could be shorter.

Of course the reality is much more complex; height is determined by many more than 2 loci, by the environment, and gene * environment interactions. This principle was a hugely important because it meant that reproduction did not necessarily remove variation from the gene pool (a fundamental problem with early evolutionary theory was the thought of "blending" - when offspring are the average of their parents)


Development of radial symmetry in starfishes and other animals

That is the field of developmental biology which deals with organizers. Cell organizers are processes, genes and signalling proteins cells use to communicate / send and receive information from their neighbors, so that their spacial distribution in the body regulates their development.
The cells also have gradients of signaling proteins inside the cytoplasm, and cell polarity, so the cells know which way round they are:
"A spatially distributed signalling cascade can create step-like activation profiles, which decay at successive distances from the cell surface, assigning digital positional information to different regions in the cell. Feedback and feedforward network motifs control activity patterns, allowing signalling networks to serve as cellular devices for spatial computations."
All metazoans use the same types of organizers to develop different patterns of cells, so starfish use the same genes as mice to organize their axes. They are early metazoan genes/ Precambrian. Here is an in depth answer to your question: www.ncbi.nlm.nih.gov/pmc/articles/PMC5307799/
The cells know where they are, because they are receiving multiple signalling proteins from further away in the animal. Here is a picture of Bicoid morphogen in fruitflies:
The signalling proteins are received from cells far away, and that signals to other cells to make different kinds of signalling proteins to organize the local neighbors.

Given the complexity of metazoan morphogenesis, there are very many organizers and we only know a few of them. The axis formation is related to the Nodal gene which uses some kind of axial/mid-line located organizers to control symmetry, there are documentd about LRO: left right organisers, in starfish its the same chemistry in a different geometry. The Nodal biochemistry: https://youtu.be/kO8k9aiQJsQ?t=189


I was letting my fingers surfed in the internet about this question and found this interesting article : http://www.caves.org/section/vertical/nh/55/TreeAnchors.pdf
Your  question is too broad so I guess the link gives a general answer.
hope this helps


What's going on when roots turn green and grow into the air?

I found this article online that does describes hibiscus plants as having a "spreading" type root system that will also form new shoots away from the parent plant ... http://homeguides.sfgate.com/type-root-hibiscus-have-49085.html

I also noticed that you have an attached orchid with aerial roots attached to the hibiscus plant.  If you are misting the orchid roots periodically, you may be dampening the surface soil in the pot and encouraging the growth of shoot forming spreading roots on the hibiscus plant to develop and grow upward.