Will I hyperventilate if I breath twice as fast at an altitude with half as much oxygen as I am used to? Will I hyperventilate if I breath twice as fast at an altitude with half as much oxygen as I am used to? If not twice as fast, should I breath any amount faster on average than usual when at high altitudes?

By definition, hyperventilation is a state of increased breathing where the exhaled $CO_2$ is greater than what is produced by the body.

Except in artificial condition or in disease process, breathing faster than the autonomously-dictated rate is going to cause hyperventilation. You have a fine-tuned control of respiration that will work out the correct breating rate for you.

Oxygen is actually irrelevant for this phenomenon, first because of the definition of hyperventilation, but also because oxygen is mostly transported through haemoglobin (98+%). This means there is a fixed quantity of oxygen that can be transported by unit volume of blood (and by breath, for a given cardiac output), and the maximum is already reached at normal breathing rate. Breathing faster does not allow for better oxygenation of the blood. (even at an higher altitude)

On the other hand, $CO_2$ is transported by the plasma, dissolved (7%), but also in the form of bicarbonate (93%) through the following equilibrium :

$$ H_2O + CO_2 \rightleftharpoons \underbrace{H_2CO_3}_\text{Carbonic acid}  \rightleftharpoons \underbrace{HCO_3^-}_\text{Bicarbonate} + H^+  $$

In the alveoli, a quantity of $CO_2$  will diffuse to the alveolar air, and be breathed out, the target being eliminating the quantity produced by the body. However, in opposition to oxygen transport, it is possible to overshoot by breathing faster, because removing $CO_2$ drives the equilibrium in direction of $H_2O + CO_2 \leftarrow  HCO_3^- + H^+ $ that is, eliminating additional $CO_2$ through the removal of bicarbonate from the blood.

This is hyperventilation, and leads to hypocapnia, causing that particular sensation of dizzyness. It is also leads to respiratory alkalosis, because, as seen in the reaction equation, this incurs the loss of protons ($H^+$).


Can NSAIDs impact negatively the healing of tendons? There are a number of articles regarding nonsteroidal anti-inflammatory drugs
 (NSAIDs) having a negative effect on healing conditions like tendonosis and tendinitis. From what I understand the channel through which they reduce inflammation disrupts healing. In general, many of them constrict vessels, thus reducing bloodflow even further to tendons. Are there other reasons, or interactions they can have with  cells that may also disrupt healing?

Are there advantages of using NSAIDs to promote healing?

I would suggest you contact your doctor if you are suffering from tendinitis.

NSAIDs are often used as part of treament for tendinitis, but like all medications they can have side effects. Therefore again if you have concerns about taking NSAIDs contact your doctor.

As for the mechinism of action of NSAIDs they don't constrict vessels but instead reduce the production of inflammatory mediators (prostoglandins) which act to dilate some vessels. These inflammatory mediators also make blood vessels more permeable so that nutrients and cells from the blood can pass through the vessel walls and carry out repairs to damage tissue. The problem however with the bodies inflammatory response is that it can be too severe, so that rather than providing healing it itself can cause damage and pain. For this reason (and many others) NSAIDs may be useful.

But again if you have concerns about taking NSAIDs or any medical condition these please consult your doctor. The internet is not an appropriate place for medical advice, your doctor is.


How long does immunity to influenza last when contracting the disease vs vaccination The long term efficacy of flu vaccines are well documented, however I cannot seem to find a good source showing how long immunity lasts when contracting the disease.

I suspect it can't be much longer than vaccines since the virus mutates so quickly.

The effect on adaptive immunity are often stronger when contracting the flu than for getting the flu vaccination. The backside of this is that the flu is a quite dangerous disease which could end fatally, so getting the vaccine is always preferrable.

Getting infected by a specific flu strain (or receive a vaccination against it) generates specific immunity against this strain. If it mutates to strong or you get infected with another strain, you will have no immunity (and will have to develop a new immune response.

It seems that immunity against the flu can be livelong (against this strain) after you went through an infection and survived it. There are two studies showing long term response against antigens from the 1918 flu pandemic. The first (summarized in reference 1, the original article is reference 2) shows specific antibodies against the reconstructed haemagglutinin protein (H1) from the 1918 virus strain.

Serum from people born 1915 or before showed specific activity against this virus antigen, even more than 90 years after the infection.

The second study analyzes cross-reactivity of antibodies against the 2009 A/H1N1 pandemic flu strain. Here the cross reactivity of people born before 1930 was the highest - the 1918 strain (with which these people most likely had contact) was also a H1N1 virus. Although these viruses mutated between 1918 und 2009, there is still enough similarity that they are recognized by H1N1 specific antibodies (see reference 2).

A study which compared antibodies responses of people who contracted the 2009 flu against people who where vaccinated against it, showed that the antibody response was more longlasting in the people who got the infection (see reference 3).

So I think it is safe to say that the immune response is stronger after the infection compared to the vaccination, but the vaccination is much safer.

References:

How Long Does Flu Immunity Last?
Neutralizing antibodies derived from the B cells of 1918 influenza
pandemic survivors
Antibody Dynamics of 2009 Influenza A (H1N1) Virus in Infected
Patients and Vaccinated People in China


Why some viruses can spread with aerosol droplets, but others some cannot Why can some viruses spread with droplet like influenza virus, but some can not like HIV?

Is it due to their physical shape or the protein of their wrapper? Is there any formalized logic decide this before test the virus in lab?

Thanks in advance!

The question you are asking, if I have it right, is about what is called the "mode of transmission" of a virus.

I won't get into too much detail but there are many many factors that play a role. The main one here (in the example of HIV vs influenza) is which cells the virus infects. Influenza infects cells of in the mouth, throat and lungs. So when it grows and ruptures these cells the virus will be let out in your throat, mouth and lungs. So the way it spreads to other people is coming out of these areas on saliva and mucus when coughed or sneezed in droplets.

HIV on the other hand infects cells of the immune system, which are mainly found in the bloodstream as well as mucus cells (that line reproductive tracks). Again without going into too much detail (because mucoid layers are also found in the stomach etc) HIV can spread only from the location where the cells are located that it infects. Because it does not generally infect cells in the mouth and throat it will not be able to access these areas. So it spreads from blood or sexual intercourse, as that is where the cells of the immune system that it infects are located.


Does the genetic expression of specific physical traits ever correlate to behaviour? Over at skeptics, there were a couple questions asked as to the correlation of specific physical traits in relation to personality/behaviour.  For instance, the simian line as well as red hair.  Now, I did my best to answer these questions, with what I understand as there being a long history of people attempting to correlate external physical characteristics with behaviour (see the disgraced "art" of phrenology for instance).

However, in answering the simian line question, I did come across some weak correlations.  It got me to wondering if this is an area of exploration in terms of perhaps one gene sequence for a physical trait somehow being tied with another gene sequence for behaviour.

So, do any physical characteristics being expressed through genes correlate to behaviour?

Aldridge et al. (2011) show a correlation between facial phenotypes and autism spectrum disorders (ASD) in a sample of 8-12 year old boys.

They studied two groups of boys, 65 that had been diagnosed with ASD and 41 who had not. They collected 3D images of the faces and looked for similar patterns among the two groups. They found a significant association between some phenotypes and ASD. But, as with most studies, the results are complex; there a distinct sub-groups within the ASD group.

Keep in mind that this is an association study -- no causation is shown.


Has the acronym DNA ever been widely understood to stand for deoxyribose nucleic acid? I have a friend familiar with evolutionary biology who was recently bragging about how much he knows.  I asked him what DNA stood for, and he answered it stood for 'deoxyribose nucleic acid'.  When I claimed it stood for deoxyribonucleic acid, he said it depends on the source you go by.  I was curious and decided to look into it, but the only source I could find using his answer was the paper "Molecular Structure of Nucleic Acids: A Structure for Deoxyribose Nucleic Acid" published in the 1950s, and no explanation regarding if and when the term was officially changed.  Can anyone shed light on the history of the term and explain if deoxyribose nucleic acid is still acceptable?

First off, that paper is the seminal discovery and publication of the structure of DNA, and is absolutely worth the read.  It's one of the most important pieces of scientific literature.

The short answer is no.  DNA stands for Deoxyribonucleic Acid.

The long answer is... this is really just picking at nits.1  DNA, deoxyribonucleic acid, is a type of nucleic acid, specifically a deoxyribose nucleic acid.  So, if your or your friend wants to be pedantic, you can call DNA a type of deoxyribose nucleic acid that stands for deoxyribonucleic acid.

You probably shouldn't, though, since if you really want to be pedantic, saying "deoxyribose" implies it's a sugar, which once it has formed the DNA backbone, it no longer technically is.  Watson and Crick clearly used the phrase your friend has, but suffice to say that British papers from the 1950s used language differently than most folks today.

As a side note, there are nucleic acid analogues, such as PNA and LNA, which generally use the "Whatever Nucleic Acid" construct for naming, but I suspect that's mostly because "peptide" is a broad category, and "locked" isn't actually a biological word.

Also, "it depends on the source you go by" is just a way of getting out of being wrong.

ETA: WYSIWYG correctly notes in the comments that it used to be called desoxyribonucleic acid, such as in this extremely important paper by Avery, MacLeod, and McCarty.

1: See what I did there?  Most people would say "nitpicking" but "picking at nits" is basically the same thing, even if almost nobody says it.


What is the cause of colours of nail Why the nails are of white colour from bottom? then why they are pink and again white in the end?

The Nightman is giving you a headstart to understand and read about nail colour.

I would like to add a different view to this question from "Colour and Pathology" point of view. Finger nails have been an excellent source of evidence for the initial physical diagnosis process. Nail colour and texture can be an indiator for a wide range of medical conditions.

You may take a look at this link : The hand in Diagnosis Process and discusses about nail pathology.. However this diagnosis gets a little tedious if the patient has colourfully painted their nails with nail polish...

I see many of the answers do include an image - well at the end it's anatomy.

Here's a relative simple and fun to read article to clarify any doubts you have about Keratin in nails being dead or not, for its colour and why it's tough.

  The cuticle and matrix are white because the melanocytes there are inactive, so there is no pigment produced. The matrix cells divide and the new cells produce a lot of keratin protein.

  The older cells fill with keratin and die, and the new cells push them out of the way – this means toward the end of your finger. This is how your nails grow.

  But our fingernail doesn’t look like individual cells. You are
   sloughing millions of skin cells each day, but for a nail the dead
   cells all mass together. Nails only wear away or must be trimmed.
   Individual cells are not lost. The solidity of the nail comes from the
   connecting of the dead cells together by junctions between the cells
   called desmosomes, and by the interlocking of the cells like jigsaw
   puzzle pieces. But there’s more.

  Individual keratin protein filaments also become connected so that the entire mass of keratin becomes one solid structure. This is called cornification, like the stratum corneum (the outer, dead layers) of your skin.

  One of the two main forms of keratin in your nails is crystalline keratin, which is rigid, stronger, and has an ordered structure - like a tinker toy cube. Transmitted light is less likely to strike an atom and bounce back when the atoms are all lined up, so this is why many crystalline lattices appear translucent.


How do Benzodiazepines induce Rewarding (Euphoric) effects? Benzodiazepines are a class of drugs that serve as positive allosteric modulators of the GABAA receptor by binding to their own "site" on the aforementioned receptor. By doing this they produce euphoria and a wide range of effects characteristic of Central Nervous System (CNS) depression (e.g. anxiolysis, sedation, amnesia, mental confusion, muscle relaxant effects).

I know that an interaction with the mesolimbic dopamine ("reward") pathway would have to come in somewhere but where? I also know that GABAergic neurons downregulate activity in the mesolimbic dopamine pathway and that this is how opioids and cannabinoids induce euphoria -- they inhibit the release of GABA from presynaptic neurons in the mesolimbic dopamine pathway. I just find that this would be confusing in the case of benzodiazepines since they increase GABA activity, presumably also in the mesolimbic dopamine pathway thus producing dysphoria and not euphoria.

I just would like to know how they manage to induce euphoria in full (what they do to increase activity in the mesolimbic dopamine pathway that thus leads to euphoria)

Please cite journal articles to substantiate your claims.

Okay, I read the question wrong.

Benzodiazepines do not bind to GABAA receptors universally. Thus the presumption that it inhibits the mesolimbic dopamine pathway may be wrong. They may not interact directly with said pathway at all.

Many subtypes for the GABAA receptor exist. The receptor consists of 5 subunits. The following subunits are known to exist: α1-6, β1-3 and γ1-3. The most common combination has two α, two β and one γ. You find ones with distinct compositions at distinct locations in the brain. All have two bindingsites for GABA, but only a subset has an additional binding site for benzodiazepines.

The benzodiazepine binding site is at the interface of an α and a γ subunit, so receptors without this structure will show no affinity for benzodiazepines. Additionally the α subunit must contain a histidine residue, which is only true for α1, α2, α3 and α5. That is paraphrased from wikipedia, where you can find the sources as well.

I still think you need to consider the idea that benzodiazepines may not interact directly with the dopaminergic reward pathway, like opiates and cocaine does. I attribute the euphoria to be an indirect effect, resulting from the muscle relaxation (which will feel like you had a good massage), and the calmness of the mind.


What is the best way from remove background signal from a band when doing Western blot image analysis? I am doing image analysis of a Western Blot in Image J. I have calculated the total intensity of my protein bands of interest through outlining each band using the rectangle tool in ImageJ, and calculating the area and mean intensity. I have multiplied the area with the mean intensity to obtain the total intensity. However, I want to remove the background signal from each protein band of interest.
The background adjusted protein signal would be calculated as: (protein band mean intensity - background band mean intensity) * (area of protein band). On my blot, I have two isoforms of my protein of interest that were detected by the antibody, and I want to subtract the background from all bands for both proteins.
The way I am calculating the background, is for each lane, making a rectangular selection near the top of the lane where there is no labelling against any protein. The length of the rectangular section is equal to the length of the lane. However I am not sure how wide the rectangle for the background should be. From what I have seen online, there is no fixed method for calculating the background signal.
Are there any ways to determine how wide you want the band for your background to be? E.g. should the width of the band for the background be equal to the width of the protein band of interest, or can it be wider than that?
Additionally, how can you know if you have made the rectangular band for the background too wide?
Any insights are appreciated.

I haven't done immunoblots for years, and didn't do much quantitative analysis of them even then, so caveat emptor. However:
1) "Are there any ways to determine how wide you want the band for your background to be?"
I would say that the central limit theorem is a good place to start. Basically, as the size of your background increases, the precision of your estimate of mean background intensity will also increase (asymptotically). So you want your background sample to be as big as possible.
This does have some assumptions:

Little regional fluctuation of mean background signal

(related) Absence of gel artifacts

So, you want your background sample to be as big as it can be without including any artifacts and as long as it is representative of the blot in the general region of your band. In practice, I imagine that taking a selection the size of your protein band is probably fine in most cases, and probably easier to explain. You just have to pick a representative piece of background to measure.
2) how can you know if you have made the rectangular band for the background too wide?
Wider than the blot is too wide. On an infinitely large blot, I think you can't make it too wide. For practical purposes, you want it to be as wide as you can get it and not overlap obvious artifacts or the edge of the blot. But again, it's probably easier to explain just selecting a piece of background as big as the protein band that is roughly near the protein band, to account for local background variation.


Is there a closed path through the circulatory system that never passes through the liver? I know the liver is responsible for doing lots of stuff to the blood, including both adding glucose and removing "weird stuff" (stuff destroyed by hepatocytes).  And I know that statistically every volume element of blood will eventually pass through the liver.
However, if you were magically minaturized a la Fantastic Voyage, and traveled with the blood flow, making ideal turning decisions at every arterial branching but never going upstream or out of the blood vessels themselves, could you completely avoid the liver?

The liver gets blood from two sources: the hepatic artery and the portal system of venous drainage from the gastrointestinal tract.
As long as you don't follow one of these paths, you'd avoid the liver. Some examples would be circulating through any of the limbs or head, but any path that avoids those two paths will do. As you point out this is statistically unlikely without your magical navigation abilities.


Is there a difference between splice-site mutations, and non-stop mutations I'm working on a bioinformatics project where a lot of the biology I've had to learn from scratch. From my current understanding, a non-stop mutation alters a stop codon such that the transcription continues, and a splice site mutation alters the region between introns and exons - where the sequence may include introns, or remove part of the exons from cancer.gov. I'm inferring therefore that these could be the same mutation type.

Is this understanding correct?

No, those kinds of mutations are quite distinct.  Also, you misstate the nature of a nonstop mutation; the change of a stop codon affects termination of translation, not transcription.  This is quite different from a splice-site mutation, which affects splicing, a form of mRNA processing that occurs between transcription and translation.


Why is EcoRI supplied with a unique buffer when it is allegedly 100% active in universal buffers? Thermo packages a unique buffer with EcoRI:

  50 mM Tris-HCl (pH 7.5)
  10 mM MgCl2
  100 mM NaCl
  0.02% Triton X-100
  0.1 mg/mL BSA

However, they also list their EcoRI enzyme as 100% active in Buffer O with no indicated star activity:

  50 mM Tris-HCl (pH 7.5 at 37°C)
  10 mM MgCl2
  100 mM NaCl
  0.1 mg/ml BSA

The same is true of 2X Tango:

  66 mM Tris-acetate (pH 7.9 at 37°C)
  20 mM magnesium acetate
  132 mM potassium acetate
  0.2 mg/ml BSA

Is there a reason one would preferably use the unique buffer over a universal one? Given that buffer compatibility is a major selling point for restriction enzymes, why would they continue to supply a unique buffer?

Activity toward the desired substrate sequence is not the only concern in evaluating a restriction enzyme buffer system. In addition, you need to be concerned about so-called "star activity", or activity of the enzyme toward other, non-desired nucleotide sequences.

For example, NEB supplies an enzyme-specific buffer for it's standard EcoRI, even though it lists 100% activity in buffer #2 of NEB's standard buffer series. But at the very bottom of the page, there's this note: "May exhibit star activity in NEBuffer 2.1 or CutSmart Buffer."

Promega has a similar warning about it's "MULTI-CORE" buffer - even though EcoRI has 100% activity in that buffer. The MULTI-CORE buffer is not recommended due to star activity - cleavage at non-standard sites.

It's a little hidden on the product data sheet, but Thermo Scientific does have a mention of star activity in the standard "Tango" buffer, and mentions star activity with overdigestion in the standard "R" buffer. There's no warning about buffer "O", but given EcoRI's propensity toward star activity, I'm guessing this is part of why they recommend a unique buffer for routine usage. Given how frequently EcoRI is used in molecular biology, it's worth using a custom buffer to get the star activity as low as possible.

From canadianer: I contacted Thermo's technical support. Despite the fact that star activity is not listed as a concern for either 2X Tango or Buffer O in the product data for EcoRI, they say that it may actually show some star activity in these universal buffers which is why they continue to supply the unique buffer for this enzyme.


Help with STRING database data I'm working with data downloaded from STRING database (string-db.org) for protein-protein interactions.
My idea is to compare the topology of connections of the same protein on different organisms.

However, I noticed that the same protein can receive different ID on each organism.

So I would like to know if there is any way to convert all ID's into just one pattern.

Thanks.

Proteins evolve and have different sequences between species, so you would have to define what you mean with "same protein". One option would be to use an orthology database like eggNOG. (eggNOG has the same protein identifiers as STRING.) Then you could figure out 1:1 correspondences between proteins.

You probably also want to read up on Roded Sharan's work, e.g. Global alignment of protein-protein interaction networks.


complete DNA transfer across different organism zygotes Consider we have a monkey zygote (i.e. single cell just fused) and a tiger zygote. If we extract the nucleus of monkey zygote and place it into tiger zygote where nucleus of tiger zygote is already removed. Is there any chance of zygote to survive and finally turn into a monkey offspring ? I tried Google for any such experiment ever conducted but seems like biology is googol to Google, no close result at all.

For more clarity it can even be considered all chromosomes transferred  instead of nucleus.

As far as I think this could be possible as all 20 amino heads must be present in zygotes of both the mammals and thus synthesizing protein should not be a problem. However I can't say anything about their respective immune system response.

This question came to my mind considering Darwin hypothesis/theory(interpret as you wish) of evolution, where even if some mutation changes the DNA sequence how much chances are there for a completely new organism if cells don't support growth natively.

Unfortunately the answer is no. Similar experiments of cross species nuclear transplants into enucleated oocytes have been attempted. Rat nuclear transfer into activated denucleated mice oocytes, rabbit oocytes etc.

The primary stumbling block appears to be incompatibility between mitochondria proteins derived from the donor nucleus and proteins derived from the host mitochondria. Mitochrondria proteins are encoded from two DNA sources, the genome within the nucleus and the genome within the mitochondria. While mammalian mitochondria proteins are very similar, there are differences. These small differences between species appears to be enough to kill a developing embryo if there is a miss match.

Attempts have been made to replace both host nucleus and host mitochondria. However complete replacement of host mitochondria has not been successful. Partial replacement of host mitochondria (mouse oocyte as host and rat nucleus with rat mitochondria as donor), appears to marginally prolong the life span of embryo. But death is still the outcome.

PS: nuclear transfer between subspecies and very closely related species does produce viable clone.  Coyote (Canis latrans) using dog (Canis lupus familiaris) oocytes. (Bos gaurus) adult nucleus donor cells and bovine (Bos taurus). My guess is that if a hybrid is possible between the two species, nuclear transplant between the two species should be possible


Validity of the August Weismann mouse-detailing experiment refuting Lamarckism Weismann conducted the experiment — described in Wikipedia — of removing the tails of 68 white mice, repeatedly over 5 generations, and reporting that no mice were born in consequence without a tail or even with a shorter tail. This was intended to refute the Lamarckian idea of of acquired characteristics.

However, surely five generations is too short a time to observe a change in an organ when the fossil record indicates that such changes in animals took millions of years. Was this not known at the time and does it invalidate the experiments?

If you are reading this after 31st July 2017 it will seem somewhat disconnected from the question. This is because the question has been extensively edited since I wrote this answer.

Anyone who is interested in the work of August Weismann should start by reading the corresponding Wikipedia page.

Ernst Mayr ranked him as the second most notable evolutionary theorist of the 19th century, after Charles Darwin.

As far as the mouse tail experiment is concerned, we learn that Weismann was concerned with disproving Lamarckianism, and that:

Weismann was aware of the limitations of this experiment, and made it clear that he embarked on the experiment precisely because, at the time, there were many claims of animals inheriting mutilations (he refers to a claim regarding a cat that had lost its tail having numerous tail-less offspring).

My grandfather used to claim that his mother was frightened by a bear whilst pregnant, which was was why he was born with bare feet but that's more likely to be due to an epigenetic effect I suppose.

Added later in response to Remi.b
I see that Charles has already addressed this to some extent, but since I have already done the research I'll post what I found:
from August Weismann, Essays Upon Heredity. Clarendon Press, Oxford, 1889
(Volume 1, Chapter 8, p. 431)

But now, after this little digression, let us return to the transmission of mutilations.
We have seen that the rudimentary tails of cats and dogs, as far as they can be submitted to scientific investigation, do not depend upon the transmission of artificial mutilation, but upon the spontaneous appearance of degeneration in the vertebral column of the tail. The opinion may, however, be still held that the customary artificial mutilation of the tail, in many races of dogs and cats, has at least produced a number of rudimentary tails, although, perhaps, not all of them. It might be maintained that the fact of the spontaneous appearance of rudimentary tails does not disprove the supposition that the character may also depend upon the transmission of artificial mutilation.
Obviously, such a question can only be decided by experiment: not, of course, experiments upon dogs and cats, as Bonnet rightly remarks, but experiments upon animals the tails of which are not already in a process of reduction. Bonnet proposes that the question should be investigated in white rats or mice, in which the length of the tail is very uniform, and the occurrence of rudimentary tails is unknown.
Before this suggestion was made, I had already attacked the
problem experimentally. Such a course might, perhaps, have been more natural to those who maintain the transmission of mutilations, to which I am opposed. Although I undertook the experiments expecting to obtain purely negative results, I thought that the latter would not be entirely valueless; and since the numerous supporters of the transmission of acquired characters do not seem to be willing to test their opinion experimentally, I have undertaken the not very large amount of trouble which is necessary in order to conduct such an experimental test.


Mitochondria - are they really separate organisms that once merged into eukaryotic cells? Theoretically, mitochondria are said to be a separate organism that is concerned with its own life and its own processes. In fact, it even duplicates individually. I know a similar question is here but I have something else apart from that to ask.

Is the presence of their own DNA/RNA - like compound justify or prove that the mitochondria was once a separate living organism?
If the mitochondria is indeed a separate living organism, then how is it controlled by the nucleus? Or is it not? Logic would suggest that since mRNA exists in the mitochondria separate from DNA in the nucleus, they have their own control over how they behave.
Often, living organisms working together have to have some sort of payment system. For example, bacteria in the body provide Vitamin K and other breakdown vitamins, and in return the body gives it a suitable home to live in. Is there any such business occurring between the individual cell and the mitochondria? Does it keep some nutrients for itself? If not, what is its mode of nutrition?
In effect, cells did exist before mitochondria joined the party. Is there any way to at least have a feasible hypothesis on why and how the cells bonded with the mitochondria or how the cells even existed in the first place without the presence of and organnelle that can break down food and convert it into energy?
Why do mitochondria have their own membrane? And that too folded? Is that to increase the surface area available for the electron transport chain, or is it for simple compactness?
Why does the mRNA in our bodies always exactly match the mRNA of our mothers and only our mothers? Can any genetic mutation change this fact?
Is it possible, that a mitochondrion can somehow escape the cell and start performing its life otherwise?
mRNA would suggest that mitochondria make their own proteins / at least some basic amino acids. If there are any such proteins, are they utilized for the cell? Or are they used for cellular respiration? Or are they kept by the mitochondria for there own means?

I will appreciate all answers!,
SmallDeveloper (a.k.a SmallScientist :) )

EDIT : Basically, I am asking 3 things:

Were mitochondria really separate organisms once?
If so, how do they get their nutrition?
How did cells exist before mitochondria came along?

Yes. But it is incorrect to call mitochondria an organism now.
Most of their genes were lost and are now encoded in the nuclear genome
It gets most of its metabolites
It is not known. See the other post for details.
Why membrane: I guess you know that. Why folded: you guessed right.
Only ovum donates mitochondria and other cytoplasmic factors. Sperm just provides the haploid genome.
No
Most of them are key respiratory enzymes


To a population with no immunity, why is smallpox or measles more deadly compared to COVID-19? Specifically, this is not a question asking how easily a virus spread in a
population (airborne, asymptomatic spread, etc), but regarding the
mechanism or the "havoc" it wreaks once inside a person's body.
Edit: The question is based on the assumption that, once a human body can readily recognize the virus signature and starts flooding the blood with anti bodies, the virus won't be a problem.

Today, We have no prior immunity to COVID; 400 years ago, Americans
had no prior immunity to smallpox either.
Both virus can be effectively combatted once the body has immunity
(recognization and anitbody production).
Yet, smallpox is so much more lethal and its damage horrifying.

I think this is an interesting question, and I've been struggling to put together a good answer to it for a while. Unfortunately, everything I came up with just boils down to "some viruses are more deadly because they kill more cells faster" which is pretty circular. A detailed understanding at the subcellular level of what happens during virus infections doesn't exist.
It's instructive here to look at the evolutionary pressures on human-infecting viruses. SARS-1 was about 10x as deadly as SARS-2, but it was contained quickly, while SARS-2 is on track to infect a substantial portion of all humans on the planet. SARS-2 is more successful because of, not in spite of, its lower lethality. Because many infections are asymptomatic, the infection can't easily be contained. If we look at things this way, the asymptomatic infections are the ones that go "according to plan" for the virus, and the severe cases and deaths are unwanted collateral damage. Severe cases of COVID are associated with the presence of viral RNA in the blood. But SARS-2 primarily enters new hosts through droplets expelled from infected hosts' respiratory systems. Any viral activity outside of the respiratory system cannot produce these droplets, and is therefore "wasted effort". This is similar to polio, which causes no symptoms when it transmits successfully by replicating in intestinal cells, but causes paralysis when it gets stuck in the dead end of its host's nervous system.
So, if viruses are most successful when they cause no disease, shouldn't they all quickly evolve into harmless versions? They don't because the "sweet spot" of asymptomatic transmission is the unstable result of an immune response that is just effective enough. If a virus fights the immune system either too hard or not hard enough, the infection will end too fast to spread effectively; due to the death of the host or the virus, respectively. Similarly, if a virus is too "aggressive" in entering cells it will damage tissues that don't lead to transmission or new infections, but if it is not aggressive enough it will not be enter those tissues it needs to make, e.g. respiratory droplets carrying new virus in the case of SARS. Since a lethal disease still results in some transmission but complete suppression by the immune system doesn't, it's more evolutionarily favorable for viruses to err on the size of causing worse disease.
Edits for changes in the question:
I think the differences between covid-19 and smallpox are a bit misleading. The big differences between the two diseases is that, while the human populations most affected by smallpox were naive to the virus, the virus was not naive to them. Smallpox is believed to have been infecting humans since at least the 3rd century BCE. It had a lot of time to evolve tricks to defeat the human immune system. And as a dsDNA virus with a 186,000 base pair genome, it had plenty of space to store those tricks. For comparison, SARS-CoV-2 has a 30 kb RNA genome, and poliovirus has a 7.5 kb RNA genome. However, Herpesviruses have been infecting humans since before humans were human, have large genomes, but only cause disease when the immune system is suppressed or nonfunctional. In those cases, however, it is quite effective at spreading throughout the host and can kill. So we see that herpesviruses also rely on the immune system of the host to stay in their sweet spot, they just have a different strategy than smallpox. Since smallpox has been exterminated and herpesvirus is in nearly every human on earth, we can say the mild strategy is the unequivocal winner, at least for now.


Terminology regarding sensory receptors I was recently asked the following question:

  Compare the following pairs of receptors in the same
  sensory system. Include in your discussion:

  The distribution in the
  sensory epithelium;
  What kind of stimulus is effective in activating
  them;
  Their physiological response properties, function and central
  connections.

  Rods and cones
  Pacinian corpuscles and free nerve endings

In particular, I was not sure what the sensory epithelium is. Is it getting at the fact that Pacinian corpsucles are subcutaneous, while free nerve endings are cutaneous and that cones are centralized at the fovea?

Alos, I am not sure what their "physiological response properties" refers to. Since they are receptors, would their responses just be the output (i.e. peripheral/foveal vision and vibration/pain sense)?

The distribution in the sensory epithelium indeed refers to the location of the different receptors. And indeed, you are also right that cones are concentrated in the fovea, and rods are mostly found more eccentrically in the retina (Kolb, 2012. I would say the free nerve endings are situated just below the epidermis, and the PCs in deeper layers of the dermis (Fig. 1). But check your notes on what your prof. wishes to hear about this.

Fig. 1. Skin receptors. source: Neupsy Key

The physiological response properties of receptors is not their output per se. It is the way they respond to stimuli, that includes their output, but also includes the sensation of physical stimuli through second messenger systems or otherwise, and eventually the output. Kolb (2012 goes into detail on the physiology of photoreceptors in quite some detail and for the physiology of touch receptors I would refer to Dougherty in Neuroscience online.

References
- Dougherty, Somatosensory Systems. in: Neuroscience online. University of Texas
- Kolb, Photoreceptors. In: Webvision. The Organization of the Retina and Visual System (2012)


How is the growth of benign tumors suppressed? A benign tumor  has an outer layer of cancerous cells beyond which are regular cells (I Think).  The Tumor must have some kind of boundary layer like a wall where somehow the cancerous cells can't affect any more normal cells outside the wall. A Benign Tumor I think can be inactive for many months; it might never grow anymore. Might it be that the cancer cells at this Benign Tumor Wall are inhibited from affecting any more cells? Could there be an Apoptosis shut-off inhibitor or a cell-death pathway shutting-off inhibitor in this case?

The primary difference between a benign tumor and a malignant tumor is that the former cannot metastasize; therefore they remain within the tissue boundaries.They grow slowly and are are not very de-differentiated thereby retaining some of the tissue organization.

Another point to be considered is that benign tumors do not cause vascularization (formation of blood vessels in the tumor tissue; triggered by secretion of VEGF), which also limits its growth.


Are (baseline) high blood levels of melatonin associated with either circadian rhythm or mood disorders? (Exogenous) melatonin is administered at night for treatment of circadian rhythm disorders, but melatonin taken during the day is linked with depression.

I would like to know if high blood levels of (endogenous) melatonin (at a steady state, throughout the day) might be linked with mood or sleep disorders (or have any effect at all), or if the body's response to melatonin adjusts accordingly.

I think the answer to this SE question is related, but I can't find the source using a reverse image search.

I found a recent PLoS article that said that none of hypochondriasis, depression, hysteria, psychopathic deviate, masculinity-femininity, psychasthenia, schizophrenia, or social intraversion (on the MMPI-2) "were associated with any melatonin parameter."

However, it does appear that "increases scores of Hypomania and Paranoia were associated with a shorter DLMO-DLMOff interval" (duration of melatonin production).

The only thing that concerns me are the significance and the effect size of the latter two results.  I can't tell whether they corrected for multiple comparisons or not.

Reference:  Burgess HJ, Fogg LF (2008) Individual Differences in the Amount and Timing of Salivary Melatonin Secretion. PLoS ONE 3(8): e3055. doi:10.1371/journal.pone.0003055


Gene of interest number of copies in transformed K. pastoris When transforming a K. pastoris strain, is there a way to predict how many copies of the gene will be integrated following the homologous recombination? More specifically is it something that a molecular biologist is able to control in a simple way, or, is it usually left to the chance (and determined afterward using gene sequencing)?
Alternatively : if I want to transform an electrocompetent wild type strain such as Pichia X33 using a plasmid vector, is the multiple integration an iterative process I control or is it random?)

Edit: Thank you all for the answers. Finally if I understand well the process is pretty random but you can control it to some extent. @gaspanic: I keep the idea of using fluorescent reporters and FACS for that ;)

To predict the number integrations is probably not possible, but you can favor multiple integrations, if that's what you are after. At least in Saccharomyces cerevisiae integration of a first plasmid appears to stimulate the insertion of additional plasmids at the same site (1). It is therefore possible to favor multiple integrations (2) by increasing the DNA-to-cell ratio in the transformation, thereby increasing the chance that any competent cell receives more than one copy of the plasmid, which could then integrate in tandem. The easiest way is to simply use more DNA, but depending on your cell competence you might need to compensate this increase by using less cells for your transformation (or simply plate less cells on each plate) as you will probably also increase the overall colony yield.
One way to actively select for multiple integrations is to use a competitive inhibitor for the selection marker. Again, in Saccharomyces cerevisiae transformations with HIS3 selection can be combined with 3-AT (3). This allows you to inhibit HIS3 activity just enough to only permit the growth of cells that have integrated a desired number of copies of the plasmid. Of course, this method is far from fool-proof, as you might also select for mutants that have increased HIS3 expression for other reasons. Edit: I actually found one paper doing this in K. pastoris (4).
Finally, if your implementation allows it you can facilitate the screening for multiple integrations by including a fluorescent protein-expressing cassette in your plasmid. That way you can easily screen for different numbers of integrations by fluorescence microscopy or FACS.
Sources:

Orr-Weaver et al. (1983): https://mcb.asm.org/content/3/4/747
Plessis and Dujon (1993): https://doi.org/10.1016/0378-1119(93)90172-Y
Wikipedia (retrieved 15 Aug 2020): https://en.wikipedia.org/wiki/3-Amino-1,2,4-triazole
Menéndez et al. (2018): https://doi.org/10.2144/00295rr05


How Does Green Tea Increase Metabolic Rate? According to the article "Green Tea Supplementation Affects Body Weight, Lipids, and Lipid Peroxidation in Obese Subjects with Metabolic Syndrome", Green tea increases metabolism and fat loss:

  Green tea beverage consumption (4 cups/d) or extract supplementation
  (2 capsules/d) for 8 weeks significantly decreased body weight and
  BMI. Green tea beverage further lowered lipid peroxidation versus age-
  and gender-matched controls, suggesting the role of green tea
  flavonoids in improving features of metabolic syndrome in obese
  patients.

Is there any information available concerning the mechanism of that metabolic increase?

Interesting question! Green tea increases metabolic rate of body because it contains antioxidants known as catechins1. Catechins are actually polyphenol flavonoids, and have been shown by Wang et al and team to affect body composition and decrease body fat in intra-abdominal area. Also, as per Khalesi et al, catechins improve blood pressure, especially when systolic pressure exceeds 130 mmHg, while some studies, such as Ellinger et al, have indicated that catechins may have effect on endothelium-dependent vasodilation which might lead to normal blood flow regulation. Another study, by Weinreb et al, shows that catechins can also reduce the risk of Parkinson's and Alzheimer's. However, their exact mode of action is unknown because of their extensive metabolism during digestion6.

Green tea also contains a little amount of caffeine. Now, as we all know, caffeine is known for its stimulating effects on the body. Caffeine, as stated by Nehlig et al, blocks the formation of adenosine in brain, thus increasing concentration of dopamine and norepinephrine in the brain which, in turn, allow quicker firing of neurons. Along with caffeine, another compound with similar effects is L-theanine, which increases the activity of GABA and leads to anti-anxiety effects, as reported by Nathan et al. Caffeine and L-theanine can together have synergistic effects on the brain and give much more pronounced effects together than individually.

A yet another, and probably less spoken of, effect of green tea, as concluded by Lee et al, is that it can even kill some bacteria and viruses (obviously, killing means preventing growth here) and thus reduces chances of bacterial and viral infections.

Obviously, there might be even more benefits of green tea than I've put here. To the precise point you were asking, we don't yet know how green tea helps in burning calories and fat oxidation. The proposed mechanisms of action are10:

catechins act on catechol-o-methyltransferase (COMT), an enzyme which degrades norepinephrine. Norepinephrine is known for regulating thermogenesis and fat oxidation. Thus inhibition of COMT by catechins may lead to prolonged effects of norepinephrine on fat metabolism.
caffeine can also affect thermogenesis, but by inhibiting phosphodiesterases & thus prolonging effects of cAMP in the cell. As a result, cAMP stimulates hormone - sensitive lipase and promote lipolysis.
catechins and caffeine can also work together and increase thermogenesis in body by 35-43% by increasing fat oxidation.

However, these are just the proposed mechanisms and more detailed studies are required to reach a conclusion.

References:

 1. Beneficial Effects of Green Tea—A Review; Carmen Cabrera, Reyes Artacho, and Rafael Giménez; Journal Of The American College Of Nutrition Vol. 25 , Iss. 2,2006

 2. Wang, H., Wen, Y., Du, Y., Yan, X., Guo, H., Rycroft, J. A., Boon, N., Kovacs, E. M.R. and Mela, D. J. (2010), Effects of Catechin Enriched Green Tea on Body Composition. Obesity, 18: 773–779. doi:10.1038/oby.2009.256

 3. Khalesi, S., Sun, J., Buys, N. et al. Eur J Nutr (2014) Green tea catechins and blood pressure: a systematic review and meta-analysis of randomised controlled trials, 53: 1299. doi:10.1007/s00394-014-0720-1

 4. Epicatechin ingested via cocoa products reduces blood pressure in humans: a nonlinear regression model with a Bayesian approach; Sabine Ellinger, Andreas Reusch, Peter Stehle, and Hans-Peter Helfrich

 5. Neurological mechanisms of green tea polyphenols in Alzheimer's and Parkinson's diseases; Orly Weinreb, Silvia Mandel, Tamar Amit, Moussa B.H. Youdim

 6. "Flavonoids". Linus Pauling Institute Micronutrient Information Center, Oregon State University

 7. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects.; Nehlig A, Daval JL, Debry G.

 8. Nathan PJ, Lu K, Gray M, Oliver C.. The neuropharmacology of L-theanine (N-ethyl-L-glutamine) a possible neuroprotective and cognitive enhancing agent. J Herb Pharmacother (2006) 6(2):21–30.10.1080/J157v06n02_02

 9. Lee H.J., Lee Y.N., Youn H.N., Lee D.H., Kwak J.H., Seong B.L., Lee J.B., Park S.Y., Choi I.S., Song C.S. Anti-influenza virus activity of green tea by-products in vitro and efficacy against influenza virus infection in chickens. Poult. Sci. 2012;91:66–73. doi: 10.3382/ps.2011-01645.

 10. Jówko E. Green Tea Catechins and Sport Performance. In: Lamprecht M, editor. Antioxidants in Sport Nutrition. Boca Raton (FL): CRC Press/Taylor & Francis; 2015. Chapter 8. Available from: https://www.ncbi.nlm.nih.gov/books/NBK299060/


What happens when the conductance of a sodium channel increases? My intuition is that, since the concentration of sodium within a cell is higher than the extracellular concentration, when conductance increases, this corresponds to the channel being open and means sodium will enter the cell. Is this correct? And what impact will this have on the membrane potential?

No, not quite. You are on the right lines, but incorrect in thinking that intracellular sodium concentration is higher.

At the resting phase of a neuron, there is less sodium inside the cell and more sodium outside the cell. An ATPase sodium potassium pump is constantly pumping 3 sodium ions outside the cell for every 2 potassium cells that enter the cell.

For voltage gated sodium channels to open, there must be a significant change in voltage, which can be triggered by the binding of neurotransmitter to receptors for example. This triggers the sodium channels open and sodium will flood into the cell due to a high concentration gradient (because there are more sodium outside than inside) but also due to an electrical gradient (the neuron is more negative on the inside; positive sodium ions will be attracted to the inside).

Because sodium is flooding into the cell, this will cause the membrane potential to become more positive (depolarised) and will eventually reach an action potential (30mV). After an action potential, the channels will become de-activated and shut. After a period of hyperpolarisation, the neuron will return to a resting state.

Source: https://en.wikipedia.org/wiki/Action_potential


How is it determined in a zygote state of foetus, that which side is mouth and which side is for anus? After the fertilization when the zygote  is in the growing state to a foetus, the main canal is introduced first, from mouth to anus. But my question is when the canal is created first how does it determine which side is for mouth and which side is for anus?

The gut tube is formed from endoderm that migrates through the primitive streak. Before this, however, the anterior-posterior axis of the embryo is defined by the formation of the streak at the beginning of gastrulation. In mice, which are phylotypic with humans at this stage, the streak forms posteriorly and then extends to the anterior. I'm not sure if you'll be able to find much research on humans, but mice and chicks are quite well studied. That said, I don't know the molecular and cellular mechanisms which define where the primitive streak forms. I don't even know if it is known. How much detail are you looking for? If I find the time, I can try and elaborate on this further. In the mean time, this review looks promising:

http://m.dev.biologists.org/content/136/5/701.long


Easy and cheap antigen/antibody couple For an application I need to find a cheap antigen and cheap correspondent antibody. The antigen can be literally any molecule that is cheap and potentially easy to produce and with a correspondent antibody that is cheap and easy to produce as well. I imagine this antigen will need to be a molecule that triggers very easily an immune response to result in a easy to produce antibody.
I have never worked in immunology so I don't know what system antigen-antibody to choose. I know pregnancy test are common so probably the antibody for Human chorionic gonadotropin (hCG) is easy and cheap to produce but I don't think hCG is.
 Are bigger molecules better than smaller ones as antigens? Any suggestion is helpful.

A good choice is the IgG/anti-IgG pair for cheap, easy to demonstrate/work with system. E.g. Goat-IgG coupled with donkey anti-goat IgG.  Just about any antibody supplier will have these.
These type of systems are the basic primary/secondary antibody bindings routinely used in immuno-assays, blotting etc. These may be mouse IgG coupled with a labeled anti-mouse IgG for example.
Reference
Wilson MS, Nie W. Electrochemical multianalyte immunoassays using an array-based sensor. Anal Chem. 2006;78(8):2507-2513. doi:10.1021/ac0518452


How do nasal and aural passages connect? I have had a bad flu with a lot of congestion.  My husband suggests a way to clear my stuffed ears is to pinch my nose shut then blow air through.  Sometimes that helps, sometimes there's just too much congestion.
What is happening exactly when I do that?  I've looked at diagrams of nasal and aural passages, but it's not clear to me what's happening when you block the nasal passage and then blow air through.  I would like to know exactly what the passage of air/fluid is.
Also, is it a bad idea to do it?
Thank you.

The eustachian tube connects the nasopharynx to the middle ear, on each side. The (naso)pharynx is basically the back of the mouth, and the middle ear is a cavity behing the eardum.

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

It is normally closed when there is no pressure difference between the middle ear and the nasopharynx, by extension between the middle ear and the air around one. Its function is to avoid a ruptured eardrum that could be caused by such difference in pressure. (This could be the case when ascending a mountain, or diving underwater, where the ambient pressure drops or increase, but not the pressure inside the middle ear)

What you are doing is closing all passages for the air to flow out (mouth and nose closed), yet trying to blow it out : this artificially increase the pressure and opens the tubes. While it is usually a passage for air, if there is a fluid buildup it could flow through it too.

Whether it is safe is a more of a medical question, which would be better suited for your physician.


Are cell lines potentially dangerous? More specifically, if a human subject was exposed to, say, a human cancerous cell line (via intravenous injection or through an open wound, for example), is it possible that they would develop any conditions associated with the cell line?

This is highly unlikely because the immune system would detect these cells and atack them as foreign. There is at least one case described in the literature in which a woman died of lung cancer after receiving a donor organ from a smoker. This is due to the fact that after transplantations people have to take drugs to suppress their immune system to avoid an immune reaction against the transplanted organ. This allows tumor cells to survive.

The same problem is true in research animals. For the transplantation of tumor cells you need mice with a severely deficient immune system (so called "SCID" (Severe Combined Immunodeficiency) mice) to allow tumor cells to grow. This is different when you work with viruses (like the human papilloma virus) which can cause cancer. Here you have to take appropriate safety measures.


Double stranded nucleic acids are more 'durable' than single stranded nucleic acids? I'm struggling with a question I've been asked.

"Why is double stranded genetic material more 'durable' than single stranded one?"

I know that double stranded genetic material is more stable due to multople strands. The single stranded isn't as stable as the double stranded since it lacks the second strand and therefore the bases are open.

Stable isn't the same as durable, and I've never heard in class that one is more durable than the other one. Did I miss something or is this just a mistake?

I'm interpreting "durability" as the DNA's resistance to physical stress, such as shearing. The Bustamante lab at UC Berkeley does a lot of very cool single-molecule biophysics looking at forces involved in protein-protein interactions and protein-DNA interactions. This Bustamante et al. review paper, Single-molecule studies of DNA mechanics includes a look at the force required to break ssDNA and dsDNA:

  Single molecules of dsDNA were broken
  with a receding water meniscus [26] at forces estimated
  to be 960 pN (correcting Young’s modulus doubles the
  published scission force of 480 pN). Short dsDNA molecules  pulled  with  an  AFM  tip  [27]  sustained  forces
  over 1700 pN.

pN = picoNewton
AFM = atomic force microscopy

dsDNA is more resistant to stretching/shearing forces because the double helix arrangement is "springy". I recommend giving the paper a read for more info. Very cool stuff.


Are there specific features of birds that cats/small predators are attracted to? I've recently heard a podcast, in which a professor describes one of the theories as to why we like abstract art. In his talk, he mentions an experiment with seagull chicks, in which the seagull chicks mistake a stick with a red dot for their mother's beak, and in the case of stick with 3 stripes actually preferred it to their mother's beak. When a stick like that is waved around a chick, it starts to peck at it, believing it is mother bird:

This experiment suggests that birds are imprinted to recognize specific patterns and interpret them as mother.

I'm in trying to create a similar experiment for cats. To do so I'm trying to understand if cats other small predators (ferrets,etc) are imprinted in a similar way - do cats recognize specific features of a bird to identify it as "bird", "prey" or "can hunt and eat"? I'm talking about stuff like - do they recognize eyes, beaks, wings or tail in a special way?

To paraphrase the question: If I'm to create a stick like above, but for cats, what features would be painted on the stick?

I know that butterflies, caterpillars and other insects have evolved to mimick "eyes" on non-vital organs to confuse birds. I'm interested if same stuff exists for small mammal predators.

Not all cat predatory behavior is innate. Researchers found that cats predatory behavior for birds vs. mice depends to a significant degree on training by the mother: if the mother taught predatory behavior with birds, the kittens grew up to be better at catching birds than at catching mice and vice versa. Supportive data shows that aside from monkeys and other primates, cats are among the most adept at learning by observing the successes and failures of other animals attempting to complete tasks to obtain a reward. This might influence, therefore, a cat's response to and attraction for objects in the air or on the floor.

Blindfolded cats can hunt mice by vibration. Paul Leyhausen, a German animal behaviorist studied domestic cats (and related felines) from the 1950's through the 1970's, and much of what is known about their predatory behavior is thanks to him.

Although their vision is not especially keen, domestic cats see well in dim light and readily perceive motion. According to Leyhausen, prey movement and the direction of movement are the only factors which innately release crouching, stalking, and catching behaviors in cats. When presented with quail, cats were far more likely to go after active quail than those stilled by tonic immobility. Cats are also more likely to go after smaller prey (mice > rats) and mice were much more likely to elicit play pawing.

Leyhausen also demonstrated that rodents were probably the natural prey of cats.

Though there has been much study of cats and predation, little is available on detail of the kind you are interested in.  My best guess for a good toy for a cat would be a smaller object that moved along the floor.

More information can be obtained from Leyhausen's book, Cat Behavior: The Predatory and Social Behavior of Domestic and Wild Cats.

Effects of the mother, object play, and adult experience on predation in cats
 The effects of experience on the predatory patterns of cats
 Tonic immobility in Japanese quail can reduce the probability of sustained attack by cats
 The behavioral bases of prolonged suppression of predatory attack in cats


What forms the base of the coral reef ecosystem? Corals are small animals that form a symbiotic relationship with algae. The algae produce sugars for the corals and are in turn provided with needed nutrients and protection from predators.

That's all great, but it doesn't explain where the amazing diversity of fish, mollusks, crustaceans, everything else comes from. As far as I can tell, the whole point of the coral's success is that their hard skeleton protects them from all but the most specialized predators.

So if the corals don't directly add (much) energy input to the coral reef ecosystem, what is it that makes the reefs so productive and diverse? Or, put another way, what makes a coral reef environment more productive than simple phytoplankton floating in the open ocean?

One role of corals is to provide structure that offers protection from predation to many prey species as well as larvae and hatchlings. Reefs also provide relief from strong currents which, again, afford protection. Many other critters such as sponges, tunicates and other sessile animals use the reef as a substrate for attachment.

Don't be fooled by the apparent inedibility of coral, many fish eat it, notably Parrotfish. To give an idea of the extent of this activity, the bleached white beaches in Palau are carbonate "sand", not silica. They are the product of millenia of Parrotfish activity on the coral. (I don't have a link, this knowledge is courtesy of the Oceanic Society guide on our snorkeling trip.) In addition to Palau, I've snorkeled Indonesia, Honduras, Hawaii and elsewhere. In every venue, multitudes of many species of Parrotfish were to be seen aggressively chomping away at coral.

Also, the reef is also a substrate for many algae which serve as a food for other varietiesw of fish. Many of the coral inhabiting algae wouldn't be recognized as such looking like bubbles, fans and other oddities unlike common kelp.

Other species also feed on coral including welks, fireworms, nudibranchs and some starfish. Here's a link:http://infolific.com/pets/coral-reef-life/eating-the-coral-reef/


Can anyone identify this caterpillar? Can anyone identify this caterpillar we found on a cauliflower? This was the only photo we could get of it.

Location : Ceres, Fife, Scotland

It might be an imported cabbageworm:

or a green-veined white:

Both exist where you are, and the former is more common than the latter. I can't tell them apart, but consulting the pages might help.


Why is high fructose corn syrup unhealthy? I understand that high fructose corn syrup was found to have detrimental effects on peoples' health. Why is this so?

Besides a lot of propaganda there is not much evidence that high fructose corn syrup (HFCS) is more dangerous than normal sugar. Lets have a look at the sugar in detail:

HFCS is produced from corn and is originally a glucose syrup. Since fructose is obviously much sweeter, the glucose is converted enzymatically into fructose (see here for more details). Before the use in food production additional glucose is added to the syrup so that typical syrups contain 55% fructose and 42% glucose or 42% fructose and 53% glucose (the remaining % are water).

If you look at saccharose (which is our ordinary sugar) then this is a disaccherid which is build from one molecule of glucose and one molecule of fructose. The enzyme sucrase breaks this molecule up into one molecule of fructose and glucose each, so reaching a 50%:50% ratio between the sugars.

As the ratios are more or less the same, it doesn't matter for the human body, where the sugar come from meaning that in this context it is more too much sugar in the food than a problem with HFCS, as also this study suggests:

Straight talk about high-fructose corn syrup: what it is and what it
ain't.

Fructose itself is not without problems as this induces the production of fats in the liver, but again, it doesn't matter for the body, where this fructose comes from:

Fructose induced lipogenesis: from sugar to fat to insulin
resistance.

For further reading I can also recommend this article on Gizmodo:

Is High Fructose Corn Syrup Really Bad for You?


Insect identification - pantry moth vs clothes moth Are the following insects a pantry moth or a clothes moth? I live in Europe, if geographical location is of importance in this case.

The insects are about 7 - 10 mm in length.

For several months I have been fighting with recurring invasion of pantry moths and those were caught in pantry moth pheromone trap. However, the specimens seem  to be smaller than the pantry moths that I have been fighting a couple of months before (I have read that clothes moths are smaller) and I have seen some flying near the wardrobes. I couldn't find traces of infestation in the food as well. Is it possible for clothes moth to be attracted by pantry moth pheromones?

Although the images are very grainy and oddly lit, the second two images look a lot like a pantry moth. Specifically, it reminds me of a very common pantry pest:

Plodia interpunctella (Indian-meal moth).

 Source: Urban & Structural Entomology, Texas A&M University, USA

Range: [source]

The Indian-meal moth can be found on all inhabited continents. Although it is primarily tropical, it can live in a range of habitats and is a very common nuisance pest in food storage facilities and people's pantries worldwide.

Description: [source]

7-10 mm long (wing span ~ 1-1.5 cm)
Wing color:
-Posterior 1/2 of wing red/brown/bronze
-Anterior 1/3 of wing is white/light gray / ochre-yellow

Separated by dark band

Body color: reddish-brown

Pest Info: [source]

Adults live 5-7 days
Females lay 60-300 eggs
Eggs hatch in 2 - 14 days
Larvae do all of the destruction

Can even eat through plastic to get to food! [source]
Common Foods: Cornmeal, flour, dried fruits, nuts, seeds, health foods, pet foods.


The effect on the efficacy and potency of a non-competetive antagonist binding to the active site of the receptor (dose-response curve) According to the book "Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy" by Golan et al, non-competetive antagonists can bind to both the allosteric site and the active site.

I know that a non-competetive antagonist that binds to the allosteric site causes a decrease in efficacy, but no decrease in potency (see figure below). Figure A shows the agonist alone and the agonist together with a competetive antagonist. This causes the dose response curve to shift to the right, thus increasing the EC50 and decreasing the potency of the agonist. Figure B shows the dose-response curve for the agonist alone and agonist together with a non-competetive antagonist that binds to an allosteric site. As you see this type of antagonist causes a decrease in efficacy, but no decrease in potency is observed.

But how does a non-competetive antagonist that binds to the active site affect the dose-response curve? Does it lead to both a decrease in efficacy and potency? Unfortunately, there is no figure in the book to answer my question.

This is a tough question. I was reading this paper Patrono, C., et al. "Clinical pharmacology of platelet cyclooxygenase inhibition." Circulation 72.6 (1985): 1177-1184. and they seemed t mention this paragraph in the introduction.

  Platelet Cycloxygenase or prostaglandin (PG) H synthase (i.e., the
  enzyme that converts arachidonate released from membrane phospholipids
  into PG endoperoxides) is the target of several antiplatelet agents
  that can reversibly or irreversibly block the activity of the enzyme
  by competing with the substrate or permanently altering the active
  site, respectively.Such drugs belong to the class of so-called
  nonsteroidal anti-inflammatory agents (e.g., indomethacin, aspirin),
  but also include a uricosuric agent, i.e., sulfinpyrazone.

So we have to look for  DRC of a NSAID to say COX. Now I was unable to find a good DRC for aspirin (If you find it, let me know in the comments below. I would love to take a look at it). But I did find DRC for other drugs that inhibit COX.

It led me to this paper Walker, M., et al. "A three-step kinetic mechanism for selective inhibition of cyclo-oxygenase-2 by diarylheterocyclic inhibitors." Biochem. J 357 (2001): 709-718. which described the inhibiton of COX2 by a NSAID called celecoxib.

  The inhibition of COX isoenzymes by NSAIDs generally conforms to one of three inhibitory mechanisms: simple reversible inhibition, as demonstrated by ibuprofen ; time-dependent reversible inhibition, which includes both weaker binding inhibitors, such as naproxen , and tight binding inhibitors, such as indomethacin and meclofenamic acid ; and irreversible covalent inhibition, as demonstrated by aspirin  and o-(acetoxy-phenyl)hept-2-ynyl sulphide ('APHS') . Most of the traditional NSAIDs display similar inhibitory mechanisms against both COX-1 and COX-2 , and are relatively non-selective. However, COX-2-selective diarylheterocyclic inhibitors demonstrate distinct inhibitory mechanisms for the two isoforms . For example, celecoxib  has been reported to be a reversible competitive inhibitor of COX-1 while demonstrating time-dependent irreversible inhibition of COX-2.

Considering the highlighted statement, I think you can consider the COX1 curve as a standard competitive inhibition and COX2 as non competitive inhibition. The resulting change is essentially the curve shape itself (being shifted to the right).

The DRCs were reported here: Tacconelli, Stefania, et al. "The biochemical selectivity of novel COX-2 inhibitors in whole blood assays of COX-isozyme activity." Current Medical Research and Opinion® 18.8 (2002): 503-511.

Interestingly the second paper (By Walker) also described how (the authors proposed) the binding occurs. A very interesting read.


A Brain Implant improves memory--but how? https://www.nytimes.com/2018/02/06/health/brain-implant-memory.html

A new therapy could improve memory by "sending electrical pulses to aid the brain when it is struggling to store new information." I'm trying to figure out how this works physically, in terms of how it actually helps the brain. I would imagine that it has something to do with the neurons getting past the threshold for firing a signal with more ease, but is this because the threshold is suddenly lower because of the presence of the current, or what?

Could anyone provide me with an explanation of the science behind this in lay terms?

Many many thanks

From what I understand, when we learn we go over things quite a few times, this is so that our brain goes over the memory cells where we store that information with electrical impulses. Thus when an electrical impulse travels over some branches they strengthen the branches, (I don't know the science behind this). This is what helps us memorise data. So if we ran lots of Impulses over the branches it could help strengthen them or fry your brain, just saying try this in a safe environment such as a lab and not in a homemade electric chair. Also like you said it helps them run easier over the brain which makes it a lot easier to remember things.

Hope this helps,

IbnJalal


Does DNA influence death (e.g. by cell aging) I know that we age because of errors in the cell replication process and these errors eventually leads to death.

If we exclude environmental factors, are there any other factors that can cause these errors? Is there for instance some kind of "programming" in our DNA of our death?

Perhaps the best type of study to examine the role of genes (DNA) in human aging are twin studies.  They have either: the same DNA (monozygotic, one egg, "identical" twins (MZ) ) or similar DNA (dizygotic twins, two eggs (DZ) ) and are perhaps exposed the same, or different environments.   I won't repeat the information in the link, above, but studies of this type guide that our DNA is not an absolute roadmap of our future.

DNA damage can be caused by exposure to excessive radiation, viruses, chemicals and just 'random events'.  Cells and tissues can also be damaged by oxidative damage - literally oxygen and related molecules that are produced within the body and can react with components of cells (e.g DNA, proteins and the lipid cell membrane).   The accumulation of these oxidized products in and around the cell disrupts tissue function and leads to many of the symptoms of aging, a process called sensescence.

We obviously cannot avoid having oxygen around us.  In the same way, our cells need the sugar glucose as a source of energy. Glucose can spontaneously react with proteins and lipids to form advanced glycation endproducts (AGEs).
 AGEs are pro-inflammatory.  In diabetes, where blood glucose levels may remain at higher than normal for extended periods, the formation of AGEs can lead to nerve and kidney damage.   The chemical reaction that is occurring is the same as when you toast a piece of bread or fry a steak.  So paradoxically, two of the ingredients essential for life - oxygen and glucose - are slowly but surely disrupting our body's function over the course of decades.   Although the body can replace some of these damaged proteins, they accumulate over time, as evidenced by the increasing lack of elasticity of older skin as collagen proteins are cross-linked.

Regular exercise, good diet and friendships all add to mental and physical health, quality of life and longevity.  So, to live a long time, don't stress, have ONE slice of cake and make new friends who will exercise with you.


What dinosaurs live during cretaceous period? I cant find website that shows all dinosaurs that lived during this time?

Tyrannosaur rex and triceratops I know but what else?

Wikipedia has a nice summary: https://en.wikipedia.org/wiki/Category:Cretaceous_dinosaurs


Photosystem I and the ETC In the light reactions of photosynthesis, Photosystem I receives electrons from the ETC after Photosystem II sends them to the ETC. Then, when Photosystem I receives light, the electron becomes excited and passes the electron back to the ETC. This leads me to my question: In the following question, are both $B$ and $E$ correct?

Which of the following are directly associated with photosystem I?
$A)$ harvesting of light energy by ATP
$B)$ receiving electrons from the thylakoid membrane electron transport chain
$C)$ generation of molecular oxygen
$D)$ extraction of hydrogen electrons from the splitting of water
$E)$ passing electrons to the thylakoid membrane electron transport chain

It appears the author of the question is trying to use "thylakoid electron transport chain" in an overly specific way. The chain from which PS I receives electrons has far more components and is different from the shorter chain to which PS I passes its electrons. But according to my copy of Biology, Campbell & Reece 7th edition, both are called "electron transport chains" and both reside in, or on, the thylakoid membrane. Perhaps the "directly" in the question refers to the fact that PS I's electron is first captured by a "primary receptor" before being passed to ferredixon, the first member of the chain to which PS I passes electrons. But, again according to Campbell, this primary acceptor is considered part of the photosystem.

I used to teach this stuff. I'd toss out the question.


Is it possible to detect whether an organism has been gene edited (by humans)? Is it possible to detect whether an organism has been gene edited? For example, if someone gene-edits a human embryo (e.g., as He Jiankui did last year), can one later detect whether the human has been gene-edited?

If you had access to the DNA of the organism's parent(s) then you could make an inference about whether the child's genome is consistent with being edited, assuming that the edit was done early enough in the embryo's existence for the edit to be present in all/most of its cells. If the organism is a chimera/mosaic, then it may be possible to detect the edit by comparing different tissues within the organism, and identifying differences which do not look like 'natural' somatic mutations.  However, I don't think we have a good handle yet on what the natural range of somatic mutations looks like, so it might be difficult to assess whether any difference found were of an engineered origin.


How do tree gnarls develop? What causes the trees to develop gnarls? I can't find anything on internet other than dictionary definitions.

Are they caused by a mold, like the burls?

If I understand what you're talking about by "gnarl", they are usually caused by a bacterium like Agrobacterium tumescens infecting and creating a gall.

Update: Forgot, also in some cases caused by insects.


Head transplant feasibility - Project HEAVEN-GEMINI There is a news circulating that in the next two years, Dr. Sergio Canavero, of the Turin Advanced Neuromodulation Group (TANG) in Italy, will perform the world's first head transplantation. A procedure which will require

  150 surgeons and nurses approximately 36 hours to complete

and after which the patient is held in coma during recovery

  The recipient will be kept in a coma for around 3-4 weeks, says Dr. Canavero, during which time the spinal cord will be subject to electrical stimulation via implanted electrodes in order to boost the new nerve connections.

Is this even feasible? If it can be done, does that imply that humans can live for a long time, if they can find a compatible donor ? What requirements are there for compatibility?

I have the impression that the MNT article is significantly over-stating the potential of this technique, at least with current technology. The mouse work by Xiaoping Ren (see this 2014 paper) seems to have a very steep death-curve post-surgery:

  Forty Kunming mice and forty C57 wild type underwent the
  AHBR  procedure.  After  transplantation,  18  mice  survived
  for 3 h after the ventilator was disconnected.

There are no details in the paper about how long the most robust mouse survived for post-surgery. I would guess that it is not an impressive number, otherwise the authors would include it. Alternatively, the 18 surviving mice may have been euthanased after three hours - the paper does not make this clear, but it is common to have a predetermined time-limit for euthanasia in experiments where animals are expected to suffer from an irreversible treatment.

  During these 3 h, the mice
  awakened and displayed normal cranial nerve function and
  characteristic responsiveness (blinking, whiskers moving, etc.).
  After the mice awoke, electroencephalogram (EEG) recordings
  were  made  directly  from  the  cortex  of  the  transplanted
  Cephalons (Figure 3). Because blood supply was maintained at
  an adequate level during surgery by anastomosing the donor
  and recipient carotid and jugular vessels, the intra- and post-
  operative EEG and ECG show electrophysiological activity.

This sounds a lot like a 'no' to 'can this technique be used to substantially extend human lifespans?', on current technology. If a human trial is approved, and is as successful as the mouse trials, the recipient will likely be dead within hours. If they survive for several hours, the level of motor control that can be expected in that time is likely restricted to unconscious motor tics (cf whisker twitching and blinking).


What is this large beetle from Shirpur, Maharastra (central India)? I found this beetle in my college in Shirpur, Maharastra (central India). What is it? It is very large, and I have never seen it before. I believe it may be Titanus giganteus but I'm not sure.

Clearly not the best picture, but from the poor quality image it does appear you have a longhorn beetle (family Cerambycidae) in the subfamily Prioninae.

They are typically large (25–70 mm) and usually brown or black. The males of a few genera sport large mandibles that are used in fights with other males, similar to stag beetles. These beetles are commonly nocturnal and are attracted to light. The majority of the Prioninae whose biology is known are borers whose larvae feed on rotting wood or roots.

For example, your specimen looks a lot like Toxeutes macleayi from Australia.

 Source: England London - Natural History Museum
I'm not sure whether other closely related species live in India (none of the related Indian species that this site mentions look like your specimen), but I would guess if you look into it you might find a local bug guide that might help you find some other related species.
Based on your location in India, I'd say one place you could start looking is through species in the genus Prionus.

they're also large, generally brown or black, are nocturnal. Additionally,

All members of the genus Prionus have twelve or more strongly toothed or even flabellate antennomeres on their large antennae.

You'll obviously need to provide a better picture for us to examine that detail of your specimen.

I also recommend you examine the list of Indian Prioninae species listed here, including relatives of similarly sized/colored species with large mandibles such as Dorysthenes huegelii and Rhaphipodus fontanieri.
Again, your picture is too low of quality for an accurate ID, but these links should likely help you parse through similar species and hopefully find your answer.


Differential Gene Expression I have a matrix two gene expression datasets, one from 10 normal individuals and ten from diseased individuals, which are normalised log fold change values--, i.e., already processed.

My question is: how do I obtain a list of differentially expressed genes?
That is the up and down expressed genes. I was thinking of getting means for each group and then sorting the average fold change values would work, but I am not sure...

Thanks.

It hard to figure out what sort of data you have. qPCR? Let me give you an example with tools involved on how I get differential genes for RNAseq data, that is whole transcriptom and for mouse that transcriptom that's about 23000 genes.

Step 1. Map raw reads to the reference genome.
Step 2. Count number of reads within the feature. Feature can be several things, but lets just take protein coding feature (feature == gene).
Step 3. Do differential expressions analysis

From step 2 you get a matrix of counts.

      sampleA_rep1 sampleA_rep2 sampleB_rep1 sampleB_rep2
gene1      2             5        20             23
gene2      10            12       50             50
gene3      20            23       4              6
..
geneN

The packages that I use are limma and/or edgeR. You can find them on bioconductor Both packages take raw counts and give you topTable of DEG, default is top 100 genes.

I recommend reading edgeR or limma manuals, there come with great explanations as well as examples. Also A scaling normalization method for differential expression analysis of RNA-seq data is original paper that explains TMM normalisation (mention a bit more in depth below)

Two things; one you need to filter genes with low counts, convert to cpm() counts per million before filtering as this takes library size (depth of sequencing) into consideration. two calcNormFactors() will do TMM

The hardest thing (I understand) in RNAseq is to get total RNA output for each sample. Because a treatment will effect the number of transcripts expressed in that sample, increasing or decreasing amount of transcript, which give you unbalanced counts. You won't know just by looking at raw counts if geneA has less counts because it's been down regulated OR because that sample after treatment has more transcripts present in the cell and geneA simply has less coverage, due to other transcripts also getting reads now. I can't really explain that too technically because I don't understand this myself, but TMM normalisation takes care of this and  gives you an estimate of degree of variability.

I know that I'm not giving that much info on actual differential testing, which was your question. edgeR has exactTest() which is Exact Tests for Differences between Two Groups of Negative-Binomial Counts , which might help you, but you might have normalise your counts differently as mentioned above. The general idea (I understand) is you need to fit a model (lmFit()) and then do the test eBayes()

Other

Degust this is very nice tool that uses limma and edgeR in the backend, but simplifies a lot of things as well as gives you nice interface to work with your data. You upload raw counts! in the format shown above
DESeq one of the other rather popular R packages that can also do differential gene testing


What species is this burrow-digging insect? These are frames from a recent recording:

Location

Urban area in Central Europe.

Abiotic factors at the time of recording

Temperature = 27°
Humidity = 51%
Wind = 16 km/h

Description

Approximate size = 6 cm 4-5 cm
Elongated shape
Distinctive orange-ish abdominal segment near the end of the abdomen
6 legs
One pair of wings (I think it's very possible that it has two pairs of wings, though, hard to see on the video or pictures)

Observed behavior

The insect seemed to be digging burrows in one of my pots (so far there are 3 holes in one pot and I also saw another burrow in a second pot). Every time I've seen it, it was alone so I assume it's not a social species.

Internet search

I ran these images through google search images and the results were (in order):

hymenopteran
insect
pest
carpenter ant

I think the closest match was the first picture but I wasn't able to get a specific species so I would appreciate any insight from experts on the matter.

That is clearly a type of wasp.  Some digging leads me to think it could be something in the genus Ammophila (a type of "thread-waisted wasp") for example Ammophila sabulosa:

However, 6 cm is huge for a wasp and twice the size of Ammophila sabulosa — are you sure about that length?


Myopia as a microscopic superpower? A few years back my Physics professor made a joke that his myopia (i.e., nearsightedness) gave him a "superpower" that allowed him to see close objects much more clearly than someone with typical eyesight. For example, reading small fine print or tiny details on a surface. The physics made sense, as a person with myopia should have a closer near focus point.

Recently, this belief was challenged by a normal-sighted friend. I did some Google-ing and couldn't find any evidence or articles confirming or refuting this belief. All I found was a lot of anecdotal evidence.

My question is: Is this belief correct? Are there any scholarly articles or similarly trustworthy sources confirming this?

Short answer
Myopes may have some benefit in terms of identifying small objects due to their ability to focus objects nearer to their retina than emmetropes, but only marginally so.

Background
The more myopic you are, the more blurred your distance vision, but the closer up you can see clearly. Hence, myopes have a range of clear vision that is closer to their eyes than emmetropes (normally sighted people) (Triad Publishing).

A young emmetropic adult can focus at an object some 10 cm away, which is defined as an amplitude of accommodation (lens adjustment) of 10 diopters.

A severely myopic eye can be up to minus 6 diopters, bringing the tally from 10 to 16 diopters, meaning you can view something up to 6 cm instead of 10 cm.

Bringing objects closer increases retinal image size and hence increases spatial detail. Going from 10 to 6 cm increases the retinal angle by 10/6 = ~1.7 x, so not even a doubling of the angle.

A random search for a magnifying glass for the visually impaired that aids in reading small print (newspapers etc.) yielded one that magnified 4x (16 diopters):

Clip on reading aid. Source: Eschenbach

Microscopes typically have lenses with magnification factors from 4x to 100x.

So in all, myopes do not have microscopic superpowers. A standard magnifying glass for the visually impaired magnifies several times more than a severely myopic eye.


How to make sure a stem cell culture is cancer free? Say I take a blood sample from an adult, extract the white cells and apply to them the process described in <this article>. Assuming this actually turns the adult white cells into stem cells, which I then transfer to a culture in order to grow an arbitrary quantity, how can I make sure in the end this culture is free of cancer stem cells? Is there a last step that can be applied which would eliminate any potential CSCs leaving only healthy cells in the culture?

Thank you.

It would not be possible to differentiate CSC from normal population non-invasively and select them out. You may do a single cell expression analysis to say if a CSC is present in a population or not but there is no magic bullet method for eliminating them. Also there are several oncogenes and some of them are also required for usual stem cell function. HAT kind of methods will not be able to eliminate potential cancer cells. Also, usual cancer chemotherapeutic drugs also affect other actively growing cell.

Bottomline: Not possible with the current level of knowledge and technology.


Server for protein structure prediction for multiple sequences Does anybody have any idea about any online server that takes in multiple amino acid sequences in fasta format and outputs the 3D structure of the input amino acid sequences in the form of helix, sheet and coil? I searched but could not find any. There are servers that take in 1 sequence. I want to get the structure of multiple sequences together...

Unfortunately it is impossible to predict the tertiary structure of proteins using raw amino acid sequence. The information required to be computed in the construction of the dynamic protein shape is too large for any computer at the moment.

There are actually a list of research facilities that are looking for people to donate their computer's idle CPU time to help sequence proteins.

Here is a list: (http://www.hyper.net/dc-howto.html).


What is the scientific name of this leaf? Has anyone seen this before? I got it from India as a gift but I have no idea what it is called or how to take care of it. Thanks

Looks very similar to Naringi crenulata which is found in India.  More information can be found on this Encyclopedia of Life page.

Image source: https://commons.wikimedia.org/wiki/File:Naringi_crenulata_leaves_and_flowers.jpg


Protoporphyrinogen (IX) formation in heme synthesis This picture shows one of the steps of heme synthesis. In this step two propanoate groups of coproporphyrinogen III are decarboxylated to form protoporphyrinogen IX. The enzyme that catalyses this step is an oxidase. Oxidase enzymes catalyze the removal of hydrogen  in the presence of oxygen to form water or hydrogen peroxdide.

So, will a water molecule form in this step? 2H+ will come from the two carboxylate groups and oxygen will combine with it to form water. Will a water molecule form in this way?

Seemingly the enzyme uses molecular oxygen in the reaction and one of the end products is water.

This reaction scheme is more detailed and presumably accurate.

http://www.hmdb.ca/reactions/3063

In addition there is also a set of papers detailing coproporphyrinogen oxidase which was also on the website, hopefully one goes into more detail on the reaction.

http://www.hmdb.ca/proteins/HMDBP00251


Osmolarity vs. Tonicity We're learning about osmoregulation in AP Biology and the terms Tonicity and Osmolarity are really confusing me. I watched this video on Khanacademy to try to understand what the difference is, and from my understanding Tonicity refers to strictly two solutions (ex: you can't take a cup with water and salt in it and claim it's hyper, hypo, or iso- tonic because there's nothing to compare it to), whereas Osmolarity refers to the composition of the single solution itself.

But then my Campbell's biology textbook completely confuses me. It has the following picture and text:

  ...osmosis, a special case of diffusion, is the movement of water across a selectively permeable membrane. It occurs whenever two solutions separated by the membrane differ in osmotic pressure, or osmolarity (total solute concentration expressed as molarity, that is, moles of solute per liter of solution).....If two solutions separated by a selectively permeable membrane have the same osmolarity, they are said to be isoosmatic. Water molecules continually cross the membrane, but under these conditions they do so at equal rates in both directions....

And then as if to clarify, they claim that tonicity refers to "solutions of known solute concentrations"...but how does this differ from osmolarity?

You're correct that tonicity needs two solutions to define.

Osmolarity (or osmotic concentration) is the measure of solute concentration, defined as the number of osmoles of solute per litre (L) of solution (Osm/L).

Tonicity, on the other hand, refers to the relative concentration of two solutions separated by a semipermeable membrane.

The difference is based what is considered for osmosis and tonicity. In case of osmosis, it is the water (or solvent) which moves across the membrane, while tonicity depends on the solutes which cannot move across the membrane. From Wikipedia:

  ... osmolarity takes into account the total concentration of penetrating solutes and non-penetrating solutes, whereas tonicity takes into account the total concentration of only non-penetrating solutes.


What does reflected onto means in the text below? The pleura lines the thoracic wall and diaphragm, where it is known as the parietal pleura. It is reflected onto the lung, where it is called the visceral pleura.

"Reflected" here describes the relationship between the continuous, but differently named parts of the pleura. The parietal pleura lines the chest wall and mediastinum (costal, cervical, mediastinal, and diaphragmatic areas marked in the image below). The visceral pleura covers the surface of the lungs (orange area below). There is a transition point at the root of the lung where the parietal pleura and visceral pleura meet. This transition is referred to typically as a reflection.

I think that the terminology is used to emphasize that the layers are continuous, but it is as if the parietal pleura bounces back off the body wall as visceral pleura.


Do teeth have the capacity to heal? Could a cavity in a human tooth "heal over" or possibly fill back in?

Yes, it can be done to a certain degree.

Cementum is capable of repairing itself to a limited degree and is not resorbed under normal conditions. Some root resorption of the apical portion of the root may occur, however, if orthodontic pressures are excessive and movement is too fast. Some experts also agree on a third type of cementum, afibrillar cementum, which sometimes extends onto the enamel of the tooth.

Cementum is produced by cells called cementoblasts.

more here:
http://en.wikipedia.org/wiki/Cementum


Cerebral/Cerebellar Cortex versus Deep Nuclei I have troubles using the terms Cortex & Deep Nuclei, and 'Nuclei' in general. From what I understand, a brain has '3 matter types in accordance to anatomical locations'

Superficial Grey matter - This is called the 'Cortex (Cerebral or Cerebellar Cortex)'

Middle White Matter
This is called 'Cerebral/Cerebellar White Matter' separating the cortex and deep nuclei

Deep Grey Matter, deep to the cortex -This is called 'Deep Nuclei' (for e.g.: Basal Nuclei of the Cerebrum, and four deep Cerebellar Nuclei (dentate, globose, emboliform, and fastigial))

Quote from the book that helps me to jump into this conclusion or summary:

  'The brain, like the spinal cord, is composed of gray and white
  matter. Gray matter - the seat of the neurosomas, dendrites, and
  synapses - forms a surface layer called the CORTEX over the cerebrum &
  cerebellum, and deeper masses called NUCLEI surrounded by white
  matter... (Saladin 2015, Unity of Form & Function, McGrawHill)

Thank you!

"Cortex" is a more general anatomical term for the outermost layer of a structure. It applies to both the cerebral and cerebellar cortex gray matter, as these are gray matter structures on the outsides of their respective parts of the brain.

Nucleus is also a more general term; in the context of neuroanatomy, it refers to a cluster of cell bodies. Typically we refer to CNS clusters of cell bodies as nuclei, and in the periphery they are called ganglia, though there are some odd exceptions like the basal ganglia (you referred to the basal nuclei in a comment, which are the same structure, but are almost always called the basal ganglia, whether or not that term is the 'best' term).

White matter, in general, is nervous tissue that appears white because it is primarily "fatty" from the lipid bilayer of cell membranes and consisting of processes like axons (especially myelinated ones) and dendrites rather than cell bodies.

I'm not aware of anyone who would call the cerebral cortex (or cerebellar cortex) a "nucleus": these areas are not shaped as clusters of cell bodies, they are shaped as sheets. The distinction is really only an anatomical one, so it makes little sense to use "nucleus" in a more general term to mean "nervous tissue consisting of cell bodies": we already have a term for that, "gray matter," and in most cases interesting to science we are talking about something more specific anyways.

I'd further say that these distinctions are really only gross anatomical ones, as one can have cell bodies outside white matter, and areas of gray matter like neocortex also include a mostly-white layer of axons and dendrites in "layer 1" but we still treat this as gray matter with respect to the whole brain.

Ultimately it doesn't matter: don't take anatomical terms more seriously than the things they are describing.