What is the meaning of expansion of T cells?

In immunotherapy, the T cells need to hit a therapeutic dose. The dose is normally determined pre-clinically or in a phase I or I/II trial. A good example is the YESCARTA label dose information:

  YESCARTA comprises a suspension of 2 × 10^6 CAR-positive viable T
  cells per kg of body weight, with a maximum of 2 × 10^8 CAR-positive
  viable T cells in approximately 68 mL (3).

YESCARTA commercial label

Lets run through a hypothetical situation based loosely on information obtained in this publication.

So say you have a cancer patient that weighs 70kg on the day they obtain a leukapheresis for their starting material. The manufacturing facility is going to say okay, we need to produced 2E6 viable CAR+ cells/kg for a 70kg patient in 68mL per the label indication. So your final product needs to have 140 million viable CAR+ cells.

The patient leukapheresis can go wildly different on a patient-specific basis due to factors such as current treatment or disease. Your separation method can result in loss. Cells die in their initial culture period pre-transduction, and they can die post-transduction. So case study in point from the paper I linked:

Their patient 029-03 ended up with 0.494E+09 cells in their leukapheresis. Transduction efficiencies aren't published for a lot of these, but lentiviruses are typically employed and efficiencies can range from 1-90% depending on numerous factors. The manufacturer needs a target efficiency of ~28% to hit 140E+06 total cells if they manage to isolate every single CD3+ cell, but if they're 85% viable for example, they still wont hit the target dose. So you need to expand the cells aka make them divide so you hit the target therapeutic dose.

You typically culture your cells in IL-2, a potent T cell stimulator, but activation can improve transduction and stimulate cell division aka expansion. You can use something like CD3/CD28 beads, for example. These provide the so-called signals 1 and 2 that stimulate T cells in a similar way antigen challenge would.

Let me know if anything is unclear.


Rationale behind Most Recent Common Ancestor (MRCA)?

any giving individual alive today will be either an ancestor to ALL of the humans (in that future time) or none of them. What is the rationale behind this?

It's a simple mathematical observation nothing more than that.

One that doesn't actually require doing any math to understand.

Take a few billion people, let them mix & breed freely within the confines of a limited environment (the world) & eventually (after enough generations) every single one of the current population will be be related & therefore descended from every single one of the original population that have any surviving descendants.

Those whose line doesn't die out will inevitably be an ancestor of every living person at a future generation, eventually.
Those who die with no offspring or have last-descendants do it for them, have no descendants.

It's just a simple statement of something that's obvious when you think on it.


What percent of biology study is dedicated to species-specific subjects like ecology and evolutionary biology?

I'm thinking of studying biology...

Did you have gone through the basic (school) level of biology and chemistry? otherwise the concepts may become hard to handle.

  especially ecological and evolutionary biology

Ecology and evolutionary biology is in fact highly information-dependent area.

Ecology is the study of habitat, lifestyle and interrelationship of different organisms. So there will come the role of different organisms in ecological relationships.

But there are other parts like statistical calculation of gene frequencies, energy uptake, etc. These parts will contain lesser amount of species-specific information.

Evolutionary biology too; have various fields and aspects, and could be studied in various ways.

If you need to study about evolution of a certain genera with fossil evidences; or estimate  the evolution of biochemical pathways; a lot of species or genus-specific information may require.

Whereas there are generalized areas, such as basic principles of evolution, its mechanisms, statistical models, etc.

(update coming soon...)


What is the difference between a myofibril and a myoblast? (In skeletal muscle)

Myoblasts are the embryonic precursors of myocytes (also called muscle cells). Myoblasts differentiate into muscle cells through a process called myogenesis.
A myofibril (also known as a muscle fibril) is a basic rod-like unit of a muscle cell. Muscles are composed of tubular cells called myocytes, known as muscle fibres in striated muscle, and these cells in turn contain many chains of myofibrils.
So, to answer your question, No. These two are different and one is the precursor of the other.


How does Haloxyfop control young grassy weeds in fields of broadleaved crops?

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

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

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

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

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


How exactly does sensory substitution work?

Tot start of with your definition:

  Sensory substitution, when one of sensory modality changes into another sensory modality to help someone restore the ability to perceive defective sensory using a working sensory modality.

I personally like to use a more subtle definition of sensory substitution (Stronks et al., 2015):

  [T]he process of obtaining information about the world through an alternative intact sensory channel [] that would normally be obtained by the deficient [sensory] system.

In other words, the information is not changed into another modality; it is simply processed by a sense normally not used for that purpose. Your definition seems to imply that the information stream is swapped. Although this is not strictly true, and hence the reason I like the second more subtle definition better, it is nonetheless true that cross-modal plasticity results in the deafferented cortical regions being taken over by other senses; for example in the blind, it has been shown that tactile and auditory information is processed in the visual regions, even down to the V1. The primary visual cortex is normally strictly associated with low-level visual processing, being the first central brain area where visual information enters the brain. Although this view is contested(V1 is also activated by tactile grids for example), in blind folks there are gross rearrangements where the somatosensory and auditory cortices take over the visual system (e.g., Pascual-Leone et al. (2005)).

To your questions

  Does this work the same way as Alternative Sensation ?

'Alternative sensation' is unfamiliar to me, it doesn't pop up in a Google search, and its nonexistence is backed up by this answer.

  Is there any pattern of which senses will probably improve according
  to which kind of senses someone's lacking

Yes. It depends on which senses are used most extensively to substitute for another sense. Training is an important factor in improving alternative sensory capabilities. In fact, it is the determining factor; the loss of a sensory system in itself does not propagate compensatory mechanisms (Stronks et al., 2015). Compensation being

  partial compensation for [the] loss of [a sense] by developing enhanced abilities with [] remaining senses

For example, training with the BrainPort Artificial Vision Device (Fig. 1), which projects electrotactile 'images' onto the tongue using 400 electrodes, gradually improves performance in the blind, all the while the somatosensory information is funneled progressively into the visual system (Stronks et al., 2016).

  Is there actually any method to train which senses someone would like
  to improve?

Pick your sensory substitution device of choice and train away; popular ones include, as said, the BrainPort (improves tactile-to-vision substitution), but also visual-to-auditory techniques like the vOICe (Striem-Amit et al., 2012). Also don't forget the guide cane, which funnels tactile information to the brain. especially the visual-to-auditory sensory substitution devices require a lot of training (Stronks et al., 2015). You can try the vOICe out yourself on an Android. However, I have tried the BrainPort myself and it is really difficult!

References
- Pascual-Leone et al. Annu Rev Neurosci (2005); 28: 377–401
- Striem-Amit, et al. PLoSONE (2012); 7(3): e33136
- Stronks et al., Brain Res (2015); 1624: 140–52
- Stronks et al., Exp Rev Med Dev (2016); 13(10): 919–31

Fig. 1. The BrainPort converts camera images into a 'grayscale' 400 pixel electrotactile image on the tongue. It partially restores visual function in the blind. Picture source: Midday Daily


Here is a tutorial to perfectly understand Hardy-Weinberg Rule! If you feel like you just need a brief reminder, you can skip the text until the section In short... and try out the exercises just to check your understanding.
Terms you should know a priori
I will not define the following terms, so make sure you understand them

locus
allele
(relative) frequency
Homozygosity and Heterozygosity

What is the Hardy-Weinberg rule?
Hardy-Weinberg rule (HWr) describes a relationship between allele frequency and genotype frequencies. I will present the maths later.
Alleles and Genotypes frequency
Let's assume we have a bi-allelic (two alleles) locus. The possible alleles are called A and B.
Notation for genotype frequencies
Note that I will use a slightly unusual notation on purpose.
Let $f_{AA}$ be the frequency of the homozygous individual caring the allele A on both haplotype (both chromosome). Let $f_{BB}$ be the frequency other homozygote. Let $F_{AB}$ be the frequency of heterozygote which inherited the A allele from the mother and the B allele from the father. Finally, $F_{BA}$ is the frequency of heterozygotes which inherited the B allele from the mother and the A allele from the father.
Most of the time people write $f_{AB}$ (or similar notation) to designate all heterozygotes irrespective of whether the A allele comes from the father or the mother. In this answer, I make the difference of which parent gave which allele. I will instead note $f_{het}$ the frequency of all heterozygotes. Therefore $f_{het} = f_{AB} + f_{BA}$. Similarly, I will note $f_{hom}$ the frequency of all homozygotes. Therefore, $f_{hom} = f_{AA} + f_{BB}$.
Notation for allele frequency
Unlike the above, I will use a class notation here.
Let the frequency of the A allele be $p$ and the frequency of the B allele be $q$.
All genotype frequencies must sum to 1
Of course, if you add up the frequency of all types of individuals in a population, you should reach 1 (or 100% if you prefer). Per consequence,
$$f_{AA} + f_{AB} + f_{BA} + f_{BB} = f_{hom} + f_{het} = 1 $$
is our first important result.
Problem 1

There is 20% of heterozygote in the population, what fraction of the population is homozygote?

Answer: (hover to see the answer)

 $f_{hom}=0.8$ (or $f_{hom}=$80%)

Problem 2

There are 10% of AA individuals and 15% of BB individuals in the population, what fraction of individuals are heterozygotes

Answer:

 $f_{het} = 0.75$ (or $f_{het} =$ 75% )

All allele frequencies must sum to one
The same is true for the allele frequency, they must sum to one. This is even easier than before. Using the above notation it means:
$$p + q = 1$$
You will note that an obvious consequence of this result is that $1-p = q$ is also true. This is the second important result.
Problem 3

The frequency of alleles which are the A allele is 0.3. What is the frequency of the B allele?

Answer:

 $q = 0.7$

Hardy-Weinberg equilibrium
Let's now talk about HWr.
HWr assumptions
HWr makes a number of assumptions that I will not detail them here. Please have a look at the post Assumptions of Hardy-Weinberg rule for more information.
HWr exercice without explanations
Here are exercises that one may consider they come too early in my explanations. Don't worry too much if you can't solve them but please take the time to try solving them. Please do not try to apply known formulas about HWr, only use your logic and the above formulas (allele frequencies must sum to 1 and genotype frequencies must sum to 1)
Problem 4

In a population, one observes that 20% of the population is homozygote for the A allele and that there are no heterozygous individuals at all. What is the frequency of the A allele?

Answer:

 $f_{A} = 0.2$

Below is a drawing of the population (assuming N=20 individuals) to help understand the answer.
AA | AA | AA | AA | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB
Problem 5

In a population, one observes that all B alleles are present in heterozygote only. The frequency of heterozygotes is 0.1. What is the frequency of the A allele?

Answer:

 $f_{A} = 0.95$

The hard part here is to first calculate $f_{B} = 0.05$. Let's draw the population (assuming only N=20 individuals) and that will likely help you out.
AA | AB | AA | AA | AA | AA | AA | AA | AA | AA | AA | AB | AA | AA | AA | AA | AA | AA | AA | AA
HWr formula
As said above, HWr describes a relationship between allele frequency and genotype frequency
Without much explanations, here are these relationships
$$f_{AA} = p^2$$
$$f_{AB} = pq$$
$$f_{BA} = pq$$
$$f_{BB} = q^2$$
Therefore,
$$f_{hom} = p^2 + q^2$$
$$f_{het} = 2pq$$
To build your intuition, you should try to consider for yourself extreme cases where one allele is fixed (fixed=reached a frequency of one). For example, what are the expected genotype frequencies when

$p=1$ and $q=0$?
$p=q=0.5$?
$p=0$ and $q=1$?

How HWr is often expressed
Mixing up the idea of the above relationships and the fact that all genotype frequencies must sum up to one, one can also write
$$p^2 + 2pq + q^2 = 1$$
As by definition $q = 1-p$, it is also common to replace write
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$
Why do these relationships make sense?
Problem 6

Imagine you are drawing alleles in a population of alleles like you would draw cards from a deck of cards! You draw a single allele. If the frequency of A allele is $p$, what is the probability of drawing an A allele?

Answer:

 $p$

Similarly, the probability of picking a B allele is $q=1-p$.
Problem 7

Ok, now. Assuming that the fact that you already drew an allele does not change the allele frequency in the population (because the population is very large), what is the probability of drawing two A alleles in a row?

Answer:

 It is $p$ for the first draw and $p$ for the second draw. The overall probability is therefore $p \cdot p = p^2$

Here we go! You just solved why $f_{AA} = p^2$. You can apply the exact same logic to find out $f_{BB} = q^2$.
Now the probability to first draw a A allele and then a B allele is $pq$. Therefore, $f_{AB} = pq$. The probability to first draw a B allele and then a A allele is $qp=pq$ as well. Therefore, $f_{BA} = pq$.
Exercise
Problem 8

In a population with two alleles for a certain locus, A and B, the allele frequency of A is 0.7. What is the frequency of heterozygotes if the population is in Hardy-Weinberg equilibrium?

(You will note I renamed the alleles to match my above notation)
Try to solve this problem yourself now!
Answer:

 It is a given that $p=0.7$. The question is what does $f_{het}$ equals to?
 Let's start by calculating $q$. $q=1-p=0.3$.
Then, let's calculate the the genotype frequencies.
$f_{AA} = p^2 = 0.49$.
$f_{BB} = q^2 = 0.09$.
$f_{het} = 2pq = 0.42$.
Here we go! We've got the answer. Let's make sure the answer makes sense by summing up the genotype frequencies to ensure we get 1.
$f_{hom} = f_{AA} + f_{BB} = 0.58$
$f_{hom} + f_{het} = 0.42 + 0.58 = 1$
All good!

Problem 9

At a bi-allelic locus, the allele A is dominant over the allele a. The phenotype associated with the dominant allele is present in 10% of the individuals of the population. What is the frequency of the allele A?

Answer:

 The genotypes coding for the phenotype associated with the dominant alleles are AA and Aa. Therefore, $f_{AA} + f_{Aa} = 0.1$ and therefore, $f_{aa} = 0.9$.
 The frequency of the allele a is $p = \sqrt{f_{aa}} = \sqrt{0.9} ≈ 0.95$.
 To conclude the frequency of the allele A is $q = 1 - p = 1 - \sqrt{0.9} ≈ 0.05$

Problem 10
You will find a HW problem involving selection at this post.
Problem 11
You will find a HW problem involving a population of triploids individuals at this post.
Problem 12
You will find a HW problem for sex-linked loci at this post

In short...
Here is a summary for a bi-allelic locus
Allele freqs sum up to one
$$p + q = 1$$

Genotype freqs sum up to one
$$f_{AA} + f_{AB} + f_{BA} + f_{BB} = f_{hom} + f_{het} = 1 $$
You will note that most often when people write $f_{AB}$, they just mean $f_{het}$ and therefore don't make the distinction between $f_{AB}$ and $f_{BA}$.

Hardy-Weinberg rule
Note that Hardy-Weinberg rule holds only under a number of assumptions (such as random mating, panmictic population, no selection, ...) that I have not detailed here (see Assumptions of Hardy-Weinberg rule for more information).
$$f_{AA} = p^2$$
$$f_{AB} = pq$$
$$f_{BA} = pq$$
$$f_{BB} = q^2$$
Therefore,
$$f_{hom} = p^2 + q^2$$
$$f_{het} = 2pq$$

Putting all together
The whole thing put together is often expressed as
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$


Can toilet or sewage aerosol transfer eggs of human parasites?

Common small protozoa that are present in infective loads in stool have not been documented in toilet aerosols. The size of the organism is going to be an issue here. As you can see from this table from the CDC, intestinal parasites (and ova) of concern to human health are larger than most droplets. Compare, E. coli and Shigella (0.5 - ~2 $\mu m$). Salmonella tends to be a litter larger (up to 5$\mu m$), but I expect those 5 $\mu m$ specimens are not the ones transmitted through aerosols. Cryptosporidium would probably be the most likely candidate, and that's one shown in the first linked study to not be present in aerosols. I wouldn't say it's impossible, but certainly transmission through aerosolized particles is less likely than for the smaller viral and bacterial organisms.


Is Sugar a stimulatant or a weak sedative?

The idea that 'dyes and preservatives' cause hyperactivity dates back to this '76 paper by one Dr. Feingold. Despite being disproved neatly in 1978, it's still around.

As far as sugar goes, I recommend this review paper covers both the arguments for and against sugar causing hyperactivity, as well as 12 double-blind placebo controlled studies showing sugar has no effect on children's actual behavior.


The bubbly structures on the dorsal sides of the digits are scutes. Birds retained them from their dinosaurian ancestors. Here is a picture of similar structures on an alligator foot:


It's probably the yellow bacterial mats, which are rich in life. The mats are a stratified ecology which varies with distance from the surface, so they are rich in many species of algea, procarote and eukariote. In Yellowstone,  the bacterial mats can range in color including brown, green, yellow and orange. They are different to precipitated minerals.

You can say "The photographer contains archaea"! So, no need to search very far.

Here is a pic of an bacterial mat habitat: https://www.sciencedirect.com/science/article/pii/S0717345817300738

You can see in some videos. Ideally we would have a a biology video demonstrating the stuff at Yellowstone to show if it's squishy, slimy, spongey, has growth rings, colord layers, cross sections... although it's only tourist videos for the moment.


harvesting fertilized eggs from Tetraodontidae species?

For DNA extraction, you would need only a few eggs. PCR would then give you all the copies of your target gene(s). A quick Google Scholar search on Takifugu fecundity revealed a paper by Yang and Chen (2008). They found that T. obscurus produced an average of 320.8 oocytes mg$^{-1}$ ovary wet weight. In comparison, T. ocellatus produced 125.2 oocytes mg$^{-1}$ ovary wet weight. Takifugu rupripes and other species are likely in a similar range, which is plenty of tissue for DNA. Kusakabe (1962) published on the fecundity of T. rubripes but the paper is in Japanese and is not readily available to me.

Beware: T. rubripes ovaries are highly toxic. Why not use other tissue instead?


Is a naive immune system equally able to handle new antigens as an educated one?

They will both go through a primary and secondary immune response. So first low affinity antibodies will bind, the corresponding b cells will undergo affinity maturation, somatic hypermutation until high affinity (perfectly fitting) antibodies are available and these antibodies will finally undergo class switching.

Depending on the antigen an innate immune response will also be triggered as part of the first line of defense. There is no difference in the immune response between these two hypothetical brothers.


Why do beta-1 and beta-2 adrenergic receptors result in two completely different effects (though both use Gs pathway)?

The autonomic nervous system is composed of the parasympathetic and sympathetic nervous systems. The sympathetic nervous system is stimulated via adrenergic receptors.
Adrenergic receptors are G protein-coupled receptors stimulated by norepinephrine (noradrenaline) and epinephrine (adrenaline).
There are 4 sub-types of adrenergic receptors:

Beta1-adrenergic receptors
Beta2-adrenergic receptors
Beta3-adrenergic receptors
Beta4-adrenergic receptors

Yes, Beta2-adrenergic agonists reduce bronchial Smooth muscle contraction.
Yes, Beta1-adrenergic agonists increase heart rate.
Here we can see activation of different tissues from different receptors, that activate the same pathway. Thus, despite the example explained - the activation of the same path-way - different responses ensue.

In the human airway - Smooth muscle cells express Beta2-adrenergic receptors the most (100%).

In human heart tissue (Cardiomyocytes/Cardiac muscle cells), of Beta-adrenergic receptors - Beta1-adrenergic receptors are expressed the most (75–80%).

"...the cAMP pathway generally promotes contraction in cardiac muscle; however, in Smooth muscle, activation of cAMP causes relaxation."

Source
cAMP inhibits myosin light chain kinase, the enzyme that is responsible for phosphorylating Smooth muscle myosin and causing contraction. Thus no contraction takes place in smooth muscles cells.
Inhibition of myosin light chain kinase increases intracellular cAMP, which further inhibits myosin light chain kinase thereby producing a lower contractile force (E.g. promoting relaxation).
Source


Is it possible to genetically alter human beings to see parts of the infrared?

Our heads are warm, so the receptors that react to infrared radiation would be set off constantly by ambient radiation, not just radiation that comes in through the eye.  Note that the animals that do see infrared are cold blooded.

So it would be a massive genetic engineering project to get working infrared vision, to either make human heads be room temperature, or to thermally insulate eyeballs from the surrounding tissue.


Why is glycine considered a nonpolar amino acid but a polar molecule?

The first part of your question illustrates a common confusion of beginners between the physiochemical properties of free amino acids in solution, and the properties of that part of an amino acid that remains after it has participated in a condensation reaction to form part of a polypeptide. They are different. (It was for that reason that I modified the question to make it clear that the ‘consideration’ of glycine as nonpolar applies to it in its protein context.)

I have prepared a diagram to clarify.

As can be seen on line 1, all free amino acids at physiological pH are charged because of the pKa of the  α-amino and α-carboxyl groups (proline, as an imino acid is the exception). The chemical features common to all amino acids are shown in blue, for the second amino acid, and the unique feature — wherein amino acids differ — is shown in red.
To show amino acid 2 in the context of a polypeptide chain, I have condensed it with two other amino acids (1 and 3) to produce a tripeptide (line 3). (This is the situation most amino acids in a long polypeptide chain will be in, as there are only two that will be at the ends.)
You can see from the colouring that what is left of the amino acid in the protein — the amino acid residue — has lost the charges of the α-amino and α-carboxyl groups, which have become parts of peptide bonds. (A molecule of water is removed in a condensation.)
The properties that a particular amino acid endows to a protein are those of the ‘R-group’— R2 in the diagram. In the case of glycine, R is H, so that in the context of proteins we regard glycine as a non-polar amino acid (The C-H bond has a negligible dipole.)
Don’t confuse R with residue. It is a side-chain, designated using a common chemical abbreviation.

The second question was “is the backbone of the macromolecule nonpolar?”.

No. The backbone of a protein has partial charges on the oxygen and nitrogen atoms of the peptide bond, as shown below. This is because it has a partial double-bonded character. These partially charged atoms can (and frequently do) form hydgrogen bonds, either with another part of the backbone (secondary structure such as α-helix or β-sheet) or with polar side-chains.

Reading

Berg et al. Section 3.2 covers the basics (although it fails to emphasize the difference in properties of amino acids and amino acid residues) and Section 3.3 covers the role of the peptide bond in protein secondary structure.


Why is Chromosome 1 called Chromosome 1?

Chromosomes were first known about from karyograms (that's the word for chromosome pictures like these) sort of like this one (1)(2):

The scientists looking at these chromosomes didn't know much about them at first. They were discovered before anything was understood about genes, but by 1922 it was thought they were the carriers of genes. Without much understanding of the chromosomes, and certainly no understanding of what they carried, scientists needed an easy way to order and compare them. They chose a straight forward option - size - and paired them up and then lined them up biggest to smallest. Because the sex chromosomes didn't fit into this scheme of matching pairs they were left to the end.

Hence Chromosome 1 is Chromosome 1 because it is the largest autosomal chromosome.

Notes:

The actual first karyogram was of a plant, this one is of a human male.
The image above is public domain, obtained from Wikipedia, and originally made by the National Human Genome Research Institute.


There are a lot of marine documentaries out there. These are some that I know of:

Shark (2 episode series in 2015);
Deep Ocean;
Life in the Blue;
Ocean of Giants (Nat Geo);
Ocean Giants (BBC);
Humpback Whales;
Ocean Voyagers (whales);
The Polar Sea;
Swimming with Killer Whales;
Ocean Wonders (no narration, just under sea footage of animal behaviour);
Martin Clunes: Man to Manta;
Nature's Great Events: Diaries (a couple episodes of marine ecology);
Dolphins: Spy in the Pod (a view on dolphin activity using dolphin-shaped cameras);

I watched these off YouTube:
Alien Reefs;
The Giants of Rurutu (whales);
Mucky Secrets: The Marine Creatures of the Lembeh Straight;
Reef Life of the Andaman;
Secrets of the Australian Ocean;
Oceans of Contrast (spends a lot of time on life on land revolving around the ocean, but there's reef life as well);
The Incredible Glowing Creatures of the Deep Sea: Documentary on Bioluminescent Sea Life;
Documentary on Coral: African Wonderful Coral Reef

Conservation type documentaries:
Sharkwater;
Mission Blue;
Chasing Coral;
Blackfish;
Sonic Sea;
A Plastic Ocean;
Shark Men (If you like reality style television series. They capture, tag and learn about sharks to protect them)

If you want a more in-depth resource for learning, you can also YouTube search "marine biology lectures"


What are the statistical tools for distinguishing molecular analogy from homology?

There are lots of statistical algorithms that allow you to evaluate the similarity between two given sequences. For instance, blast allows you a rapid comparison between your sequence and other sequences in a database; while Clustal, with a similar functioning, allows you to compare a set of given sequences between them. They are very simple algorithms, but very fast and useful, and basically they score an alignment by counting how many positions between the two entries are the same. Other algorithms function in a similar fashion, but they use hidden Markov models to compare your sequence with a consensual sequence in order to identify motifs and domains. I'm sure there are even more advanced programs, but I don't know them and don't think it's the point.

Homology usually refers to things that share the same origin, while analogy refers to things that do the same function but their origin isn't shared. While the algorithms I've described you only search for similarity or identity, you must notice a few things:

a) Homology of function doesn't necessarily correlate with high similarity. Two proteins can have the same global structure and their sequences be completely different. The three-dimensional structure is the same, and probably there'll be key amino acids that will remain very similar. This is very obvious in many proteases, which share only the three catalytic amino acids (catalytic triad) between them, and vary enormously even between strains of the same species.

b) Protein domains vary in size from a few dozen to a few hundred amino acids. The odds that exactly the same sequence evolves in two separate moments are very low. Especially in highly conserved domains, which usually carry out key functions.

c) Proteins usually have a modular structure with more than one domain. New proteins often evolve by switching and combining domains by translocation. So, even if the same domain has evolved in two separate times, the association between these two "twin" domains with other domains will probably reveal its unusual origin.

That's why usually the term molecular analogy is not used, and if so, it would refer for example to structurally different domains that catalyze the same reaction or that share the same structure. Note that even if the analogy as you describe isn't impossible by itself, the software won't be able to differentiate them unless the sequence appears associated with others. Furthermore, the origin of many of the current protein families is so far in the past that it's quite impossible to reconstruct it, even more so with the high diversity in prokaryotes.


The Most Recent Common Ancestor (MRCA) of birds and mammals was the first amniotes.

Fossil record

The latest known fossil of amniotes are 312 million years old (Bentou and Donoghue, 2007).

Genetic data

From EOL, using data from The Paleobiology Database, the first amniote is in between 314.6 and 323.2 million years old. Those results are a little bit older than the latest known fossil which very much makes sense.

The (apparent) contradiction in the sources you found

  This site seems to imply it was at least 250 milions of years ago.

They actually say 250 to 320 millions years. This broad estimates match the above studies and data.

  This scientific article mentions 600 milion years but the sentence is a little unclear.

It is actually a news feature published by a science writer (former neuroscientist according to her twitter account), not a researcher. She indeed made the claim (Even so, 600 million years of evolution and radically different brain architectures separate birds from humans.). There is no reference for the claim and based on above evidences, it appears at first to be a mistake. It is not impossible though that she considered the evolutionary time in both branches in her statement but that would be very unusual If two lineages diverged $t$ years ago, then they both evolved for $t$ years and it could arguably be said that they are separate by $2 t$ years of evolution. If this is what she meant, then the claim is correct but quite misleading.


How to confirm secondary structure formation of Precursor miRNA on gel?

Disclaimer: Although I have attempted northern blots for miRNA, I haven't actually done the kind of experiment you are talking about.

First of all you need controls.

A negative control: a same length RNA that will not fold (you can introduce some mutations in your pre-miRNA sequence to disrupt the base pairing). You can use the miRNA secondary structure prediction tools for rationally designing such controls.
A positive control: perhaps a folded pre-miRNA that is crosslinked. Frankly, I haven't come across anyone using such crosslinking agents to study RNA secondary structure. I had however, seen some old papers on this topic (Wagner and Garrett, 1978, Rabin and Crothers, 1979). You may also try some conditions (salt concentrations etc) under which the RNA will fold (studied using biophysical assays).

Now, you cannot run agarose gels. You would need long polyacrylamide gels ~15%. You also need to use the right buffers. 0.5-1x TBE supposedly works. You may want to run your sample in two conditions: denaturing (with 8M urea) or non-denaturing. You can refer to this protocol (Petrov et al. 2013).

Your positive control should migrate faster than the negative control. If your RNA is folded (fully or partially) it should migrate between the positive and negative controls in the non-denaturing gel. In the denaturing gel, your RNA should migrate at the same level as the negative control. Positive control (if it works) should not be affected by urea.

Also, the gel heats up during electrophoresis which in turn can dentature RNA. You may want to run the non-denaturing gel in the cold room.

Having said all this, I would advise that instead of putting in so much effort in gel based assay you can use more sensitive equipment to study RNA folding. There are many biophysical studies on in vitro RNA folding. You can check them out.


What constitutes the determination of a normal blood glucose level?

Determining what is considered to be "normal" is quite challenging indeed. Both the ADA and the WHO look at upgrading diagnosis limits and both have a conservative approach, primarily due to the difficulties in conducting large scale studies and the anomalies between assumptions of plasma glucose distribution and what is probably actually present in populations. Digging through, I found a very good WHO document here:

http://www.who.int/diabetes/publications/Definition%20and%20diagnosis%20of%20diabetes_new.pdf

I am not going to regurgitate from this document, but I believe Issue 2 provides a detailed answer to your question detailing several determination methodologies.

As to your second question on age/sex variations, are you asking if the criteria are different? At least with reference to FPG, they don't appear to be so.


In Japan, the official average body temperature is 36.0 °C. Why so different from that of Europe?

Factors that can lower body temperature:

low environment temperature
low metabolic rate
hypothyroidism

I couldn't find any relevant study addressing the Japanese people situation, but:

  There is significant variation in metabolic rate in humans, independent of differences in body size, body composition, age, and gender. Although it has been generally held that the normal human "set-point" body temperature is 37 degrees C, these interindividual variations in metabolic rate also suggest possible variations in body temperature [1].

And here's a factor that increases body temperature:

  The present experiment investigated the effects of skin pressure by foundation garments (girdle and brassiere) on the circadian rhythms of core temperature and salivary melatonin. [...] The results suggest that skin pressure by clothing could markedly suppress the nocturnal elevation of salivary melatonin, resulting in an increase of rectal temperature [2].

Whether there are differences between Japanese and other people in metabolic rate and /or clothing behavior remains unclear.

References:

Rising R, Keys A, Ravussin E, Bogardus C. Concomitant interindividual variation in body temperature and metabolic rate. Am. J. Physiol. 1992 Oct;263(4 Pt 1):E730-4. PubMed PMID: 1415692.
Lee YA, Hyun KJ, Tokura H. The effects of skin pressure by clothing on circadian rhythms of core temperature and salivary melatonin. Chronobiol. Int. 2000 Nov;17(6):783-93. PubMed PMID: 11128295.


For your first question

Both enzymes, are components of Epidermal growth factor receptor (EGFR) signalling pathway.

MMP is a matrix metalloproteinase, that triggers EGFR signalling, this can be done by a mechanism called transactivation

So, A signal from G-coupled receptor, or cytokine receptor could activate the cleavage of MMP,  then MMP converts to a ligand for EGFR activation

For example Angiotensin II type 1 receptor (AT1R) and type 2 receptor (AT2R) which are GPCR, there are evidence for crosstalk with EGFR, look for this paper. This could be linked with hypertension or inflamation. Also cancer, could trigger EGFR receptors by NMP's.

And finally tissue inhibitors of metalloproteinases (TIMPs) are the negative regulator of MMP's

This are only an overview of the whole biological process involving MMP, so I think there is no single answer to your question, but you can delimit the topic for a specific disease, and look for papers at google scholar.


What type of insect is this? Is it ant or something else?

Such a queer species. I thought it was an ant. But it is actually a spider.

These spiders belong to Salticidae family,commonly called ant-mimicking spiders / jumping spiders.

  They are  Batesian mimics of ants, such as Sphecotypus in the Clubionidae.

They do not feed on their model organisms and keep them at an acceptable distance.

This one is from Myrmarachne sp. There are more than 20 species found in India.

Source:

Wikipedia
Myrmarachne


Do mutations in one bacterial strain have the same effect in other strains within the same species?

Different strains of the same species have differents genotypes (ie different alleles and therefore express different proteins).So if your protein A in strain 1 has some effect, it could have the same effect in strain 2, but not necessarily.
Indeed lets imagine that protein A interact with protein B in strain 1 to produce an effect. If protein B is absent in strain 2, or different, protein A will have no effect. My point is if you have a mutation in one strain, the same mutation would not necessarily have the same effect (although it is very likely) in an another strain beacause both strain don't express the same proteome.


I'm trying to identify a tree i saw in Taormina, Sicily, Italy. Can anyone help?

It looks like the Silky oak, Grevillea robusta, which is btw not related to our indigenous oaks (quercus).
It's native only to eastern Australia, so planted in Sicily.
https://pommepal.wordpress.com/tag/silky-oak/


Does muscle growth trigger angiogenesis?

Muscle is heavier than fat so actually it does. Muscle growth directly increases angiogenesis. Particularly the mechanism relies on hypoxia, any tissue with less than adequate blood supply secretes factors which result in angiogenesis. This is seen frequently when muscle is bulking as this increases the oxygen requirement but is also seen in heart muscle where subsequent to a heart attack tissue which isn't dead but mildly suffering caused new blood vessels to grow to supply this tissue (as the other ones are blocked which was the cause of the heart attack in most cases).


A question on exclusion of study participants for an Exome genotyping array

When you design the arrays, you need to have probes on the surface complementary to the sequence you want to detect. Depending on what you want to detect, you need to design these probes with known sequence on a known position.
If you want to detect single nucleotide polymorphisms (SNP), then you need a library of known SNPs on your ChIP, which are basically the position of the SNP and the surrounding sequence.

SNPs can be roughly grouped into two subgroups, common (I call them like this) and rare (frequency in the population lower than 0.1%). The problem with this ChIP based method is that it can only detect SNPs which are already known (or at least are located close to known SNPs with which they in linkage disequilibrium). So if you want to detect rare SNPs in your population sample, you need a big group of people from which you take the SNPs into you ChIP design. If you look at the numbers, one rare variant will only be present in about 12 of the 12.000 persons used in the design.

Your study group is then different from the group of people, which where used to make the ChIP design. Here you take people with a certain background (high lipid levels for example) and then compare, if people which had coronary heart problems have SNPs in common which might be connected to this disease. This can help to identify a mutation in a protein which is the risk factor.


Looking for source: Biologic reactions of people saying "no"

Most of the claims that "saying no is good for one's health" are grounded in psychology. In other words, they are  not experimentally verifiable. Likewise, health here refers not only literally to physical health, but also to psychological health, which in itself is something hard to define.
Surely, in situations of high stress saying "no" can actually result in some measurable responses, in which case it can be studied within the context physiology and neuroscience. However, this would address only a small part of the situationd covered by the original claim - discarding any effects on psychological health as well as long-lasting effects on the physical health.
To summarize: for a scientific study the claim needs to be made more specific, i.e., apply to well-defined situations and responses.
Disclaimer
I feel that a clarification is needed, lest what I wrote above is interpreted as a negative view of psychology.
I am not claiming that all of the psychology is outside of the scientific method, but a big part of it is - at least outside of being possible to study in a laboratory setting. And this is by no means unimportant part, in terms of the role it plays in our society. While words not scientific often carry negative connotation, in practice any scientist should recognize that scientific method has its limitations - many phenomena (psychological, social, economic, etc.) are not sufficiently reproducible and controllable to study experimentally, yet too important to dismiss.


What is the ultimate source of ADP/ATP in humans?

Phosphorus is a very common nutrient, found in high levels in proteins, which are in such foods as milk and milk products, meat, beans, lentils, nuts, and grains, especially whole grains. Phosphorus is found in smaller amounts in vegetables and fruit, as well. Adenosine can be found in many of the same foods, both as free ATP/ADP/AMP, and as part of the DNA found in all animal and plant-based foods (are there any other kinds?).

Adenine (the nucleotide base before the addition of ribose creates adenosine) is synthesized via the purine synthesis pathway, whose ultimate product is IMP, or inosine monophosphate. IMP is then converted to adenylosuccinate, then to AMP, which is then phosphorylated to ATP. It should be noted that, as is the case in most biosynthetic pathways, this one requires ATP to power it along, meaning it takes ATP to make ATP.


What are the advantages of using interphase cells rather than metaphase cells for gene mapping purposes using FISH?

In metaphase, chromosomes are at their highest level of condensation. FISH relies on being able to dissociate the two strands of DNA to anneal a sequence-specific probe. So, my guess is that it is technically easier to achieve a good FISH staining in interphase, when chromosomes are much less densely condensed. There might be other reasons I am not aware of (I am not a geneticist).


What molecular processes are involved in pseudopodial extension?

The extracellular cue signal must be relayed to the cell by Rho family of GTPases, like in the case of filopodia and lammelipodia. This causes local actin polymerization leading to extension of pseudopodium.

For a casual reference you can check the wikipedia page on Rho family of GTPases. Cell biology books like MBOTC also have information on mechanism of cytoskeletal dynamics.


Why does it take so long for the human brain to develop from an evolutionary point of view?

We can say that brain and our nerve system is the first system in embryo that starts to develop and as you said this system is continuing to develop until after birth.
So here is a question that why our brain don't develop completely before the birth ?  Evolution has gone so far as to limit the development of the brain in the human embryonic phase and to allow it to continue into the postnatal phase. This helps the infant to be born and ease the birth both for mother and the new born because if the brain had fully grown, the size of the head would have made problem in birth. Now, after birth, the brain continues to grow and develop majorly between ages 2-3 and becomes more mature after that . The ability of the brain to grow over the years gives us the ability to adapt to different environments , learnings and new issues and other capabilities That happens with the subsequent creation and pruning of dendritic spines.


How can tree branches grow upwards against gravity?

This review paper might help answer your question: http://www.plantphysiol.org/content/120/2/343.full

It seems that starch-filled organelles called amyloplasts sediment in the cell according to the pull of gravity, and in doing so this gives the cell some form of basic up-down polarisation.  If my memory serves correctly, this can then cause changes to the growth of the cell in the branches, meaning the side of the cell opposite the amyloplasts grows slower and the side closest the amyloplasts grows faster, causing the upwards curvature of the branches seen in your tree.


Which is better against genetic mutations? Asexual or Sexual Reproduction?

Mutations can be caused by much more than just recombinatory events--polymerase fidelity, DNA damage repair, even environmental factors can have a huge impact on DNA damage. While most DNA polymerases have an error rate of around one mutation per billion, there are different levels of fidelity among different polymerases (McCulloch and Kunkel, 2008).

Regarding the fidelity of crossover/recombination events, it is true that these events increase the likelihood of a lethal or detrimental mutation. However, recombination is not a random process. Recombination hotspots are chromosomal locations where the rate of recombination can be hundreds of times higher than other locations. These hotspots are generally in "safe" locations, not in the middle of a crucial gene, etc. There are also recombinase enzymes specific to certain sites of recombination.

As to "which is better", I don't think the answer is as straightforward as you might think. You might think a sexually-reproducing eukaryote with a very high-fidelity DNA polymerase and safe, specific recombination hotspots would be ideal. That situation is generally what we find in nature, so you're (probably) correct. However, at the other extreme, think of a virus*. Viruses have a much, much, much higher rate of mutation than eukaryotes--orders of magnitude higher. This is how a virus survives, basically out-evolving the host's defenses. A high rate of mutation works for a virus, and a low rate of mutation works for a multicellular eukaryote.

*Of course, there is always debate about whether or not viruses are alive. However, they definitely reproduce.


From inflammation to sickness and depression: when the immune system subjugates the brain

Cytokines are essentially signalling molecules of the immune system. Broadly speaking these can be classed as pro- or anti-inflammatory. Pro-inflammatory cytokines promote inflammation, and anti-inflammatory cytokines inhibit inflammation.

Inflammation (again, broadly speaking) is associated with the 'innate' immune response - this is the immediate response by neutrophils and macrophages (among others), and these cells release a variety of molecules designed to damage cells around them. This is great if those cells are bacterial, or damaged host cells that need removing, but not so great if that is 'normally' functioning tissue.

Aging is associated with increased systemic inflammation - i.e. a greater proportion of pro- to anti-inflammatory cytokines. The causes of this aren't entirely certain, but it could be that the adaptive immune response (i.e. the memory T-/B- cells) is not as effective in older ages so the innate response is more important, or that it is just simply left 'unchecked'. Either way, the result this that the pro-inflammatory response can end up damaging host tissues, including the brain, without the corresponding repair instigated by anti-inflammatory cells/cytokines.

Any anti-inflammatory medication (e.g. aspirin, ibuprofen, or glucocorticoids) will, in theory, reduce inflammation, but by suppressing the immune system the risk of infection naturally rises, and there may be unforeseen consequences to prolonged use (the immune system does a lot more than just fend of bacteria - e.g. it is essential for tissue maintenance and regeneration), so I am by no means suggesting the use of anti-inflammatories to protect brain function!


A friend has informed me this is from the redstem Filaree, and there are some cool time-lapse videos on Youtube of their spinning behavior when they are exposed to water, which is thought to help them burrow into the soil.  (I'm just glad it didn't get a chance to burrow into the kitty!)


Why is Aorta sometimes called Compression chamber?

The aorta is a compression chamber because it is an important drive for diastolic perfusion. To keep the blood flowing constantly, and not only during systole (as would be the case with a rigid aorta), the high elasticity of the aortic walls allows it to dilate as a consequence of the high systolic pressure. This allows the aorta to accumulate blood in its proximal part, which is then propelled by the passive elastic contraction of the aorta during diastole.


Why do red blood cells contain haemoglobin and not myoglobin?

Just to expand slightly on the answer by Jack Aidley:

Have a look at this section from Stryer's Biochemistry text book, particularly Fig 10.17, where you can see that haemoglobin has evolved to have a high affinity for oxygen at the O2 concentrations present in the lungs, but a low affinity at the O2 concentrations present in the peripheral tissues. This is achieved by binding oxygen co-operatively. This means that haemoglobin can release 60-70% of its bound oxygen. Under the same conditions myoglobin, were it be used in red blood cells as an oxygen carrier, would release much less.

Incidentally the Figure linked to shows a comparison between haemoglobin and a hypothetical protein which shows 50% saturation at the same concentration of oxygen but which binds oxygen non-cooperatively (like myoglobin).

A more direct comparison of haemoglobin and myoglobin  - found here -  is shown below:

edit added to respond to shigeta's response

I don't understand some of the statements from shigeta so here are my views - if I am wrong, I would (genuinely) like to be corrected, since I have to teach this stuff.

  ..."what is particularly useful about Hb's cooperativity is that the last oxygen is harder to pull off the Hb tetramer than the first."

This statement contradicts my understanding of the oxygen-binding behaviour of haemoglobin. In the deoxygenated state the protein is in the conformation known as the T (for tense) state, and this is a low affinity state. The binding of an oxygen molecule to one of the haem groups in one of the globin subunits of the tetramer increases the affinity, so that subsequent binding of oxygen becomes easier. The details of how this happens are still debated, but I think what I have said so far is accepted by everyone.

Here is an equation to represent the binding of the first oxygen molecule to the haemoglobin tetramer:

O2 + [Hb]4 <--> [Hb4]O2

If deoxygenated Hb has a low affinity for oxygen then that equilibrium must lie to the left hand side - in other words the right to left reaction (release) is faster than the right to left reaction (binding). This is not consistent with the idea that haemoglobin hangs on to its last oxygen.

  "The heart, which is the first organ in the blood cycle after the lungs uses a lot of oxygen - if hemoglobin were not cooperative, it might take all the oxygen from hemoglobin just after the beat when it uses oxygen when in distress, creating a block of hemoglobin which is completely without bound oxygen."

This is based on an erroneous view of the circulation - it implies that all of the blood passes through the coronary artery before getting to the rest of the body. Oxygenated blood leaves the heart via the aorta. Although it is true that the first branch off the aorta is the coronary artery, most of the blood doesn't enter this branch, but proceeds into the remainder of the circulation. In this sense the coronary circulation (by which I mean coronary artery>coronary veins - the heart's own blood supply) is in parallel with the rest of the circulatory system, not in series with it. At rest, just 5% of the heart's output goes into the coronary circulation.

According to this review, Regulation of Coronary Blood Flow During Exercise, (I am simplifying a lot here, but this statement does appear in the review and is not taken out of context): "Increased myocardial oxygen demands during exercise are met principally by augmenting coronary blood flow." At rest the heart is already extracting most of the oxygen from its blood supply (see here for some interesting data) so again there is no question of the heart extracting much more - it simply needs more blood, and of course the increased heart rate will contribute to this. There is also scope for directing a greater proportion of heart output through the coronary circulation, but I have been unable to find any quantitative statements about that. Interestingly, if you take a look at the data in the 1st table of the data here you will see that, at rest, 22% of the heart's output goes into the renal circulation, but that much less oxygen is extracted from that blood (about one ninth of how much is extracted from the blood going through the cardiac circulation). This represents a source of potential increased blood to be diverted to the heart at the expense of a reduction in renal filtration.

  "Also - Hemoglobin is pretty clearly an evolutionary adaptation where four myoglobins came together to form a cooperative oxygen binder, so at one time probably myoglobin was the oxygen carrier. There are some primitive animals which have no distinct hemoglobin, just myoglobin like carriers."

I agree it is clear that haemoglobin and myoglobin evolved from a monomeric myoglobin-like ancestor, and that the appearance of a tetrameric molecule created the potential for co-operative oxygen binding. I am not as convinced by the rest of the sentence. I think we have to agree first on what we mean by an oxygen carrier. What I mean is a protein that is a component of a circulatory system. I know of no evidence that a myoglobin like molecule could perform this function. This arises directly from the shape of a simple binding curve (a rectangular hyperbola). For the protein to be saturable at atmospheric oxygen concentrations it has to have a certain Kd, and this precludes significant release of oxygen at physiologically useful concentrations. You either have a protein which can unload effectively but will not ever become saturated with oxygen, or you have a molecule that is able to become saturated but cannot ever unload except at every low oxygen concentrations. That is the remarkable thing about haemoglobin - the appearance of cooperative binding allowed for a more switch-like interconversion between a high affinity state, for loading up, and a low-affinity state, for unloading.

Now, if you wish to include intracellular oxygen transport in your definition of "carrier" then we enter a whole other debate about the role of myoglobin, but I have gone on for far too long already, so I'll stop there.


Computational approaches for making hypotheses about the effects of genetic engineering? Experiment planning methods?

I suspect that what you are asking for is years in the future yet. Bear in mind that the use of CRISPR-CAS9 is just entering clinical trials for a very few, well studied diseases. Almost all the work with CRISPR-CAS9 is still limited to model organisms and tissue cultures.

Are you referring to Adiposis Dolorosa?  Apparently the cause is not actually known yet. It's thought to be heritable, but it isn't known to be associated with a single gene or family of genes. The most common technique for analyzing what genes and gene mutations cause disease is Genome Wide Association Studies (GWAS), so you might use that as a staring point for your searches.

There are several computer programs that try to model what pathological effects a given mutation will have, but these are pure research at this point, and typically require extensive training for each gene or protein product. Try searching for "sequence based pathology prediction". However you may not find much related to Adiposis Dolorosa since the causative genes are apparently not known yet.


can we say that pumps are carriers that need ATP?

Yes, you can consider pumps are carriers used for active transportation (needing ATP).

A carrier is a specific type of transport proteins. They differ from channels or pores in the fact that during a certain instant, carriers only have one side of the protein open1. While pores are continuously open, and channels are either open or closed2.

Carriers can be involved in active transport3 or facilitated diffusion (passive)4. But as you mentioned, pumps always are used for active transport. Pumps, as Bryan pointed out in the comments, are just a name given to some transport proteins that use active transport, but not all active transport proteins are labeled as pumps.

I hope this clarified things for you.


What determines testosterone exposure in womb, baby's genetics or mom's body?

Fetal testis produces testosterone from cholesterol. There is a peak of production around 15 weeks of gestation (the "masculinization programming window"). So the genotype of the fetus can affect testosterone levels directly via effects on the biosynthesis of the hormone, or indirectly by defective regulation of the pathway's activity.

However, exposure to chemicals in the mother's environment is also thought to play a part in determining testosterone levels. The classic example of this is the phthalate esters used as plasticizers.

  Scott et al. (2009) Steroidogenesis in the Fetal Testis and Its Susceptibility to Disruption by Exogenous Compounds. Endocrine Reviews 30: preprint freely available here.


Can a cell survive temporarily without oxygen?

This is really interesting because the answer largely depends on the severity of the damage, the length of the damaging condition, the type of damage incurred, and the type of cell incurring the damage.

For a real life example, irreparable DNA damage as by irradiation or drugs tends to be lethal to a cell. The severity of the damage may affect how long a cell has to live, however. For example, PBMC we irradiated with X gy tend to stay alive for 10-15 days (they actually don't divide though, due to the damage). Why did we pick that number? Too low a dose the cells persist, and too high you obliterate them. For reference, my experiements require my PBMC to be alive for a few days but disappear from the culture over time, so X gy is just an optimized value. Gy (gray) is an SI value for dose of ionizing radiation.

What you call a temporary denial of oxygen is actually referred to as intermittent hypoxia, or in a prolonged case just hypoxia. Human cells regularly survive in hypoxia by altering their metabolic pathways when OxPhos can't be utilized anymore. These changes are assisted by oxygen-sensing molecules that change the transcriptional profile of the cell. HIF1a comes to mind, a hypoxia inducible factor, which is regularly induced by PI3K and MAPK (typical cellular signals). It's typically kept in check by other oxygen sensitive proteins like VHL, but in hypoxia the effects of HIF1a action are entirely beneficial. So when the cell returns to "normoxia" it can typically reprogram into OxPhos (caveats exist, tumors for example).

So to answer your question yes, the cells will survive (in nutrient deprivation, too, but with a different mechanism), but they have to make a lot of changes first.


How can some residues in the active site of enzymes be protonated with a pKa < 7?

Generally speaking, even though physiological pH is generally ~7.4, this is not necessarily the pH inside the enzyme active site. The enzyme's catalytic machinery may experience a completely different pH for one of two reasons: 1) because the enzyme is located in a place where the pH is simply not 7.4, and 2) The enzyme's amino acid composition shifts either the pH in the active site or the pKa of the active site residues relative to the surrounding environment such that the effective local pH in the catalytic site is lower or higher than 7.4.

For example, there are places in humans, such as the stomach or around muscle cells during anaerobic respiration where the pH is actually acidic relative to the standard physiological pH of 7.4, due to the presence of HCl or lactic acid respectively. Additionally, certain subcellular organelles, such as lysosomes, also are relatively acidic, since they are a site for breaking down proteins into amino acids.

However, the case presented in this paper seems to be an example of the second situation, where an enzyme that is in a pH neutral environment relies on one or more protonated amino acids to perform catalysis. This is relatively common. Basically, the enzyme's active site has an amino acid composition that when folded correctly, alters the local pH around the catalytic residues to favor catalysis. For example, in the enzyme acetylcholinesterase, the active site serine is rendered nucleophilic by being positioned next to a glutamate and a histidine, in an arrangement referred to as a catalytic triad. The glutamate is an acidic residue, and its close proximity to the histidine means that it will stabilize the protonated form of the histidine. Energetically, this makes protonation of the histidine very favorable. This causes the histidine to take a proton from the active site serine. Now that serine's oxygen is deprotonated, it can act as a strong nucleophile. After the serine forms a covalent interaction with the substrate, the histidine will facilitate a similar nucleophilic attack by a water molecule, regenerating the enzyme and completing the catalytic cycle.

Something similar is seen with the beta-lactamase TEM-1. In this case, TEM-1 uses a lysine (pKa ~11) instead of histidine (pKa ~6), so multiple acidic residues are in the active site to facilitate the deprotonation of the lysine during the catalytic cycle. In effect, the amino acid composition of the active site allows for the shuffling of protons needed for catalysis.

So to summarize, while physiological pH is widely regarded to be 7.4, an enzyme's catalytic machinery may experience a very different pH through either the cellular/physiological localization, or through the amino acid composition of the active site. In the latter case, the presence of acidic or basic residues can alter the protonation state of other acidic or basic residues, meaning the effective pKa of these residues or the effective pH around them is higher or lower than 7.4.


Difference between dysentery and bloody diarrhea

Diarrhoea
Diarrhea is loosely defined as passage of abnormally liquid or unformed stools at an increased frequency. For adults on a typical Western diet, stool weight >200 g/d can generally be considered diarrheal. Diarrhea may be further defined as  acute  if <2 weeks,  persistent  if 2–4 weeks, and  chronic  if >4 weeks in duration.
~Harrison's principles of internal medicine, 20$^{th}$ edition, page 261.

Dysentry
Dysentery is bloody diarrhoea, i.e. any diarrhoeal episode in which the loose or watery stools contain visible red blood. Dysentery is most often caused by Shigella species (bacillary dysentery) or Entamoeba histolytica (amoebic dysentery).
~WHO definition

One can also follow WHO definition of diarrhea for practical purposes but still I mentioned it from Harrison as it is more specific and quantified.
'Blood in stools' generally describe visible blood in stool, and the quantity of stool passed here can be normal like in upper GI bleeding if compared to diarrhoea or dysentry.
Diarrhoea can be classified into four major categories: Secretory, Osmotic, Malabsorbtive, and Exudative, in which exudative diarrhoea show such features of bloody stool.(~ Robbins basic pathology 9$^{th}$ edition page 577).
In fact, it is also clearly mentioned in Harrison in the topic of diarrhoea that:-

Invasive bacteria and  Entamoeba histolytica  often cause bloody diarrhea (referred to as  dysentery).

Conclusively, bloody diarrhoea and dysentry are the same.


Vitamins located closely under the peel?

There are some vitamins in the peel of some fruits/vegetables. The color of many fruits and vegetables is the result of high carotene concentration in the peel. $\beta$-carotene is converted by the human body into retinal, which is a form of vitamin A [1].

Another example is vitamin C. Guava and citrus category fruits contain high amounts of ascorbic acid in their peel and orange's peel contains greater amounts of vitamin C than its juice [2].

There are also other compounds in fruits peel like B vitamins and minerals [2].

  This implies that they are more healthier when not pealed.

In most situations, yes. The peel can absorb insecticide sprays and can also contain high amounts of fibers which can cause indigestion [2]. The peel can contain allergens [3].

  And does it make sense to concentrate important substances there, where they might get lost when the peel is damaged?

Yes. For example carotene plays a role in photosynthesis [1]. Fibers improve mechanical properties of the peel, thus protecting the fruit.

References:

Wikipedia contributors, "Carotene," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Carotene&oldid=625015773 (accessed September 14, 2014).
Umesh Rudrappa, www.nutrition-and-you.com. Fruit peel nutrition facts
Wikipedia contributors, "Peel (fruit)," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Peel_(fruit)&oldid=624708837 (accessed September 14, 2014).


Calculating pairwise Fst from allele frequencies

The original Wright's formulation
$$Fst=\frac{var(p)}{\bar p}$$
, where $\bar p = \frac{1}{J} \sum_{j=1}^J p_{j}$ and $var(p) = \frac{1}{J}\sum_{j=0}^J (p-\bar p)^2$ is the variance in frequencies among populations.
This original formulation is valid only for a bi-allelic locus. Nei (1973) generalizes this definition to loci that have more than two alleles.
Nei (1973) general formulation
I recommend to have a look a the paper (Nei 1973), it is a really nice paper.
Nei shows that defining that within Subpopulation gene diversity (a.k.a. expected heterozygosity) $H_S$ and the Total gene diversity (a.k.a. expected heterozygosity) $H_T$ as
$$H_S = \frac{1}{J}\sum_{j=1}^J \frac{1}{I}\sum_{i=1}^I p_{ij}^2$$
$$H_T = \frac{1}{I}\sum_{i=1}^I \left(\frac{1}{J} \sum_{j=1}^J p_{ij}\right)^2$$
, where $I$ is the number of alleles and $J$ is the number of populations. Then Wright's definition of $F_{ST}$
$$F_{ST} = \frac{var(p)}{p(1-p)}$$
generalizes (for cases with more than one allele) into
$$Fst = \frac{H_T-H_S}{H_T}$$
Have a look at Nei 1973 to understand why they are equivalent.
Weir and Cockerham (1984) formulation for several loci
Averaging $Fst$ over several loci is more complicated than one would expect at first place. The solution is given in Weir and Cockerham 1984.
The formulation is a little cumbersome so I just invite you to have a look at the paper.


What magnification do I need to see blood cells?

Just my 2-cents worth as visual add-on to @MattDMo 's answer:

Blood smear showing red blood cells and two white blood cells at 400x. Source: Microscope Master

Human red blood cells 1000x. Source: Wikipedia

Human white blood cells 2000x. The small dots (red arrow) are Diplococcus gonorrhea bacteria (Neisseria gonorrhoeae), each ~0.5 micrometers in diameter. Some of the neutrophils have phagocytosed bacteria. Source: Waynes World

Red blood cells visualized by scanning electron miscroscopy. Source: Pinterest.
Note: for illustrative and comparative purposes only; electron microscopy is not the most advisable method for home use.


How to estimate mRNA counts from Relative Promoter Units (RPU) or RNAP per second (PoPS) in E. coli?

I could not find any paper that discusses these issues. So this answer is just based on my guess.

From the this page:

  Transcription rate is generally a parameter associated with a
  particular transcript and has units of transcripts per unit time. In
  contrast, PoPS is essentially transcription rate at a particular
  location on the DNA. The value of PoPS just downstream of a coding
  region should be equal to the coding region's transcription rate.
  However, there are certain positions at which a transcription rate
  doesn't necessarily make sense yet PoPS does. For instance, as
  biological engineers, we care about the rate at which RNA polymerase
  moves through a terminator (or the PoPS downstream of a terminator)
  but yet most people don't talk about the transcription rate of a
  terminator.

What we want is the transcription rate for every gene. You can estimate it using PoPS corresponding to that terminator.

Now, at steady state the mRNA concentration would be the rate of formation divided by the rate of degradation (removal): rf / rd.

Since the study that you are referring to, calculates PoPs, I would guess that it is based on some standard BioBricks parts. You are likely to have have mRNA degradation rates associated with these transcripts (even protein formation and degradation rates, possibly). If you don't have the mRNA degradation rate then at least for long lived mRNAs, you can assume the rate of removal to be same as the dilution rate (loge2 / doubling time). Substitute this in the equation for steady state and you should get mRNA concentration.

Steady state protein counts would be: mRNA counts × protein formation rate / protein removal rate.


Difference between Appendix and the Cecum?

In herbivores the Cecum is an area that stores plant matter and helps digest it via symbiotic bacteria. Carnivores have smaller Cecums because meat is easier to digest than plant matter. In humans the Cecum is also an anatomical landmark that delineates the change from small intestine (a digesting organ) to the large intestine (mostly a capacity/storage organ).

The Appendix is a small, previously thought "superfluous" fleshy worm-shaped organ at the junction between the small and large intestines. Recent research posits that the appendix is sort of a harbor for a person's gut flora that can re-populate the intestines should the existing bacteria die or get removed (diarrhea being the most common cause). It can also become infected, inflamed, and require surgery to remove (Appendicitis).


Short answer
Butterflies can see behind them.

Background
Merry et al. (2006) have estimated the field of view of the butterfly, by investigating the Orange Sulphur butterfly (Colias eurytheme):

Colias eurytheme. Source: Massachusetts Butterfly Club

The authors found that this butterfly has a very large visual field, encompassing
93% of the spherical space around the animal. There was a small blind spot behind the head not seen by either eye. Another study by the same group showed similar results in another species of butterfly, the Empress Leilia (Asterocampa leilia). Here is a picture of the estimated binocular field of view of the Orange Sulphur, revealing that the animals' vision is virtually spherical, with only a small blind spot at the back (the white area):

Source: Merry et al., 2006. Grey is the field of view, white the blind spot posteriorly. Cardinal directions are indicated (Dorsal, Ventral, Posterior, Left and Right).

Here are a few pictures of other species of butterfly that show the protruding compound eyes covering a large field of view:

Sources: Alex Sukonkin and PhotographersDirect

The feature of large visual fields in insects is, however, not restricted to butterflies (Lutowski & Warrant, 2002). Another insect I often try sneak upon to take pictures are dragon flies, and more often than not they fly away regardless of the angle I approach them. They too have these large compound eyes with a field of view extending to the back:

Source: Nature North

References
- Lutowski & Warrant, J Comp Physiol 2002;188:1-12
- Merry et al., J Insect Physiol 2006;52:240–8


Does inhaling glue (glue sniffing) reduce appetite?

Short answer
Various inhalants, most notably organic solvents including those used in paint and glue suppress appetite.

Background
From the Division of Alcohol and Drug Abuse I learned the following:

  Initial effects [of various inhalants] include nausea [...], and a loss of appetite.

And the Humanitarian Irin News reports the following on Nepali street youths:

  The adhesive glue contains toluene, [an] intoxicating hydrocarbon [...]. The solvent [...] causes hallucinations as well as dampening hunger pangs [...].

Indeed, acute exposure to organic solvents has been associated with a loss of appetite (Gregerson, 1998), and chronic exposure to toluene in the industrial workforce has also been linked to appetite suppression (Kishi et al., 1993).

References
- Gregerson, Am J Industr Med (1998); 14(6): 681–701
- Kishi et al., Environmental Res (1993); 62(2): 303–13


Which one is true about sunflowers, "follow the sun across the sky" or "always face east"?

Both are correct.

The issue here is the developmental stage of the flower, that is, if it is a immature or a mature flower (actually, not a flower but an inflorescence instead).

Immature or young flowerheads do display heliotropism. However, as the flower matures, it stops showing heliotropism and becomes "fixed", always facing east.

This is a photo of the sunset. If the mature flowers (or inflorescences) still displayed heliotropism, they would be facing the sun (at the west). However, they face the opposite side (east):

Also, to be honest with the sources, the first link (Science ABC) you provided does make that clear. You can read next to the end:

  Mature sunflowers finally stop displaying heliotropism.

So, there is no contradictory information here.

A good source of information, with videos, can be found at this page of Berkeley University, which says:

  As the sunflower matures and the flower opens up, overall growth slows down and the plants stop moving during the day and settle down facing east. This seems to be because, as overall growth slows down, the circadian clock ensures that the plant reacts more strongly to light early in the morning that in the afternoon or evening, so it gradually stops moving westwards during the day.

Source: https://nature.berkeley.edu/news/2016/08/sunflowers-move-clock


Why is the null hypothesis of trait evolution Brownian motion?

I think that the simple answer to this question is that the present comparative methodology was largely established by Felsenstein 1985, American Naturalist. For mathematical convenience, he suggested Brownian motion as a null hypothesis, because "...the variance of the distribution of change of a branch is proportional to the length of time of the branch...", and then "...it is easy to see that the differences between pairs of tips... must be independent." Also: "...after one unit of time, the contrast [between a pair of tips] has expectation 0 and [easily defined] variance..."
He explicitly discusses whether Brownian motion is a reasonable model in the section "What if we lack an acceptable statistical model of character change?"
I would suggest reading that paper in more detail if you are interested in the details of Brownian motion applied to phylogenies.
A recent historical perspective on this influential paper can be found here.
For a more extensive bibliography/more details you can see here.


Perhaps not though the tree of life website, but the Open Tree of Life exists to fulfil this need. You can export newicks of nodes which you are interested in.


Is this silverfish? My apartment very dry

Remi is right that it's a silverfish, and here's some macrophotography of Lepisma Saccharina.


No.

Very early in the development of an organism, it is just a clump of cells.  Then those cells communicate, and determine where they are in the clump, which determines their eventual fate in the full organism.  In mammals, for instance, cells split into three different layers, and the skin and nerve cells develop from cells in the outermost layer...etc.

You can't just dump a bunch of stem cells somewhere and expect them to know where they are and what they should be developing into.


The species name of this insect is the gooseberry saw fly. There are three related species, I think this is the pale spotted gooseberry sawfly because it has a pale green head. They usually have black dots as well, but this might develop when the larvae grow. At least, this is what I observed once in my garden.


If your primers are not specific enough, you should design other primers. Try shifting a few bases upstream or downstream. Also, you can add a few extra bases to your primer, you can safely reach 68C as annealing temperature.

If you want your PCR to be able to distinguish a single base mismatch, then the mismatch should occur at the 3' of your primers, ideally one of the three last bases.

If your goal is just to quantify the initial DNA, then RT-PCR will be ok. But if you want to detect the composition of the different polymorphisms, then you should go for sequencing.


How many atoms has the smallest known bacterium?

Let's take the example of the model bacterium E. coli, for which one can find the numbers for a wet cell of a dry mass of 0.28pg. If you have a feeling for how much smaller the smallest known bacterium is compared to E. coli, you can ballpark things.

The number of carbon atoms in a single E. coli cell is approx. 7x10^9 carbon atoms.
The ratio of elements in E. coli is C : H(1.77) : O(0.49) : N(0.24) .

More simply, if you multiply the ratios by 4, you get the ratios of approximately 4 carbons, 7 hydrogen, and 2 oxygen atoms for each nitrogen atom.

Taken together, there are approximately the following number of atoms in an E. coli cell:

C: 7 x 10^9

H: 1.23 x 10^10

O: 3.5 x 10^9

N: 1.75 x 10^9

That is around 2.4 x 10^10 individual atoms. As you may have noticed, these numbers do not have any bearing on the complexity of the system whatsoever. They also do not provide any insight into the intrinsic biological plasticity and dynamics of the system.


Why does V. cholerae produce a human specific choleragen?

Vibrio cholerae originated in the Sundarbans, a very large wetland at the mouth of the Bay of Bengal. Although it can exist as free living, it is much more fecund when associated with tiny crustaceans called copepods. In 1760, the East India Company settled and sprawled, hewing the mangroves and planting rice. So, that was the first opportunity of note introducing V. cholerae to a major species of land animal, humans. The frequent contact with a sizable population of humans, plus time, allowed V. cholerae to evolve the traits to become a parasite.

For example, a hair-like filament evolved which allowed the cells to clump together forming colonies that could stick to the gut. At that point, perhaps with additional traits, V. cholerae became a zoonosis. That is, a disease we acquire from animals, copepods in this case, but not directly from other humans. Further evolution over time gave it the traits to spread directly between humans making it a true human pathogen.

So, humans were the species that became available and V. cholerae evolved to take advantage.

This is a minute fraction of the whole story as related in the 2016 book Pandemic by Sonia Shah. She is a science writer, the book is extremely well referenced. Since this is your second question on this, I suspect you may well be interested in the book.


Creep is correct. I sent an email asking this question to The Tortoise Group, which is a non-profit organization whose mission statement is:

Improving the lives of wild and desert tortoises through education.

The Executive Director replied:

It's a bale for turtles and a creep for tortoises. I am sure they could have come up with a better name!

If you have additional questions, there's a wealth of scientific information on their website.


How does hemoglobin-free blood transport oxygen?

Snails, like most molluscs, have a protein called hemocyanin dissolved directly in the hemolymph ("blood"). Hemocyanins are copper-containing metalloproteins: the binding site for a single O2 molecule contains two copper atoms. Unlike hemoglobin, where reversible oxygen binding is accomplished without a change in the oxidation state of the Fe(II) atoms in the heme prosthetic groups, in hemocyanin the copper undergoes a transition from colourless Cu(I) in the deoxygenated state to blue Cu(II) when oxygenated.

Incidentally, there are certain species of fish that manage with little or no hemoglobin - icefish.


What is the chemical composition / empirical formula of Herpes Simplex 1?

The Herpes viruses have a unique four-layered structure: a core containing the large, double-stranded DNA genome is enclosed by an icosapentahedral capsid which is composed of capsomers. The capsid is surrounded by an amorphous protein coat called the tegument. It is encased in a glycoprotein-bearing lipid bilayer envelope 1.

You can watch an animation of infection and steps of replication here, and below the video, they say that

  HSV is a nuclear replicating, icosahedral, enveloped DNA virus. The HSV envelope contains at least 8 glycoproteins. The matrix or tegument which contacts both the envelope and the capsid contains at least 15-20 proteins[2].

In this definition of the structure, they at least assigned some values to the makeup. Additionally, in wikipedia, the viral genome is listed which I would recommend you take a look at as well. It can be found here but here is the synopsis of the table

UL1 through UL56
US1 through US12
RS1, ICP0, LRP1, LRP2
RL1, LAT

Additional resources:

HSV Genome 2nd link
The use of microarrays to analyze gene expression
Structural properties of HSV promoters
Animation of the Construction of a HSV-1 DNA Microarray for Global Analysis of Transcript Abundance
Animation of the Time-dependant Changes in HSV-1 Transcript Abundance During Productive Infection
Some Genetic Functions Encoded by Herpes Simplex Virus type 1
Herpes Simplex Virus Oligonucleotide Probes used in the DNA-microarray


To expand on Remi.b's answer, groups are defined based on all the species we know about. This includes extinct species. So in your example, the group {B,C} is paraphyletic regardless of whether A goes extinct or not.

But what if A went extinct ages ago and we don't know about it at all? In that case we would only have B and C to base a group on, and they are the only descendants of their common ancestor that we know about, so we would indeed define {B,C} as monophyletic.

The question comes when we discover A's existence, and that it is more closely related to B than to C. At that point we have a choice: expand the definition of group {B,C} to include A, in which case the group becomes {{A,B},C} and is monophyletic, or keep the group {B,C} and accept that we were wrong about it being monophyletic, it was really paraphyletic all along.

You can see these processes happen as paleontology and cladistics advance. Birds used to be classified differently from dinosaurs, but as our knowledge of how birds are descended from dinosaurs increased paleontologists chose to classify them as a subset of dinosaurs, keeping the group "dinosaurs" monophyletic.

On the other hand as our understanding of how mammals/birds are descended from reptiles and tetrapods are descended from fish increased, making both of those groups paraphyletic, the attempts to redefine them as clades have largely failed, so they are now considered paraphyletic groups. "Amniotes" has replaced "reptiles" as the name of the clade containing reptiles, mammals and birds, and "Craniata" is the monophyletic group containing various fish and tetrapods.


With the help of Bristol Stool Chart (BSC) and full explanation of conditions related to different stool sizes from this link you could have a full understanding over stool size.

  » Type 1: Separate hard lumps, like nuts Typical for acute
  disbacteriosis. These stools lack a normal amorphous quality, because
  bacteria are missing and there is nothing to retain water. The lumps
  are hard and abrasive, the typical diameter ranges from 1 to 2 cm
  (0.4–0.8”), and they're painful to pass, because the lumps are hard
  and scratchy. There is a high likelihood of anorectal bleeding from
  mechanical laceration of the anal canal. Typical for post-antibiotic
  treatments and for people attempting fiber-free (low-carb) diets.
  Flatulence isn't likely, because fermentation of fiber isn't taking
  place.

  » Type 2: Sausage-like but lumpy Represents a combination of Type 1
  stools impacted into a single mass and lumped together by fiber
  components and some bacteria. Typical for organic constipation. The
  diameter is 3 to 4 cm (1.2–1.6”). This type is the most destructive by
  far because its size is near or exceeds the maximum opening of the
  anal canal‘s aperture (3.5 cm). It‘s bound to cause extreme straining
  during elimination, and most likely to cause anal canal laceration,
  hemorrhoidal prolapse, or diverticulosis. To attain this form, the
  stools must be in the colon for at least several weeks instead of the
  normal 72 hours. Anorectal pain, hemorrhoidal disease, anal fissures,
  withholding or delaying of defecation, and a history of chronic
  constipation are the most likely causes. Minor flatulence is probable.
  A person experiencing these stools is most likely to suffer from
  irritable bowel syndrome because of continuous pressure of large
  stools on the intestinal walls. The possibility of obstruction of the
  small intestine is high, because the large intestine is filled to
  capacity with stools. Adding supplemental fiber to expel these stools
  is dangerous, because the expanded fiber has no place to go, and may
  cause hernia, obstruction, or perforation of the small and large
  intestine alike.

  » Type 3: Like a sausage but with cracks in the surface This form has
  all of the characteristics of Type 2 stools, but the transit time is
  faster, between one and two weeks. Typical for latent constipation.
  The diameter is 2 to 3.5 cm (0.8–1.4”). Irritable bowel syndrome is
  likely. Flatulence is minor, because of disbacteriosis. The fact that
  it hasn't became as enlarged as Type 2 suggests that the defecations
  are regular. Straining is required. All of the adverse effects typical
  for Type 2 stools are likely for type 3, especially the rapid
  deterioration of hemorrhoidal disease.

  » Type 4: Like a sausage or snake, smooth and soft This form is normal
  for someone defecating once daily. The diameter is 1 to 2 cm
  (0.4–0.8”). The larger diameter suggests a longer transit time or a
  large amount of dietary fiber in the diet.

  » Type 5: Soft blobs with clear-cut edges I consider this form ideal.
  It is typical for a person who has stools twice or three times daily,
  after major meals. The diameter is 1 to 1.5 cm (0.4–0.6”).

  » Type 6: Fluffy pieces with ragged edges, a mushy stool This form is
  close to the margins of comfort in several respects. First, it may be
  difficult to control the urge, especially when you don‘t have
  immediate access to a bathroom. Second, it is a rather messy affair to
  manage with toilet paper alone, unless you have access to a flexible
  shower or bidet. Otherwise, I consider it borderline normal. These
  kind of stools may suggest a slightly hyperactive colon (fast
  motility), excess dietary potassium, or sudden dehydration or spike in
  blood pressure related to stress (both cause the rapid release of
  water and potassium from blood plasma into the intestinal cavity). It
  can also indicate a hypersensitive personality prone to stress, too
  many spices, drinking water with a high mineral content, or the use of
  osmotic (mineral salts) laxatives.

  » Type 7: Watery, no solid pieces This, of course, is diarrhea, a
  subject outside the scope of this chapter with just one important and
  notable exception—so-called paradoxical diarrhea. It‘s typical for
  people (especially young children and infirm or convalescing adults)
  affected by fecal impaction—a condition that follows or accompanies
  type 1 stools. During paradoxical diarrhea the liquid contents of the
  small intestine (up to 1.5–2 liters/quarts daily) have no place to go
  but down, because the large intestine is stuffed with impacted stools
  throughout its entire length. Some water gets absorbed, the rest
  accumulates in the rectum. The reason this type of diarrhea is called
  paradoxical is not because its nature isn‘t known or understood, but
  because being severely constipated and experiencing diarrhea all at
  once, is, indeed, a paradoxical situation. Unfortunately, it‘s all too
  common.

  Interestingly, the interpretations and explanations of the BSF scale
  that accompany the original chart differ from my analysis. To this I
  can only say: thanks for great pictures, but, no thanks for the
  rest...

  Excerpted from Fiber Menace, page 117-120; BSF Chart: wikipedia.org

But to make it more clear:

Reasons behind thicker and harder stool:

Lower fiber food
Lower liquid intake
Lower physical activity
Lack or lower amount of bacteria related to retaining water inside rectum and colon
Medication:

  Many medications have constipation as a side effect. Some include (but
  are not limited to) opioids also known as narcotics, diuretics,
  antidepressants, antihistamines, antispasmodics, anticonvulsants, and
  aluminum antacids. Certain calcium channel blockers such as nifedipine
  and verapamil can cause severe constipation due to dysfunction of
  motility in the rectosigmoid colon.

Metabolic and muscular

  Metabolic and endocrine problems which may lead to constipation
  include: hypercalcemia, hypothyroidism, diabetes mellitus, cystic
  fibrosis, and celiac disease. Constipation is also common in
  individuals with muscular and myotonic dystrophy.

Structural and functional abnormalities

Any physical digestive tract line problem which cause interference of stool movement. Like cancer or some kind of inflammation that could ban the canal

  Constipation has a number of structural (mechanical, morphological,
  anatomical) causes, including: spinal cord lesions, Parkinson, colon
  cancer, anal fissures, proctitis, and pelvic floor dysfunction.

  Constipation also has functional (neurological) causes, including anismus, descending perineum syndrome, and Hirschsprung's disease. In
  infants, Hirschsprung's disease is the most common medical disorder
  associated with constipation. Anismus occurs in a small minority of
  persons with chronic constipation or obstructed defecation.

Psychological

  Voluntary withholding of the stool is a common cause of
  constipation.The choice to withhold can be due to factors such as fear
  of pain, fear of public restrooms, or laziness. When a child holds in
  the stool a combination of encouragement, fluids, fiber, and laxatives
  may be useful to overcome the problem.

Edit:

In the second provided link you could get how cross-sectional diameter changes based on what you eat or how you behave with your body mentally or physically if you are a healthy person.

But as you are interested more on cross-sectional size of stool and reason behind it, consider the fact that colons and rectum are water absorber. The more stool stays there the more thick and dry it gets. So if you ate more fiber you will probably have softer stool and thinner caliber as the result of pressure of the rectum canal. Because some bacteria which are active in the fibers of stool are water absorbers too and the reason behind why doctors insist on eating more probiotic products is to keep these bacteria present and stable and also to get vitamins from their activities. So you could change your caliber only by eating more fiber more water and having more physical activities and also for consistent thick and dry stool (constipation) individual must share the problem with doctor because it could bring more dangerous problems in future or maybe it's a sign of some other serious disease that person's body is already dealing with. Most of the time it's nothing but our diet and hours we are sitting for variety of reasons or maybe focusing on another activitys (work, computer games, disabilities, watching tv and so on and so forth).

https://en.wikipedia.org/wiki/Constipation
https://www.gutsense.org/constipation/normal_stools.html


Is our genome decaying (see "Genetic Entropy"), and, if so, is this evidence for our genome being "young"?

If I understand the question correctly, you are asking why random mutations (most of the non-silent ones are deleterious) cannot create information and improve the overall fitness of the organism.

This is a common creationist statement, and has been shown to be incorrect in many different ways. The best way this can be shown to be false is by simply applying natural selection.

E. coli has a beneficial mutation rate of $10^{-5}$ per genome-generation (source) and a detrimental mutation rate of $2×10^{-4}$ per genome-generation (source).

Therefore, at first glance, the claim that the "genome is deteriorating" appears plausible. However, natural selection quickly acts on these mutants with deleterious mutations due to their low fitness. Therefore, the deleterious mutations are removed from the gene pool and are replaced with their beneficial counterparts instead.

If we define "information" as beneficial adaptations to the environment, random mutations themselves do not directly create the information. It is the application of natural selection that allows the fitness of the organism to increase despite the presence of random mutations.


According to wikipedia there are two different way to distinguish stage of the disease. One is from McCallan and one from the World health organisation (WHO). For the second one, on WHO website, you can find their grading card with eyes images. You can download it with also a little description.

Hope it helps.


These are plant pathogens commonly known as scale insect (Coccoidea). Among the genera mentioned to infect Dracaena marginata here and here the most likely candidate is Pinnaspis.

They are close relatives of aphids and psyllids (and more distantly -- also to true bugs). Cochineal is probably the most famous representative of the superfamily. Scale insects suck host's sap and can be quite dangerous to the plant. Adult females are immobile and the spreading is performed by nymphs and (when present) males.

As far as I know they are harmless to humans. When digested (products of) at least cochineal can cause allergic reaction in some persons.


How do you break up cell clumps when passaging?

I find that I only get clumps (with HeLa and similar cell types) if I leave them in Tryple too long. Generally I leave them in room-temp (not hot) Tryple for ~8 minutes, then I angle the dish, lid off, so that I can see the "sheen" of cells on the dish (this happens in the hood, of course). Then I blast the sheen with Tryple using a 1000ul pipetter, which de-adheres the cells. These are generally much less clumped than if I let the Tryple de-adhere the cells.


Do repeated freeze-thaw strip nutrition from vegetables/food?

Repeated freeze-thaw has virtually no effect on macronutrients, such as proteins, lipids, and sugars, because these are broken down to their basic building blocks (such as amino acids and simple sugars) upon food digestion anyway.

According to this paper freeze-thaw has no effect on micronutrients, such as vitamins, as well.

What affects nutritious quality is the length of time the food remains frozen. Most household freezers maintain a temperature of -20°C. At this temperature, the food doesn't get spoiled by bacteria, but degradation of vitamins still occurs, albeit at a slower rate. This is critical for some unstable vitamins, such as vitamin A and C. But elements such as iron, calcium, zinc, and phosphorus are not affected at all.

If you want to prevent vitamin degradation for a very long time, you need a freezer that maintains food at -80°C. This is only if you want to keep the food frozen for many months though.